The document provides guidance on performing a cardiovascular examination, including taking a history, inspecting the precordium, palpating the chest, and auscultating heart sounds. It details the specific areas to examine by palpation and auscultation, and what abnormalities in findings may indicate different cardiovascular conditions. The examination techniques are described step-by-step, emphasizing the importance of patient comfort and obtaining accurate information.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
A comprehensive echocardiographic examination includes two-dimensional imaging, Doppler imaging, and M-mode imaging. Three-dimensional imaging is also increasingly used as a supplement. The examination obtains standard views of the heart from multiple transducer locations and angles in order to assess cardiac structure and function.
This document outlines the steps for performing a cardiovascular examination, including inspection, palpation of pulses, auscultation of heart sounds, and assessment for common cardiovascular problems. The exam involves checking general appearance, eyes, face, precordium, and ankles. Key pulses, jugular venous pressure, heart sounds, murmurs and extra sounds are auscultated systematically. Common presenting complaints like chest pain, breathlessness, palpitations, and syncope are discussed.
This document provides an overview of electrocardiography (ECG), including how an ECG works, the basics of recording an ECG, ECG leads, normal ECG waveforms and intervals, interpreting an ECG, common abnormalities, and how to report an ECG. It discusses topics such as the cardiac conduction system, Einthoven's triangle, the 12-lead ECG, determining heart rate and axis, normal sinus rhythm, P waves, QRS complex, ST segment, T waves, and the QT interval.
The document discusses electrocardiography (ECG). It defines ECG as the graphical recording of electrical activity of the heart from body surface electrodes. It notes ECG is immediately available, non-invasive, and inexpensive. The document outlines uses of ECG including assessing heart rate, arrhythmias, blocks, chamber enlargement, electrolyte imbalance, and drug effects. It discusses key aspects of ECG like waves, intervals, axis, and ST segment elevation. Overall, the document provides an overview of ECG, its uses, principles, and how to interpret common findings.
Left ventricular hypertrophy is an increase in the mass of the left ventricle that can be caused by hypertension, hypertrophic cardiomyopathy, aortic stenosis, or athletic training. It is defined on an ECG as increased voltages in certain leads. Risk factors include age, gender, high blood pressure, obesity, and genetic factors. If left untreated, LVH can lead to heart failure, arrhythmias, heart attack, or sudden cardiac death. Right ventricular hypertrophy is the enlargement of the right ventricle and can be caused by pulmonary hypertension, congenital heart defects, or lung diseases. Both LVH and RVH are diagnosed using ECG criteria and can cause chest pain, palpitations
This document provides a summary of basics of electrocardiography (ECG/EKG). It discusses the history and development of ECG technology. It describes the components of a normal ECG waveform including the P, QRS, and T waves. It explains how to determine heart rate from an ECG and identify different arrhythmias based on the waveform. Key anatomical structures involved in heart's electrical conduction system are also outlined.
The document discusses the anatomy, causes, diagnosis, and management of aortic regurgitation (AR). It provides details on the location of the aortic valve, variants such as bicuspid aortic valve, and common causes of AR including rheumatic heart disease. Physical exam findings, echocardiography parameters, and indications for surgery to replace the aortic valve are summarized. Medical management including vasodilator therapy to reduce afterload is also reviewed.
A comprehensive echocardiographic examination includes two-dimensional imaging, Doppler imaging, and M-mode imaging. Three-dimensional imaging is also increasingly used as a supplement. The examination obtains standard views of the heart from multiple transducer locations and angles in order to assess cardiac structure and function.
This document outlines the steps for performing a cardiovascular examination, including inspection, palpation of pulses, auscultation of heart sounds, and assessment for common cardiovascular problems. The exam involves checking general appearance, eyes, face, precordium, and ankles. Key pulses, jugular venous pressure, heart sounds, murmurs and extra sounds are auscultated systematically. Common presenting complaints like chest pain, breathlessness, palpitations, and syncope are discussed.
This document provides an overview of electrocardiography (ECG), including how an ECG works, the basics of recording an ECG, ECG leads, normal ECG waveforms and intervals, interpreting an ECG, common abnormalities, and how to report an ECG. It discusses topics such as the cardiac conduction system, Einthoven's triangle, the 12-lead ECG, determining heart rate and axis, normal sinus rhythm, P waves, QRS complex, ST segment, T waves, and the QT interval.
The document discusses electrocardiography (ECG). It defines ECG as the graphical recording of electrical activity of the heart from body surface electrodes. It notes ECG is immediately available, non-invasive, and inexpensive. The document outlines uses of ECG including assessing heart rate, arrhythmias, blocks, chamber enlargement, electrolyte imbalance, and drug effects. It discusses key aspects of ECG like waves, intervals, axis, and ST segment elevation. Overall, the document provides an overview of ECG, its uses, principles, and how to interpret common findings.
Left ventricular hypertrophy is an increase in the mass of the left ventricle that can be caused by hypertension, hypertrophic cardiomyopathy, aortic stenosis, or athletic training. It is defined on an ECG as increased voltages in certain leads. Risk factors include age, gender, high blood pressure, obesity, and genetic factors. If left untreated, LVH can lead to heart failure, arrhythmias, heart attack, or sudden cardiac death. Right ventricular hypertrophy is the enlargement of the right ventricle and can be caused by pulmonary hypertension, congenital heart defects, or lung diseases. Both LVH and RVH are diagnosed using ECG criteria and can cause chest pain, palpitations
This document provides a summary of basics of electrocardiography (ECG/EKG). It discusses the history and development of ECG technology. It describes the components of a normal ECG waveform including the P, QRS, and T waves. It explains how to determine heart rate from an ECG and identify different arrhythmias based on the waveform. Key anatomical structures involved in heart's electrical conduction system are also outlined.
The document provides information on aortic valve disease including anatomy, etiology, and pathophysiology. It describes the key components of the aortic root including the aortic annulus, cusps, sinuses, and sinotubular junction. The three main causes of aortic stenosis are discussed as congenital bicuspid valve with calcification, calcification of a normal trileaflet valve, and rheumatic disease. The pathophysiology of aortic stenosis involves left ventricular pressure overload leading to hypertrophy and eventually decreased ejection fraction if severe stenosis is not corrected.
This document provides guidance on performing a vascular examination, including:
1) It outlines the key anatomy of the arterial and venous systems and common pathologies.
2) It describes the equipment, patient positioning, and steps needed for a full examination, including inspection, palpation, auscultation, and testing pulses and blood pressures.
3) Examination techniques are provided to assess the peripheral arterial system, abdominal aorta, and lower limb venous system for varicosities, reflux, and sites of incompetence.
Aortic incompetence is an anatomical defect of the aortic valve where the cups are deformed, sclerotic, calcified, decreased in volume, and unable to close the aortic orifice properly. This allows blood to flow backward from the aorta into the left ventricle during diastole, increasing the intraventricular pressure and blood volume. Over time this causes left ventricular hypertrophy and dilation, displacing the heart borders and apex beat to the left. Symptoms include a diastolic murmur, water hammer pulse, increased arterial pressure, and displaced apex beat. Diagnosis is made through ECG, chest x-ray, and echocardiogram showing valve abnormalities and ventricular changes.
