The document provides an overview of cardiovascular conditions including ischemia, infarction, coronary artery disease, myocardial infarction, and cardiac arrhythmias. It discusses diagnostic testing and evaluation, management, treatment options, and medications for these conditions. Key points include diagnostic markers for infarction like cardiac enzymes, symptoms of angina and myocardial infarction, management of conditions through diet, medication, procedures like angioplasty and bypass surgery, and treatment of arrhythmias through medications, cardioversion, defibrillation, and pacing.
An 81-year-old woman with a history of hypertension, diabetes, heart disease and abdominal pain was admitted to the hospital for worsening abdominal pain. Her ECG showed signs of a previous heart attack. Cardiac enzyme levels were elevated, leading to a diagnosis of a non-ST elevation myocardial infarction (NSTEMI). Angiography revealed blockages in her coronary arteries, which were treated with stent placement. NSTEMIs are less severe than ST elevation MIs and are usually caused by partial blockages that damage part of the heart muscle.
This document discusses angina pectoris, myocardial infarction, and coronary artery disease. It defines angina pectoris as chest pain associated with temporary ischemia caused by inadequate oxygen supply to the myocardium due to narrowed coronary arteries. It describes the different types of angina and their characteristics. Medical interventions for angina include medications to relieve symptoms and procedures like cardiac catheterization and percutaneous transluminal angioplasty to open blocked vessels.
1) The document describes a case presentation of an 81-year-old male admitted with acute chest pain. Physical examination and investigations confirmed ST elevation myocardial infarction (STEMI) with hyperkalemia.
2) It then provides an overview of acute coronary syndrome (ACS) management, covering topics like pathophysiology, clinical presentation, diagnosis, and treatment of unstable angina/NSTEMI and STEMI.
3) Key diagnostic tests for ACS evaluation discussed include ECG, cardiac biomarkers, and stress testing. Management involves risk factor modification, antiplatelets, anticoagulants, and revascularization when appropriate.
This document provides information on acute coronary syndrome (ACS). ACS refers to a spectrum of clinical presentations ranging from ST-segment elevation myocardial infarction (STEMI) to non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina. It is usually caused by acute coronary atherothrombosis. Risk factors include smoking, high cholesterol, diabetes, and family history. The document discusses gender differences in ACS presentation and outlines treatments including anti-ischemic drugs, antiplatelet therapy, anticoagulants, and revascularization procedures. It also covers STEMI and NSTEMI diagnosis and management.
Cardiogenic shock is a low cardiac output state resulting from inadequate tissue perfusion despite adequate left ventricular filling pressures. It is usually caused by acute myocardial infarction which accounts for about 80% of cases. Clinically, it is defined by sustained hypotension with signs of hypoperfusion and a systolic blood pressure less than 90 mmHg for at least 30 minutes or the need for vasopressor/inotropic support. The mortality rate for cardiogenic shock remains high at over 80% despite advances in management. Early diagnosis and aggressive treatment including revascularization, inotropic support, and mechanical circulatory support are aimed at improving outcomes.
This document discusses guidelines and recommendations for measuring and managing hypertension. It defines hypertension as a systolic blood pressure of 140 mmHg or higher, or a diastolic blood pressure of 90 mmHg or higher based on the average of two or more readings. The goals of treatment are to reduce cardiovascular risk, end organ damage, and mortality. Treatment involves lifestyle modifications like weight loss, reduced sodium intake, exercise, and limiting alcohol as well as pharmacotherapy including diuretics, ACE inhibitors, ARB, beta blockers, calcium channel blockers, and other antihypertensive drugs.
This document provides an overview of the management of acute stroke. It defines stroke and transient ischemic attack, and discusses the epidemiology, classification, risk factors, pathophysiology, clinical presentation, diagnosis, management, complications and prognosis of stroke. The management involves resuscitation, reperfusion therapies like thrombolysis and thrombectomy, treating complications, secondary prevention including blood pressure and diabetes control, and rehabilitation. The document emphasizes the importance of specialized stroke units and timely management to improve outcomes for patients with acute stroke.
An 81-year-old woman with a history of hypertension, diabetes, heart disease and abdominal pain was admitted to the hospital for worsening abdominal pain. Her ECG showed signs of a previous heart attack. Cardiac enzyme levels were elevated, leading to a diagnosis of a non-ST elevation myocardial infarction (NSTEMI). Angiography revealed blockages in her coronary arteries, which were treated with stent placement. NSTEMIs are less severe than ST elevation MIs and are usually caused by partial blockages that damage part of the heart muscle.
This document discusses angina pectoris, myocardial infarction, and coronary artery disease. It defines angina pectoris as chest pain associated with temporary ischemia caused by inadequate oxygen supply to the myocardium due to narrowed coronary arteries. It describes the different types of angina and their characteristics. Medical interventions for angina include medications to relieve symptoms and procedures like cardiac catheterization and percutaneous transluminal angioplasty to open blocked vessels.
1) The document describes a case presentation of an 81-year-old male admitted with acute chest pain. Physical examination and investigations confirmed ST elevation myocardial infarction (STEMI) with hyperkalemia.
2) It then provides an overview of acute coronary syndrome (ACS) management, covering topics like pathophysiology, clinical presentation, diagnosis, and treatment of unstable angina/NSTEMI and STEMI.
3) Key diagnostic tests for ACS evaluation discussed include ECG, cardiac biomarkers, and stress testing. Management involves risk factor modification, antiplatelets, anticoagulants, and revascularization when appropriate.
This document provides information on acute coronary syndrome (ACS). ACS refers to a spectrum of clinical presentations ranging from ST-segment elevation myocardial infarction (STEMI) to non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina. It is usually caused by acute coronary atherothrombosis. Risk factors include smoking, high cholesterol, diabetes, and family history. The document discusses gender differences in ACS presentation and outlines treatments including anti-ischemic drugs, antiplatelet therapy, anticoagulants, and revascularization procedures. It also covers STEMI and NSTEMI diagnosis and management.
Cardiogenic shock is a low cardiac output state resulting from inadequate tissue perfusion despite adequate left ventricular filling pressures. It is usually caused by acute myocardial infarction which accounts for about 80% of cases. Clinically, it is defined by sustained hypotension with signs of hypoperfusion and a systolic blood pressure less than 90 mmHg for at least 30 minutes or the need for vasopressor/inotropic support. The mortality rate for cardiogenic shock remains high at over 80% despite advances in management. Early diagnosis and aggressive treatment including revascularization, inotropic support, and mechanical circulatory support are aimed at improving outcomes.
This document discusses guidelines and recommendations for measuring and managing hypertension. It defines hypertension as a systolic blood pressure of 140 mmHg or higher, or a diastolic blood pressure of 90 mmHg or higher based on the average of two or more readings. The goals of treatment are to reduce cardiovascular risk, end organ damage, and mortality. Treatment involves lifestyle modifications like weight loss, reduced sodium intake, exercise, and limiting alcohol as well as pharmacotherapy including diuretics, ACE inhibitors, ARB, beta blockers, calcium channel blockers, and other antihypertensive drugs.
This document provides an overview of the management of acute stroke. It defines stroke and transient ischemic attack, and discusses the epidemiology, classification, risk factors, pathophysiology, clinical presentation, diagnosis, management, complications and prognosis of stroke. The management involves resuscitation, reperfusion therapies like thrombolysis and thrombectomy, treating complications, secondary prevention including blood pressure and diabetes control, and rehabilitation. The document emphasizes the importance of specialized stroke units and timely management to improve outcomes for patients with acute stroke.
This document provides an overview of non-ST elevation myocardial infarction (NSTEMI), including its pathophysiology, clinical presentation, diagnostic testing, and management. It defines NSTEMI as unstable angina with evidence of myocardial necrosis seen through elevated cardiac markers. It discusses the role of electrocardiograms, cardiac biomarkers like troponin and CK-MB, as well as treatments including thrombolysis, percutaneous coronary intervention, and coronary artery bypass grafting in the acute management of NSTEMI. It also reviews risk factor evaluation, secondary prevention strategies, and long-term management of NSTEMI.
Exercise stress testing can be used to identify cardiovascular endurance and the likelihood of coronary artery disease. There are several types of stress tests that use equipment like treadmills, bicycles, or arm ergometers along with electrocardiogram monitoring. The tests aim to determine if physical exertion causes ischemia or inadequate oxygen supply to the heart. Results are reported as negative, positive, or inconclusive based on changes in the ECG tracing during physical exertion. Precautions must be taken as the tests carry a risk of inducing dangerous cardiac events.
Cardiac arrhythmias can be caused by abnormalities in heart rate, rhythm, origin of impulses, or conduction. The main mechanisms are reentry, automaticity, parasystole, and triggered activity. Reentry requires two pathways that form a loop with a block in one pathway and slow conduction in the other. Common arrhythmias include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardia. First-line drugs for treating arrhythmias include lignocaine, amiodarone, adenosine, beta-blockers, and calcium channel blockers. These drugs work via different mechanisms such as blocking sodium, potassium, or calcium channels to suppress arrhythmias.
Dr. Rohit and Dr. Sagar presented on shock, defining it as inadequate tissue perfusion resulting from an imbalance in oxygen delivery and consumption. They discussed the main types of shock - hypovolemic, cardiogenic, obstructive, and distributive - and the pathogenesis of each. Key signs of shock include tachycardia, tachypnea, poor pulses, and altered mental status. Early goal-directed resuscitation within the "golden hour" is important for outcomes. Management involves addressing the underlying cause, optimizing preload and cardiac output, and monitoring for resolution of shock.
1) Exercise stress testing is used to detect myocardial ischemia through monitoring changes in the ECG and physiological parameters during exercise.
2) Key parameters include heart rate, blood pressure, oxygen consumption and the presence of ECG changes like ST segment depression or elevation.
3) Abnormal responses include inadequate heart rate or blood pressure increase, chest pain, significant ST changes and ventricular arrhythmias, which can indicate coronary artery disease.
This document discusses the diagnosis and treatment of acute coronary syndrome. It provides statistics showing that over 1.5 million hospital admissions in the US each year are due to acute coronary syndromes, with the majority being unstable angina or NSTEMI. It then discusses the clinical presentation, ECG changes, cardiac biomarker increases, and definitions of STEMI. It emphasizes the importance of rapid diagnosis of STEMI using high-sensitivity troponin tests. Finally, it outlines the routine medical therapies for STEMI including antiplatelets, anticoagulants, nitrates, beta blockers, ACE inhibitors, ARBs, aldosterone antagonists, and high-intensity statins.
This document discusses the diagnosis and treatment of acute coronary syndrome. It provides statistics showing that over 1.5 million hospital admissions in the US each year are due to acute coronary syndromes, with the majority being unstable angina or NSTEMI. It then discusses the clinical presentation, ECG changes, cardiac biomarkers, and definitions used to diagnose STEMI according to recent guidelines. Treatment involves both routine medical therapies as well as reperfusion through primary PCI or thrombolytics to restore blood flow in STEMI patients.
1. Acute coronary syndrome (ACS) encompasses unstable angina and myocardial infarction, and is caused by reduced blood flow in the coronary arteries, often due to atherosclerosis.
2. Clinical features of ACS include chest pain and discomfort, but it can also be "silent" in some high-risk groups. Diagnosis involves ECG, cardiac troponin levels, and coronary angiography.
3. Treatment depends on whether the ACS is STEMI (ST elevation on ECG) or NSTEMI/unstable angina. For STEMI, primary percutaneous coronary intervention is the treatment of choice if readily available to restore blood flow, along with dual antiplatelet therapy and antico
Blood pressure is the pressure exerted by circulating blood on the walls of blood vessels. It is typically measured in millimeters of mercury (mmHg). Normal blood pressure is less than 120/80 mmHg. Blood pressure is regulated through both immediate mechanisms like baroreceptor reflexes and delayed mechanisms involving the kidneys, renin-angiotensin system, and other hormones. Factors that affect blood pressure include cardiac output, peripheral resistance, blood volume, vessel elasticity, and viscosity. Hypertension is defined as high blood pressure over 140/90 mmHg and can increase the risk of heart disease and stroke if left untreated.
This document discusses various types of shock including cardiogenic, distributive, obstructive, and hypovolemic shock. It provides details on the etiology, pathophysiology, clinical presentation, diagnostic evaluation and management of each type. Key goals in the first hour of resuscitation for septic shock are outlined, including maintaining circulation and organ perfusion through fluid resuscitation and vasoactive drugs if needed. Trials of various monoclonal antibodies and drugs for treating sepsis are briefly summarized, most showing little benefit. Hemodynamic variables are compared across different shock states.
The document discusses Acute Coronary Syndrome (ACS), which includes Unstable Angina/Non-ST-segment elevation myocardial infarction (UA/NSTEMI) and ST-segment elevation myocardial infarction (STEMI). UA/NSTEMI is caused by a reduction in oxygen supply or increase in demand due to plaque rupture or spasm. STEMI occurs when there is complete thrombotic occlusion of a coronary artery. Both involve chest pain but STEMI presents with ST-segment elevation on ECG. Treatment for both includes anti-ischemic, anti-thrombotic medications, and coronary revascularization if high-risk features are present.
This document provides information on angina pectoris (chest pain), including its types, causes, symptoms, pathogenesis, and treatment options. It discusses the classification and mechanisms of action of various antianginal drug classes - nitrates, beta-blockers, calcium channel blockers, potassium channel activators, and others. Adverse effects and uses are described for representative drugs in each class. The classifications covered are nitrate compounds, beta-blockers, calcium channel blockers, potassium channel activators, and miscellaneous drugs including antiplatelet and cytoprotective agents.
A 75-year-old diabetic male presented with chest pain and other symptoms of acute coronary syndrome. The most probable diagnosis is myocardial infarction. Relevant investigations include ECG, biochemical markers like CK-MB and troponin, and echocardiogram. Management involves medical therapy in emergency, possible fibrinolysis or PCI, and long term preventative treatment. Complications can include heart failure, cardiogenic shock, arrhythmias if not properly managed.
This document provides an overview of various cardiac medications, including their classifications, mechanisms of action, indications for use, dosages, and potential adverse effects. It discusses drugs that work on the cardiovascular system like beta blockers, calcium channel blockers, ACE inhibitors, diuretics, inotropes, antiarrhythmics, and anticoagulants. The document also provides a case study example and discusses preparation for cardiac catheterization.
