The document discusses the diagnosis and management of primary hypertension, including defining diagnostic criteria, describing diagnostic procedures such as clinical exams, blood pressure measurements, laboratory tests, and imaging studies to identify target organ damage, and outlining treatment pathways including lifestyle modifications and medication management. Target organ damage of the heart, brain, kidneys, eyes, and peripheral arteries from long-term high blood pressure is also reviewed.
The document discusses hypertensive emergencies and urgencies. It defines hypertensive emergencies as severe high blood pressure with impending or progressive organ damage, while urgencies involve severe elevation in BP without organ damage. Various intravenous antihypertensive medications are reviewed for treating emergencies, including vasodilators like sodium nitroprusside, nicardipine, and nitroglycerin, as well as adrenergic inhibitors like labetalol, esmolol, and phentolamine. The ideal drug lowers blood pressure without compromising organ blood flow and has a rapid onset and offset of action with minimal side effects. Treatment goals and medication choices depend on the underlying cause and end organ
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
This document discusses antiarrhythmic drugs. It begins by defining arrhythmias as abnormal heartbeats that can be too slow, fast, irregular or early. It then discusses the sites in the heart where arrhythmias can originate, such as the sinus node or ventricles. The mechanisms of arrhythmia are described as automaticity, reentry, after depolarization or enhanced pacemaker activity. The document reviews the Vaughan-Williams classification system for antiarrhythmic drugs and provides examples of drugs from each class. It also discusses specific antiarrhythmic drugs like amiodarone, beta blockers, lidocaine, calcium channel blockers and more.
This document discusses hypertensive urgency and emergency. Hypertensive urgency is severely elevated blood pressure without target organ damage, with symptoms like headache and dizziness. Treatment involves slowly lowering blood pressure over hours to days. Hypertensive emergency is elevated blood pressure that results in organ damage to the brain, heart, or kidneys, requiring immediate treatment to lower blood pressure within minutes to hours to prevent further damage. Specific treatments depend on the affected organ and may include drugs like labetalol, nicardipine, and sodium nitroprusside. The main difference between urgency and emergency is that emergency involves organ damage while urgency does not.
Hypertensive crisis refers to severely elevated blood pressure that can lead to organ damage and is categorized as hypertensive urgency or emergency depending on the presence of end-organ damage; treatment of urgency involves gradual oral medication while emergency requires immediate intravenous drugs to reduce blood pressure to prevent further damage; careful diagnosis and monitoring of blood pressure and organs is needed along with selecting appropriate drugs based on the situation.
An electrocardiogram (ECG) records the electrical activity of the heart. It can evaluate the heart's automaticity, conductivity, and excitability, but not contractility. The ECG is generated by ion fluxes across cell membranes during cardiac activation and recovery. It represents the vector sum of dipoles created by depolarization waves. A standard 12-lead ECG provides different views of the heart through limb and precordial leads. The P wave represents atrial depolarization, the QRS complex represents ventricular depolarization, and the ST-T wave represents ventricular recovery.
Shock is characterized by reduced systemic tissue perfusion and oxygen delivery, creating an imbalance between oxygen delivery and consumption. Prolonged oxygen deprivation can lead to cellular hypoxia and biochemical derangements. There are several types of shock including hypovolemic, cardiogenic, septic, neurogenic, and hypoadrenal shock. Mean arterial pressure depends on cardiac output and systemic vascular resistance. Parameters like lactate, blood pressure, heart rate, respiratory rate, urine output are used to classify shock into compensated, decompensated, and irreversible stages. Treatment involves identifying and treating the underlying cause while aggressively resuscitating with fluids and vasopressors.
1. Hypertensive emergencies involve severe, symptomatic elevation in blood pressure that causes end organ damage to organs like the brain, kidneys, eyes, and heart. Hypertensive urgencies involve severe elevation in blood pressure without symptoms or end organ damage.
2. Hypertensive encephalopathy is the most common hypertensive emergency and involves severe blood pressure elevation that causes cerebral edema and neurological symptoms like lethargy and seizures.
3. Etiologies of hypertensive emergencies in children include renovascular diseases, congenital renal anomalies, preeclampsia, drugs like cocaine and amphetamines, and endocrine diseases.
The document discusses hypertensive emergencies and urgencies. It defines hypertensive emergencies as severe high blood pressure with impending or progressive organ damage, while urgencies involve severe elevation in BP without organ damage. Various intravenous antihypertensive medications are reviewed for treating emergencies, including vasodilators like sodium nitroprusside, nicardipine, and nitroglycerin, as well as adrenergic inhibitors like labetalol, esmolol, and phentolamine. The ideal drug lowers blood pressure without compromising organ blood flow and has a rapid onset and offset of action with minimal side effects. Treatment goals and medication choices depend on the underlying cause and end organ
A brief synopsis of acute decompensated heart failureDr Emad efat
This document provides an overview of acute decompensated heart failure (ADHF). It defines ADHF as a clinical syndrome characterized by the development of respiratory distress due to rapidly accumulated fluid in the lungs. The document categorizes heart failure based on systolic vs diastolic function, left vs right sided, acute vs chronic onset, and NYHA functional classification. Common symptoms, physical exam findings, causes, risk factors, differential diagnoses, and initial investigations are described. Imaging findings on chest x-ray indicative of different stages of heart failure are also summarized.
This document discusses antiarrhythmic drugs. It begins by defining arrhythmias as abnormal heartbeats that can be too slow, fast, irregular or early. It then discusses the sites in the heart where arrhythmias can originate, such as the sinus node or ventricles. The mechanisms of arrhythmia are described as automaticity, reentry, after depolarization or enhanced pacemaker activity. The document reviews the Vaughan-Williams classification system for antiarrhythmic drugs and provides examples of drugs from each class. It also discusses specific antiarrhythmic drugs like amiodarone, beta blockers, lidocaine, calcium channel blockers and more.
This document discusses hypertensive urgency and emergency. Hypertensive urgency is severely elevated blood pressure without target organ damage, with symptoms like headache and dizziness. Treatment involves slowly lowering blood pressure over hours to days. Hypertensive emergency is elevated blood pressure that results in organ damage to the brain, heart, or kidneys, requiring immediate treatment to lower blood pressure within minutes to hours to prevent further damage. Specific treatments depend on the affected organ and may include drugs like labetalol, nicardipine, and sodium nitroprusside. The main difference between urgency and emergency is that emergency involves organ damage while urgency does not.
Hypertensive crisis refers to severely elevated blood pressure that can lead to organ damage and is categorized as hypertensive urgency or emergency depending on the presence of end-organ damage; treatment of urgency involves gradual oral medication while emergency requires immediate intravenous drugs to reduce blood pressure to prevent further damage; careful diagnosis and monitoring of blood pressure and organs is needed along with selecting appropriate drugs based on the situation.
An electrocardiogram (ECG) records the electrical activity of the heart. It can evaluate the heart's automaticity, conductivity, and excitability, but not contractility. The ECG is generated by ion fluxes across cell membranes during cardiac activation and recovery. It represents the vector sum of dipoles created by depolarization waves. A standard 12-lead ECG provides different views of the heart through limb and precordial leads. The P wave represents atrial depolarization, the QRS complex represents ventricular depolarization, and the ST-T wave represents ventricular recovery.