This document discusses different types of heart block. It defines heart block as an abnormal heart rhythm where the heart beats too slowly due to blocked electrical signals between the upper and lower chambers. The types of heart block are described as first, second, and third degree. First degree heart block causes a prolonged PR interval but no symptoms. Second degree heart block can be Mobitz type I or II, with type II being more significant. Third degree or complete heart block causes complete dissociation between the upper and lower chambers and requires a pacemaker.
The mitral valve lies between the left atrium and left ventricle. Mitral stenosis is usually caused by rheumatic fever which causes scarring of the mitral valve leaflets and commissures. In early mitral stenosis, the leaflets can open but have restricted motion. Over time, the leaflets become thickened and rigid, reducing valve opening. This causes symptoms like dyspnea and pulmonary hypertension. On examination, findings may include an irregular pulse from atrial fibrillation, elevated jugular venous pressure, accentuated S1, and a diastolic murmur. Severe mitral stenosis can lead to right heart failure and complications like hemoptysis.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
The document discusses aortic regurgitation, including its anatomy, etiology, pathophysiology, epidemiology, clinical manifestations, diagnosis, and management. Key points include:
- Aortic regurgitation occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole.
- Causes include conditions like infective endocarditis, bicuspid aortic valve, hypertension, and Marfan syndrome.
- In acute severe cases, a rapid increase in left ventricular preload can cause pulmonary edema and cardiogenic shock. Chronic cases involve left ventricular dilation and hypertrophy to compensate for the increased preload over time.
- Physical exam may
ECG Rhythm Interpretation
ST Elevation and non-ST Elevation MIs
ECG Changes
ECG Changes & the Evolving MI
Left Ventricular Hypertrophy
Normal Impulse Conduction
Bundle Branch Blocks
Valvular heart disease refers to abnormalities of the heart valves that result in obstruction of blood flow or backflow of blood. Echocardiography plays a key role in evaluating valve function and structure non-invasively. Common valvular abnormalities include aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. Treatment depends on severity and symptoms, ranging from medical management to surgical repair or replacement of the affected valve.
This document provides an overview of basic echocardiography. It discusses the history and development of echocardiography, how ultrasound images are generated, the different transducer positions and standard views used in echocardiography exams, and the modalities of echocardiography including 2D, M-mode, and Doppler echocardiography. It also covers transesophageal echocardiography, epicardial imaging, intracardiac echocardiography, and stress echocardiography.
Atrial flutter is an abnormal heart rhythm where the atria beat too fast, usually between 240-340 beats per minute. It often occurs in patients with underlying heart conditions that cause enlargement or damage to the atria, such as rheumatic heart disease, congenital heart disease, or COPD. Common symptoms include palpitations, chest discomfort, and fatigue. Treatment options include medications to slow the heart rate or restore normal rhythm, cardioversion, catheter ablation, or implanting a pacemaker.
A 53-year-old man presented with shortness of breath and was found to have severe mitral stenosis, moderate aortic stenosis, severe aortic regurgitation, and moderate pulmonary hypertension. He underwent double valve replacement and is now doing well. Physical examination revealed an irregular pulse, murmurs, and cardiomegaly on chest x-ray, and echocardiogram demonstrated the valvular abnormalities.
Peripheral artery disease (PAD) is a common circulatory problem where narrowed arteries reduce blood flow to the limbs, most commonly affecting the legs. It is usually caused by atherosclerosis and risk factors include smoking, diabetes, and hypertension. Symptoms may range from intermittent leg pain with walking to leg ulcers or gangrene. Diagnosis involves tests like ankle-brachial index and angiography. Treatment focuses on risk factor modification through medication, exercise and lifestyle changes, with surgical or minimally invasive procedures for more severe cases.
The document discusses various types of cardiac arrhythmias including bradyarrhythmias like sinus bradycardia, sick sinus syndrome, and different degrees of atrioventricular block. It also discusses tachyarrhythmias such as sinus tachycardia, atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. It provides details on the characteristic electrocardiographic patterns, underlying causes, clinical presentations, and management approaches for each of these arrhythmias.
Aortic stenosis is a narrowing of the aortic valve opening that obstructs blood flow from the heart into the aorta. It has several causes including a congenitally abnormal bicuspid aortic valve, age-related degeneration and calcification of the valves, or rheumatic heart disease. Diagnosis involves echocardiography to measure the severity based on aortic valve area and pressure gradients. Severe aortic stenosis carries a poor prognosis without intervention, with 50% mortality within 3 years of symptom onset. Treatment options include surgical aortic valve replacement or the minimally invasive transcatheter aortic valve replacement procedure.
This document defines and describes sick sinus syndrome, which is a dysfunction of the sinoatrial node that can cause abnormal heart rhythms like bradycardia, tachycardia, and alternating slow and fast rhythms. It may be caused by certain drugs, aging, or underlying heart conditions. Symptoms can include fatigue, dizziness, and fainting. Diagnosis involves an electrocardiogram showing arrhythmias. Treatment options include medications or a pacemaker if symptoms are severe. The document also briefly discusses different types of heart block.
Aortic regurgitation is a condition where the aortic valve leaks, causing blood to flow back into the left ventricle from the aorta during diastole. It can be chronic or acute, with chronic causes including rheumatic heart disease, infections, and connective tissue disorders. Symptoms are usually mild at first and include palpitations and fatigue, but can progress to cardiac failure. Signs include a high-volume pulse, elevated systolic blood pressure with low diastolic pressure, a diastolic murmur heard at the heart base, and signs of left ventricular volume overload. Echocardiography can confirm the diagnosis and severity. Treatment involves managing heart failure symptoms medically, but severe
The document provides guidance on performing and interpreting 12-lead electrocardiograms (ECGs). It outlines the proper procedure for applying electrodes, including skin preparation and placement of limb and chest leads. Key aspects that must be checked include verifying the leads are attached correctly, the ECG is free of artifact, and identifying any critical findings such as arrhythmias or ST segment changes. Interpreting the ECG requires evaluating the rhythm, measuring the heart rate, identifying normal and abnormal waveforms, and relating findings to the patient's condition.
The document provides guidance on taking a thorough patient history. Key points include:
1) Listen to the patient and allow them to speak freely without interruption to provide the diagnosis.
2) Ask open-ended questions and be selective about direct questioning to avoid missing important details.
3) Mandatory questions for any presenting complaint include onset, duration, aggravating/relieving factors, and associated symptoms.
4) It is important to ask about symptoms in other body systems as the presenting complaint may be caused by an undiagnosed illness elsewhere.
functional assessment and physical examination of the cardiovascular systemSrimanta Haldar
This document provides an overview of procedures for examining patients for potential cardiological disorders. It describes taking a history and performing a physical exam, including assessing symptoms, measuring vital signs, examining the heart and vessels, and auscultating heart sounds. Common cardiac pulses, murmurs, and abnormalities are defined. The goal is to evaluate symptoms and signs to identify potential cardiac issues.