Angina pectoris is a clinical syndrome characterized by chest pain or pressure due to insufficient blood flow to the heart muscle. It is usually caused by an imbalance between myocardial oxygen supply and demand. There are different types of angina including stable, unstable, and variant angina. Risk factors include family history, diabetes, hypertension, smoking, and high cholesterol. Diagnosis involves ECG, stress test, and angiography. Treatment focuses on decreasing oxygen demand on the heart and increasing supply by using nitrates, beta blockers, calcium channel blockers, antiplatelet drugs, and statins. Emergency treatment for unstable angina may include thrombolytics. Lifestyle changes and medication aim to prevent future cardiac events associated with untreated
This document discusses the management of coronary artery disease and acute coronary syndrome. It begins with the anatomy of the heart and coronary blood vessels. It then defines acute coronary syndrome as unstable angina or myocardial infarction caused by plaque rupture and thrombosis. Risk factors for coronary artery disease are outlined. The diagnostic approach involves assessing symptoms, signs, electrocardiogram changes and cardiac biomarker levels. Treatment focuses on reopening the blocked vessel with medications, fibrinolytics or percutaneous coronary intervention. Chronic stable angina from established coronary artery disease is also discussed.
Immersive Learning That Works: Research Grounding and Paths ForwardLeonel Morgado
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
Evidence of Jet Activity from the Secondary Black Hole in the OJ 287 Binary S...Sérgio Sacani
Wereport the study of a huge optical intraday flare on 2021 November 12 at 2 a.m. UT in the blazar OJ287. In the binary black hole model, it is associated with an impact of the secondary black hole on the accretion disk of the primary. Our multifrequency observing campaign was set up to search for such a signature of the impact based on a prediction made 8 yr earlier. The first I-band results of the flare have already been reported by Kishore et al. (2024). Here we combine these data with our monitoring in the R-band. There is a big change in the R–I spectral index by 1.0 ±0.1 between the normal background and the flare, suggesting a new component of radiation. The polarization variation during the rise of the flare suggests the same. The limits on the source size place it most reasonably in the jet of the secondary BH. We then ask why we have not seen this phenomenon before. We show that OJ287 was never before observed with sufficient sensitivity on the night when the flare should have happened according to the binary model. We also study the probability that this flare is just an oversized example of intraday variability using the Krakow data set of intense monitoring between 2015 and 2023. We find that the occurrence of a flare of this size and rapidity is unlikely. In machine-readable Tables 1 and 2, we give the full orbit-linked historical light curve of OJ287 as well as the dense monitoring sample of Krakow.
This document provides an overview of non-ST elevation myocardial infarction (NSTEMI), including its pathophysiology, clinical presentation, diagnostic testing, and management. It defines NSTEMI as unstable angina with evidence of myocardial necrosis seen through elevated cardiac markers. It discusses the role of electrocardiograms, cardiac biomarkers like troponin and CK-MB, as well as treatments including thrombolysis, percutaneous coronary intervention, and coronary artery bypass grafting in the acute management of NSTEMI. It also reviews risk factor evaluation, secondary prevention strategies, and long-term management of NSTEMI.
Exercise stress testing can be used to identify cardiovascular endurance and the likelihood of coronary artery disease. There are several types of stress tests that use equipment like treadmills, bicycles, or arm ergometers along with electrocardiogram monitoring. The tests aim to determine if physical exertion causes ischemia or inadequate oxygen supply to the heart. Results are reported as negative, positive, or inconclusive based on changes in the ECG tracing during physical exertion. Precautions must be taken as the tests carry a risk of inducing dangerous cardiac events.
Cardiac arrhythmias can be caused by abnormalities in heart rate, rhythm, origin of impulses, or conduction. The main mechanisms are reentry, automaticity, parasystole, and triggered activity. Reentry requires two pathways that form a loop with a block in one pathway and slow conduction in the other. Common arrhythmias include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardia. First-line drugs for treating arrhythmias include lignocaine, amiodarone, adenosine, beta-blockers, and calcium channel blockers. These drugs work via different mechanisms such as blocking sodium, potassium, or calcium channels to suppress arrhythmias.
Dr. Rohit and Dr. Sagar presented on shock, defining it as inadequate tissue perfusion resulting from an imbalance in oxygen delivery and consumption. They discussed the main types of shock - hypovolemic, cardiogenic, obstructive, and distributive - and the pathogenesis of each. Key signs of shock include tachycardia, tachypnea, poor pulses, and altered mental status. Early goal-directed resuscitation within the "golden hour" is important for outcomes. Management involves addressing the underlying cause, optimizing preload and cardiac output, and monitoring for resolution of shock.
1) Exercise stress testing is used to detect myocardial ischemia through monitoring changes in the ECG and physiological parameters during exercise.
2) Key parameters include heart rate, blood pressure, oxygen consumption and the presence of ECG changes like ST segment depression or elevation.
3) Abnormal responses include inadequate heart rate or blood pressure increase, chest pain, significant ST changes and ventricular arrhythmias, which can indicate coronary artery disease.
This document discusses the diagnosis and treatment of acute coronary syndrome. It provides statistics showing that over 1.5 million hospital admissions in the US each year are due to acute coronary syndromes, with the majority being unstable angina or NSTEMI. It then discusses the clinical presentation, ECG changes, cardiac biomarker increases, and definitions of STEMI. It emphasizes the importance of rapid diagnosis of STEMI using high-sensitivity troponin tests. Finally, it outlines the routine medical therapies for STEMI including antiplatelets, anticoagulants, nitrates, beta blockers, ACE inhibitors, ARBs, aldosterone antagonists, and high-intensity statins.
This document discusses the diagnosis and treatment of acute coronary syndrome. It provides statistics showing that over 1.5 million hospital admissions in the US each year are due to acute coronary syndromes, with the majority being unstable angina or NSTEMI. It then discusses the clinical presentation, ECG changes, cardiac biomarkers, and definitions used to diagnose STEMI according to recent guidelines. Treatment involves both routine medical therapies as well as reperfusion through primary PCI or thrombolytics to restore blood flow in STEMI patients.
1. Acute coronary syndrome (ACS) encompasses unstable angina and myocardial infarction, and is caused by reduced blood flow in the coronary arteries, often due to atherosclerosis.
2. Clinical features of ACS include chest pain and discomfort, but it can also be "silent" in some high-risk groups. Diagnosis involves ECG, cardiac troponin levels, and coronary angiography.
3. Treatment depends on whether the ACS is STEMI (ST elevation on ECG) or NSTEMI/unstable angina. For STEMI, primary percutaneous coronary intervention is the treatment of choice if readily available to restore blood flow, along with dual antiplatelet therapy and antico
Blood pressure is the pressure exerted by circulating blood on the walls of blood vessels. It is typically measured in millimeters of mercury (mmHg). Normal blood pressure is less than 120/80 mmHg. Blood pressure is regulated through both immediate mechanisms like baroreceptor reflexes and delayed mechanisms involving the kidneys, renin-angiotensin system, and other hormones. Factors that affect blood pressure include cardiac output, peripheral resistance, blood volume, vessel elasticity, and viscosity. Hypertension is defined as high blood pressure over 140/90 mmHg and can increase the risk of heart disease and stroke if left untreated.
This document discusses various types of shock including cardiogenic, distributive, obstructive, and hypovolemic shock. It provides details on the etiology, pathophysiology, clinical presentation, diagnostic evaluation and management of each type. Key goals in the first hour of resuscitation for septic shock are outlined, including maintaining circulation and organ perfusion through fluid resuscitation and vasoactive drugs if needed. Trials of various monoclonal antibodies and drugs for treating sepsis are briefly summarized, most showing little benefit. Hemodynamic variables are compared across different shock states.
The document discusses Acute Coronary Syndrome (ACS), which includes Unstable Angina/Non-ST-segment elevation myocardial infarction (UA/NSTEMI) and ST-segment elevation myocardial infarction (STEMI). UA/NSTEMI is caused by a reduction in oxygen supply or increase in demand due to plaque rupture or spasm. STEMI occurs when there is complete thrombotic occlusion of a coronary artery. Both involve chest pain but STEMI presents with ST-segment elevation on ECG. Treatment for both includes anti-ischemic, anti-thrombotic medications, and coronary revascularization if high-risk features are present.
This document provides information on angina pectoris (chest pain), including its types, causes, symptoms, pathogenesis, and treatment options. It discusses the classification and mechanisms of action of various antianginal drug classes - nitrates, beta-blockers, calcium channel blockers, potassium channel activators, and others. Adverse effects and uses are described for representative drugs in each class. The classifications covered are nitrate compounds, beta-blockers, calcium channel blockers, potassium channel activators, and miscellaneous drugs including antiplatelet and cytoprotective agents.
A 75-year-old diabetic male presented with chest pain and other symptoms of acute coronary syndrome. The most probable diagnosis is myocardial infarction. Relevant investigations include ECG, biochemical markers like CK-MB and troponin, and echocardiogram. Management involves medical therapy in emergency, possible fibrinolysis or PCI, and long term preventative treatment. Complications can include heart failure, cardiogenic shock, arrhythmias if not properly managed.
This document provides an overview of various cardiac medications, including their classifications, mechanisms of action, indications for use, dosages, and potential adverse effects. It discusses drugs that work on the cardiovascular system like beta blockers, calcium channel blockers, ACE inhibitors, diuretics, inotropes, antiarrhythmics, and anticoagulants. The document also provides a case study example and discusses preparation for cardiac catheterization.
Angina pectoris is a clinical syndrome characterized by chest pain or pressure due to insufficient blood flow to the heart muscle. It is usually caused by an imbalance between myocardial oxygen supply and demand. There are different types of angina including stable, unstable, and variant angina. Risk factors include family history, diabetes, hypertension, smoking, and high cholesterol. Diagnosis involves ECG, stress test, and angiography. Treatment focuses on decreasing oxygen demand on the heart and increasing supply by using nitrates, beta blockers, calcium channel blockers, antiplatelet drugs, and statins. Emergency treatment for unstable angina may include thrombolytics. Lifestyle changes and medication aim to prevent future cardiac events associated with untreated
This document discusses the management of coronary artery disease and acute coronary syndrome. It begins with the anatomy of the heart and coronary blood vessels. It then defines acute coronary syndrome as unstable angina or myocardial infarction caused by plaque rupture and thrombosis. Risk factors for coronary artery disease are outlined. The diagnostic approach involves assessing symptoms, signs, electrocardiogram changes and cardiac biomarker levels. Treatment focuses on reopening the blocked vessel with medications, fibrinolytics or percutaneous coronary intervention. Chronic stable angina from established coronary artery disease is also discussed.
Immersive Learning That Works: Research Grounding and Paths ForwardLeonel Morgado
We will metaverse into the essence of immersive learning, into its three dimensions and conceptual models. This approach encompasses elements from teaching methodologies to social involvement, through organizational concerns and technologies. Challenging the perception of learning as knowledge transfer, we introduce a 'Uses, Practices & Strategies' model operationalized by the 'Immersive Learning Brain' and ‘Immersion Cube’ frameworks. This approach offers a comprehensive guide through the intricacies of immersive educational experiences and spotlighting research frontiers, along the immersion dimensions of system, narrative, and agency. Our discourse extends to stakeholders beyond the academic sphere, addressing the interests of technologists, instructional designers, and policymakers. We span various contexts, from formal education to organizational transformation to the new horizon of an AI-pervasive society. This keynote aims to unite the iLRN community in a collaborative journey towards a future where immersive learning research and practice coalesce, paving the way for innovative educational research and practice landscapes.
Evidence of Jet Activity from the Secondary Black Hole in the OJ 287 Binary S...Sérgio Sacani
Wereport the study of a huge optical intraday flare on 2021 November 12 at 2 a.m. UT in the blazar OJ287. In the binary black hole model, it is associated with an impact of the secondary black hole on the accretion disk of the primary. Our multifrequency observing campaign was set up to search for such a signature of the impact based on a prediction made 8 yr earlier. The first I-band results of the flare have already been reported by Kishore et al. (2024). Here we combine these data with our monitoring in the R-band. There is a big change in the R–I spectral index by 1.0 ±0.1 between the normal background and the flare, suggesting a new component of radiation. The polarization variation during the rise of the flare suggests the same. The limits on the source size place it most reasonably in the jet of the secondary BH. We then ask why we have not seen this phenomenon before. We show that OJ287 was never before observed with sufficient sensitivity on the night when the flare should have happened according to the binary model. We also study the probability that this flare is just an oversized example of intraday variability using the Krakow data set of intense monitoring between 2015 and 2023. We find that the occurrence of a flare of this size and rapidity is unlikely. In machine-readable Tables 1 and 2, we give the full orbit-linked historical light curve of OJ287 as well as the dense monitoring sample of Krakow.
PPT on Alternate Wetting and Drying presented at the three-day 'Training and Validation Workshop on Modules of Climate Smart Agriculture (CSA) Technologies in South Asia' workshop on April 22, 2024.
Microbial interaction
Microorganisms interacts with each other and can be physically associated with another organisms in a variety of ways.
One organism can be located on the surface of another organism as an ectobiont or located within another organism as endobiont.
Microbial interaction may be positive such as mutualism, proto-cooperation, commensalism or may be negative such as parasitism, predation or competition
Types of microbial interaction
Positive interaction: mutualism, proto-cooperation, commensalism
Negative interaction: Ammensalism (antagonism), parasitism, predation, competition
I. Mutualism:
It is defined as the relationship in which each organism in interaction gets benefits from association. It is an obligatory relationship in which mutualist and host are metabolically dependent on each other.
Mutualistic relationship is very specific where one member of association cannot be replaced by another species.
Mutualism require close physical contact between interacting organisms.
Relationship of mutualism allows organisms to exist in habitat that could not occupied by either species alone.
Mutualistic relationship between organisms allows them to act as a single organism.
Examples of mutualism:
i. Lichens:
Lichens are excellent example of mutualism.
They are the association of specific fungi and certain genus of algae. In lichen, fungal partner is called mycobiont and algal partner is called
II. Syntrophism:
It is an association in which the growth of one organism either depends on or improved by the substrate provided by another organism.
In syntrophism both organism in association gets benefits.
Compound A
Utilized by population 1
Compound B
Utilized by population 2
Compound C
utilized by both Population 1+2
Products
In this theoretical example of syntrophism, population 1 is able to utilize and metabolize compound A, forming compound B but cannot metabolize beyond compound B without co-operation of population 2. Population 2is unable to utilize compound A but it can metabolize compound B forming compound C. Then both population 1 and 2 are able to carry out metabolic reaction which leads to formation of end product that neither population could produce alone.
Examples of syntrophism:
i. Methanogenic ecosystem in sludge digester
Methane produced by methanogenic bacteria depends upon interspecies hydrogen transfer by other fermentative bacteria.
Anaerobic fermentative bacteria generate CO2 and H2 utilizing carbohydrates which is then utilized by methanogenic bacteria (Methanobacter) to produce methane.
ii. Lactobacillus arobinosus and Enterococcus faecalis:
In the minimal media, Lactobacillus arobinosus and Enterococcus faecalis are able to grow together but not alone.