Shock is characterized by reduced systemic tissue perfusion and oxygen delivery, creating an imbalance between oxygen delivery and consumption. Prolonged oxygen deprivation can lead to cellular hypoxia and biochemical derangements. There are several types of shock including hypovolemic, cardiogenic, septic, neurogenic, and hypoadrenal shock. Mean arterial pressure depends on cardiac output and systemic vascular resistance. Parameters like lactate, blood pressure, heart rate, respiratory rate, urine output are used to classify shock into compensated, decompensated, and irreversible stages. Treatment involves identifying and treating the underlying cause while aggressively resuscitating with fluids and vasopressors.
1. Hypertensive emergencies involve severe, symptomatic elevation in blood pressure that causes end organ damage to organs like the brain, kidneys, eyes, and heart. Hypertensive urgencies involve severe elevation in blood pressure without symptoms or end organ damage.
2. Hypertensive encephalopathy is the most common hypertensive emergency and involves severe blood pressure elevation that causes cerebral edema and neurological symptoms like lethargy and seizures.
3. Etiologies of hypertensive emergencies in children include renovascular diseases, congenital renal anomalies, preeclampsia, drugs like cocaine and amphetamines, and endocrine diseases.
Organophosphate (OP) compounds irreversibly inhibit acetylcholinesterase (AChE), leading to accumulation of acetylcholine and overstimulation of muscarinic and nicotinic receptors. Clinical features include muscarinic, nicotinic, and central nervous system effects. Diagnosis is based on exposure history and low AChE levels. Treatment involves atropine for muscarinic effects, pralidoxime for reactivation of AChE, supportive care, and monitoring for intermediate syndrome or delayed neuropathy. Prevention focuses on safe use of pesticides and other OP sources.
Hyperaldosteronism, also known as Conn syndrome, is the most common cause of secondary hypertension, accounting for 5-13% of cases. It is characterized by hypokalemia in around half of patients with aldosterone-producing adenomas and 17% of patients with bilateral hyperplasia. Diagnosis involves measuring plasma renin activity and plasma aldosterone concentration along with confirmation tests such as saline loading, saline infusion, or fludrocortisone suppression. Adrenal vein sampling may be used if surgical treatment is an option to determine if hyperaldosteronism is unilateral or bilateral.
Hypertension, also known as high blood pressure, is a major public health problem worldwide. It is a chronic medical condition in which the blood pressure in the arteries is persistently elevated. While there is no cure, lifestyle modifications and medication can help prevent and manage hypertension. The goal of treatment is to reduce cardiovascular and renal risks and complications through lowering blood pressure. Treatment typically involves a combination of lifestyle changes and medications, with regular monitoring needed to control the condition.
This document discusses various types of supraventricular arrhythmias including sinus arrhythmia, premature atrial contractions, atrial flutter, atrial fibrillation, AV nodal reentry SVT, and AV reentry SVT. It provides details on the characteristics, mechanisms, and features seen on ECG for each type. Common arrhythmias in neonates such as premature atrial contractions, atrial flutter, and different forms of supraventricular tachycardia are also mentioned. The classification of tachycardias based on site of origin and rhythm is summarized.
This document discusses hypertensive emergencies, which are severe cases of high blood pressure that result in acute organ damage. It defines categories of hypertensive states and provides details on etiology, pathophysiology, presentation, workup, and treatment of hypertensive emergencies. Treatment involves identifying the affected organ system and gradually lowering blood pressure over hours to days to prevent further organ injury, using intravenous medications like nitroprusside, labetalol, or nicardipine depending on the situation. Specific guidance is provided for rapidly lowering blood pressure in conditions like hypertensive encephalopathy, intracerebral hemorrhage, and ischemic stroke.
Idiopathic Parkinson's disease is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms. Motor symptoms include tremors, rigidity, akinesia, and postural instability. Non-motor symptoms often precede motor symptoms and include loss of smell, sleep disturbances, mood changes, and autonomic dysfunction. Pathology involves the loss of dopaminergic neurons in the substantia nigra and presence of Lewy bodies. Diagnosis is based on physical exam findings and imaging can assess neuronal loss. Treatment focuses on dopamine replacement therapy with levodopa and dopamine agonists to improve motor symptoms while other therapies aim to improve non-motor symptoms and complications from long-term treatment.
This document provides a history of the electrocardiogram (EKG/ECG) and describes how it is used to evaluate cardiac electrical activity and identify various cardiac conditions. Some key points:
- The EKG was developed in the late 19th/early 20th century, with scientists like Matteucci, Marey, and Einthoven contributing to its invention and clinical use.
- An EKG records the heart's electrical activity through electrodes on the skin and can be used to detect arrhythmias, ischemia, infarction, and other conditions.
- It analyzes the P wave, QRS complex, ST segment, and T wave to evaluate conduction and identify abnormalities.
Acute dystonia is defined as involuntary muscle contractions causing abnormal movements or postures. It is often caused by drugs that block dopamine receptors or disrupt dopamine-cholinergic balance in the basal ganglia. Symptoms vary but include trismus, risus sardonicus, torticollis, and opisthotonus. Treatment involves diphenhydramine, benztropine, or lorazepam to relieve symptoms, with diphenhydramine as first line. Differential diagnoses include conversion disorder, seizures, meningitis, and other conditions involving muscle spasms or contractions.
Cardiac tamponade is a serious medical condition where blood or fluid fills the space between the sac surrounding the heart (pericardium), putting extreme pressure on the heart and preventing it from filling with blood properly. This can lead to organ failure, shock, and even death if not treated. Causes include infectious diseases, malignancies, anticoagulation medications, and connective tissue diseases. Symptoms include chest pain, difficulty breathing, fainting, and pale/gray skin color. Diagnosis involves physical exam, imaging like echocardiograms, and lab tests. Treatment consists of oxygen, fluids, medications, and procedures to drain excess fluid from the pericardial space.
DIAGNOSIS & MANAGEMENT OF PULMONARY HYPERTENSIONKamal Bharathi
Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left or both ventricles not solely caused by abnormal loading conditions or ischemic heart disease. It has an annual incidence of 5-8 per 100,000 people and is more common in males, blacks, and those with hypertension or chronic beta-agonist use. Causes include genetic mutations, viral or autoimmune myocarditis, toxins, and metabolic abnormalities. On pathology, it shows cardiac dilatation and loss of myocytes leading to decreased wall thickness and increased fibrosis. Treatment involves managing heart failure symptoms and its underlying causes. Prognosis depends on factors like functional classification, ejection fraction, and biomarkers, with some patients experiencing improvement or stabilization
Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.
Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS).
Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.
This document discusses the management of hypertensive emergencies and urgencies. It defines hypertensive emergencies as marked blood pressure elevation with acute life-threatening organ damage, requiring rapid BP reduction in an ICU. Hypertensive urgencies involve significant but not life-threatening BP elevation without acute organ dysfunction, allowing gradual oral medication-based BP reduction over hours. The document reviews ideal intravenous antihypertensive agents, special considerations for neurological, cardiovascular and other emergencies, and the treatment of hypertensive urgencies.
