Acute left ventricular failure is sudden worsening of dyspnea or congestive heart failure caused by conditions that increase left ventricular pressure like aortic stenosis or acute valve regurgitation. It leads to pulmonary edema as hydrostatic pressure in lungs exceeds plasma oncotic pressure, causing fluid to exude into alveoli. Patients experience terrifying breathing difficulties and pink frothy sputum. On exam, they are pale, sweaty and tachycardic with rales and S3 gallop, indicating severe dysfunction. Treatment focuses on oxygen, diuretics, morphine and positioning to relieve anxiety and dyspnea while reducing preload on the heart.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
Pulmonary edema is often caused by congestive heart failure. When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs. As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction
Contains 17 clinical situations of prolonged fever and discussion of various differential diagnosis based on them. Also gives the key points in the diagnosis of a prototype diagnosis and the usefulness of a relevant investigation modality in identifying these conditions. This power point presentaion is based on the chapter in Harrison's Text Book on Internal Medicine chapter on Fever of Unknown Origin
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
1. Acute Left Ventricular Failure
Definition:
Acute left ventricular failure is defined as sudden onset of dyspnea at rest
or worsening dyspnoea of pre-existing chronic congestive cardiac failure
occurring in patients with a cardiac condition. It is not a disease but a syndrome
and complication of heart disease.
Acute pulmonary edema is another term used synonymously with the
same meaning. This can also mean that the left ventricle has not failed but the
left atrium alone has failed as in the case of mitral stenosis.
Acute pulmonary edema can also be due to non-cardiac causes. Non-
cardiac pulmonary edema can occur in adult respiratory distress syndrome and
organo phosphate insecticide poisoning. Neurogenic pulmonary edema follows
neurological causes.
Etiology:
Acute left ventricular failure can occur in any condition, which increases
the left ventricular pressure to significantly high levels like aortic valve stenosis,
systemic hypertension, or any condition, which produces an acute volume over
load of the left ventricle as in acute mitral or aortic valve regurgitation.
Coronary artery heart disease is another important cause of acute left
ventricular failure by causing diastolic dysfunction of the left ventricle.
Pathology:
Acute left ventricular failure may be precipitated by a major event like
acute myocardial infarction or a minor event like the onset of atrial fibrillation in
chronic valvular heart disease. The increase in left ventricular diastolic pressure
causes a passive increase in pressure in the left atrium and the pulmonary veins.
This is transmitted to the pulmonary capillaries.
When the hydrostatic pressure in the pulmonary capillaries exceeds the
oncotic pressure of plasma, which is approximately 25 to 27 mmHg, the fluid
exudes from the pulmonary capillaries into the alveoli, causing pulmonary
edema. This stimulates the respiration through a series of autonomic reflexes
resulting in increase in respiratory rate.
In the case of mitral stenosis since the development of pulmonary venous
hypertension is very slow, occurring over a period of several years, this is
followed by the development of pulmonary arterial hypertension. This actually
protects the patient from developing acute pulmonary edema.
Symptoms:
Acute left ventricular failure presents with sudden onset of dyspnoea at
rest. It then rapidly progresses to orthopnoea and severe respiratory distress, the
patient sitting up and gasping for breath.
Acute pulmonary edema is the classical description of a terrifying
experience. The patient will describe it as a sensation of fighting for breath. This
might occur after mid night after a few hours of sleep. Patient sits up with acute
onset of breathlessness. Sitting or standing will only give little or no relief. There
will be cough and wheezing and plenty frothy expectoration of pink or blood
stained sputum.
2. Confusion and memory impairment can occur in later stages. Severe
prostration, acute anxiety and feeling of impending death can also occur. Death
is likely in all untreated patients, who have not received immediate treatment.
Signs:
The patient appears to be pale and agitated. The extremities are cold and
sweating. He is acutely dyspnoeic and orthopnoeic. The pulse rate is increased
out of proportion to the general condition of the patient. There may be pulsus
alternans in severe left ventricular failure. This means the alternating pulse beats
have lower volume. Extreme tachycardia and bradycardia are ominous in the
setting of acute left ventricular failure.