The synergistic relationship between E. faecalis and L. arobinosus occurs in which E. faecalis require folic acid
PPT on Direct Seeded Rice presented at the three-day 'Training and Validation Workshop on Modules of Climate Smart Agriculture (CSA) Technologies in South Asia' workshop on April 22, 2024.
Describing and Interpreting an Immersive Learning Case with the Immersion Cub...Leonel Morgado
Current descriptions of immersive learning cases are often difficult or impossible to compare. This is due to a myriad of different options on what details to include, which aspects are relevant, and on the descriptive approaches employed. Also, these aspects often combine very specific details with more general guidelines or indicate intents and rationales without clarifying their implementation. In this paper we provide a method to describe immersive learning cases that is structured to enable comparisons, yet flexible enough to allow researchers and practitioners to decide which aspects to include. This method leverages a taxonomy that classifies educational aspects at three levels (uses, practices, and strategies) and then utilizes two frameworks, the Immersive Learning Brain and the Immersion Cube, to enable a structured description and interpretation of immersive learning cases. The method is then demonstrated on a published immersive learning case on training for wind turbine maintenance using virtual reality. Applying the method results in a structured artifact, the Immersive Learning Case Sheet, that tags the case with its proximal uses, practices, and strategies, and refines the free text case description to ensure that matching details are included. This contribution is thus a case description method in support of future comparative research of immersive learning cases. We then discuss how the resulting description and interpretation can be leveraged to change immersion learning cases, by enriching them (considering low-effort changes or additions) or innovating (exploring more challenging avenues of transformation). The method holds significant promise to support better-grounded research in immersive learning.
Sexuality - Issues, Attitude and Behaviour - Applied Social Psychology - Psyc...PsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Discovery of An Apparent Red, High-Velocity Type Ia Supernova at 𝐳 = 2.9 wi...Sérgio Sacani
We present the JWST discovery of SN 2023adsy, a transient object located in a host galaxy JADES-GS
+
53.13485
−
27.82088
with a host spectroscopic redshift of
2.903
±
0.007
. The transient was identified in deep James Webb Space Telescope (JWST)/NIRCam imaging from the JWST Advanced Deep Extragalactic Survey (JADES) program. Photometric and spectroscopic followup with NIRCam and NIRSpec, respectively, confirm the redshift and yield UV-NIR light-curve, NIR color, and spectroscopic information all consistent with a Type Ia classification. Despite its classification as a likely SN Ia, SN 2023adsy is both fairly red (
�
(
�
−
�
)
∼
0.9
) despite a host galaxy with low-extinction and has a high Ca II velocity (
19
,
000
±
2
,
000
km/s) compared to the general population of SNe Ia. While these characteristics are consistent with some Ca-rich SNe Ia, particularly SN 2016hnk, SN 2023adsy is intrinsically brighter than the low-
�
Ca-rich population. Although such an object is too red for any low-
�
cosmological sample, we apply a fiducial standardization approach to SN 2023adsy and find that the SN 2023adsy luminosity distance measurement is in excellent agreement (
≲
1
�
) with
Λ
CDM. Therefore unlike low-
�
Ca-rich SNe Ia, SN 2023adsy is standardizable and gives no indication that SN Ia standardized luminosities change significantly with redshift. A larger sample of distant SNe Ia is required to determine if SN Ia population characteristics at high-
�
truly diverge from their low-
�
counterparts, and to confirm that standardized luminosities nevertheless remain constant with redshift.
CLASS 12th CHEMISTRY SOLID STATE ppt (Animated)eitps1506
Description:
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Candidate young stellar objects in the S-cluster: Kinematic analysis of a sub...Sérgio Sacani
Context. The observation of several L-band emission sources in the S cluster has led to a rich discussion of their nature. However, a definitive answer to the classification of the dusty objects requires an explanation for the detection of compact Doppler-shifted Brγ emission. The ionized hydrogen in combination with the observation of mid-infrared L-band continuum emission suggests that most of these sources are embedded in a dusty envelope. These embedded sources are part of the S-cluster, and their relationship to the S-stars is still under debate. To date, the question of the origin of these two populations has been vague, although all explanations favor migration processes for the individual cluster members. Aims. This work revisits the S-cluster and its dusty members orbiting the supermassive black hole SgrA* on bound Keplerian orbits from a kinematic perspective. The aim is to explore the Keplerian parameters for patterns that might imply a nonrandom distribution of the sample. Additionally, various analytical aspects are considered to address the nature of the dusty sources. Methods. Based on the photometric analysis, we estimated the individual H−K and K−L colors for the source sample and compared the results to known cluster members. The classification revealed a noticeable contrast between the S-stars and the dusty sources. To fit the flux-density distribution, we utilized the radiative transfer code HYPERION and implemented a young stellar object Class I model. We obtained the position angle from the Keplerian fit results; additionally, we analyzed the distribution of the inclinations and the longitudes of the ascending node. Results. The colors of the dusty sources suggest a stellar nature consistent with the spectral energy distribution in the near and midinfrared domains. Furthermore, the evaporation timescales of dusty and gaseous clumps in the vicinity of SgrA* are much shorter ( 2yr) than the epochs covered by the observations (≈15yr). In addition to the strong evidence for the stellar classification of the D-sources, we also find a clear disk-like pattern following the arrangements of S-stars proposed in the literature. Furthermore, we find a global intrinsic inclination for all dusty sources of 60 ± 20◦, implying a common formation process. Conclusions. The pattern of the dusty sources manifested in the distribution of the position angles, inclinations, and longitudes of the ascending node strongly suggests two different scenarios: the main-sequence stars and the dusty stellar S-cluster sources share a common formation history or migrated with a similar formation channel in the vicinity of SgrA*. Alternatively, the gravitational influence of SgrA* in combination with a massive perturber, such as a putative intermediate mass black hole in the IRS 13 cluster, forces the dusty objects and S-stars to follow a particular orbital arrangement. Key words. stars: black holes– stars: formation– Galaxy: center– galaxies: star formation
EWOCS-I: The catalog of X-ray sources in Westerlund 1 from the Extended Weste...Sérgio Sacani
Context. With a mass exceeding several 104 M⊙ and a rich and dense population of massive stars, supermassive young star clusters
represent the most massive star-forming environment that is dominated by the feedback from massive stars and gravitational interactions
among stars.
Aims. In this paper we present the Extended Westerlund 1 and 2 Open Clusters Survey (EWOCS) project, which aims to investigate
the influence of the starburst environment on the formation of stars and planets, and on the evolution of both low and high mass stars.
The primary targets of this project are Westerlund 1 and 2, the closest supermassive star clusters to the Sun.
Methods. The project is based primarily on recent observations conducted with the Chandra and JWST observatories. Specifically,
the Chandra survey of Westerlund 1 consists of 36 new ACIS-I observations, nearly co-pointed, for a total exposure time of 1 Msec.
Additionally, we included 8 archival Chandra/ACIS-S observations. This paper presents the resulting catalog of X-ray sources within
and around Westerlund 1. Sources were detected by combining various existing methods, and photon extraction and source validation
were carried out using the ACIS-Extract software.
Results. The EWOCS X-ray catalog comprises 5963 validated sources out of the 9420 initially provided to ACIS-Extract, reaching a
photon flux threshold of approximately 2 × 10−8 photons cm−2
s
−1
. The X-ray sources exhibit a highly concentrated spatial distribution,
with 1075 sources located within the central 1 arcmin. We have successfully detected X-ray emissions from 126 out of the 166 known
massive stars of the cluster, and we have collected over 71 000 photons from the magnetar CXO J164710.20-455217.
EWOCS-I: The catalog of X-ray sources in Westerlund 1 from the Extended Weste...
1-medical-surgical_compress.pdf
1. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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CARDIOVASCULAR
Ischemia: lacking Blood supply
Infarcted: Absence of blood supply; tissue damage (Infarcted
cardiac tissue releases enzymes)
1. DIAGNOTICS:
1.1 CARDIAC ENZYMES:
1.1.1 CK-MB: elevation indicates myocardial
damage: elevates within 24
4-6 hrs; peaks in 18-
hrs
1.1.2 LDH: occurs in 24 hrs and peaks in 48-72 hrs
1.1.3 TROPONIN I: 0-0.4 ng/mL; EARLIEST in 2-4
hrs; most sensitive
1.2 COMPLETE BLOOD COUNT: WBC RBC, H&H,
HDL, LDL, Triglyceride Level
1.3 Electrolytes: K, Na, Ca, Phosphorus (In renal), Mg
1.4 BUN & CREATININE: the heart stops, stops the
perfusion to other organs especially the kidney
1.5 CXR: enlarged heart
1.6 ECG: electrical activity of the heart; Simply remove
metals but in reality no real effect
*ADD: NCLEX ECG; Written and what to do with it
1.7 Coagulation Tests: In pharmacology
1.8 CARDIAC CATHERTERIZATION: assess the
obstruction in the blood vessels or coronary arteries
1.8.1 FEMORAL ARTERY: you don’t insert the
whole catheter; place dye to determine where
the obstruction starts
1.8.2 NOW predisposed to bleed: Pressure dressing
and Sand bag (10 pounds of pressure) unto
the area: HIGH PRESSURE ARTERY; The
client may complain of bed wetting but may
refer to bleeding;
1.8.3 It can also form Hematoma (Due to the
pressure and moving around) in the inguinal
artery (LOWER EXTREMITIES) so monitor
the peripheral pulses (Pedal Pulses: Dorsalis
Pedis. Posterior Tibialis) ’
; if you can t palpate,
you use a DOPPLE; 4-6 hrs immobilized on
bed
1.8.4 Ask patient if allergic to Dye
CORONARY ARTERY DISEASE
1. AGINA: is the symptom of CAD; Chest pain results
from Myocardial Ischemia: most common symptoms
of CAD; Concept: DEMANDS EXCEEDS SUPPLY
1.1 TYPES
1.1.1 STABLE: Pain goes away when
precipitating factors are removed; pain
relieved by REST and NTG
1.1.2 UNSTABLE: Increased activity
severity, duration and frequency; might
not be relieved by NTG (2 capsules);
May proceed to MI
1.1.3 PRINZMETAL/ VARIANT/
VASOSPASTIC: may occur at rest
(usually secondary to
VASOCONSTRICTION ie Cold
environment)
1.2 CAUSE: Anything that increases the HR,
Increases oxygen Demand (Anything that causes
Stress, Stimulation or Excitement)
1.3 3E’s: EXERTION, EMOTION, EATING
1.3.1 Increase metabolism increases HR; SFF
1.3.2 Walking is the only possible exercise
1.3.3 Overjoyed can cause increase HR
1.3.4 Sexual Activity
1.3.5 Artherosclerosis (MOST COMMON
CAUSE); Thromboembolism
1.4 ASSESSMENT
1.4.1 Pain: SUBSTERNAL, Crushing or
compressing; may radiate to the LEFT
arms, jaws or back also in shoulder;
;
usually after exertion, excitement or
exposed to cold
1.4.2 MEN: Substernal pain
1.4.3 WOMEN: Lower/ Epigastric region
pain; May be diagnosed as GERD not
Angina; Higher cause of death in
women due to Misdiagnosis
1.4.4 Anxiety: Diaphoresis, dyspnea,
tachycardia, palpitations, epigastric
distress (ATYPICAL/ uncommon
manifestation; Mostly for women)
1.5 DX
1.5.1 Increased Cholesterol, LDL and
triglycerides
1.5.2 CARDIAC ENZYMES: usually
WITHIN NORMAL LEVELS
1.5.3 Coronary arteriography shows
narrowing coronary arteries
1.5.4 ECG: ST segment depression, T-wave
inversion
*In NON-STEMI and ANGINA: both are Non ST elevated
and may become depressed; so you don’t know the difference;
The only thing that will tell you that it is MI is CARDIAC
EZYMES that show presence of infarction
1.6 MANAGEMENT
1.6.1 Low fat, Low cholesterol; SFF
1.6.2 Administer 02 to decrease 02 demand
1.6.3 Maintain Bed rest and SEMI
FOWLER’s position: Reduce cardiac
workload (with bathroom privilege:
may walk but until bathroom only)
1.6.4 Encourage weight reduction and
smoking cessation (vasoconstriction)
1.7 MEDICATION
1.7.1 NTG: 3 Months; Take 5 minutes max of
three then go to the ER or call 911
1.7.2 Anticoagulants: Heparin (APTT,
Protamine Sulfate); Coumadine (PT, Vit
K)
1.7.3 Ca Channel Blockers (VND)
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2. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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1.7.4 Beta Blockers (propranol)