Hypertensive emergencies require rapid blood pressure reduction to prevent target organ damage, while hypertensive urgencies only require gradual reduction over 24 hours without end organ involvement. The case study describes a patient presenting with acute pulmonary edema secondary to hypertensive emergency and acute kidney injury. He was intubated and given intravenous nitrates, frusemide and morphine to rapidly reduce blood pressure and relieve pulmonary congestion over several hours.
This document discusses heart arrhythmias and how anti-arrhythmic drugs work to treat them. It provides details on:
1) The electrophysiology of normal heart contraction and how disturbances can cause arrhythmias.
2) Classification systems for anti-arrhythmic drugs based on their mechanisms of action, such as blocking specific ion channels.
3) How different classes of drugs can alter properties like conduction velocity, refractoriness, and automaticity to restore normal rhythm or prevent dangerous arrhythmias.
The document provides information on the management of hypertensive crisis. It begins with outlines of topics covered which include introduction, etiology, pathophysiology, clinical evaluation, workup, and management. It then goes into further detail on these topics. The key points are:
1) Hypertensive crisis is defined as a sudden rise in blood pressure that causes end organ damage and is classified as either a hypertensive urgency or emergency.
2) Common causes include poorly controlled essential hypertension and renal disease.
3) Rapid evaluation is needed to identify end organ damage to the heart, kidneys, brain, or vasculature.
4) Treatment involves slowing lowering blood pressure, usually over hours
- The document discusses the anatomy and physiology of the heart's conduction system and how it generates the normal cardiac rhythm. It describes the roles of the sinoatrial node, atrioventricular node, Bundle of His, and Purkinje fibers in conducting electrical impulses through the heart.
- Various types of cardiac arrhythmias are defined based on disruptions to the heart's normal conduction system. These include premature beats, rhythms originating from the atria, AV junction, or ventricles. Characteristics like P wave presence/morphology, rate, and regularity are used to identify arrhythmias.
- A 12-lead electrocardiogram (EKG or ECG) is used to
Parkinson's disease is a brain disorder that causes shaking, stiffness, and difficulty with movement. It results from the death of dopaminergic neurons in the substantia nigra, which leads to a decrease in dopamine levels. Common symptoms include tremors, rigid muscles, slow movement, and impaired balance. While the exact causes are unknown, genetic and environmental factors may play a role. There is no cure for Parkinson's disease, but treatments like L-Dopa and Carbidopa can help manage symptoms.
Primary hypertension accounts for 90% of hypertension cases. It is defined as high blood pressure without an identifiable secondary cause. The main pathophysiological drivers of primary hypertension are an overactive renin-angiotensin-aldosterone system and endothelial dysfunction. This leads to increased peripheral resistance and higher blood pressure. Over time, uncontrolled high blood pressure can damage target organs like the heart, brain, kidneys, and blood vessels, potentially causing complications like heart failure, stroke, and kidney disease. Managing risk factors and treating hypertension can help prevent its progression and reduce complications.
Three large international hypertension trials involving over 80,000 patients will improve understanding of hypertension management. The trials compare different drug classes and treatment strategies. They found that diuretics are as effective as newer drugs in lowering blood pressure and risk of cardiovascular events. The trials also showed tight blood pressure control, below 130/80 mmHg, provides better outcomes.
Organophosphate (OP) compounds irreversibly inhibit acetylcholinesterase (AChE), leading to accumulation of acetylcholine and overstimulation of muscarinic and nicotinic receptors. Clinical features include muscarinic, nicotinic, and central nervous system effects. Diagnosis is based on exposure history and low AChE levels. Treatment involves atropine for muscarinic effects, pralidoxime for reactivation of AChE, supportive care, and monitoring for intermediate syndrome or delayed neuropathy. Prevention focuses on safe use of pesticides and other OP sources.
Hyperaldosteronism, also known as Conn syndrome, is the most common cause of secondary hypertension, accounting for 5-13% of cases. It is characterized by hypokalemia in around half of patients with aldosterone-producing adenomas and 17% of patients with bilateral hyperplasia. Diagnosis involves measuring plasma renin activity and plasma aldosterone concentration along with confirmation tests such as saline loading, saline infusion, or fludrocortisone suppression. Adrenal vein sampling may be used if surgical treatment is an option to determine if hyperaldosteronism is unilateral or bilateral.
Hypertension, also known as high blood pressure, is a major public health problem worldwide. It is a chronic medical condition in which the blood pressure in the arteries is persistently elevated. While there is no cure, lifestyle modifications and medication can help prevent and manage hypertension. The goal of treatment is to reduce cardiovascular and renal risks and complications through lowering blood pressure. Treatment typically involves a combination of lifestyle changes and medications, with regular monitoring needed to control the condition.
This document discusses various types of supraventricular arrhythmias including sinus arrhythmia, premature atrial contractions, atrial flutter, atrial fibrillation, AV nodal reentry SVT, and AV reentry SVT. It provides details on the characteristics, mechanisms, and features seen on ECG for each type. Common arrhythmias in neonates such as premature atrial contractions, atrial flutter, and different forms of supraventricular tachycardia are also mentioned. The classification of tachycardias based on site of origin and rhythm is summarized.
This document discusses hypertensive emergencies, which are severe cases of high blood pressure that result in acute organ damage. It defines categories of hypertensive states and provides details on etiology, pathophysiology, presentation, workup, and treatment of hypertensive emergencies. Treatment involves identifying the affected organ system and gradually lowering blood pressure over hours to days to prevent further organ injury, using intravenous medications like nitroprusside, labetalol, or nicardipine depending on the situation. Specific guidance is provided for rapidly lowering blood pressure in conditions like hypertensive encephalopathy, intracerebral hemorrhage, and ischemic stroke.
Idiopathic Parkinson's disease is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms. Motor symptoms include tremors, rigidity, akinesia, and postural instability. Non-motor symptoms often precede motor symptoms and include loss of smell, sleep disturbances, mood changes, and autonomic dysfunction. Pathology involves the loss of dopaminergic neurons in the substantia nigra and presence of Lewy bodies. Diagnosis is based on physical exam findings and imaging can assess neuronal loss. Treatment focuses on dopamine replacement therapy with levodopa and dopamine agonists to improve motor symptoms while other therapies aim to improve non-motor symptoms and complications from long-term treatment.
This document provides a history of the electrocardiogram (EKG/ECG) and describes how it is used to evaluate cardiac electrical activity and identify various cardiac conditions. Some key points:
- The EKG was developed in the late 19th/early 20th century, with scientists like Matteucci, Marey, and Einthoven contributing to its invention and clinical use.
- An EKG records the heart's electrical activity through electrodes on the skin and can be used to detect arrhythmias, ischemia, infarction, and other conditions.
- It analyzes the P wave, QRS complex, ST segment, and T wave to evaluate conduction and identify abnormalities.