The document provides information on aortic valve disease including anatomy, etiology, and pathophysiology. It describes the key components of the aortic root including the aortic annulus, cusps, sinuses, and sinotubular junction. The three main causes of aortic stenosis are discussed as congenital bicuspid valve with calcification, calcification of a normal trileaflet valve, and rheumatic disease. The pathophysiology of aortic stenosis involves left ventricular pressure overload leading to hypertrophy and eventually decreased ejection fraction if severe stenosis is not corrected.
This document provides guidance on performing a vascular examination, including:
1) It outlines the key anatomy of the arterial and venous systems and common pathologies.
2) It describes the equipment, patient positioning, and steps needed for a full examination, including inspection, palpation, auscultation, and testing pulses and blood pressures.
3) Examination techniques are provided to assess the peripheral arterial system, abdominal aorta, and lower limb venous system for varicosities, reflux, and sites of incompetence.
Aortic incompetence is an anatomical defect of the aortic valve where the cups are deformed, sclerotic, calcified, decreased in volume, and unable to close the aortic orifice properly. This allows blood to flow backward from the aorta into the left ventricle during diastole, increasing the intraventricular pressure and blood volume. Over time this causes left ventricular hypertrophy and dilation, displacing the heart borders and apex beat to the left. Symptoms include a diastolic murmur, water hammer pulse, increased arterial pressure, and displaced apex beat. Diagnosis is made through ECG, chest x-ray, and echocardiogram showing valve abnormalities and ventricular changes.
This document discusses different types of heart block. It defines heart block as an abnormal heart rhythm where the heart beats too slowly due to blocked electrical signals between the upper and lower chambers. The types of heart block are described as first, second, and third degree. First degree heart block causes a prolonged PR interval but no symptoms. Second degree heart block can be Mobitz type I or II, with type II being more significant. Third degree or complete heart block causes complete dissociation between the upper and lower chambers and requires a pacemaker.
The mitral valve lies between the left atrium and left ventricle. Mitral stenosis is usually caused by rheumatic fever which causes scarring of the mitral valve leaflets and commissures. In early mitral stenosis, the leaflets can open but have restricted motion. Over time, the leaflets become thickened and rigid, reducing valve opening. This causes symptoms like dyspnea and pulmonary hypertension. On examination, findings may include an irregular pulse from atrial fibrillation, elevated jugular venous pressure, accentuated S1, and a diastolic murmur. Severe mitral stenosis can lead to right heart failure and complications like hemoptysis.
Ventricular tachycardia is a fast heart rhythm originating from the ventricles with a rate over 100 bpm. It is classified based on duration (sustained vs non-sustained), morphology (monomorphic, polymorphic, sinusoidal), and symptoms. Causes include structural heart disease, electrolyte abnormalities, drugs, and prolonged QT interval. Diagnosis involves ECG criteria showing ventricular origin. Treatment depends on hemodynamic stability and may include antiarrhythmic drugs, implantable cardioverter-defibrillator, catheter ablation, or surgery. Recurrent ventricular tachycardia is managed long term with devices, drugs, and treatment of underlying causes.
The document discusses aortic regurgitation, including its anatomy, etiology, pathophysiology, epidemiology, clinical manifestations, diagnosis, and management. Key points include:
- Aortic regurgitation occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole.
- Causes include conditions like infective endocarditis, bicuspid aortic valve, hypertension, and Marfan syndrome.
- In acute severe cases, a rapid increase in left ventricular preload can cause pulmonary edema and cardiogenic shock. Chronic cases involve left ventricular dilation and hypertrophy to compensate for the increased preload over time.
- Physical exam may
ECG Rhythm Interpretation
ST Elevation and non-ST Elevation MIs
ECG Changes
ECG Changes & the Evolving MI
Left Ventricular Hypertrophy
Normal Impulse Conduction
Bundle Branch Blocks
Valvular heart disease refers to abnormalities of the heart valves that result in obstruction of blood flow or backflow of blood. Echocardiography plays a key role in evaluating valve function and structure non-invasively. Common valvular abnormalities include aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. Treatment depends on severity and symptoms, ranging from medical management to surgical repair or replacement of the affected valve.
This document provides an overview of basic echocardiography. It discusses the history and development of echocardiography, how ultrasound images are generated, the different transducer positions and standard views used in echocardiography exams, and the modalities of echocardiography including 2D, M-mode, and Doppler echocardiography. It also covers transesophageal echocardiography, epicardial imaging, intracardiac echocardiography, and stress echocardiography.
Atrial flutter is an abnormal heart rhythm where the atria beat too fast, usually between 240-340 beats per minute. It often occurs in patients with underlying heart conditions that cause enlargement or damage to the atria, such as rheumatic heart disease, congenital heart disease, or COPD. Common symptoms include palpitations, chest discomfort, and fatigue. Treatment options include medications to slow the heart rate or restore normal rhythm, cardioversion, catheter ablation, or implanting a pacemaker.
A 53-year-old man presented with shortness of breath and was found to have severe mitral stenosis, moderate aortic stenosis, severe aortic regurgitation, and moderate pulmonary hypertension. He underwent double valve replacement and is now doing well. Physical examination revealed an irregular pulse, murmurs, and cardiomegaly on chest x-ray, and echocardiogram demonstrated the valvular abnormalities.
Peripheral artery disease (PAD) is a common circulatory problem where narrowed arteries reduce blood flow to the limbs, most commonly affecting the legs. It is usually caused by atherosclerosis and risk factors include smoking, diabetes, and hypertension. Symptoms may range from intermittent leg pain with walking to leg ulcers or gangrene. Diagnosis involves tests like ankle-brachial index and angiography. Treatment focuses on risk factor modification through medication, exercise and lifestyle changes, with surgical or minimally invasive procedures for more severe cases.
The document discusses various types of cardiac arrhythmias including bradyarrhythmias like sinus bradycardia, sick sinus syndrome, and different degrees of atrioventricular block. It also discusses tachyarrhythmias such as sinus tachycardia, atrial fibrillation, atrial flutter, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation. It provides details on the characteristic electrocardiographic patterns, underlying causes, clinical presentations, and management approaches for each of these arrhythmias.
Aortic stenosis is a narrowing of the aortic valve opening that obstructs blood flow from the heart into the aorta. It has several causes including a congenitally abnormal bicuspid aortic valve, age-related degeneration and calcification of the valves, or rheumatic heart disease. Diagnosis involves echocardiography to measure the severity based on aortic valve area and pressure gradients. Severe aortic stenosis carries a poor prognosis without intervention, with 50% mortality within 3 years of symptom onset. Treatment options include surgical aortic valve replacement or the minimally invasive transcatheter aortic valve replacement procedure.
This document defines and describes sick sinus syndrome, which is a dysfunction of the sinoatrial node that can cause abnormal heart rhythms like bradycardia, tachycardia, and alternating slow and fast rhythms. It may be caused by certain drugs, aging, or underlying heart conditions. Symptoms can include fatigue, dizziness, and fainting. Diagnosis involves an electrocardiogram showing arrhythmias. Treatment options include medications or a pacemaker if symptoms are severe. The document also briefly discusses different types of heart block.