1.8 TREATMENT
1.8.1 Percutaneous Transluminal Corornary
Angioplasty (PTCA)
1.8.2 Intravascular Stenting: Done to prevent
restenosis after PTCA; Given
Coumadin, ASA (prevent clotting;
lifetime medication for stents)
2. MI
*Loose circulation to whole body: Brain and Kidneys
(U/O monitor)
2.1 CAUSES
2.1.1 Total occlusion of one of the coronary
arteries causing ischemia, injury and
NECROSIS
2.1.2 Infarction most common to the LV
2.1.3 RF: same risk of Angina
2.1.4 Not relieved by rest or NTG
2.2 LEVINE’S SIGN: clutching at the chest due to
Pain; Most likely having an MI
2.3 ASSESSMENT
2.3.1 Crushing substernal pain (radiate to jaw,
back and arms; unrelieved by rest and
NTG)
2.3.2 Dyspnea, Diaphoresis
2.3.3 Hypoxia causes Arrhythmias (V
Fibrillation: MC cause of Death)
*PULSELESS V- -
TACH and V FIB: Shockable rhythm
2.4 DX
2.4.1 Diagnostic evaluation: ECG shows
deep, wide Q wave (All layers are
infarcted: epi, myo and endocardium),
Elevated or depressed ST-segment, T-
wave inversion
2.4.2 Coupled with Cardiac Enzymes, you
will be able to determine the presence
of MI; Increased Cardiac Enzymes
2.5 MANAGEMENT
2.5.1 Bedrest with Bedside Commode (used
as a chair and makes it easier to
defecate and urinate; just beside the
bed)
2.5.2 CABG: Saphenous Vein
(Contraindicated with varicose Veins);
Internal Mammary Artery (may be
used); The number CBG x5 meaning 5
vessels were bypassed
2.5.3 Angioplasty
2.5.4 Low calorie, low cholesterol, low fat
diet
2.5.5 Monitor labs (ABG, CK, electrolyte and
Troponin)
2.5.6 02
2.5.7 CPR (if patient becomes unconscious
and defibrillate when ECG shows V
Fibrillation)
*CPR within um of 15 minutes
5-10 minutes; Brain maxim
anoxic; Longer, becomes stroked-out (vegetable)
2.6 CPR
2.6.1 Assess consciousness: hey hey are you
ok: Unresponsive
2.6.2 Check the Pulse: Carotid Pulse for at
least 10 seconds
2.6.3 Assess Respiration: rise and fall [New:
MONITOR for absence of breathing or
abnormal breathing {GASPING for
breath}]
2.6.4 Call for help: CODE
2.6.5 Start Chest Compression: 30:2
Compression to Breathe; ;
2 INCHES
HIGH QUALITY CPR Adequate rate
and Adequate Depth: 100-120
compressions per minute;
2.6.6 Advance Airway (Ambubag): 1 breathe
every 6 seconds; Avoid excessive
ventilation; REMEMBER TO COUNT
2.6.7 ABC: Compression, Airway, Breathing
2.6.8 New: 2 minutes of Full compression not
unless someone brings the Defibrillator
2.6.9 Defibrillator: Apex and Sternum (for
the paddles and lubricate); Once placed
on the chest, APPLY 10 lbs of pressure;
Setting must be on MODE:
ASYNCHRONIZED (It does not
matter where it will hit; the rhythm is
chaotic; No need to be careful; Shock
will hopefully go back to any rhythm
good for perfusion); JOULES: It
depends on the defibrillator being used;
2.6.9.1 MONOPHASIC: One way and
does not travel back to the heart;
360 Joules
2.6.9.2 BIPHASIC: Goes back and forth
with an AC Current with lesser
joules or damage to the muscles;
200 Joules
*CARDIOVERSION: SYNCHRONIZED
2.6.9 if does not wake up: KEEP CPR and Inject
needed meds: EPINEPHRINE; Then Continue
Defibrillation with same joules
2.7 MEDICATION
2.7.1 MONA
2.7.2 MORPHINE: vasodilator and
analgesics (reduces Myocardial 02
demand)
2.7.3 O2
2.7.4 NTG
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3. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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2.7.5 ASA: Anti-Platelet
2.7.6 Beta Blocker and CA Channel
2.7.7 Thrombolytics: Given 3 4 hrs
- after
S/SX
2.7.8 Anticoagulant
2.8 VENTRICULAR FIBRILLATION: Chaotic
Discharge; rate >300/min, may result to clinical
death; IMMEIDIATE DEFIBRILATION and
EPINEPHRINE
CARDIAC ARRYTHMIAS
- Abnormal electrical conduction or automaticity that
changes cardiac rhythm rate
- PROPERTIES: [1] Automaticity (initiating its own
heart beats); [2] Conductivity (Traveling from one
point to another); [3] Contractility (the ability to
empty the content of the heart)
- SA NODE: the intrinsic pacemaker of the heart
IMPULSE WAVE ACTIVITY
SA NODE
HR: 60-100
bpm
P-wave Atrial
Depolarization:
Contraction
AV NODE
HR: 40-60
bpm
Time travel &
Impulse from SA to
AV:
PR interval: 0.12-
20 seconds
BUNDLE
OF HIS
PURKINJE
FIBERS:
20 40bpm
-
QRS: 0.4-0.12
Seconds
Ventricular
Depolarization
T-Wave Ventricular
Repolarization:
Resting Heart
CARDIAC DYRRYTHMIAS
TYPES LABEL BPM MGMT
SINUS
Normal Sinus
Rhythm
All the
available
waves
(PQRST)
Sinus
Bradycardia
Still from SA
Node; But
slower;
Sleeping
Asymtomatic:
No tx
Symptomatic:
Atropine S04
Sinus
Tachycardia
Exertion
ATRIAL
Atrial Flutter P-wave Jagged
Saw teeth
250-
350
Quinidine (Na
channel
Blocker)
Atrial
Fibrillation
Jiggling;
Beating to fast,
shaking
atrium;
Presence of
Blood clot
>350 Anti-
coagulants
PAC Ectopic Heart
beat
VENTRICULAR
Ventricular
Tachycardia
All QRS 101-
250
Lidocaine;
VTach Pulse:
Cardioversion
VTach w/o
Pulse:
Defibrillation
Ventricular
Fibrillation
Chaotic
HEART BLOCK
First Degree
Heart Block
Prolonged PR
interval
HR at
40 50
-
No treatment
Second
Degree
Type 1:
Wincklebach
PR interval:
Long, longer,
longest drop
No treatment
Type 2 PR Interval:
Norma,
normal,
normal, drop
If requires tx if
VR falls too
low to
maintain
adequate CO
Third Degree No impulse
form SA node
reaches the
ventricles; no
association;
cant determine
which wave is
which
Pace makers
*IMPAIRED TISSUE PERFUSION: all Cardiac
Dysrhythmias
1. CAUSES
1.1 Congenital, Drug toxicity, Electrolyte
imbalances (HYPOKALEMIA: most dangerous;
Sister is Magnesium so also low); Heart Disease
(MI, CHF)
2. TREATMENT
2.1 Anti arrhythmic card
, Synchronized ioversion,
CPR, Defibrillation
2.2 ICD (Implanted Cardiac Defibrillator; detects
fibrillation and shocks; for post VFIb/MI
patients), Transcutaneous pacing
3. CARDIOVERSION: 50-200 Joules only
3.1 Synchronized mode: you wait for a particular or
certain wave; WAIT FOR THE R-WAVE
3.2 DON’T HIT the T-WAVE (the heart is resting)
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4. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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4. MANAGEMENT:
4.1 Monitor hypoperfusion: to prevent cardiac
anoxia and renal failure
4.2 Initiate CPR
4.3 If trained, defibrillate VFIB and Pulseless
VTACH
5. PACEMAKER
5.1 Atrium or Ventricles inserted
5.2 Electronic device that causes cellular
depolarization and cardiac contraction
5.3 MODES
5.3.1 Fixed: 60-100 bpm no matter what
5.3.2 Demand: Shocks if below the setting
(will only work if higher or lower)
5.4 INDICATIONS:
5.4.1 Tachyarrythmia
5.4.2 Symptomatic Bradyarrythmias
5.4.3 Heart Blocks
5.5 PACING
5.5.1 Single Chamber: one chamber atrium or
ventricular
5.5.2 Double Chamber: Both
5.5.3 A paced: the wave at the Atrial
5.5.4 V paced: before the QRS; ventricular
5.5.5 AV pace: if both the atrium and the
ventricle
5.6 NX MGMT
5.6.1 Monitor ECG following implantation
and VS
5.6.2 5-10 year battery Life; The symptoms
returns with arrhythmia (the battery is
dying)
5.6.3 Signs of pacemaker failure:
DIZZINESS AND FAINTING
5.6.4 Sterile technique in changing the
dressing
5.6.5 Avoid going near an electric device: NO
MRI, NO Microwaves (6 feet away);
Use cellphone on the unaffected side;
NO CONTACT SPORTS; No tight
clothes
CHF
- Inability of the heart to pump adequate blood into the
systemic circulation to meet metabolic demands:
CONGESTION
- The Heart can’t pump the blood forward, then will
cause back-up
- RCHF: Systemic Signs; Cardiac Cirrhosis
- LCHF: Pulmonic Signs
1. CAUSES
1.1 Atherosclerosis in the Descending Aorta
1.2 MI
1.3 COPD: Damaged and fibrotic; the blood cannot
enter due to damage so causing back-up to the
RV; this causes COR PULMONALE: the heart
got damaged due to the lungs (very specific to
RIGHT SIDED HEART FAILURE)
1.4 HTN
1.5 Fluid Overload
1.6 Pulmonary HTN
1.7 Valvular Insufficiency: this will result to CHF
due to Endocarditis
2. MANAGEMENT
2.1 Low sodium; I&O, weights, restrict fluid (1L a
day)
2.2 Assess CV status and VS to detect decreased
cardiac output
2.3 Keep in Semi-fowler’s position
3. MEDICATION
3.1 Inotropic: (Best Dug; Initial
DIGOXIN
medication) Normal Level: 0.5-2 mg/mL; Check
BANDAV; Check for toxicity; Antidote
DIGIBIND
3.2 Analgesics (morphine for pulmo edema)
3.3 Beta Blockers
3.4 Diuretics: FUROSEMIDE
ENDOCARDITIS
- All layers of the heart can get infected; You also
damage the heart
- MC cause: Bacteria; GABHS; From Strept throat
- Risk for Clots and CHF: MANAGE as CHF
- TX: Give antibiotics
PERICARDITIS
- Inflammation of the pericardium
- SPACE: has fluid to decrease fluids
- Inflammation and Histamine causes the movement
from Intravascular to the Interstitial Space: BP goes
down causing CARDIAC TAMPONADE
- Viral, Fungal, Bacterial
- MGMT: ATB, Steroids, Salicylate (the inflammatory
effect); But if the heart contains blood, do not give
Aspirin (causes more bleeding)
- Pain on respiration
CARDIAC TAMPONADE
- Rapid unchecked rise in intrapericardial pressure due
to blood or fluid accumulating in pericardial sac
1. ASSESSMENT
1.1 Anxiety
1.2 Dyspnea, tachycardia,
1.3 REDUCED ARTERIAL BP; Narrow pulse
pressure
1.4 Distended neck vein
1.5 Pallor or cyanosis
2. DX: CXR shows cardiomegaly and widened
mediastinum
3. MANAGEMENT: PERICARDIOCENTESIS
(needle aspiration) of the pericardial sac
*PLEURAL EFFUSION: Pleural: parietal and visceral: has a
space where pleura has fluid; Thoracentesis
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5. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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VALVULAR HEART DISEASE
- Can result from endocarditis and inflammation then
HF
1. TYPES
1.1 STENOSIS or NARROWING: does not open
due to or hardening (CHF)
stiffening
1.2 INSUFFICIENCY: Incomplete closure of the
valve (CHF)
1.3 PROLAPSE OF THE VALVE: protrudes into
the La (MC in Mitral/ Bicuspid valve)
2. FORMS
2.1 Aortic insufficiency: Left Sided CHF
2.2 Mitral insufficiency: Left Sided CHF
2.3 Mitral Stenosis
2.4 Mitral Valve Prolapse
2.5 Tricuspid Insufficiency
3. MANAGEMENT
3.1 PORCINE: Pork grafting for valves; Temporary
3.2 Prosthetic: Permanent
3.2.1 HANCOC: Tricuspid
HTN
1. CLASSIFICATION OF BP FOR ADULTS
SYSTOLIC DIASTOLIC
Optimal 120 80
Normal <130 <85
High 130 139
- 85 89
-
STAGE 1 140 159
- 90 99
-
STAGE 2
(+20)
160 179
- 100 109
-
STAGE 3
(+10)
>180 >110
*To diagnose with HTN; 2 Consecutive reading over a 2-week
period
2. ASSESSMENT
2.1 Essential: no particular reason
2.2 Asymptomatic
2.3 Elevated BP
2.4 Dizziness
2.5 H/A
2.6 L Ventricular Hypertrophy
2.7 HF
2.8 Cerebral Ischemia
2.9 RENAL FAILURE
*Renal ischemia: low blood supply; It will release RENIN à
Angiotensin I ACE
à à ANGIOTENSIN II: High BP
2.10Visual Disturbances inc. Blindness: in the
FRONTAL LOBE
2.11Epistaxis : Pressure in the BV
3. DX
3.1 Increased BUN, creatinine, Na and cholesterol
4. ANEURYSM: GOAL: maintain NORMAL BP;
Don’t make it rupture
4.1 TYPES
4.1.1 Saccular: one side pouch
4.1.2 Fusiform: Both sides
4.1.3 Dissecting
4.1.4 False Aneurysm
4.2 SURGERY: Clipping of Aneurysm; Coiling (did
not treat just block not really stop the aneurysm)
5. MANAGEMENT
5.1 Regular exercise to reduce weight
5.2 Low sodium diet and limitation of alcohol
5.3 Assess CV status and VS; Take an average of 2
or more readings to establish HTN
5.4 Assess neurologic Disorders and observe for
changes that may indicate alteration in cerebral
perfusion (CVA)
5.5 Monitor I&O and weight
6. MEDICATION
6.1 Maintain quiet environment to reduce stress:
AWAY FROM NX station and elevator
ARTERIAL DISEASES
1. REYNAUD’S DISEASE: Vasospasms of the
arterioles and arteries of the extremities
(Oxygenated Blood); Ischemic à NECROSIS
1.1 ETIOLOGY
1.1.1 Cold [ICE]; Stress; Smoking
1.2 UPPER EXTREMITIES
1.3 ASSESSMENT
1.3.1 Blanching of ext. followed by cyanosis:
WHITE à à
BLUE RED
1.3.2 Reddened tissue
1.3.3 Numbness, tingling sensation
(Paresthesia: Impaired circulation)
1.4 MANAGEMENT
1.4.1 Stop Smoking
1.4.2 VASODILATORS
1.4.3 Avoid Precipitating factors
1.4.4 Warm Clothing
1.4.5 Avoid injuries to hands and fingers
2. BUERGER’S DISEASE/ THROMBO
ANGINITIS OBLITERANS: occlusive disease of
the median and small arteries and veins by clot
formation
2.1 RF: 30-35 y/o; Males; Men who SMOKE
2.2 ETIOLOGY:
2.2.1 Unknown, smoking, males
2.3 LOWER EXTREMITIES
2.4 ASSESSMENT
2.4.1 Intermittent Claudication
2.4.2 Ischemic Pain occurring in the digits
while at rest
2.4.3 Cool, Numb, tingling sensation
2.4.4 Diminished pulse at distal extremities
2.4.5 Ulceration
2.5 Amputation
2.6 MANAGEMENT
2.6.1 Instruct to stop smoking
2.6.2 Monitor Pulses
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6. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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2.6.3 Avoid injury to extremities
2.6.4 Administer vasodilators as prescribed
3. VARICOSE VEINS
- Distended protruding veins that appears darkened and
tortuous; Vein walls weaken and dilate, the valves
become incompetent
- VARICOSE: Veins full of blood
- In the RECTUM: Hemorrhoids
- In the ESOPHAGUS: Esophageal varices
3.1 ETIOLOGY
3.1.1 Prolonged standing (Pooling of blood) /
sitting (impede the circulation
especially when the popliteals are at the
edge of the sit)
3.1.2 PREGNANT Obesity
and : Increase
abdominal pressure
3.1.3 Congenital absence of valves
3.1.4 Constrictive Clothing
3.2 INCIDENCE