Acute dystonia is defined as involuntary muscle contractions causing abnormal movements or postures. It is often caused by drugs that block dopamine receptors or disrupt dopamine-cholinergic balance in the basal ganglia. Symptoms vary but include trismus, risus sardonicus, torticollis, and opisthotonus. Treatment involves diphenhydramine, benztropine, or lorazepam to relieve symptoms, with diphenhydramine as first line. Differential diagnoses include conversion disorder, seizures, meningitis, and other conditions involving muscle spasms or contractions.
Cardiac tamponade is a serious medical condition where blood or fluid fills the space between the sac surrounding the heart (pericardium), putting extreme pressure on the heart and preventing it from filling with blood properly. This can lead to organ failure, shock, and even death if not treated. Causes include infectious diseases, malignancies, anticoagulation medications, and connective tissue diseases. Symptoms include chest pain, difficulty breathing, fainting, and pale/gray skin color. Diagnosis involves physical exam, imaging like echocardiograms, and lab tests. Treatment consists of oxygen, fluids, medications, and procedures to drain excess fluid from the pericardial space.
DIAGNOSIS & MANAGEMENT OF PULMONARY HYPERTENSIONKamal Bharathi
Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ≥25 mm Hg at rest, measured during right heart catheterization. There is still insufficient evidence to add an exercise criterion to this definition. The term pulmonary arterial hypertension (PAH) describes a subpopulation of patients with PH characterized hemodynamically by the presence of pre-capillary PH including an end-expiratory pulmonary artery wedge pressure (PAWP) ≤15 mm Hg and a pulmonary vascular resistance >3 Wood units. Right heart catheterization remains essential for a diagnosis of PH or PAH. This procedure requires further standardization, including uniformity of the pressure transducer zero level at the midthoracic line, which is at the level of the left atrium. One of the most common problems in the diagnostic workup of patients with PH is the distinction between PAH and PH due to left heart failure with preserved ejection fraction (HFpEF). A normal PAWP does not rule out the presence of HFpEF. Volume or exercise challenge during right heart catheterization may be useful to unmask the presence of left heart disease, but both tools require further evaluation before their use in general practice can be recommended. Early diagnosis of PAH remains difficult, and screening programs in asymptomatic patients are feasible only in high-risk populations, particularly in patients with systemic sclerosis, for whom recent data suggest that a combination of clinical assessment and pulmonary function testing including diffusion capacity for carbon monoxide, biomarkers, and echocardiography has a higher predictive value than echocardiography alone.
Dilated cardiomyopathy is defined as dilatation and impaired contraction of the left or both ventricles not solely caused by abnormal loading conditions or ischemic heart disease. It has an annual incidence of 5-8 per 100,000 people and is more common in males, blacks, and those with hypertension or chronic beta-agonist use. Causes include genetic mutations, viral or autoimmune myocarditis, toxins, and metabolic abnormalities. On pathology, it shows cardiac dilatation and loss of myocytes leading to decreased wall thickness and increased fibrosis. Treatment involves managing heart failure symptoms and its underlying causes. Prognosis depends on factors like functional classification, ejection fraction, and biomarkers, with some patients experiencing improvement or stabilization
Acute heart failure (AHF) is defined as rapid onset of new or worsening signs and symptoms of heart failure. It represents a life-threatening condition requiring treatment for fluid overload and hemodynamic compromise. Presentation may be initial diagnosis with symptoms and signs of AHF or acute decompensation of pre-existing cardiomyopathy. Hemodynamic instability results from disorders of the myocardium, valves, conduction system or pericardium, in isolation or combination. Potentially treatable causes, e.g. acute coronary syndromes, must be diagnosed and managed early for restoration of function.
Physiological changes associated with AHF result in reduced cardiac output and end-organ hypoperfusion. Once potentially treatable causes are managed, stratification of patients by clinical presentation guides further therapeutic intervention. AHF patients can be categorized as either ‘wet’ or ‘dry’ by clinical fluid status assessment, and either ‘cold’ or ‘warm’ according to perfusion status. In combination, these features identify four patient groups (‘warm-wet’, ‘warm-dry’, ‘cold-dry’, ‘cold-wet’) that guide therapy and facilitate prognostication. ‘Warm-dry’ patients rarely require intensive care for AHF treatment but may benefit from escalation of oral therapeutic regimen. Patients who examine as ‘cold-dry’ may benefit from fluid challenge, and/or inotropic agent infusion. ‘Warm-wet’ patients present with predominantly congestive or hypertensive symptoms which benefit from diuresis and vasodilatation. Patients who present ‘wet-cold’ with normal blood pressure (SBP >90) may benefit from vasodilators and diuretics, with inotropic agents for refractory symptoms. Hypotensive ‘wet-cold’ patients (classic cardiogenic shock) require inotropy with or without vasopressor agents, effective diuresis and early consideration of mechanical circulatory support (MCS).
Definitive therapies for AHF depend on underlying cause, and may include coronary artery intervention, valve repair, rhythm control to restore atrio-ventricular synchrony or management of pericardial tamponade. Patients with severe AHF not responsive to standard therapies should be considered for temporary MCS while candidacy for more durable option is explored by the multi-disciplinary team.
This document discusses the management of hypertensive emergencies and urgencies. It defines hypertensive emergencies as marked blood pressure elevation with acute life-threatening organ damage, requiring rapid BP reduction in an ICU. Hypertensive urgencies involve significant but not life-threatening BP elevation without acute organ dysfunction, allowing gradual oral medication-based BP reduction over hours. The document reviews ideal intravenous antihypertensive agents, special considerations for neurological, cardiovascular and other emergencies, and the treatment of hypertensive urgencies.
Hypertensive emergencies require rapid blood pressure reduction to prevent target organ damage, while hypertensive urgencies only require gradual reduction over 24 hours without end organ involvement. The case study describes a patient presenting with acute pulmonary edema secondary to hypertensive emergency and acute kidney injury. He was intubated and given intravenous nitrates, frusemide and morphine to rapidly reduce blood pressure and relieve pulmonary congestion over several hours.
This document discusses heart arrhythmias and how anti-arrhythmic drugs work to treat them. It provides details on:
1) The electrophysiology of normal heart contraction and how disturbances can cause arrhythmias.
2) Classification systems for anti-arrhythmic drugs based on their mechanisms of action, such as blocking specific ion channels.
3) How different classes of drugs can alter properties like conduction velocity, refractoriness, and automaticity to restore normal rhythm or prevent dangerous arrhythmias.
The document provides information on the management of hypertensive crisis. It begins with outlines of topics covered which include introduction, etiology, pathophysiology, clinical evaluation, workup, and management. It then goes into further detail on these topics. The key points are:
1) Hypertensive crisis is defined as a sudden rise in blood pressure that causes end organ damage and is classified as either a hypertensive urgency or emergency.
2) Common causes include poorly controlled essential hypertension and renal disease.
3) Rapid evaluation is needed to identify end organ damage to the heart, kidneys, brain, or vasculature.