Aortic regurgitation is a condition where the aortic valve leaks, causing blood to flow back into the left ventricle from the aorta during diastole. It can be chronic or acute, with chronic causes including rheumatic heart disease, infections, and connective tissue disorders. Symptoms are usually mild at first and include palpitations and fatigue, but can progress to cardiac failure. Signs include a high-volume pulse, elevated systolic blood pressure with low diastolic pressure, a diastolic murmur heard at the heart base, and signs of left ventricular volume overload. Echocardiography can confirm the diagnosis and severity. Treatment involves managing heart failure symptoms medically, but severe
The document provides guidance on performing and interpreting 12-lead electrocardiograms (ECGs). It outlines the proper procedure for applying electrodes, including skin preparation and placement of limb and chest leads. Key aspects that must be checked include verifying the leads are attached correctly, the ECG is free of artifact, and identifying any critical findings such as arrhythmias or ST segment changes. Interpreting the ECG requires evaluating the rhythm, measuring the heart rate, identifying normal and abnormal waveforms, and relating findings to the patient's condition.
The document provides guidance on taking a thorough patient history. Key points include:
1) Listen to the patient and allow them to speak freely without interruption to provide the diagnosis.
2) Ask open-ended questions and be selective about direct questioning to avoid missing important details.
3) Mandatory questions for any presenting complaint include onset, duration, aggravating/relieving factors, and associated symptoms.
4) It is important to ask about symptoms in other body systems as the presenting complaint may be caused by an undiagnosed illness elsewhere.
functional assessment and physical examination of the cardiovascular systemSrimanta Haldar
This document provides an overview of procedures for examining patients for potential cardiological disorders. It describes taking a history and performing a physical exam, including assessing symptoms, measuring vital signs, examining the heart and vessels, and auscultating heart sounds. Common cardiac pulses, murmurs, and abnormalities are defined. The goal is to evaluate symptoms and signs to identify potential cardiac issues.
This document discusses scleroderma, a chronic autoimmune disease characterized by fibrosis of the skin and internal organs. It defines the two main types as limited scleroderma, which affects the hands, face and forearms, and diffuse scleroderma, which affects the whole body. Raynaud's phenomenon, skin thickening, gastrointestinal issues, lung fibrosis and pulmonary hypertension are common clinical features. The document provides details on pathogenesis, prevalence, risk factors, clinical assessment criteria and organ-specific complications of scleroderma.
1. The document describes the examination of a patient with signs of infective endocarditis including splinter hemorrhages, purpura, and Janeway lesions.
2. Finger clubbing is described in four stages from increased ballotability to thickening of the distal finger resembling a drumstick. Clubbing can be caused by various cardiac and respiratory conditions.
3. The examination of arterial pulses, jugular venous pulsation, carotid pulsation, apical impulse, heart sounds, murmurs and additional sounds are outlined.
HOPPING ALLAH ACCEPT MY TRIAL TO HELP OTHERS
TO MY WIFE AND MY KIDS , AIMING TO LEAVE SOME GOOD THINKS IN THIS LIFE AND FOR OUR COUNTRY WHICH IS SCREAMING
MAGDI AWAD SASI
This document provides details on examining patients with cardiovascular symptoms. It describes how to take a history, including presenting symptoms, previous illnesses, habits, and family history. The physical exam involves inspection, pulse examination, blood pressure measurement, jugular vein examination, chest examination, and heart auscultation. Specific cardiovascular conditions can cause chest pain, dyspnea, fatigue, palpitations, and syncope. Findings on exam include pulses, jugular vein pressure, heart sounds, murmurs, and peripheral signs. The goal is to evaluate symptoms, signs, and history to understand a patient's cardiovascular condition.
This document provides guidance on performing a cardiovascular examination. It outlines the basic approach, including general observations, examination of pulses, blood pressure, eyes/face, neck, legs, and praecordium. Specific techniques are described for palpation, auscultation, and accentuating murmurs. Potential case scenarios involving aortic stenosis, mitral regurgitation, and aortic regurgitation are reviewed. The summary emphasizes performing the exam systematically and using any inability to detect findings as a learning opportunity.
Cardiomyopathy is a disease of the heart muscle that can cause mechanical and electrical dysfunction. It has many causes including genetic disorders, infections, and metabolic issues.
The prognosis for cardiomyopathy is generally poor if left undiagnosed until advanced stages. Diagnostic tools include echocardiography, chest x-rays, and cardiac catheterization.
Dilated cardiomyopathy is the most common type and is characterized by the enlargement of heart chambers and thinning of the walls. It can lead to heart failure if not properly managed with medications like ACE inhibitors, beta blockers, diuretics, and devices like defibrillators if needed. The prognosis is poor with 50% of patients dying within
This document discusses portal hypertension and esophageal varices. It begins by defining portal hypertension as increased blood pressure within the portal venous system, usually caused by cirrhosis of the liver obstructing blood flow. Esophageal varices develop as collateral blood vessels when portal pressure exceeds 12 mmHg. The document then covers causes of portal hypertension, risk factors for bleeding varices, clinical presentation, investigations including endoscopy, and treatment approaches focusing on preventing or managing bleeding from varices.
This document provides an overview of how to examine the cardiovascular system through history, examination of vital signs, inspection, palpation, and auscultation. It details how to examine the pulse, blood pressure, jugular venous pulse, apex beat, and heart sounds. It describes normal findings as well as abnormalities that may be found and how to characterize different types of murmurs. The examination is supported by additional tests like ECG, chest x-ray, and echocardiogram.
Detaliled approach to ascitic patients in liver cirrhosiscardilogy
This document provides detailed information on ascites, including causes, mechanisms, diagnosis, and complications. It discusses that ascites is generally caused by cirrhosis in 85% of cases and results from salt and water retention due to increased aldosterone levels and increased lymph formation from sinusoidal hypertension. Diagnosis involves paracentesis to examine ascitic fluid and measure factors like white blood cell count to check for spontaneous bacterial peritonitis. Complications of ascites include infections, hemorrhage, and spontaneous bacterial peritonitis.
Detailed approach to thyroid gland and parathyroid glandscardilogy
The document discusses thyroid and parathyroid disorders, including:
- Hyperthyroidism is caused by an overproduction of thyroid hormones and can be due to Graves' disease or toxic nodules. Symptoms include weight loss, heat intolerance, tremors, palpitations, and protruding eyes.
- In Graves' disease, the thyroid is enlarged and soft, and patients may experience lid retraction, exophthalmos, eye swelling, and limitations in upward gaze. Malignant exophthalmos is a medical emergency with risk of vision loss.