3.2.1 Female, Pregnant
3.2.2 35-40 y/o
3.2.3 Not necessarily Hereditary
3.3 S/SX
3.3.1 Rare to Have pain
3.3.2 MC Heaviness in the Lower
Extremities; Leg edema (due to
pooling)
3.4 MANAGEMENT
3.4.1 elevation 15-30 minutes
3.4.2 Compression with support stockings:
Has a gradient that has pressure;
Measured circumference of the calves
3.4.3 SCLEROTHERAPY: it involves
injection of a sclerosing agent in to the
varicose vein: Scleroses the vein
3.4.4 SURGERY: vein stripping and ligation
to relive pain, reduce swelling or
provide cosmetic results
3.4.5 EARLY AMBULATION: prevent
thrombophlebitis
HEMATOLOGIC
BLOOD COMPONENTS
STEM CELL: An originating cell; Capable of becoming another
type of cell
↓ ↓
Lymphoid Myeloid
↓ ↓ ↓
B-CELL T-CELL RBC, PLATELET,
WBC
Plasma Cells:
Antibodies or
immuno-
globulins
1. Helper: Activate B
and Killer T-Cells
2. Cytotoxic/ Killer
3. Suppressor: not
working: Immune
diseases
Differentiated: has functions and trasnsforms into another cell
1. ANEMIA
- Decrease in the number of RBC
1.1 TYPES
1.1.1 BLOOD LOSS: Hemorrhagic (>500
ml)
1.1.2 HEMOLYTIC: increased destruction
1.1.2.1 Sickle Cell
1.1.2.2 Thallacemia
1.1.3 MANUFACTURING
Pernicious
IDA
Aplastic Anemia
1.2 CONCEPT: Tissue Hypoxia: Underlying
cause of all manifestations accompanying
anemia
1.3 S/SX:
1.3.1 Pallor, Easy fatigability, Dyspnea, H/A
APLASTIC ANEMIA (PANCYTOPENIA)
- Damage to the bone marrow: Chemotherapy or
radiation
- Decrease in or damage to the marrow stem cells
- RENAL FAILURE: due to loss of erythropoietin
- Results in anemia, leukopenia, Thrombocytopenia
1. CAUSES: medications, chemicals, radiation
2. MANAGEMENT:
2.1 Remove the cause Supportive
2.2 BONE MARROW TRANSPLANT: from
the marrow; SITE OF ASPIRATION: Iliac
Crest
*BONE MARROW REJECTION: Graft vs Host Disease
(GVHD); The one rejecting is the BONE MARROW or the
marrow
*ORGAN REJECTION: the body rejects the organ
2.3 PERIPHERAL BLOOD STEM CELL
TRANSPLANTATION
*NEUPOGEN: ;
Filgrastin WBC production
*EPOGEN production
: RBC
LEUKEMIA
- Malignant disorder of hematopoietic system that
involves the bone marrow and the lymph nodes
- Characterized by uncontrolled proliferation of
immature WBC
- TOO MUCH WBC PRODUCTION: Anemia and
Thrombocytopenia; due to decrease RBC and
platelets
1. TYPES: classified by onset and severity and by
precursor cells
1.1 Acute ML: MC in Adults; Aplastic Anemia
1.2 Acute LL: MC in Children; Dangerous;
Very prone to infections; No defense
1.3 Chronic ML
1.4 Chronic LL
2. DX: BONE MARROW BIOPSY: Leukemic
Blast Cells
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3. MANAGEMENT
3.1 Chemotherapy
3.2 Radiation
3.3 Bone Marrow Transplantation: GVHD
*ADD: Study Blood Transfusion
LYMPHOMA
- Lymphatic problems
- LYMPHADENPATHY (Kulani): Phagocytosis;
Inflammation of the Lymph Node
- Lymphatic System: goes to the heart and turns
systemic
A. HODGKINS
• Proliferation of REED-STERNBERG cells in
a single lymph node then travel to other lymph
nodes: AFFECT B-CELLS
1. CAUSE: EPSTEIN BARR VIRUS
(Transmitted through Saliva by Kissing;
KISSING’S DISEASE); Starts as
INFECTIOUS MONOCLEOSIS (15-20 y/o);
FLU LIKE SYMPTOMS since it is viral; May
cause CA and needing Chemotherapy;
HIGHER CHANCE OF CURE
2. PROGRESSION
2.1 STAGE 1: Single Lymph Nodes/ Cervical
Lymph Nodes
2.2 STAGE 2: 2 or more lymph nodes on the
same side of the diaphragm (Still Good
Prognosis)
2.3 STAGE 3: Both sides of the Diaphragm
2.4 STAGE 4: Disease disseminated, spreads
to other extralymphatic organs like
SPLEEN (POOR PROGNOSIS)
3. S/SX
3.1 EARLIEST: Bone Pain and cyanosis of
face and neck; Enlarged, painless, Non
tender, firm, and movable lymph nodes
3.2 LATE: Hepatomegaly; Splenomegaly;
Difficulty of breathing; facial edema;
enlargement of the LE
*EXTRA-LYMPHATIC ORGANS: LIVER AND THE
SPLEEN
4. DX: Swab test
B. NON-HODGKINS
• Affects B and T-cells
• Tumors occurs throughout the lymph nodes and
lymphatic organs in an unpredictable pattern
1. S/SX: Prominent, painless generalized
lymphadenopathy
2. DX: Lymph Node Biopsy
3. MANAGEMENT: Radiation/
Chemotherapy; Transfusion RBS; Admin
02 and Rest
*MC Lymphoma in AIDS: NON-HODGKINS
*MC Cancer in AIDS: KAPOSI’S SARCOMA
MULTIPLE MYELOMA
- Abnormal proliferation of plasma cells (Precursors to
Antibodies)
- Immature and malignant WBC invade the bone
marrow, Lymph nodes and liver, spleen and
kidneys (HIGHLY VASCULAR, through the blood);
THE BONE MARROW IS INVADED and leads to
blood destruction throughout the body: Multiple
fractures, Increased Serum Ca & Kidney Stones (RF)
- BENCE JONES CHON in urine, Increased BUN,
Creatinine Hypercalcemia
1. S/SX: pancytopenia; pathologic fracture
(fracture secondary to another disease);
hepatomegaly, renal Calculi, Severe Bone
pain
2. MANAGEMENT
2.1 Bone Marrow Transplant
2.2 HD, Chemotherapy, Radiation
2.3 Encourage Fluid intake
2.4 Maintain seizure precaution due to
hypocalcemia
*PROTATE SPECIFIC ANTIGEN: for prostate cancer
RESPIRATORY
1. DIAGNOSTIC
1.1 Skin testing: Mantoux Testing (test of the
person is Exposed to the Client); 48 to 72 hrs;
Positive: Indolation (SWOLLEN AND HARD):
Measure 10 mm or more; AIDS or
Immunocompromised: 5 mm
*Once exposed, always exposed, no ne d to repeat Mantoux
e
test
1.2 CXR: preliminary only
1.3 SPUTUM EXAM: To determine positive for
TB; early AM, Cough, rinse mouth with water;
Gargle and Don’t swallow
*FOR THOSE WHO CAN’T COUGH: CPT, Bronchodilators
1.4 THORACENTESIS: position upright at side of
the bed, lean on overhead table; NEED FOOT
STOOL, to stabilize legs; IF not Pneumothorax
1.5 BRONCHOSCOPY: NPO before and after until
the gag reflex returns; or else ASPIRATION
2. INTERVENTION
2.1 OXYGEN THERAPY: Nasal Cannula (2-3);
Face mask (3L); Humidify if high
concentrations, tracheobronchial suctioning
2.2 CHEST PHYSIOTHERAPY
2.3 INCENTIVE SPIROMETRY: Done 10x every
hour, waking hours
2.4 CLOSED CHEST TUBES
(THORACOSTOMY)
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EPISTAXIS
- Don’t hyperextend; no ice compress
- Sit-up lean forward and head tilted down
- Pressure over the soft tissue of the nose
- Cold Compress
- Avoid Nose Blowing
- Nasal pack with Neosynephrine (Vasoconstrictor; 3-5
days; A1 Agonist)
TONSILITIS
- Inflammation of the tonsils; GABHS
- S/SX: sore throat, difficulty or pain in swallowing,
fever
- MGMT: ATB, Anti-pyretic, Saline Gargles
- Surgery: Tonsillectomy: POST-OP CARE: HOB to
450
elevate to reduce swelling; avoid citrus and
carbonated drinks: irritate the incision; Ice chips,
small sips of cold fluid, popsicle (First day); Soft
foods on (Second day)
*PEDIA: Prone position to facilitate drainage of blood due to
risk of aspiration and they do not have good swallowing
LARYNGITIS
*ADD: Laryngeal Cancer and Surgery of the Larynx
- inflammation and swelling of mucous membrane of
the larynx
- CAUSE: infection, improper use of voice, smoking
- S/SX: hoarse voice, throat irritation, dry non
productive cough
- MGMT: ATB, stop smoking, Removal of cause
(don’t speak, don’t whisper)
COPD
- A group of diseases that include: Chronic
Bronchiectasis; Chronic Asthma; Chronic Bronchitis,
Emphysema
- Causes: Airborne irritants and pollution, SMOKING,
allergens; Chronic RT infection
- ASSESSMENT
1. Barrel Chest (Antero-posterior Diameter
increased) and clubbing (excessive trapping of
air and cyanosis)
2. Cough, evectional dyspnea
3. Wheezing and crackles
4. Weight loss (unable to eat due to SOB); SFF
only, Increased myocardial oygen demand
5. Sputum production (amount, color consistent)
6. Use of accessory muscles: Main muscle is
DIAPHRAGM but extra: sternocleidomastoid,
scalene, trapezius, intercostal muscles
7. Posturing (leaning forward): better to breathe
leaning forward since it displaces the heart, less
pressure on the lungs
8. Pursed lip breathing (remove C02)
9. Can cause COR PULMONALE (R-CHF)
- DIAGNOSTICS
1. CXR: congestion and hyperinflation
2. ABG: respiratory acidosis and hypoxemia
- TREATMENT
1. CPT, Postural Drainage, Incentive Spirometry
2. FLUID INTAKE to 3L/ day if not
contraindicated (Contraindicated: If you have
COR PULMONALE/ CHF)
3. 02 at 2 3 L/day
-
4. Diet high in CHON, Vit C, Calories, Nitrogen
(CHO yields C02 so not much on these food
item)
5. Instruct diaphragmatic or abdominal and pursed
lip breathing ( inhale and
Instruct Consciously,
feel the / increase out;
abdomen go out The
diaphragm at the same time goes down; to relax
and decrease C02)
6. Suction
7. Encourage SFF to prevent dyspnea
8. Stop Smoking
9. Avoid person infection
10. RECEIVE IMMUNIZATION: Pneumonia
vaccine (Pneumovax: Only every 5 years); Flu or
Influenza (every year since viruses are faster to
mutation)
- MEDICATION
1. Bronchodilators: instruct oral and inhalants
2. Steroids
3. Anti-Leukotrienes
4. Mast Cell Stabilizers
5. Mucolytic
6. Expectorant
I. CHRONIC BRONCHITIS
1. Persistent cough for at least 3 MONTHS a year
for 2 successive years;
*IMPAIRED AIRWAY CLEARANCE: Bronchitis
2. S/SX: Edema of the mucous membrane; Hyper-
secretion of mucus; BLUE BLOATERS
(cyanosis; BLOATING: it can cause COR
PULMONALE, passageway is too narrow)
3. PREDIPOSING FACTORS: Cigarette smoking
& Bacterial infection
II. EMPHYSEMA
1. Level of the alveoli, the air went in and not out
the inelastic alveoli: OVER distended and non-
functional alveoli leading to rupture; Retaining
C02 and Carbonic Acid (respiratory acidosis);
BULLAE: air trapped alveoli
*IMPAIRED GAS EXCHANGE: Emphysema
2. S/SX: PINK PUFFER (vasodilation on the face;
carb on dioxide retention; PUFFER: due to
PURSED LIP breathing, prolonged expiration to
blow off all C02); Chronically Hypoxic
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3. NORMAL: Stimulus to breathe is increased C02
4. COPD: Stimulus to breathe is low p02
5. MGMT: 02 = 1-2 L/min
III. ASTHMA
- HYPERSENSITIVITY REACTION: Edema of the
mucous Membrane, Hypersecretion of mucus &
Bronchoconstriction (More dangerous than
Bronchitis since the muscle constrict the airway +
mucus production = AIRWAY OBSTRUCTION &
Respiratory Acidosis)
- Retention of C02 and air trapping
- Hypoxia
- Avoidance of the triggers
IV. BRONCHIECTASIS
- MC cause: Bacterial infection
- The bronchioles are over distended; No
bronchoconstriction
- Hypersecretion of mucus and edema formation
STATUS ASTHMATICUS
- Type of asthma not relived by normal bronchodilator
- High Fowler’s position; Monitor VS; Monitor
respiratory status; EPINEPHRINE/
AMINOPHYLLINE (Xanthine) IV; If not epi then
use aminophylline
PNEUMONIA
- Refers to bacterial, viral, parasitic or fungal infection
that cause inflammation of alveolar spaces and
increase in alveolar fluids. Ventilations decrease as
secretion the thicken
- CAUSES: Aspiration, Chemical irritants and Various
organisms
- ASSESSMENT
1. Chills, fever SOB, tachypnea, Accessory muscle
use
2. Sputum (rusty, green or bloody pneumococcal
pneumonia and yellow green with
bronchopneumonia);
3. Crackles, Ronchi, Pleural friction Rub (rubbing
sand paper) on auscultation; Cough and malaise
- DX: CXR: Consolidation; Diffuse patches; Sputum
Culture to determine what microorganism (bacterial
or other wise); WBC and ESR (due to inflammation)
are elevated
- MGMT: CPT, PD, IS; Diet high CHN, High calorie,
Force Fluids; Admin 02, Semi fowlers to facilitate
breathing and lung expansion; Change position
frequently and ambulate as tolerated to mobilize
secretions
- LOBAR PNEUMONIA: only one lobe of the lungs
- BRONCHOPNEUMONIA: patches of
consolidation all over the lungs
- HANDWASHING and proper disposal of secretion
PNEUMOCYSTIS CARINII PNEUMONIA
- MC cause of death in AIDs and form of pneumonia;
opportunistic to HIV
- MICROOGANISM: Pneumocystitis jiroveci
- Leading cause of death among HIV patient
- ASSESSMENT: fatigue, low grade, intermittent
fever, non-productive cough, dyspnea, anorexia,
weight loss
- MGMT: Pentamidine and Bactrim; monitor I&O;
Anti-pyretic; Administer 02, monitor hypoxemia
PLEURAL EFFUSION AND EMPYEMA
- Pleural Effusion: excess of fluids in the pleural
space
- Empyema: accumulation of pus and necrotic tissue
in the pleural space
- CAUSE: bacterial or fungal infection, RF, Hepatic
Disease with ascites
- ASSESMENT:
1. Pleuritic Chest Pain that is sharp and increases
with inspiration;
2. Decreased breathe sounds (lung is being
compression; Absent: if too much fluid;
ATELECTASIS), Dyspnea, fever, malaise; DRY
non productive cough caused by bronchial
irritation or mediastinal shifting to unaffected
side
- TX: Thoracentesis & Thoracotomy; Chest tube
Drainage
- MGMT: tell the pt. to expect stinging sensation from
the insertion
PNEUMOTHORAX
- SPONTANEOUS: The rupture of bleb (Bullae), MV
(mechanical ventilator; OVERINFLATION and
rupture; positive pressure MV), Internal cause
*Negative Pressure: MG; Iron Lung Machine: POLIO
- OPEN: Came from a source outside: Gunshot;
opening through the chest allows air to flow between
pleural space and outside of the body
- -
TENSION: Build up of air in pleural space that can’t
escape
*Stab wound: remove, if ever, cover with a VENTED gauze
(3 sides closed but one side open; this will let air out as well;
may cause TENSION PNEUMOTHORAX if completely
sealed)
- MEDIASTINAL SHIFTING: The HR is increased,
BP is low and the RR low; The heart trachea and
lungs to the unaffected side
are moved
- The difference with open and close VS Tension:
.