4) Treatment involves slowing lowering blood pressure, usually over hours
- The document discusses the anatomy and physiology of the heart's conduction system and how it generates the normal cardiac rhythm. It describes the roles of the sinoatrial node, atrioventricular node, Bundle of His, and Purkinje fibers in conducting electrical impulses through the heart.
- Various types of cardiac arrhythmias are defined based on disruptions to the heart's normal conduction system. These include premature beats, rhythms originating from the atria, AV junction, or ventricles. Characteristics like P wave presence/morphology, rate, and regularity are used to identify arrhythmias.
- A 12-lead electrocardiogram (EKG or ECG) is used to
Parkinson's disease is a brain disorder that causes shaking, stiffness, and difficulty with movement. It results from the death of dopaminergic neurons in the substantia nigra, which leads to a decrease in dopamine levels. Common symptoms include tremors, rigid muscles, slow movement, and impaired balance. While the exact causes are unknown, genetic and environmental factors may play a role. There is no cure for Parkinson's disease, but treatments like L-Dopa and Carbidopa can help manage symptoms.
Primary hypertension accounts for 90% of hypertension cases. It is defined as high blood pressure without an identifiable secondary cause. The main pathophysiological drivers of primary hypertension are an overactive renin-angiotensin-aldosterone system and endothelial dysfunction. This leads to increased peripheral resistance and higher blood pressure. Over time, uncontrolled high blood pressure can damage target organs like the heart, brain, kidneys, and blood vessels, potentially causing complications like heart failure, stroke, and kidney disease. Managing risk factors and treating hypertension can help prevent its progression and reduce complications.
Three large international hypertension trials involving over 80,000 patients will improve understanding of hypertension management. The trials compare different drug classes and treatment strategies. They found that diuretics are as effective as newer drugs in lowering blood pressure and risk of cardiovascular events. The trials also showed tight blood pressure control, below 130/80 mmHg, provides better outcomes.
The document discusses the circulation in the lungs and pulmonary hypertension. It describes the double blood supply and drainage of the lungs from the pulmonary and bronchial arteries and veins. It discusses the types of pulmonary arteries and how they change in size and composition from the main pulmonary artery towards the capillaries. It also summarizes pulmonary hypertension, its genetics, pathobiology involving endothelial dysfunction, smooth muscle proliferation, remodeling, inflammation and thrombosis.
This document discusses different types of research studies and their purposes. It describes observational studies like cross-sectional, case-control and cohort studies. It also discusses experimental studies like randomized controlled trials. Key aspects of valid research studies discussed include accuracy, precision, and minimizing biases and errors. The ideal research study is described as accurate, free of bias and confounding, with no sampling errors and appropriate confidence intervals and p-values.
This document summarizes various cardiac pathologies. It discusses problems related to inadequate cardiac output such as leaks in the cardiovascular system, irregular heart rhythms, obstructions to blood flow, and valve problems. Congenital heart diseases are also examined, noting they result from mixing of oxygenated and unoxygenated blood and can be caused by genetic or environmental factors like infections. Specific congenital defects like atrial septal defects and tetralogy of Fallot are described. Other cardiac conditions reviewed include ischemic heart disease, hypertension, cardiomyopathy, pericardial diseases, infective endocarditis, and rheumatic fever.
This document discusses the evaluation of a patient presenting with palpitations. It begins by defining palpitations and describing the general and systemic examination findings that should be assessed. These include vital signs, heart auscultation findings, and an ECG. It then lists key clinical findings associated with different arrhythmias and cardiovascular conditions that could cause palpitations. The document concludes by discussing the differential diagnosis of palpitations, which can be due to arrhythmias, psychiatric conditions, medications, nonarrhythmic cardiac causes, or extracardiac etiologies. A thorough history, physical exam, and testing are needed to determine the underlying cause.
This document discusses febrile convulsions, which are seizures caused by a rapid rise in body temperature due to an external infection in children between 9 months and 5 years old. Simple febrile convulsions typically last less than 15 minutes and occur once per fever, while complex convulsions last over 15 minutes or recur within 24 hours. Treatment involves controlling the fever with medications and treating the underlying infection. Prophylactic anti-seizure medications are sometimes used for children at higher risk of developing epilepsy. The risk of future seizures or epilepsy is increased if the first febrile seizure occurred before age 1, the temperature was lower, or there is a family history or other risk factors.
Ophthalmoscopy allows examination of the inside of the eye. It is done using an ophthalmoscope to view the retina and optic disc. It was invented in 1851 and has since improved. During the exam, the pupil is dilated and the ophthalmologist views the retina through different aperture settings and filters on the ophthalmoscope. They examine the optic disc, retina, blood vessels and look for any abnormalities. Common findings include signs of diabetes, hypertension, glaucoma, or other eye conditions. The ophthalmoscopy exam is important for evaluating eye health and detecting underlying diseases.
Management of bronchial asthma in children Shaju Edamana
This document discusses the management of bronchial asthma in children. It defines asthma as a chronic inflammatory airway disorder characterized by episodes of coughing, wheezing, and shortness of breath in response to triggers. It outlines the clinical presentation of asthma in children and discusses alternative causes of wheezing. Diagnostic procedures and classifications of asthma control are also presented. The document recommends inhaled medications as preferred treatment delivered by various devices based on a child's age. It stresses the importance of education, monitoring, and follow-up to maintain asthma control. Acute exacerbations should be treated with oxygen, inhaled bronchodilators, systemic corticosteroids, and possibly anticholinergics.
The document discusses the perioperative management of diabetes mellitus. It provides criteria for diagnosing diabetes, discusses how surgery and diabetes affect metabolism, and outlines recommendations for preoperative evaluation and glycemic control in the perioperative period. The goals are to maintain good glycemic control, prevent complications, and shift patients back to their usual diabetes medications and diet as quickly as possible after surgery.
The document discusses hypertension, including definitions of systolic and diastolic blood pressure, factors that affect blood pressure such as cardiac output and vascular resistance, short and long-term regulation of blood pressure, classifications of hypertension, risk factors, signs and symptoms, diagnostic tests, treatment goals and lifestyle modifications to control hypertension such as weight loss, exercise, sodium restriction, and moderation of alcohol intake. It provides information on hypertension for healthcare professionals to educate patients.
This document provides guidelines for diagnosing hypertension through diagnostic evaluations. It discusses establishing blood pressure levels, identifying secondary causes, and evaluating cardiovascular risk through measurements, medical history, physical exam, and investigations. Specific guidelines are provided for office and ambulatory blood pressure monitoring, interpreting results, and assessing for target organ damage through tests like ECG, echocardiogram, carotid ultrasound, and lab work.
This document discusses congestive heart failure (CHF). It provides epidemiological data on CHF, showing it affects millions of people worldwide and costs billions of dollars annually. It defines CHF as the heart's inability to meet circulatory demands and classifies it based on location (left vs right heart) and time course (acute vs chronic). Causes of acute and chronic CHF include myocardial infarction, hypertension, valvular diseases, and cardiomyopathies. The pathophysiology of CHF involves systolic and diastolic dysfunction that can lead to ventricular hypertrophy, dilation, and neurohormonal activation causing further organ damage.