- Clinical examination of the thyroid involves inspection, palpation, percussion and auscultation to evaluate for signs of enlargement, consistency
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect multiple organ systems. SLE most commonly affects women in their 20s and 30s. The course of SLE is unpredictable, with periods of illness alternating with remission. Common initial symptoms include fatigue, fever, joint pain, and weight changes. SLE can cause skin rashes, oral ulcers, hair loss, serositis, lung involvement including pleurisy, heart involvement such as pericarditis, and kidney disease. The prognosis for SLE has improved in recent decades due to medical advances, with survival rates of approximately 95% at 5 years and 90% at 10 years. SLE is treated symptomatically mainly with
All ACUTE LYMPHOBLASTIC LEUKEMIA BY DR MAGDI SASIcardilogy
1. The document provides information about acute lymphocytic leukemia (ALL), the most common type of cancer in children. It describes the symptoms, signs, classification, and risk factors of ALL.
2. Common symptoms of ALL include fever, fatigue, easy bruising, frequent infections, and bone/joint pain. Physical signs may include pallor, organ enlargement, and lymphadenopathy.
3. ALL is classified according to the type of lymphocytes involved (B-cell vs T-cell lineage) and cellular features. The vast majority of ALL cases involve B-cell lymphocytes. Risk factors for ALL are generally unknown for most people.
1. Acute renal failure (ARF) can be caused by pre-renal factors which decrease blood flow to the kidneys (75% of cases), renal damage to the kidney parenchyma itself (10-20% of cases), or post-renal obstruction of urine flow (2-15% of cases).
2. Common causes of pre-renal ARF include hypovolemia, decreased cardiac output, sepsis, renal artery occlusion, and certain drugs. Renal causes include various types of glomerulonephritis, interstitial nephritis caused by drugs and infections, and acute tubular necrosis from ischemia or toxins. Post-renal ARF can be due to
1. Examine the general appearance of the patient including height, weight, build, position in bed, and level of consciousness. Note any pallor, cyanosis, jaundice, clubbing, edema.
2. Examine the neck for jugular venous pulse, thyroid enlargement, lymph nodes. Position the patient semi-sitting and inspect for distention of neck veins above the clavicle.
3. Inspect the hands and nails for signs of anemia, cyanosis, clubbing and examine the conjunctiva for pallor, jaundice or hemorrhages. Ask the patient to look up and down to examine the sclera and conjunctiva fully.
1. Fatty liver of pregnancy typically occurs late in pregnancy and is associated with preeclampsia. Immediate termination of pregnancy is essential for possible recovery of the patient.
2. Prognosis in fulminant hepatic failure is affected by age, etiology, clinical course, and occurrence of secondary complications such as bleeding and hypoglycemia. Poor prognostic signs include increased prothrombin time and decreased pH.
3. Causes of death in fulminant hepatic failure include renal failure, respiratory failure, neurological complications such as cerebral edema, gastrointestinal hemorrhage, bacterial infection, and hemodynamic complications.
ACUTE and CHRONIC AORTIC INSUFFICIENCY-DR MAGDI SASI 2016cardilogy
1) Acute aortic regurgitation is caused by sudden damage to the aortic valve and presents with severe pulmonary edema, decreased cardiac output, and hypotension as the normal left ventricle cannot handle the sudden volume overload.
2) Chronic aortic regurgitation develops over time as the left ventricle enlarges to compensate for the backflow of blood, eventually leading to heart failure if left untreated. Patients experience exertional dyspnea and fatigue.
3) Infective endocarditis is a common cause of both acute and chronic aortic regurgitation, often causing destruction of the aortic valve leaflets. Other causes include aortic dissection and connective tissue diseases.
This document provides information on examining the cardiovascular system. It discusses the anatomy of the heart and describes how to examine jugular venous pressure. A normal jugular venous pressure is less than 8 cm above the right atrium. The document outlines the steps to measure jugular venous pressure including inspecting the internal jugular vein and measuring the highest point of pulsation in relation to the sternal angle. Elevated jugular venous pressure indicates abnormal cardiac function or pressures in the right heart.
This document provides guidance on assessing the cardiovascular system through physical examination. It describes how to inspect general appearance, check for cyanosis, examine the face, hands, pulse, blood pressure, chest, abdomen, and other areas. It also discusses auscultating heart sounds at various locations and what alterations may indicate, as well as investigating with electrocardiography, echocardiography, and other tests. Physical assessment of the cardiovascular system is important for evaluating a patient's condition, documenting findings, and guiding treatment and care.
The document provides guidance on assessing the carotid pulse, jugular venous pulse, praecordium, and auscultation of heart sounds and murmurs. It describes how to feel the carotid pulse and assess its volume and character. It also explains how to visualize the jugular venous pulse, including positioning the patient and what the normal findings are. The praecordium should be inspected for shape and pulsations, and palpated for thrills and abnormal pulsations. Heart sounds and murmurs should be auscultated in standard areas and positions using the diaphragm and bell to identify any abnormalities.
This document provides instructions for performing various clinical skills assessments including: resuscitation, assessing peripheral pulses, measuring blood pressure, examining the cardiovascular and respiratory systems, performing an electrocardiogram, assessing peak flow, and using a vitalograph machine. Key steps are outlined for each skill, such as procedures for opening an airway, performing chest compressions, locating and feeling different pulse points, correctly applying a blood pressure cuff, examining heart sounds and murmurs, and interpreting vital sign readings.
health assessment theory cardiovascular and abdomin.pdfAbdAlhamid4
This document provides guidance on performing a cardiovascular assessment. It describes indications for assessment, necessary equipment, areas of inquiry for patient history, positioning the patient, taking vital signs, inspecting the chest, auscultating heart sounds at multiple sites, assessing perfusion, examining extremities, and assessing the abdomen. The goal is to evaluate a patient's cardiovascular status, identify abnormalities, and ensure individual patient needs are met.
This document provides guidance on performing a cardiovascular examination, including:
1. Examining the general appearance, vital signs, jugular venous pressure, peripheral edema, and hands of the patient.
2. Performing a local heart examination using the IPPA sequence of inspection, palpation, percussion, and auscultation of the four heart valve areas.
3. During auscultation, commenting on heart sounds, extra sounds like murmurs, and lung bases.
The document provides an overview of how to assess the heart. It describes the heart's anatomy and location. Heart sounds are produced by valve closure, with S1 resulting from AV valve closure and S2 from semilunar valve closure. The assessment involves inspection, percussion, and auscultation of the heart sounds at different locations on the chest. Variations in assessment for geriatric patients and possible collaborative problems are also outlined.
This document outlines the general principles and procedures for performing a physical examination. The physical exam aims to understand a patient's physical and mental well-being by systematically collecting objective information through examination techniques. Key components include assessing vital signs like pulse, blood pressure, temperature and respiratory rate. Other assessments include examining general appearance, oral cavity, hair, nails, lymph nodes, edema, clubbing, pallor, icterus and cyanosis. The exam is conducted in a private, relaxed environment with the patient's consent and reassurance.
This document provides instructions for performing various clinical skills assessments including: resuscitation, assessing peripheral pulses, taking blood pressure, performing a cardiovascular examination, assessing the respiratory system, performing peak flow and vitalograph tests. The key steps are outlined for each skill with the goal of assessing vital signs, breathing, circulation and identifying any abnormalities.