When inspiring it’s the same (the lungs and heart
move to unaffected side and affected lung is small or
not inflated); When the lung is expiring, this will
normally inflate the affected but in tension, the heart
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and lung will still continue being in mediastinal
shifting
- ASSESSMENT: Dyspnea, decreased 02 at;
Diminished or absent breath sound; Sharp chest pain
that increases with exertion; tracheal shift to
unaffected side (tension); SUCKING SOUNDS
WITH OPEN CHEST WOUND
- MGMT: apply vented dressing; Position in High
Fowlers; Prepare for chest tube placement until the
lungs has fully expanded; Monitor hypotension,
tachycardia and tachypnea (mediastinal shifting);
Administer 02 and Monitor chest tube drainage
system
CHEST TUBE
- Returns negative pressure to intrapleural space
- Used to remove abnormal accumulation of air and
fluid from pleural space
- CHAMBERS
1. COLELLCTION CHAMBER: Drainage
2. WATER AND SEAL CHAMBER: Tip of the
tube under water (2cm) allowing fluid and air
from entering the pleural space; Immersed so
that the air will not go back; Water will show
INTERMITTENT BUBBLING
3. SUCTION CONTROL CHAMBER: gentle
bubbling normal high
; only used when there are
amounts of mucous but does not drain; Attached
to suctioning apparatus; Expected to have
CONTINOUS BUBBLING
- WATER OCCILATES/ TIDALING: moves up
when the patient inhales and moves down as the
patient exhales; To see if the bottle system is moving
- NO OSCILLATION or TIDALING: [1]
obstruction in the system (kinked or pt. is lying down
on the tube; Thick secretions like pus); [2] lung has
expanded meaning to more secretions to suck; To
determine if not effusion subsided: CXR
*ONE BOTTLE: Drainage and water sealed into one
*TWO-BOTTLE: Drainage and Water seal
- MGMT: Monitor the drainage; Keep tubes free of
leaks, dependent loops or other obstructions; Do not
strip or milk tubes unless specified by the doctor
(Milking: Pressing; Stripping: continual pressing
from start for bubbling
until end); Check : Intermittent
bubbling is normal while continuous bubbling is air
leak; If water is used in the suction chamber, check
the continuous bubbling which indicates the system is
working
*If the bottle brakes, immerse the tube unto water; A
BOTTLE OF STERILE WATER: must be placed on the bed
side; Clamping will cause pressure then TENSION
PNEUMOTHORAX
*if pulled out: use Vented gauze and call MD
*if removed after use: use occlusive dressing; take a deep
breath and pull; use petrolatum dressing or dry dressing
LUNG CANCER
- The lungs are highly vascular since it oxygenates the
body
- TYPES:
1. NON SMALL CELL: MC;
1.1 Adenocarcenoma
1.2 Squamous- Cell Carcinoma
1.3 Large Cell Carcinoma
2. SMALL CELL
- CAUSES: Smoking (pack/year/history; Exposure to
environmental and occupational pollutants);
MINERS: Mineral deposits into the lung tissue
PACK YEARS:
# packs per day X Number of years smoked
1 PACK = 20 cigarettes
- EARLIEST MANIFESTATION: Productive Cough
- LATE MANIFESTATION: hemoptysis: eroding lung
tissues
- S/SX: Dyspnea, hoarseness, chest pain, anorexia, and
weight loss, weakness
- SURGERY: SIZE matters
PNEUMONECTOMY
SECTION DESCRIPTION
Wedge resection /
Segmentectomy
Only near the part of the
tumor
Lobectomy Entire lobe has been
infiltrated
*These surgeries WILL have CHEST TIUBES
*UNAFFECTED SIDE: position, there is a chest tube and
make the lung re-inflate properly
Pneumonectomy Whole side of the lung
*NO CHEST TUBE: no lung no bleeding, no anything
* AFFECTED SIDE: position; allow the remaining lung to
expand
*TB: 2 weeks of RIPES and then can now socialize; no more
isolation
*EMPHYSEMA: alveoli; DYPNEA ON REST
*Bronchitis: Chronic productive cough
*Asthma: WheezingMUSCULOSKELETAL DISORDERS
*ADD: proper body mechanics
TRAUMA
- All signs of trauma will cause inflammations
SPRAIN: ; tendons
overstretching
STRAIN: Over twisting; joints and ligaments
Dislocated: when outside; total
Subluxation: partial dislocation
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FRACTURE
- the move it the more it will brake
- SIGNS: Injury will cause inflammation; Loss of
motion; edema, crepitus (rubbing against another
bone), shortening of the extremity
- IMPACTED: one bone is rubbing on another (Sound
is called Crepitus)
- STAGES OF BONE HEALING
1. HEMATOMA: immobilize, the only thing that is
keeping it together is blood clots; Inflamed (First 3
days; don’t place a cast since it will compress the
site; PLACE a POSTERIOR MOLD: which is a hard
board and bandages wrapped around it)
2. GRANULATION TISSUE STAGE: Osteoblasts go
to the site; Bones are made of protein and at this
stage protein will be laid down; WHOLE CAST are
now placed here since inflammation has decreased
3. CALLUS STAGE Calcium deposition
: START of ;
partial weight bearing can now be done (PROM; only
the done for fractures on joints; the more sedentary
you are; the more calcium will go out the body)
4. REMODELING: ossification and remodeling
MANAGEMENT
*SPLINT: it is above and below the JOINT; ex if radial
fracture: long arm cast
STIFFNES OF THE JOINT: Contracture
- MGMT: immobilize ( )
SPLINT : the more you move,
the more you break; NECK (cervical: IMMOBILIZE
THE NECK, ASAP); Cervical Collar: prevent injury
to phrenic nerve
*PHRENIC NERVE: C2 C3
-
- RICE (educe inflammation; Rest Ice, Compression,
Elevation)
- Reduction: Realignment of the bone
1. OPEN: surgery to realign the bone
2. CLOSE: Casting/ traction
CAST CARE
- Types:
1. PLASTER OF PARIS: it looks like gauze but
chalky in consistency; place in water then
squeeze then mold it in place; DRIES: 24-48 hrs:
Do not touch the cast when wet; USE THE
PALM of the hand when molding or moving it
around; Cement/ heavy
2. FIBERGLASS: it is plastic, synthetic; Wet the
gauze and little bit of water; DRIES: 20 min;
Plastic/ Light
- MGMT: Monitor the extremities for circulatory
impairment inserted
(1-2 fingers must be to
determine if the cast is not too tight):
COMPARTMENT SYNDROME
5P’s
1. PAIN
2. PALLOR
3. PARESTHESIA
4. PULSELESSNESS
5. PARALYSIS
- Monitor for any drainage on the cast; Instruct to keep
the cast clean and dry; DO NOT WET THE
PLASTER OF PARIS CAST, will make it soft; For
Fiberglass, you can wet it but it is discouraged, the
outside can be cleaned but the inside cannot dry
properly; Instruct not to insert anything in the cast; do
not write anything on the cast
- INFX:
1. Monitor for Drainage
2. Monitor HOTSPOTS: touch the cast it must be
cold but when it feels warm that is the infected
are
*NO POWDER: will contribute to infection
- Instruct to do ISOMETRIC EXERCISES (alternate
contraction and relaxation)
TRACTION: Act of pulling into the proper location
1. Ensure the weights are hanging freely
2. Maintain continuous traction (once you pull it don’t
let it go; misaligned: will heal into that position
[MALUNITED/ MALUNION] or does not stick
together [NO UNION])
3. Must always have a counter-traction: the need for
balance (ONLY 10% of the patient’s Body weight)
- BRYANT’S TRACTION: for children <3y/o; the
feet are held up; The buttocks of the baby must be off
the mattress, not touching the bed meaning NO
PULL; Place a mobile to stimulate the baby
- SKIN TRACTION
1. CERVIVCAL TRACTION: Skin type; cervical
2. PELVIC TRACTION: for lumbar spine
- SKELETAL TRACTION
1. CRUTCHFIELD TONG: Drilled into the skull
for traction
2. BST: Clean the pin since there is an entry for
microorganisms;
2.1 PIN CARE: Do not clean with hydrogen
peroxide: will cause anaerobic infection;
No betadine: this will oxidize and rust the
pins; Apply ATB; place antiseptic
*SKIN TRACTIONS: are temporary, for minor injuries
*SKELETAL TRACTION: severe injuiries
CRUTCHES
- The crutches not up to the AXILLA: this will cause
BRACHIAL PLEXUS COMPRESSION
(paresthesia of the fingers)
- MEASUREMENT:
1. 2 INCHES below axilla
2. 2-3 INCHES into the side; 6-12 inches into the
front
3. ELBOW FLEXION (20-30 degrees)
- Exercises to prepare for CW:
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1. Hand muscles exercise (all the weight in the
palm of your hands to stabilize)
2. Arm muscle exercise
- Stair Climbing
1. UP: good leg with bad leg
à crutches
2. DOWN : bad leg à crutches with good leg
“UP WITH THE GOOD, DOWN WITH THE BAD”
*If the patient is non-weight bearing: 3-point gait, may also
use Swing to (crutch forward and swing to the point of the
crutch) & Swing Through (crutch forward and pass the
crutches)
*If patient is partial weight bearing: 4-point gait
*2-point Gait: as if walking; faster version of 4-point gain
CANE
- Cane held on the stronger side or unaffected side
- Cane walks together with the weak leg
COMPLICATION OF FRACTURES
1. FAT EMBOLISM: systemic fat lobules into the
circulation; As the bone fractures, the fat is adhered
unto by platelets and becomes a blood clot, then an
embolism; MC in long bone fractures (ribs, tibia,
pelvis)
1.1 S/SX: Chest pain, CHANGE IN LOC;
Tachypnea, Tachycardia, Petechae on neck and
the anterior chest (INTRAVASCULAR
THROMBOSIS)
1.2 MGMT: DBE and CE; 02 Supplementation;
Intubation
2. INFECTION/ OSTEOMYELITIS
2.1 TYPE: Acute and Chronic
2.2 Signs of infection: Fever and chills
2.3 Infection may turn the bone necrotic:
SEQUESTRUM (Surgery: Sequestrectomy: A
type of debridement of necrotic bone)
2.4 MGMT: NOT UNTIL YOU REMOVE THE
NECROTIC BONE, will the bone heal; IV ATB:
6-8 weeks then to ORAL
switch
3. COMPARTMENT SYNDROME
3.1 Tight cast; Neurovascular compression
3.2 MGMT: 5P’s; Monitor for ATN (Acute
Tubular Necrosis: may lead to RF;
MYOGLOBIN: Any single time that the muscle
is hurt, myoglobin is released; Myoglobin is very
small and can go to the renal tubules and cause
damage)
3.3 SURGERY: Faciotomy (Straight into the fascia
to relieve the compression)
HIP FRACTURE
- Proximal 3rd
fracture of the femur
- Common among elderly women
- HIP REPLACEMENT TYPES:
1. Total Hip Replacement: all parts
2. Partial Hip replacement: except acetabulum
- POST-OP
1. DISLOCATION: Always Abducted (place
pillows between the legs); Abduction will
displace prosthesis for 8 weeks; When asleep
2. Avoid bending or cross legs
3. Use trochanter roll to prevent external rotation
AMPUTATION
- Surgical removal of the part of the limb; LIMB is
very vascular and bleeds after; PRESSURE
DRESSING must be in place
- POST-OP
1. Monitor VS for BLEEDING
2. Evaluate for Phantom Limb Sensation and pain;
explain to the patient’; “Its is no longer there but
it will take some time to go away”
3. During the FIRST 24hrs, elevate the stump;
After the 48 hr, flat on bed to prevent FLEXION
HIP CONTRACTURES
4. After 48 hrs, instruct also to be on PRONE
POSITION, several times a day (PRONE: 3x a
day; 5-10 minutes)
5. Maintain application of ACE WRAP to promote
stump shrinkage (FINGURE OF 8)
- POST OP COMPLICATION; hemorrhage, Infection
and Contracture
-
*DISARTCULATION: removal of the entire joint with the
extremities
RHEUMATOID ARTHRITIS
- Autoimmune and hereditary (IMMUNE
COMPLEX); The Cytotoxic T- -
Cell & B Cells attack
the Synovial membrane
- Can occur in children; Juvenile Rheumatoid
Arthritis (JRA)
- Bilateral and symmetrical, inflammatory;
SYSTEMIC
- Usually affects the joints symmetrically (on both
sides equally), may initially begin a couple of joints
only and most frequently attacks the WRIST,
HALNDS, ELBOWS, SHOULDERS, KNEES AND
ANKLES
- Progressive, Lifetime disorder
- SYNOVITIS: formation of scar tissue and BONY
ANKYLOSES (causing contractures due to stiffness)