The document defines hypertension and discusses changes made to definitions in guidelines from 2003 and 2017. It also covers the epidemiology of hypertension, risk factors, mechanisms, etiologies (essential vs. secondary), diagnosis, evaluation, target organ damage, clinical presentation, and patient workup. The summary provides an overview of key points:
1. The document defines normal, prehypertension, stage 1 and 2 hypertension based on guidelines from 2003 and 2017.
2. Hypertension is the most prevalent risk factor for cardiovascular disease, affecting about 30% of people over 18 and 50% over 60.
3. Patient evaluation for hypertension includes history, exam, and tests to define blood pressure levels, identify risk factors,
1) The document discusses heart failure, including definitions, classifications, epidemiology, and treatment. It summarizes key findings from the PARADIGM-HF trial which compared the drug Entresto to enalapril.
2) The PARADIGM-HF trial found Entresto reduced the risk of cardiovascular death or hospitalization for heart failure by 20% compared to enalapril.
3) Specifically, Entresto reduced the risk of cardiovascular death by 20% and first hospitalization for heart failure by 21% compared to enalapril.
The document discusses consensus documents on catheter-based renal denervation (RDN) for treatment of resistant hypertension. It summarizes that there are 7 consensus documents from scientific societies and groups published between 2012-2014 that cover domains such as the pathophysiology of hypertension, rationale for RDN, candidate selection criteria, procedural aspects, efficacy assessment, safety data, and recommendations. There are still many unmet needs including randomized blinded studies, long-term data on efficacy and safety, and impact on patient outcomes. Overall the consensus documents provide guidance on RDN but more research is still required.
This document discusses the management of hypertensive emergencies in children. It defines hypertension and hypertensive crises, and outlines the urgency vs emergency distinction. It describes the prevalence of hypertension in children, potential causes, pathophysiology, and complications involving end organ damage if left untreated. Initial diagnostic approach involves assessing for end organ injury and its severity, with the immediate goal of therapy being to decrease blood pressure quickly in emergency situations.
This document summarizes dizziness and syncope. Dizziness is a common complaint that can have many causes including vertigo, disequilibrium, and presyncope. A careful history and exam can often determine the etiology as central, peripheral, or psychiatric. Syncope is the transient loss of consciousness and posture due to decreased brain perfusion. The evaluation of syncope focuses on identifying potentially life-threatening cardiac causes through history, exam, EKG and selected testing. Neurocardiogenic or vasovagal syncope is often diagnosed clinically without extensive testing. Admission is recommended for high risk patients but many can be safely discharged with careful evaluation.
This document summarizes dizziness and syncope. Dizziness is a common complaint that can have many causes including vertigo, disequilibrium, and presyncope. A careful history and exam can help determine if the cause is central or peripheral. Syncope is a brief loss of consciousness that also has multiple potential etiologies like cardiac arrhythmias, neurocardiogenic, orthostatic, and idiopathic. The diagnostic workup involves history, exam, EKG and may include testing like tilt table, monitoring or imaging depending on risk factors. Admission is recommended for high risk patients but many can be safely discharged with careful evaluation and follow up.
Critical Congenital Heart Disease (CCHD) refers to several heart defects present at birth that require intervention. Some key points:
- CCHD includes defects where blood flow depends on an open ductus arteriosus after birth, such as Tetralogy of Fallot.
- Clinical presentation varies but may include cyanosis, heart murmur, respiratory distress. Diagnosis involves tests like echocardiogram, EKG, chest x-ray.
- Management depends on the specific defect but may include prostaglandin E1 to keep the ductus arteriosus open, then surgery to repair the anatomical issues. Early detection through newborn pulse oximetry screening can help identify cases
Introduction and pathophysiology of hypertension in elderly. Differences among hypertension in adults and elderly in terms of symptoms, treatment consideration. Issues and Challenges among elderly patients. Stroke among Elderly population. Issues and challenges in stroke elderly population.
The document discusses patent ductus arteriosus (PDA), which is a persistent opening between the aorta and pulmonary artery that is normally present before birth. After birth, the ductus arteriosus usually closes within the first few days/weeks of life. If it remains open, it results in PDA. PDA allows blood to flow from the aorta back to the pulmonary artery, resulting in increased pulmonary blood flow. The document outlines the signs, symptoms, investigations and management including medical closure with indomethacin or ibuprofen in preterms or surgical ligation in older infants. Complications like congestive cardiac failure or pulmonary hypertension are also discussed.
Approach to young hypertensive patientsChandan Kumar
1. The document discusses hypertension in young adults, including definitions of different types of elevated blood pressure (e.g. hypertensive urgency, emergency), risk factors, clinical presentation, causes (primary vs. secondary), evaluation approach, and ambulatory blood pressure monitoring.
2. Most young adults with hypertension have primary/essential hypertension with no identifiable cause, though secondary hypertension can occur in about 10% of cases. Evaluation aims to confirm the diagnosis, assess cardiovascular risk, detect target organ damage, and identify secondary causes.
3. Ambulatory blood pressure monitoring provides blood pressure readings outside the office and can help identify white coat hypertension or masked hypertension, which have implications for risk stratification and treatment.
Heart failure Update as per, 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the
Management of Heart Failure and 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
Hypertensive Encephalopathy and Emergenciessazzad92
This document discusses hypertensive encephalopathy and hypertensive emergencies. It defines hypertensive encephalopathy as a condition caused by very high blood pressure that results in neurological symptoms. It describes the pathogenesis, symptoms, investigations, diagnosis, and treatment, which involves slowly lowering blood pressure over 24-48 hours. Hypertensive emergencies involve acute severe blood pressure elevations that cause end organ damage and require admission and rapid blood pressure control within hours to prevent further damage. The document outlines the clinical features, diagnosis, and treatments for hypertensive emergencies depending on the affected organ.
This document provides guidelines for evaluating and managing patients presenting with syncope. It defines syncope and differentiates it from other transient loss of consciousness conditions. Syncope is categorized into three major types - neurally-mediated, orthostatic hypotension, and cardiovascular-mediated. The guidelines recommend a systematic approach involving identifying life-threatening causes, evaluating for etiology, and risk stratifying patients if the cause remains unclear. Key aspects of history taking and physical exam are outlined to help identify potential causes. Recommended tests include ECG, cardiac monitoring, echocardiogram, and tilt table testing depending on patient characteristics and presentation.
This document summarizes a lecture on the treatment of congestive heart failure. It defines heart failure classifications according to the New York Heart Association. For acute heart failure, the main treatment goals are treating life-threatening conditions and improving quality of life through vasodilation, organ protection, and volume control. Chronic heart failure treatment aims to improve quality of life, reduce disability, and increase longevity. Evidence-based drug therapies recommended for chronic heart failure include ACE inhibitors, beta-blockers, and aldosterone antagonists. Other options discussed include surgical treatments like heart transplantation and resynchronization therapy, as well as developing treatments like stem cell therapy. The document emphasizes the importance of home care programs for long-term heart failure
The document discusses diagnostic procedures for congestive heart failure, including clinical exams, echocardiography, blood tests, cardiac imaging like angiography and MRI, and hemodynamic monitoring. Key diagnostic tests are clinical exams, echocardiography to assess heart structure and function, blood tests like BNP to support diagnosis, and additional cardiac imaging tests like angiography to evaluate underlying heart conditions. Hemodynamic monitoring provides cardiac functional parameters but has limited clinical use due to its invasiveness.