The systemic blood pressure maybe altered in acute left ventricular failure
due to the underlying cause itself. In aortic stenosis, the systolic pressure will be
low, the diastolic pressure normal and the pulse pressure narrow. In systemic
hypertension, which is another cause for acute left ventricular failure, the systolic
as well as the diastolic blood pressure will be elevated.
But in case of acute left ventricular failure due to other causes, the blood
pressure is not significantly changed. Only in severe acute left ventricular failure,
the cardiac output is reduced and the systolic pressure is lowered.
The jugular venous pressure also does not show an increase unless there
is right ventricular failure or fluid over load in association. The jugular pulse
waves also remain unaltered in isolated acute left ventricular failure.
The apex beat is usually shifted downwards and outwards in most cases
of acute left ventricular failure and the character of the apex is usually heaving in
nature. On percussion of the heart cardiomegaly is detected and in presence of
pericardial effusion the percussed out left heart border is outside the palpated
apex.
The First and second heart sounds are normally heard or altered
depending upon the underlying cardiac lesion. Tachycardia invariably evident
and sometimes associated with irregularity as in the case of atrial fibrillation,
which is another important cause or precipitating factor in acute left ventricular
failure.
The diagnostic hallmark of acute left ventricular failure is the presence of a
third heart sound or a ventricular gallop. This is best heard over the apex in the
left lateral position with the breath held in expiration. The presence of a third
heart sound indicates the presence of severe left ventricular dysfunction.
There may be a murmur heard depending upon the presence of
underlying heart lesion. For example a mid-diastolic murmur of mitral stenosis or
ejection systolic murmur of aortic stenosis may be heard.
Another clinical finding that is diagnostic of acute left ventricular failure is
the presence of bilateral fine crepitations over the lung base. This is sometimes
more extensive and heard all over the lung fields as in acute pulmonary edema.
If there is significant bronchospasm there will be bilateral rhonchi also. This might
create confusion in the diagnosis as acute bronchial asthma which also presents
in a similar fashion.
3. Treatment:
Supportive treatment:
The patient with acute left ventricular failure is always a very anxious and
dyspnoeic. Hence he should be comfortably positioned and supported with a
backrest in the propped up position. Patient may be given a mild sedative like
alprazolam if needed
Oxygen administration:
Oxygen inhalation should be started immediately using a face mask or nasal
probes containing high concentration of oxygen flowing a at a rate of 4-6 liters
per hour.
Morphine:
Morphine sulphate is administered as slow IV injection after diluting with
dextrose. Morphine of one ampoule containing 15 mg of the drug, is diluted in 9
ml of dextrose. One ml will then contain 3 mg. It is given as slow IV injection and
repeated at 15 minutes intervals till the patient is either relieved from dyspnoea
or sedated.
Diuretics;
Diuretics such as frusemide 40 mg are given intravenously as a first line of
treatment. They can be repeated at short interval till desired action is obtained.
Precaution should be taken against the induction of hypokalemia. Diuretics
increase the urinary excretion of sodium and reduce the blood and plasma
volume
Digoxin
Digoxin is indicated in all cases of acute left ventricular failure except in the
setting of acute myocardial infarction, where it is contraindicated. It is the drug of
choice when heart failure is associated with atrial fibrillation, Digoxin tablet
containing 0.25mg is administered either as a slow digitalization if the patient is
already on a daily maintenance dose of the drug or as a rapid digitalizing dose.
0.5 to 0.75mg is given initially fooled by 0.25mg after eight hours and 8hrly for 4
doses and then reduced to a maintenance dose of one tablet a day
Nitrates:
Nitrates are indicated in acute left ventricular failure due causes other than aortic
stenosis. Tablets of isosorbide dinitrate are given as thrice daily doses of 10mg.
Care should be taken to avoid hypotension or syncope. Vasodilators like nitrates
are more useful in chronic heart failure than acute heart failure.
Physiological venesection:
After all other measures fail the technique of reducing the venous return by
rotating tourniquet should be applied. It can reduce the venous return up to 20%.
Rubber tourniquet or blood pressure cuffs are tied to the three limbs and rotated
at intervals of fifteen minute.
Surgical venesection is the last resort in trying to relieve the acute left
ventricular failure in bedside settings. 100 to 150 ml of blood is let out by
venepuncture and there by reducing the pre load.