(permanent)
- Remission and Exacerbation (FLARE UP: stressed or
ill; the body will release these T-Cells to defend)
- IMMUNE COMPLEXES: RH Factor (Auto-
Antibodies)
- PANNUS FORMATION: highly vascular
granulation
- On and off then damage at area à healing à healed
but keep on fracturing à scar formation à
Ankylosis and Pannus Formation
- JOREN’S SYNDROME: Systemic effect of RA;
Dryness of the eyes and the vagina
- S/SX: painful warm, swollen joints with limited
motion; STIFF in the morning after periods of
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inactivity; SWAN NECCK deformity; Bouteniere’s
Deformity; Ulnar Deviation
- DX: Increased WBC, RF + (Auto Antibodies);
Elevated ESR; effusion in the joint (Arthrocentesis)
- MANAGEMENT
1. Bed Rest
2. PROM
3. Heat stiffness and cold for inflammation; Warm
Shower in the AM
4. PT
5. Splint painful joints
- MEDICATION: Aspirin (the 4 effects); NSAIDS
(Ibuprofen); Corticosteroids; DMARDS (Disease
Modifying Anti Rheumatic Drugs):
Immunosuppressants, Methotrexate, Sulfasalazine,
GOLD therapy
- SURGERY: Synovectomey & Arthroplasty
*SLE: you it is
damage anything with COLLAGEN ( found
everywhere; SYSTEMIC; Butterfly Rash)
OSTEOARTHRITIS
- Degeneration of articular cartilage
- MC in Obese Clients
- Involves weight bearing: HIPS; Knees; Fingers;
Vertebra (Lower Back)
- S/SX
1. Joint pain aggravated by use; relieved by rest
2. Stiffening of joints
3. Formation of bony outgrowths
(OSTEOPHYTES); HEBERDEN’S (Distal IP)
and BOURCHARD’S NODES (Proximal IP)
4. Decreased ROM and CREPITUS
- MANAGEMENT
1. Relieve strain and further trauma to joints
2. Cane or walker, if indicated
3. Joint replacement as needed
4. Proper Body Mechanics
5. Avoid Excessive weight bearing and standing
6. PT
7. Relief of pain (NSAIDS)
8. CHONTROTIN: repairs the cartilage AND
GLUCOSAMINE
- TYPES OF HIP REPLACEMENT
1. TOTAL HIP: All parts
2. patella
PARTIAL: except
- PASSIVE ROM MACHINE: for continuous
movement and stop contracture of the knee
replacement
GOUT
- Disorder of purine metabolism
- Uric acid crystals in the JOINT: TOPHI
- S/SX: Joint pain, redness, ankle and great toe (MC)
- MANAGEMENT
1. Rest
2. Low purine and increase fluids
3. PHARMACOTHERAPY
3.1 Acute Attack: Colchicine and NSAIDS
3.2 Uricosuric Drugs: Excretes Uric acid:
Probenecid (Benemid)
3.3 Allopurinol (Zyloprim): Inhibits the
formation of uric acid
HERNIATED NUCEUS PULPOSUSU/ SLIP DISK
- NUCLEUS PULPOSIS: the jelly inside the vertebral
disk
- ANNULUS FIBROSUS: this holds the nucleus
fibrosis
- CAUSES: lifting, degeneration of the disc (loses
water content); also caused by sitting down
- AREAS
1. Cervical: Shoulder pain radiating to the hand;
Weakness and Paresthesia; Weight bearing on
the NECK/ HEAD; On cervical Traction
2. Lumbosacral: back pain radiating across buttocks
and down the leg (SCIATIC NERVE; Sciatica);
weakness ad paresthesia; Muscle spasm in the
Lumbar region; on pelvic Traction
- MANAGEMENT
1. Bed rest on firm mattress with board
2. Traction
3. Local Application of het
4. Lumbosacral corset (BACK BRACE)
5. Prevent complication of Immobility
- SURGERY: Laminectomy with Discectomy;
SURGICAL FUSION (Spinal fusion with rod
insertion)
- POSTOP:
1. Turn the patient as a whole (LOG ROLLING
TECHNIQUE)
2. LUMBAR: HOB, flat, supine with legs slightly
flexed
3. CERVICAL: HOB elevated, with neck
immobilized with collar or sandbag
GASTROINTESTINAL HEPATOBILLIARY
&
- Mouth into the Anus; Unsterile
GERD
- The food is refluxing up to the esophagus; Gastric
contents flow upwards to esophagus
- Common for obese and pregnant women
- Any activity that increase intra abdominal pressure
(Overeating, bending, tight clothing), Foods that
relax the cardiac sphincter (Alcohol, peppermint,
caffeine, high fat diet [fats are not easily digestible,
stays longer in the stomach]), lying down after eating
- ASSESSMENT: Dyspepsia; Dyspepsia;
ODYNOPHAGIA (painful swallowing); Esophagus;
Eaophagitis
- MANAGEMENT:
1. Avoid alcohol, peppermint, caffeine, high fat
diet;
2. 15-30 minutes High Fowler (Supine opens the
sphincter due to pressure)
3. Lose weight
4. Avoid over-eating and tight fitting clothes
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*SWALLOW AIR: carbonated drinks, chewing gum and
eating fast
*HERNIA: protrude; Can also cause GERD due to opening of
the sphincter
*Ambulation increases Peristalsis
PEPTIC ULCER
- GASTRITIS: inflamed only but later forms
ulceration causing GI bleeding; The deeper it gets
then erodes the mucosa
- PERITOTINITIS: from the contents of stomach will
cause septicemia à SEPTIC SHOCK
- STRESS, STIMULATED or EXCITED (SNS):
Gastric Ischemia; CURLING’S ULCER (for GI) and
CUSHINGS (inc. ICP); Both are still related to
gastric ischemia
- Increases release of gastric acid or HCL: hot and
spicy; Food with MILK (It is rich in protein; You
need pepsin to breakdown CHON, pepsin stimulates
the parietal cells to release HCL); Alcohol, Cigarette
Caffeine, Drugs: NSAIDS, ASA, Steroids; NUMBER
1 CAUSE IS H. PYLORI (90 %)
- KINDS
1. DUONDENAL: Hyperacidity; MC Duodenal
and most acidic
2. GASTRIC: Decreased Mucous; Hyposecretion
of HCL
*Don’t give reduced; H2; PPI and antacids to GASTRIC
ULCERS, it will not help
- DUODENAL: Nothing buffers the food; no food
makes it painful; 2-4 hours after eating; Wakes up in
the middle of the night due to pain
- GASTRIC: no mucous and more painful when you
eat; 1-2 after eating
- MGMT
1. Relieve the pain
2. Lifestyle modification
- MEDICATION:
1. ANTACIDS: Neutralize Gastric Acids
1.1 Magnesium, Aluminum, Calcium
*Magnesium Based Antacid: Diarrhea
*Aluminum Based Antacid: Constipation
2. DECREASE ACID PRODUCTION
2.1 Proton Pump inhibitors (Esomeprazole):
Most effective for DUODENAL!
2.2 H2 Blocker (Cimetidine, Ranitidine)
3. PROVIDE PROTECTIVE COATING OVER
ULCERATIVE SITE
3.1 Sucralfate (Carafate)
4. INCREASE MUCOUS PRODUCTION
4.1 Misoprostol (Cytotec): GATRIC!
5. ANTIBIOTICS
5.1 Amoxicillin
5.2 Metronidazole (Flagyl)
- SURGERY: VAGOTOMY (Sever the vagus nerve
which enervates the parietal cells; Inhibits release of
HCl)
1. BILROTH I (Cut the stomach and attach to the
duodenum) & II (cut the stomach and attach to
the jejunum; Shorter; Very Prone to DUMPING
SYNDROME): Ga tric resection
s
2. TOTAL GASTRECTOMY (Pernicious
Anemia: loss of intrinsic factor for B12)
- POST OP:
1. Maintain on NPO; TPN (Pure glucose 50 %;
Check CBG every 6 hours; DO NOT D/C
abruptly stop; only good for 24 hrs [Wait longer
and may cause SEPTICEMIA and change the
whole tubing system]; make sure to infuse D10%
to wait for next TPN)
*72 hours: for normal IV VS TPN is 24 hrs
*D50: is for UNCONSCIOUS HYPOGLYCEMIC
2. Maintain on fowler’s position for comfort and to
promote drainage
3. NGT for drainage
4. Monitor dressing for drainage (bleeding)
5. Assess bowel sounds
DUMPING SYNDROME
- Prevent dumping syndrome: rapid emptying gastric
content contents into the small intestines which has
been anastomosed to the gastric stump
- The fluid goes to the stomach which decreased
INTRAVASCULAR VOLUME and goes to the
stomach; Majority of blood to the stomach and causes
Dizziness (decreased cerebral perfusion);
Tachycardia and LOW BP
- CAUSE: ingestion of food HIGH in CHO and
electrolytes, which must be diluted in the Jejunum;
Ingestion of Fluids at mealtimes (DIET: low CHO or
simple sugar; Drink after meals)
- ONSET: 15-30 minutes after meals so lie down!
- S/SX: 3D’s; Diarrhea, Dizziness, Diaphoresis; N/V,
palpitations
MGMT: SFF; Chew food thoroughly; Lie down after
meals; Low CHO diet; Do not drink fluids during
meals;
APPENDICITIS
- Obstruction of the VERMIFORM APPENDIX;
FECALITH (MC cause of Appendicitis; small piece
of feces; since it should not contain anything);
BARIUM (drink fluids after or it may dislodge in this
area)
- S/SX
1. Acute abdominal pain (RIQ); McBurney’s Point
2. N/V/A
3. Rigid Abdomen with guarding
4. Rebound Tenderness
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5. Elevated WBC count, Fever
6. Sudden cessation of pain means rupture: NO
ANALGESICS if there are no DX for it
*PALPATION of the LEFT lower abdomen causing pain in
RIQ
*BLUMBERG’S SIGN: rebound Tenderness; Peritonitis
*ROVSING’S SIGN: palpate on the Left it hurts more on the
RIGHT
- MANAGEMENT:
1. Bed rest
2. NPO
3. NO NARCOTICS initially will mask the pain
4. NO ENEMA/ Laxatives: can cause perforation;
High pressure into the intestinal tract and cause
rupturing
5. ATB TX
6. Surgery: Appendectomy
INFLAMMATORY BOWEL DISEASES
- AUTOANTIBODIES to the GI
CROHN’S DISEASE ULCERATIVE COLITIS
(ulcer: Bleeding, Colitis:
Inflammation of COLON)
Autoimmune Autoimmune
Ileum & Ascending:
Digestion, Metabolism and
Partly elimination; FAT is
metabolized in the illeum;
They cannot absorb FAT
(STEARRHOEA); Also Fat
soluble ADEK deficiency; No
Vitamin K (Bleeding)
Rectosigmoid:
Elimination problem only
RIGHT Lower quadrant pain Left Lower Quadrant Pain
3-5 watery stools 15-20 BLOODY Diarrhea
(Shock and F&E Balance)
TRANSMURAL
INVOLVEMENT: All layers
have already been involved
SHALLOW ULCERATION:
few layers only
Ileostomy Colostomy
COBBLESTONE
APPEARANCE/ SKIP
LESIONS:
not all segment, there are
parts without
CONTINOUS PATTERNS:
all the parts of the
rectosigmpoid are inflamed
STEROIDS & FLAGYL STEROIDS & FLAGYL
*CHEMOTHERAPY: is used also for their
immunosuppressant effect
- MANAGEMENT:
1. Rest the bowel
2. Control the inflammation
3. TX INFX
4. Correct Malnutrition: Chron’s: ADEK
5. Alleviate Stress: causes exacerbation
6. Provide Symptomatic Relief
- MEDICATIONS: DMARDS:
AMINOSALICYLATE(Sulfazaline), ATB, Steroids,
Immunosuppresants
- SURGERY
1. CHRON’S PROCTOCOLECTOMY: total
removal of the Intestines; Liquid stools
Large
and may irritant incision
2. CONTINENT ILEOSTOM/ KOCK’S
POUCH: the bag is inside: the intestines are
used to create the pouch; there is a whole;
Continent (Can be manually drained through
CATHERTER); With a flat stoma on the right
side of the abdomen (Drained every 2-4 hours)
2.1 ADVANTAGE
2.1.1 No need to wear an external pouch
2.1.2 Minimal kin Problems
2.1.3 No flatus or leakage of stool
- PRE-OP
1. Reduce the bacteria in the intestinal tract to
prevent infection: NEOMYCIN
2. Reduce colon content: low residue diet,
laxatives, enema
3. Decompress GI tract
- COLOSTOMY CARE
1. Skin Care: cleanse with mild soap and water
2. Odor control: no gassy foods or smelly
(asparagus)
3. Control gas: no eggs; place charcoal or baking
soda to deter scent
4. Colostomy Irrigation: to stimulate peristalsis; to
establish a regular pattern; Almost the same as
enema but inserted into the colostomy; can only
be done ONCE a DAY or may cause diarrhea
- COLOSTOMY IRRIGATION
1. DO NOT INSERT NO MORE THAN 4 inches
2. Do not force catheter into the stoma
3. Elevate solution 12-18 inches
4. 500
Irrigate only with -1000ml of warm tap water
5. Do not irrigate more than once a day
- STOMA CARE:
1. COLOR: pinkish, reddish with slight edema for
5-7 days
2. PURPLE: is cyanotic
3. Beefy red: inflamed infected
LIVER CIRRHOSIS
- Scarring if the liver; irreversible damage to the liver
- CAUSES:
1. Laennec (Alcohol);
2. post Hepatitis (VIRAL): Fibrosis;
3. Biliary Obstruction (chronic bile obstruction
causes cirrhosis);
4. Cardiac (R-CHF)
- LIVER CIRCULATION:
1. Lymphatic artery: BLOOD is 20% oxygenated
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2. Portal Vein: From the GI tract 80%
unoxygenated Blood (needs more of unoxy)
- Once the liver is damage, causes PORTAL
HYPERTENSION because the blood cannot enter.