1. Medical Science Tanzania Lectures
Management of primary
Hypertension
1. Diagnostic procedures
March 2013 Prof. G. Hennersdorf DGK ESC SES
2. Hypertension subsets
Primary Hypertension
Dysregulation of neurohormonal (RAS) systems
Triggering Target Organ Damage
Heart
Left ventricular hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart failure
Brain
Stroke or transient ischemic attack
Kidney:
Chronic kidney disease
Peripheral arterial disease
Eye
Retinopathy
March 2013 Prof. G. Hennersdorf DGK ESC SES
3. Hypertension subsets
• Secondary Hypertension
– Organ mediated
• Renal disorders (parenchymatic, vascular)
• Glands (thyroid; adrenal)
• Cardiac (aortic regurgitation)
• Vessel abnormalities (Aortic coarctation)
• Pregnancy (gestation, eclampsia)
• Others (drug addiction)
March 2013 Prof. G. Hennersdorf DGK ESC SES
4. Definition of arterial Hypertension HPT
systolic blood pressure diastolic blood pressure
Normal <140 and <90
(diabetic) <130 <80
Age =>80 150 90
mild HPT 140-179 and/or 90-104
borderline HPT 140-159 90-94
intermediate >=180 >=105
severe HPT
and/or
isolated systolic >=160 <90
HPT(ISH**) 140-159 and
*WHO 2000 ** isolated systolic hypertension
March 2013 Prof. G. Hennersdorf DGK ESC SES
5. Prevalence of arterial hypertension (%)
50
45
40 44
35
30 32 Germany
subsaharan Africans
25
26 US
20 Afroamericans
20
15
10
5
0
per cent age
March 2013 Prof. G. Hennersdorf DGK ESC SES
6. Prevalence
of hypertensive stroke
Subsaharan Africa (Tanzania) 1,6%
Western Countries (US) 1,7%
March 2013 Prof. G. Hennersdorf DGK ESC SES
7. Hypertension Diagnosis
• clinical diagnosis
• advanced measures
• pathways and flowcharts
March 2013 Prof. G. Hennersdorf DGK ESC SES
8. Hypertension Diagnosis
• Clinical Diagnosis
• Advanced Measures
• Pathways and Flowcharts
March 2013 Prof. G. Hennersdorf DGK ESC SES
9. Hypertension Diagnosis:
normal changes of BP
Sleeping: BP falls and Running: BP rises and Alcohol and tobacco
rises when waking up decreases to normal misuse, drug addiction: BP
during recovery phase with rises and triggers
positive training effects hypertension!
protecting from
hypertension
March 2013 Prof. G. Hennersdorf DGK ESC SES
10. Hypertension Diagnosis
Hypertension by itself doesn‘t hurt!
• History:
– General signs and symptoms should reveal level of risk
and suspicion of TOD*s
• Head ache, Dizziness, visus abnormalities, hst. of stroke, hst.
of fainting (syncope) brain damage
• Palpitation, Dyspnea, chest pain, nocturnal dysuria, hst. of MI
heart (damage) failure, CAD
• Leg pains: Walking, rest pain, peripheral (damage) disease
• Family history, physical activity, history of smoking habits,
alcohol abuse
• History of medication *target organ damage
March 2013 Prof. G. Hennersdorf DGK ESC SES
11. Hypertension Diagnosis
• Physical examination
– Inspection, palpation and auscultation
• Chest: lungs and heart (congestion, murmurs, rhythm)
• Neurological status: consciousness, motion
abnormalities, reflexes, speech
• Peripheral pulses: carotid murmurs, abdominal
murmurs (renal disease?), ankle-brachial-index ABI
• Hyperlipidemia: xanthelasm, arcus senilis, ear lobe
creases
• Joints: gout
March 2013 Prof. G. Hennersdorf DGK ESC SES
12. Hypertension Diagnosis
• Physical examination
– Measuring blood pressure: necessary at each visit
start, whenever seeing the doctor!
This is the most important examination procedure,
therefore be careful, be skilled, be an expert
March 2013 Prof. G. Hennersdorf DGK ESC SES
13. Hypertension Diagnosis
• The correct measurement
of blood pressure depends on
– Patient
– Environment
– Device
– Procedure
March 2013 Prof. G. Hennersdorf DGK ESC SES
14. Hypertension Diagnosis
• The correct measurement of blood pressure
– Patient (first visit)
– Environment
– Device
– Procedure
March 2013 Prof. G. Hennersdorf DGK ESC SES
15. Hypertension Diagnosis
• Silence, Sedation (?)
• No coffee, no smoking for at least 60 min.
before reading
• Supine position (for at least 10 min.)
March 2013 Prof. G. Hennersdorf DGK ESC SES
16. Hypertension Diagnosis
• The correct measurement of blood pressure
– Patient
– Environment
– Device
– Procedure
March 2013 Prof. G. Hennersdorf DGK ESC SES
17. Hypertension Diagnosis
• Dry, calm, separate (?) room
• Avoid fast movements of the personnel
• Quiet, warm setting
March 2013 Prof. G. Hennersdorf DGK ESC SES
18. Hypertension Diagnosis
• The correct measurement of blood pressure
– Patient
– Environment
– Device
– Procedure
March 2013 Prof. G. Hennersdorf DGK ESC SES
19. Hypertension Diagnosis
• Devices for the physician:
– Mercury (Hg; best device!)
– Aneroid (needs regular calibrations vs. Hg)
– Ultrasound (esp. children)
– Oscillometry (forearm-wrist devices)
March 2013 Prof. G. Hennersdorf DGK ESC SES
20. Hypertension Diagnosis: mercury device
Scaled mercury manometer
Cuff
Air bulb pumping accessory
March 2013 Prof. G. Hennersdorf DGK ESC SES
22. Hypertension Diagnosis
• Cuff size: 2/3 of arm length (smaller cuffs result in higher
pressures!)
• Cuff position: unclothed arm, tight and strong, deflated
• Choose mercury manometer; aneroid devices should be
calibrated against Hg every 6 month!
• for children choose smaller cuffs or ultrasound devices
March 2013 Prof. G. Hennersdorf DGK ESC SES
23. Hypertension Diagnosis
• The correct measurement of blood pressure
– Patient
– Environment
– Device
– Procedure
March 2013 Prof. G. Hennersdorf DGK ESC SES
24. Hypertension Diagnosis: anatomy of brachial
auskultation area
a.brachialis
membrane area
medial,just above the
joint (epicondylus
medialis)
March 2013 Prof. G. Hennersdorf DGK ESC SES
25. Hypertension Diagnosis
• Brachial measurement
– Inflation quickly 20 mm Hg over expected SBP or as
recognized by palpation of the radial pulse
(disappearance)
– Deflation slowly (3 mm Hg /s)
– Readings:
first reading both left and right arm, difference not being
above 20 mm Hg
at least 2 readings from the arm with the higher pressure
– listen to disappearance of Korotkow noise (muffling may
occur: take the attenuation point)
March 2013 Prof. G. Hennersdorf DGK ESC SES
26. Hypertension Diagnosis: anatomy of radial
palpation area
a.radialis
palpation area
March 2013 Prof. G. Hennersdorf DGK ESC SES
27. Hypertension Diagnosis
• Radial pulse palpation, if only SBP
measurements are needed:
– shock or hypotension (if palpable!)