Makos green systemic examination osce wiseKeneth Hesbon
The document provides guidance for conducting a cardiovascular examination, including key areas to inspect, palpate, percuss and auscultate. It describes examining the patient's general appearance, hands, pulse, blood pressure, head, neck, chest, back and ankles. Important signs and clinical findings are defined for each area. Common cardiac pathologies and their physical exam findings are also outlined.
This document provides guidance on performing a peripheral vascular examination, including examining the arms and legs to check for signs of vascular disease. It describes how to inspect and palpate pulses in the upper and lower limbs, listen for bruits, and perform additional tests like Buerger's angle test. The document also covers examining the venous system, including inspection for varicose veins, palpating for fascial defects, and tests like Trendelenburg's test to check for venous incompetence.
General physical examination involves assessing the patient's general appearance, vital signs, and examining the hands, scalp/face/neck, lymph nodes, and edema. Examining the hands focuses on signs like clubbing, cyanosis, and nail changes. Examination of the face evaluates features such as jaundice, pallor, and oral lesions. Neck examination includes assessing carotid pulses, jugular venous pressure, thyroid, and lymph nodes. Vital signs include pulse, blood pressure, respiratory rate, temperature, oxygen saturation, and blood glucose.
This document provides instructions for performing a cardiovascular examination. It outlines how to check the pulse rate and rhythm, listen for arterial bruits, take blood pressure readings, examine jugular venous pressure, auscultate the heart, and interpret findings like murmurs. The goal is to evaluate a patient's cardiovascular system through inspection, palpation, percussion, and auscultation.
This document provides instructions for examining the cardiovascular system, including the heart and neck vessels. It describes the anatomy of the heart and major neck structures. Examination techniques are outlined for inspecting, palpating, percussing and auscultating the heart and neck vessels. Specific assessment methods are described for the carotid artery, jugular venous pulse, jugular venous pressure, apical impulse, heart sounds, and listening for extra sounds or murmurs. Abnormal findings are contrasted with normal findings. Maintaining cardiovascular health through lifestyle changes is emphasized.
The document provides an introduction to Doppler ultrasound and how it is used to assess blood flow in arteries. It discusses:
- The Doppler principle and how sound wave frequency is altered by moving objects like blood cells
- How Doppler ultrasound works to determine blood velocity in vessels
- How to perform an ankle brachial pressure index (ABPI) test using Doppler to calculate the ratio of ankle to brachial systolic pressures
- How to interpret ABPI results and what they indicate about arterial disease severity
- Factors that can affect the accuracy of Doppler assessments
Monday final abdominal examination final pptroheedakhan81
This document provides information on assessing the abdomen, anus, and rectum. It discusses the key components of the examination, including inspection, auscultation, percussion, and palpation. Inspection involves observing the abdomen for signs like scars, striae, jaundice, and hernias. Auscultation listens for bowel sounds and bruits. Percussion determines the liver and spleen size and checks for fluid. Palpation feels the abdomen for masses, tenderness, guarding, and rigidity. The rectal examination and specific assessment findings are also outlined.
This document provides information on cardiovascular history taking and physical examination. It discusses important symptoms of heart disease like dyspnea, palpitations, edema, and chest pain. It also outlines the steps for examining arterial pulses, blood pressure, jugular venous pressure, auscultation of heart sounds, and palpation of the precordium. The physical exam aims to evaluate symptoms, risk factors, and detect any abnormalities that could indicate cardiac issues.
This document provides information on performing a general survey and measuring vital signs. It describes aspects to observe in a general patient survey, such as appearance, posture, and gait. It then discusses the importance of measuring weight, height, temperature, blood pressure, heart rate, rhythm, and respiratory rate as vital signs. For each vital sign, it explains the proper technique for measurement and provides normal ranges. It also describes abnormalities that may be observed, such as orthostatic hypotension or irregular pulses.
This document discusses non-infectious diseases, specifically coronary heart disease and atherosclerosis. It describes how atherosclerosis develops as fatty deposits build up in artery walls, restricting blood flow. This can lead to heart attacks, angina, or cardiac arrest if arteries become fully blocked. The document outlines treatments for coronary heart disease like angioplasty, bypass surgery, medications, and in rare cases, heart transplants. It also examines risk factors for developing heart disease and the global distribution and costs of treating cardiovascular diseases.
1) The document reviews the anatomy and physiology of the cardiovascular system and describes methods for assessing cardiovascular status including health history, physical exam techniques like inspection, palpation, percussion and auscultation, and diagnostic tests.
2) The physical exam involves assessing things like vital signs, jugular vein pulsations, heart sounds and murmurs auscultated over the precordium.
3) Diagnostic tests discussed include electrocardiograms, echocardiograms, stress tests and cardiac catheterization.
This document provides information on assessing the cardiovascular system. It begins with an introduction on the importance of cardiovascular assessment by nurses. It then covers anatomy and physiology of the heart, including the valves and blood circulation. Physical examination techniques are outlined, including inspection, palpation, percussion and auscultation. Common abnormalities that may be found on assessment are listed. Finally, additional investigation methods are mentioned, such as electrocardiograms, blood tests and cardiac imaging.
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Cardiovascular history and examination
1. MAGDI AWAD SASI 2013
BY DR. MAGDI AWAD SASI
Detailed analysis of cardiovascular examination 2012
Cardiovascular History
Record the date and time the history was taken.
Name, Age, Occupation(s)
Presenting Problem/ Complaint
Remember the questions you need to ask about each symptom?
There are 4 main cardiovascular symptoms:
1. Chest pain (character, radiation)
2. Shortness of breath (exercise tolerance, orthopnoea, paroxysmal nocturnal
dyspnoea)
3. Presence and extent of oedema (ankle, leg or sacral)
4. Palpitations (tap out rhythm, any dizziness or blackouts)
Systemic Review
During the history consider (and ask about) the main risk factors for Ischaemic
Heart Disease:
1. Smoking
2. Hypertension
3. Diabetes mellitus
4. Hyperlipidaemia
5. Family history
Past Medical History (may ask under presenting complaint)
e.g. angina, myocardial infarction, bypass operation, rheumatic fever, stroke,
intermittent
claudication
Social History
Smoking (pack years), alcohol, stairs
Family History
At what age did the relative have illness?
Drug History
Allergies
2. MAGDI AWAD SASI 2013
INTRODUCTION
W - Wash your hands.
I - Introduce yourself (full name and role). Greet the patient with their
title and surname.
P - Permission. Explain that you wish to examine their heart.
E - Expose the necessary parts of the patient. Ideally the patient should be
undressed from the waist up taking care to ensure the patient is not cold or
unnecessarily embarrassed.
R - Reposition the patient. In this examination the patient should be
supine and reclined at 45 degrees.
In the cardiovascular examination a lot of information can be obtained by
looking for peripheral signs of cardiovascular disease.
The examination is therefore split into a
A.peripheral examination and B. examination of the precordium.
Adequate exposure and a quiet environment are critical.