- S/SX: GI Symptoms: N/V, Anorexia, decreased
energy (cannot metabolize and Glucose
CHO
properly); HEPATOMEGALY (Fatty Liver; caused
by the loss of the liver to metabolize fats); Decrease
albumin (CHON) (shifting due to
production: edema
decreased colloidal pressure) ascites; decreased
production of clotting, bleeding anemia
*ANTIBODIES are made out of CHON, since you can’t
metabolize proteins, you will be prone to Infections
* CLOTTING FACTORS ARE ALSO MADE OF CHON
- Obstruction of Bile flow: Decreased absorption of
fats and ADKEK; VITAMIN K is for clotting: THEY
DIE of HEMMORHAGIC STROKE
- Decreased conjugation of Bilirubin: ACHOLIC
stools, tea Colored Urine
• RBC (120 days) à HEME + BILIRUBIN à
Unconjugated bilirubin à not water soluble
(cannot be excreted) à Glucoronyl Transferase
• In the Liver converts it into CONJUGATED
BILIRUBIN: goes to the liver to be recycled
and the remaining becomes STERCOBILIN
(gives the color or the liver); Which in turn
causes ACHOLIC STOOLS
• The one left with the liver and goes to the blood
HYPERBILIRUBENEMIA; then to the kidneys
causing HYPERBILIRUBINEMIA which is
TEA COLORED URINE
- Decreased deamination of CHON Ammonia
- can’t be
converted to urea
• AMMONIA is toxic to the Nervous System;
Deamination in the Liver to converts it into
water soluble UREA
• This will increase the BUN
- S/SX OF HEPATIC ENCEPALOPATHY
1. Confusion
2. Forgetfulness
3. Peripheral: ASTERIXIS
- Liver also has something to do with Sex Hormone
use: Males (gynecomastia) and Females (hirsutism);
The Sex hormones are destroyed
- MANAGEMNT
1. Correct electrolyte imbalance
2. Reduction of ammonia formation:
2.1 NEOMYCIN, LACTULOSE
2.2 CHON restriction, tap water enema
*MODERATE CHON but lower with hepatic Encephalopathy
*HIGH BIOLOGICAL CHON: MEAT
*LOW BIOLOGICAL CHON: Beans or monngo in CHN
*If you use LOW biological, you will eat a lot and cause more
feces so you use High biological to decrease stool
3. NGT to suction
4. Potassium Sparring: Spirinololactone
(CIRRHOSIS has increased sodium and
Hypokalemia)
5. Paracentesis
6. BEDREST: to reduce metabolic demands to the
liver
7. High CHO, High Calorie Diet
ESOPHAGEAL VARICES
- When the client eats the varices can be hit and cause
bleeding without chance of clotting
- STEGSTAKEN BLAKEMORE TUBE: it puts
pressure on the esophagus and stomach; there are two
balloons; No blood supply and causes ESPHAGEAL
VARICES (Deflate 5 minutes 10 hrs per day
in 8- ); if
ever the patient pulls out cut the balloons SCISSORS
on bed side
*what do you need in BED SIDE Thyroidectomy:
Trachesotomy Set
- MANAGEMENT
1. IV FLUIDS
2. Anti Emetics
3. Stegstaken-Blakemore
PANCREATITIS
- Inflammation: AUTODIGESTION by the trapped
enzymes; Obstruction and edema; Interstitial
hemorrhage and tissue necrosis
- CAUSES
1. Chronic Alcoholism
2. Gallstone
3. Infection
4. DRUGS: Chlorothiazine, Glucocorticods –
PROVOKE PANCREATITIS
- May hurt due to the trapped pancreatic enzyme
- S/SX:
1. Steady, severe epigastric pain: back, aggravated
by fatty meal and recumbent position
2. Vomiting which does not relieve epigastric pain
3. Fever
4. Abdominal pain
5. Elevated lipase and amylase: Characteristic
Indicator
6. Elevated WBC, blood sugar (since the pancreas
creates the insulin; causing DM) and bilirubin
- SIGNS OF PERITONEAL BLEEDING
1. CULLEN’S SIGN: discoloration of abdomen
and peri-umbilical region
2. TURNER’S SIGN: Bluish discoloration of the
flanks
- SIGNS OF PERITONITIS: Blumberg’s Sign
(rebound tenderness)
- MANAGEMENT
1. Client will be free from pain or less: NPO:
prevents auto-digestion; ANALGESIS: Demerol
(drug of choice); NO Morphine causes spasm of
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the sphincter of oddi; ANTICHOLINERGIC:
Probanthine: decrease secretion and relax
sphincter of Oddi
2. Client will be free form shock: IV FLUIDS
3. TPN and Insulin as needed and Vitamins
4. Stop drinking alcohol
- SURGERY: WIPOL’S SURGERY: head of
pancreas and and part duodenum
*ADD: Pancreatic CA
CHOLELITHIASIS
- Stone formation in the gall bladder
- CHOLECYSTITIS: inflammation of the gall bladder
usually precipitated by gallstones (Cholelithiasis)
- CHOLEDOCHOLITHIASIS: Stone formation at the
common bile duct
(CHOLEDOCHOLTITHOTOMY)
- Incidence (5Fs)
1. Female
2. Forty (age: 40 and above)
3. Fair Complexion
4. Fertile
5. Fat
- Fatty Foods and Dehydration: Liquid bile but
becomes dehydrated due to low fluids
- The COMMON BILE DUCT: cannot be removed but
only remove the stone (T-TUBE)
- MANIFESTATION: Epigastric distress; Abdominal
Distention; RUQ pain after fatty meal; REFERRED
PAIN to Shoulder
- MURPHY’S SIGN: with pain when palpated during
DB
- MANAGEMENT: Pain: DEMEROL (drug of
choice): Do not give Morphine: causes spasm of the
sphincter of oddi
- NON SURGICAL
1. DISSOLUTION TX: Chemodeoxycholic Acis
(chenosiol), Ursodiol PO: 4-6 months to take
effect and dissolve and few could be dissolve
2. ESWL: followed by oral dissolution; 1500
shockwaves delivered in 1 2 hours done on
-
selective basis; <3 stones; Instruct to remain
motionless for 20 minutes-1 hour;
ABDOMINAL AREA WILL BE BRUISED;
Also for Kidney stones
*HIGH INCISION OF OPEN CHOLE: does not promote
DBE and will cause Pneumonia and Atelectasis; Open:
monitor for respiratory distress
- -
POST OP
1. Maintain a patent NGT
2. Assess T-Tube if common bile duct is
manipulated (500mL/ dy for 1st
few days):
Drains the bile until the COMMON BILE DUCT
IS NOLONGER INFLAMMED; green discharge
*How to know if the CBD is no longer inflamed: Clamp the T-
Tube and let the patient eats; He will be able to tolerate the
feeding; So if the client cannot tolerate (N/V), clamp
automatically
3. Position: Low to SF
4. Monitor dressing
5. Clamp Tube as ordered: open ready ti eat
6. DBE
7. EARLY ambulation
8. FAT FREE DIET for 6 weeks
GENITOURINARY
KIDNEYS: Urine formation; Excretion of waste products
- URINE is the vehicle to remove waste ;
products
Waste Product: CHON metabolites (in metabolizing
CHON: UREA (80%; BUN), Creatinine, Phosphate,
Sulfates, Uric Acid); ALL OF WHICH WILL
CAUSE METABOLIC ACIDOSIS
- REGUALTION of electrolytes: Sodium and
Potassium; 80% of K is by the kidneys (this
excreted
is the reason why diuretics loose all the K in the
body)
*30-60 mL/Hr is the normal U/O; 720 ml Minimum amount of
urine per day; Less than that is Oliguria; None is Anuria
- Regulates Acid Base Balance
- : Deep and Rapid
breathing (KUSSMAUL’S RESPIRATION: anytime
you have metabolic acidosis not only DKA or
HHNS)
- Control of water balance: ADH (Vasopressin):
Edema
- Control of BP: RAAS; Increased BP with kidney
damage; HTN
- Regulation of RBC Production: Anemic
DIAGNOSTICS
1. Labs
1.1 Routine Urinalysis
1.2 Creatinine Clearance
1.3 Blood studies: BUN (8-25 mg/dL), Serum
Creatinine (0.6-1.3 mg/dL), Creatinine Clearance
(85-135 ml/min), serum electrolytes
1.4 Cystoscopy
1.5 Abdominal X-ray (KUB)
*ADD: all Laboratory procedures and Diagnostic Procedures
RENAL FAILURE
1. TYPES:
1.1 Acute: can be reversed; sudden loss of
functioning
1.2 Chronic: more dangerous; gradual, progressive
2. CAUSES:
2.1 PRERENAL: is decreased or
perfusion
decreased blood supply
2.2 RENAL: damage directly to the kidneys; Renal
Calculi or medications
2.3 POSTRENAL: obstr the
uction nd up flow
a
kidney
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ACUTE RENAL FAILURE
1. PHASES
1.1 OLIGURIC/ ANURIC PHASE (Chronic is
stuck here) -
: 8 15 days output <400ml/day;
-
Toxins accumulate: METABOLIC acidosis;
Increased BUN, Crea, Hyperkalemia
1.1.1 Decreased: pH, bicarb and Na anad Ca
1.1.2 AZOTEMIA: elevated serum level of
UREA, creatinine and uric Acid
1.2 DIURETIC PHASE: extends from the time
daily output >400 mL/day; BUN stops
increasing, U/O >3-5L/day, hyponatremia you
(
are now urinating Na and K), change in LOC;
hypokalemia, changes in LOC
1.3 RECOVERY (Chronic RF will never go to this
phase): extends from the first day BUN falls to
the day it returns to normal
2. MANAGEMENT
2.1 Dialysis monitor F7E, Acids and bases observe
for fluid overloads
2.2 Moderate protein restriction, high on calories,
CHO, Low K
*KAYEXELATE (Sodium Polystyrene Sulfonate):
hyperkalemia, exchange Na for K ions in GIT
2.3 Monitor cardiac status, I&O, weigh daily
2.4 Fluid restriction
2.5 Diuretic Therapy
CHRONIC RENAL FAILURE
STAGES OF CRF
1. DIMISHED RENAL RESERVE
1.1 Normal serum BUN and Creatinine
1.2 No symptom
1.3 Other kidney Compensates
2. RENAL INSUFFICIENCY
2.1 GFR is only 25% normal
2.2 Azotemia: mild; Anemia
2.3 Decreasing Creatinine Clearance
3. END STAGE RENAL DISEASE
3.1 GFR <10%
3.2 SEVERE AZOTEMIA
MANIFESTATIONS
1. Azotemia; Metabolic Acidosis
2. ALOC due to accumulation of waste
3. Irregular HR
4. Yellow to bronze skin due to altered metabolic
process
5. Dry and scaly skin with severe itching due to uremic
frost
6. Proteinuria, Glycosuria
7. Diminished erythropoietin secretion: Anemia
8. Renal Phosphate excretion and VIT D synthesis are
diminished; K secretion increases
9. Heart Failure; Pulmonary edema
10. Kussmaul’s Respiration
MANAGEMNT
1. Kidney transplant
2. Dialysis, Monitor I&O, F&E
3. Low CHON Diet: Limit accumulation of end
products of CHON metabolism
4. Fluid restriction
5. Ant Diuretics
iHTN and
6. EPOGEN
7. Antipuritics; Good skin Care
DIALYSIS
HD
1. Access Site: takes 4-6 weeks to mature so use an
central Venous Catheter
1.1 AV Fistula
1.2 Av Graft
1.3 Central Venous Catheter (IJ, Subclavian,
Femoral)
2. MANAGEMNT
2.1 Monitor venous access
2.2 Weigh before and after the procedure
*DRY WEIGHT: the weight of the patient without excess
water; based by the physician; so ex. Dry weight of 5 L and
simply remove 5kg from the real weight and place that into the
machine
3. Monitor Disequilibrium Syndrome: too fast removal
of waste causes Confusion and weakness
4. Monitor for Shock and hypovolemia
5. Auscultate for Bruits and palpate for thrills
6. Don’t use arm for BP, IVT or venipuncture
PD
- Introduction of specially prepared dialysate solution
into the abdominal cavity where the peritoneum acts
as a semi-permeable membrane
- CHON may leak out
- MANAGEMENT: Assess Vs every 15 minutes then
after every hour; Weigh; Let patient void before
procedure; Warm dialysate to prevent cramps
1. Access Site: [1] STERILE INSERTION (if not
peritonitis); [2] Concepts: INFLOW (10 minutes),
DWELLING TIME (20 min - 30 minutes) &
OUTFLOW (15-20 minutes)
2. Drainage is less than infused: Turn side to side or
Ambulate
UTI
- Stasis of the urine in the bladder and of urine
reflux
back into the bladder
- UPPER UTI = SUPRAPUBIC PAIN: Urethritis
- LOWER UTI = FLANK PAIN: cystitis, urethritis
- MC is ASCENDING TYPE
- Females > Males (shorter urethra)
- Instrumentation and obstruction also common causes;
Also sexual intercourse promotes development of
UTI
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19. MEDICAL-SURGICAL NURSING
UNIVERSITY*OF*SANTO*TOMAS*–*COLLEGE*OF*NURSING*|*FJCP*2017*|
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- MANIFESTATIONS:
1. Frequency, Urgency, Dyuria
2. Hypogastric Pain
3. Malaise
4. Fever, Chills
5. N/V
6. Low back pain
7. Urinalysis Findings
- MANAGEMENT
1. C and S before ATB
2. Increase Fluid intake
3. Acidify the urine
*ACID ASH: CPP: Cranberry, Plums & Prunes
*Buco Juice is only a DIURETICS
*ALKALINE ASH: Citrus fruits
4. Perineal Hygiene
5. Regular Bladder emptying
6. Hot sitz bath
UROLITHIASIS/ NEPHROLITHIASIS
- Formation of stones in the urinary tract
- RF:
1. Calcium: Diets high in calcium; immobilization
(if you don’t move, the calcium is removed from
the bones into the serum)
2. Urinary Stasis
3. Dehydration
4. Uric Acid
- TYPE OF STONE
1. URIC ACID
CALCIUM OXALATES, PHOSPHATES
- MANIFESTATION
1. Hematuria: late sign
2. Colicky pain
3. N/V; Dysuria
- MANAGEMENT
1. Fluids
2. Strain urine
* STRAIN the urine and send it to the lab to determine the
stone
3. Encourage ambulation
4. Pain Control
5. DIET
5.1 Calcium: Acid Ash
5.2 Cystine: Alkaline Ash
5.3 Uric Acid: Low purine
*Vegetables: contain oxalates so don’t give to calcium
OXALATE stones!
6. SURGERY: Urolithotomy/ Nephrolithotomy;
NEPHROSTOMY TUBE: At the flank to drain
the urine while it is healing/ inflamed; Same idea
as a T TUBE; ESWL
BPH
- Slow enlargement of the prostate; 40 y/o and above
- Nocturnal: number 1 reason;
- CAUSES: hormonal changes or factors; age related
changes
- Urethral compression occurs with sign of urinary
obstruction urinary stasis
à à UTI
- INTERFERENCE IN URINATION
- MANIFESTATIONS
1. Urinary frequency
2. Nocturia
3. Bladder distention
4. Bladder Calculi
- MANAGEMENT:
1. Terazosin: to promote urination; ALPHA
BLOCKER
2. ATB for UTI
3. Administer Finasteride (Proscar: reduces size)
- SURGERY
1. TURP
1.1 Suprapubic: incision in the abdomen and blader
1.2 Retropubic: abdominal incision
1.3 Perineal: near the rectum; highest risk of
contamination and incontinence
*1% Impotent after surgery
- POST-OP
1. Cystoclysis: to remove the clots; Maintain urine to
pinkish red; if red, too little, too little, too fast; 3
WAY CATHERTER: infusion, balloon and drainage
bag
2. Normal to have bladder spasms
PROSTATE CANCER
- Slow malignant in the prostate gland that spreads by
direct invasion of the tissue and can metastasize to
bony pelvis and spine
- Elevated serum acid phosphatrase and serum PSA
(Prostate Specific Antigen) and CEA
(Carcinoembryonic Antigen)
- BIOPSY: Reveals malignancy, MRI-CT
- Give: Diethystilbrstrol (estrogen) to reduce
testosterone
- Radiation and Radical Prostectomy
- ORCHIECTOMY: to also decrease production of
testosterone
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