– Posture evaluation (syncope diagnosis)
– sudden information about systolic blood
pressure
Does NOT replace regular measurements!
March 2013 Prof. G. Hennersdorf DGK ESC SES
28. Hypertension Diagnosis
Radial blood pressure devices for self measurements:
instructions, training and commitment of the patient
are necessary. Scheduled repeat calibration!!
March 2013 Prof. G. Hennersdorf DGK ESC SES
29. Hypertension Diagnosis
• How many doctor‘s readings?
– Office visit: at least 3 readings in order to reduce white
coat BPR
– At home (self control): at least 5 readings per day with
protocol):
• After bedrest,
• After breakfast
• Late in the morning
• late afternoon
• Before bed rest
March 2013 Prof. G. Hennersdorf DGK ESC SES
30. Hypertension Diagnosis:patient
commitment
Have a blood pressure protocol booklet ready,
when your patient visits office last time.
Ask the patient to use it regularly and carefully
Ask the patient to show at next visit
therapy control Pt. compliance
March 2013 Prof. G. Hennersdorf DGK ESC SES
31. Hypertension Diagnosis
date time SBP/DBP pulse remarks-medication
Main contents of BP booklet
March 2013 Prof. G. Hennersdorf DGK ESC SES
32. Hypertension Diagnosis
• Clinical Diagnosis
• Devices for measurement
• Advanced Measures
• Pathways and Flowcharts
March 2013 Prof. G. Hennersdorf DGK ESC SES
33. Hypertension Diagnosis
• Advanced BP-measures
– 24 h monitoring
– Telemetry
– Exercise (treadmill) Tests
March 2013 Prof. G. Hennersdorf DGK ESC SES
34. Hypertension Diagnosis
• Advanced BP-measures
– 24 h monitoring
– Telemetry Sleep Wake up
– Exercise Blood pressure
High incidence of
MACCE
March 2013 Prof. G. Hennersdorf DGK ESC SES
35. Hypertension Diagnosis
24h-BP-Monitoring
Daytime 7:00 am – 10:00 pm 20 min intervals
During the night 10 pm – 6:00 am 30 min intervals
minimum of 80/24 h
measurements
March 2013 Prof. G. Hennersdorf DGK ESC SES
36. Hypertension Diagnosis
24h-BP-Monitoring
Normal values
Daytime mean < 135/85 mm Hg
Frequency of values over 20 -25%
140/90 mm Hg
Night dipping 10-15%
Total mean <130/80 mm Hg
Recommendations of the german hypertension society
March 2013 Prof. G. Hennersdorf DGK ESC SES
37. Hypertension Diagnosis
• Advanced BP-measures
– 24 h monitoring
– Telemetry (mostly investigational,needs
invasive measurement)
– Exercise
future use: telemedicine
electronic data transmission by telephone and/or computer
in order to leave the patient not uncontrolled
or to give him safety to contact his doctor in case of emergency
March 2013 Prof. G. Hennersdorf DGK ESC SES
39. Hypertension Diagnosis
Exercise equipment Exercise protocol
March 2013 Prof. G. Hennersdorf DGK ESC SES
40. Hypertension Diagnosis
• Validation of exercise test concerning BP changes:
if
– SBP = 200 mm Hg when reaching 100 W level (10
METS), or
– no recovery to normal values within 5 min observation
time, or
– DBP >= 110 mm Hg at any level (before: do not
perform test, during: stop test!)
Result: exercise hypertension; persistent hypertension
March 2013 Prof. G. Hennersdorf DGK ESC SES
41. Hypertension Diagnosis
• advanced diagnostic procedures:
target organ damage
– Heart: Chest Xray, ECG, Ultrasound, MD-CT, MRT
– Brain: Carotid Duplex Ultrasound, CT, MRT
– Renal: blood tests, urinalysis
– Peripheral vessels: arm-ankle-ratio (<=1), retinal
background
March 2013 Prof. G. Hennersdorf DGK ESC SES
42. Chest Xray:
left heart enlargement
Prominent aortic knob
Dilated aortic root
Enlarged (hypertrophic)
left ventricle
March 2013 Prof. G. Hennersdorf DGK ESC SES
46. Retinopathy: hypertension
Crossing phenomenon
GUNN
Silver reflecting artery
March 2013 Prof. G. Hennersdorf DGK ESC SES
47. Target Organ Damage Diagnosis
Ankle Brachial Index ABI
SBP arm
-------------------
SBP leg (ankle, a. tibialis post.)
Normal value: 120/150 = 0.8
Pathological: 120/80 = 1.5
Peripheral
arterial
disease
US flow transducer
March 2013 Prof. G. Hennersdorf DGK ESC SES
48. Hypertension Diagnosis:
Laboratory tests
• Basic tests:
– Blood tests: full blood count, thyroid gland (T3), kidney, liver,
glucose, electrolytes
– Urinary test: protein, albumin, sedimentum
– Special urinary test. microalbuminuria
• Advanced :
– (secondary Hptn.)renine, aldosterone, katecholamines
– quantitative urinalysis (quantative albuminuria, clearances, Na +,
Cl-)
March 2013 Prof. G. Hennersdorf DGK ESC SES
49. Hypertension Diagnosis
• advanced diagnostic procedures:
mainly secondary Hptn.
– Hormone assays (thyroid, adrenal, pituitary gl.)
– Vascular bed diagnosis (renovascular):
• Abdominal CT
• Abdominal angiography
March 2013 Prof. G. Hennersdorf DGK ESC SES
50. Hypertension Diagnosis
• Clinical Diagnosis
• Devices for measurement
• Advanced Measures
• Pathways and Flowcharts
March 2013 Prof. G. Hennersdorf DGK ESC SES
51. Hypertension Diagnosis:
Flow Chart
consider sec.HPTN
History, office
readings Persistently raised BP
yes
CXR, US, renal Target organ damage?
tests
no
high
patient passport Home BP measurement Start treatment
Information/instruction
low
abnormal
24h Monitoring
normal
Continue repeat visits
March 2013 Prof. G. Hennersdorf DGK ESC SES
52. Hypertension Diagnosis: pathways and
networks
BP Control, blood tests
OPD
treatment control
visit
Hospital Nurse office
admission patient Home care
Emergency, BP Control
First, advanced dgn Treatment control
Start of treatment Instructions
Clinic/office Scheduling appointments
BP Control, blood tests
treatment control
53. Cardiovascular Diseases
Hypertension Management
part I
The End
March 2013 Prof. G. Hennersdorf DGK ESC SES