Peripheral Examination
End of the Bed
• Examine the patient for signs of breathlessness or distress.
• It is also important to look at the surrounding environment for oxygen, fluid
restriction signs or GTN spray.
Hands
• To assess warmth, sweating and whether there is peripheral cyanosis.
• Examine the nails for clubbing or signs of infective endocarditis (splinter
haemorrhages, Osler’s nodes and Janeway lesions).
• Palpate the radial pulse and assess the rate and rhythm.
Rate , rhythm , volume, special character, synchronicity, radiofemoral delay
Small volume = stenotic lesion mitral and aortic stenosis.
Large volume = regurgitation lesion mitral and aortic regurgitation.
3. MAGDI AWAD SASI 2013
Types of pulses
Slow rising pulse (delayed up strokes / parvus et tardus) A
carotid arterial pulse that is reduced (parvus) and delayed (tardus) argues for
aortic valvular stenosis. Occasionally this also may be accompanied by a
palpable thrill. If ventricular function is good, a slower upstroke correlates with a
higher transvalvular gradient. In left ventricular failure, however, parvus and
tardus may occur even with mild aortic stenosis (AS).
Pulsus bisferience = AR + AS
Pulsus paradocsus = acute sever asthma or cardiac tamponade
Pulsus paradoxus is an exaggerated fall in systolic blood pressure during quiet
inspiration
Pulsus alternans = LVF
Pulsus alternans is the alternation of strong and weak arterial pulses
despite regular rate and rhythm.
Collapsing pulse= hyperdynamic circulation
A high volume pulse that hits the fingers suddenly and falls away just
as quickly. It is exaggerated by raising the arm well above the level of the
heart. This is a sign of aortic regurgitation. The pulse is examined with the arm
by the patient’s side; then briskly raise the arm
• Measure the blood pressure. If the
blood pressure is raised compare both arms.
Face
• Check eyes for corneal arcus and xanthelasma.
• Inspect the conjunctivae for anaemia.
• Check for mouth and tongue for central cyanosis.
4. MAGDI AWAD SASI 2013
Check Jugular Venous Pressure (JVP)
o With the head resting back on the pillow ask the patient to turn the head to the
left while the head of bed is elevated to 45.
1 Think anatomically. The right IJ runs between the two heads (sternal and
clavicular) of the sternocleidomastoid muscle (SCM) and up in front of the ear.
2 Take your time. Look at the area in question for several minutes while the
patient's head is turned to the left. The carotid artery is adjacent to the IJ, lying just
medial to it . The carotid impulse coincides with the palpated radial artery
pulsation and is characterized by a single upstroke timed with systole. The venous
impulse (at least when the patient is in sinus rhythm and there is no tricuspid
regurgitation) has three components a, c and v waves. When these are transmitted
to the skin, they create a series of flickers that are visible diffusely within the
overlying skin. In contrast, the carotid causes a single up and down pulsation.
Furthermore, the carotid is palpable. The IJ is not and can, in fact, be obliterated by
applying pressure in the area where it emerges above the clavicle.
3. Shine a pen light tangentially across the neck. This sometimes helps to
accentuate the pulsations.
4 . Hepatojugular reflux If you are still uncertain, apply gentle pressure to
the right upper quadrant of the abdomen for 5 to 10 seconds. This elicits Hepato-
Jugular Reflux which, in pathologic states, will cause blood that has pooled in the
liver to flow in a retrograde fashion and fill out the IJ, making the transmitted
pulsations more apparent. Make sure that you are looking in the right area when
you push as the best time to detect any change in the height of this column of blood
is immediately after you apply hepatic pressure.
5 . The Angle of Louis
5. MAGDI AWAD SASI 2013
The angle is the site of the joint which connects the manubrium with the rest
of the sternum.
First identify the supra-sternal notch, a concavity at the top of the
manubrium.
Then walk your fingers downward until you detect a subtle change in the
angle of the bone, which is approximately 4 to 5 cm below the notch. This is
roughly at the level of the 2nd intercostal space.
The vertical distance from the top of the column to this angle is added to 5cm,
the rough vertical distance from the angle to the right atrium with the patient
lying at a 45 degree angle.
The sum is an estimate of the CVP.Normal is 7-9 cm.
o Look for pulsation along the right internal jugular vein.
o The height of the pulsation is measured vertically in cm from the sternal angle.
Add 5cm to get the JVP.
o You should know how the JVP can be differentiated from carotid pulsation
6. MAGDI AWAD SASI 2013
Explain what you're doing (& why) before doing it .
Expose the minimum amount of skin necessary - this requires "artful" use of gown
& drapes (males & females)
Examining heart & lungs of female patients:
Ask pt to remove bra prior (you can't hear the heart well thru fabric)
Enlist patient's assistance, asking them to raise their breast to a position that
enhances your ability to listen to and palpate the heart
Don't rush, act in a callous fashion, or cause pain
PLEASE... don't examine body parts thru gown as:
1. It reflects Poor technique
2. You'll miss things
3. You'll lose points on scored exams .
7. MAGDI AWAD SASI 2013
INSPECTION
The examination should be conducted in a warm, quiet room. Place the patient in a supine position with
the upper body elevated 30 to 45 degrees after all clothing has been removed from the chest. Explain to
the patient that you are going to examine the heart. Warm your hands and stethoscope, but warn the
patient that your hands may be cool at first. The most comfortable and satisfactory position for most
examiners is on the patient's right side
The praecordium is the front of the chest overlying the heart.
A. Look for abnormal chest shape
Normal chest =anterior posterior diameter 1/3- 2/3 of side to side
Barrel shaped = anterior posterior equal to side to side
COPD, Bronchial asthma , Bronchiectasis
Pigeon chest = pectus incavatum= sternum protruded out
Funnel chest= pectus excavatum = sternum depressed
B. Look for skin , scar , pulsation ,Pacemaker
Midline – sternotomy scar – CABG/valve replacement.
Left – thoracotomy scar (diagonal from under left breast to left axilla) – mitrial
valvectomy for mitrial stenosis.
Pacemaker – under skin inferior to left clavicle.
Apical pulsation , parasternal pulsation , epigastric pulsation
C. Look for respiratory movement
Thoraco abdominal in female , Abdominothoracic in male
Any change gives a clue to pathological process.
D.Look for accessory muscles
Contracted sternomastoid , recession of intercostals muscles that gives a
clue that the patient is dyspneic or he had a chronic respiratory disease
with chronic dyspnea.
Note
This is the same even for chest inspection that for CVS concentrate on
pulsation and for chest lok for respiratory movement.
8. MAGDI AWAD SASI 2013
PALPATION
1.Palpate trachea
2.Apex beat = Point of Maximum Impulse (PMI)
It is the lower most , outer most and most forceful pulsation.
LOCATE the apex beat accurately with the flat of and fingers of your right hand.
Try to pin down the precise location with the tip of your index finger. The normal
sized and functioning ventricle will generate a penny sized impulse Count down
the ribs from the sternal angle= 2ND
intercostals space. The normal apex beat
should be in the 5th intercostal space in the mid clavicular line. Decide if the apex
beat is normal or displaced.
Locate the line “axillary, midclavicular “ , space “ 5th
,6th
,7th
“ and character
“ tapping,foreceful heaving or unsustained “.
.Apex beat not palpable
Normal cause Obesity , thick chest , behind rib
Pathological cause barrel chest ,pericardial effusion,dextocardia
.Rotating the patient to a left lateral decubitus position tips the heart
towards the chest wall and makes the apex beat easier to feel.
9. MAGDI AWAD SASI 2013
1.Mitral stenosis
produces a particularly characteristic cardiac apical impulse. The apical
impulse often has a sharp tapping nature. This is because the first heart
sound is loud because of forceful closure of the mitral valve and this forceful
closure is transmitted to the chest wall as a ‘tap’. Same line and same
space “ tapping”
2.Aortic stenosis- pressure load “heaving”
A forceful or ‘thrusting’ apex, either in the normal position or slightly
displaced to 6th
intercostals space. This is usually due to concentric LV
hypertrophy as a result of conditions such as aortic stenosis or hypertension.
same line and change space. “forceful sustained”
3. Mitral and aortic regurgitation- volume load
The apical impulse may be displaced to the left and have a more diffuse
heaving nature. This is usually when there is volume overload. A similar
type of apex beat is often seen when there is sever LV dysfunction and the
ventricle is enlarged. If the patien has an audible gallop rhythm this can
sometimes also be palpated with a hand placed over the cardiac apex. Line
and space changed.
“forceful unsustained”
D. Constrictive pericarditis , which is rare in many developed countries,
but common in the developing world, can produce in-drawing of the
intercostals spaces during systole because the LV is tethered to the chest
wall by the diseased pericardium.
Summary:
For apex beat , check line , space and character.
Palpation of the precordium of a female patient is best
done by placing the palm of your right hand directly
beneath the patient's left breast such that the edge of
your index finger rests against the inferior surface of the
breast. Tell that patient what you are about to do (and
why) before actually performing this maneuver.
Remember that with age tissue turgor often declines,
causing the breasts to hang below the level of the heart.
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Palpate the 2nd
left intercostals space “pulmonary area” for palpable 2nd
heart sound which normally not felt.
In pulmonary hypertension , the pulmonary artery dilates and produces
an impulse in the second left intercostals space and the loud pulmonary
component of the S 2 may also be appreciated as a sharp snapping
feeling in this area.
3.THRILL
It is a palpable vibratory sensation, often compared to the purring of a cat, and
typical of murmurs caused by very high pressure gradients. These, in turn,
lead to great turbulence and loudness.
Hence, thrills are only present in pathologic murmurs whose intensity is greater
than 4/6. It should be checked in the four areas by palmer surface of the right
hand at the junction of metacarpophalangeal surfaces.
The commonest cause of a thrill is aortic stenosis.
If present there should be an easily audible murmur present on auscultation.
In mitral area= diastolic thrill , in aortic area= systolic thrill
11. MAGDI AWAD SASI 2013
1.Aortic area: “AA” 2nd
parasternal right intercostals space
2.Pulmonary area “ PA”:2nd
parasternal left intercostals space
3.Tricuspid area “TA” : 4th
paraeternal left intercostals space
4. Mitral area “MA” : 5th
left intercostals space-apex beat
4.HEAVE
Left parasternal (right ventricular) heave
A signifi cantly hypertrophied and/or dilated RV will produce
an abnormal impulse at the lower end of the sternum,
usually to the left side. In a patient with lung disease and
an abnormal RV this physical sign may be absent because
the over-infl ated lung acts as a cushion between the heart
and the chest wall and therefore prevents the impulse being
transmitted to the surface. Heaves represent ventricular hypertrophy
and feel as if your hand is being lifted of patient’s chest.
Figure 1 AREAS TO BE PALPATED FOR THRILL
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Auscultation
. Don’t auscultate over clothes or gown.
. Warm your hands and stethoscope.
. The most satisfactory position for examiner is on the patient's right side.
. Become comfortable with your stethoscope.
. Learn how to use it correctly bell and diaphragm.
. The most important "part" is what sits betwen the ear pieces!
. Be isolated from surrounding and keep ear pieces tight to your ears.
.4 areas need to be auscultated 2 times change from diaphragm to bell.
. 2 positions need to be done by the patient other than supine.
. 2 radiation of the murmurs need to be checked.
. Start from mitral area “apex beat”. OR aortic area!
. start from MA - TA – PA – AA
.
These areas, although known as the mitral, tricuspid, pulmonary and
aortic areas, in fact have no anatomical meaning. They are the key
areas where the heart sounds and murmurs radiating from these
valves are traditionally considered to be best heard. Be prepared to
hunt around slightly to find the optimum position for your stethoscope
but don’t move too quickly or you could miss a sound.
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Technique of auscultation
A. Start from mitral area by putting the diaphragm of stethoscope and
Listen systematically to the cardiac cycle i.e. 1st and 2nd heart
sounds (S1 and 2) and listen in the systolic and diastolic intervals
for added sounds and murmurs. Time events with simultaneous
palpation of the carotid.
B. Roll your patient slightly onto his left side and listen in the 5th
ICS with the bell for the low frequency mid diastolic murmur of
mitral stenosis. (Listen in full expiration).
C. Auscultate in the axilla with the diaphragm for radiation and
comparative loudness of a systolic murmur. (e.g. the pan -
systolic murmur of mitral regurgitation radiates to the axilla.)
D. Go to TA then PA then AA ask patient to sit , lean forward
and exhale the air to check AA and listen at left lower sternal
edge for high frequency diastolic murmur of aortic regurgetation
E. auscultate with the diaphragm over both
carotids for bruits and radiation of
murmurs, (the ejection systolic murmur of
aortic stenosis radiates to the neck.)
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F. Use both the bell and diaphragm appropriately in the 4 areas –
That the bell should only be placed lightly on the skin.
The bell at the apex for low frequency sounds (i.e. murmurs)
The diaphragm at the base for high frequency sounds.
HEART SOUNDS
Heart sounds are discrete bursts of auditory vibrations of varying intensity
(loudness), frequency (pitch), quality, and duration.
Start by listening to the heart sounds. To help you differentiate between the heart
sounds they should be timed against the carotid pulse.
SUMMARY
S1 =1st
heart sound best heard in MA
Muffled with MR as it is masked by pansystolic murmur
Very loud in MS with rumbling diastolc murmur
Timed with carotid pulsation
S2 =2nd
heart sound heard in AA
Loud in PA in pulmonary HTN, loud in AA in systemic HTN
Timed with carotid pulsation “delay”
Soft A2 in AS , AR
S3 = Left ventricular failure-gallop rhythm
S4 = noncompliant ventricle LVH
S3 AND S4 DIASTOLIC SOUNDS , LOW PITCHED.
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S1 & S2 ARE NORMAL SOUNDS . S3&S4 ARE PATHOLOGICAL.
• The first heart sound is
. The sound of the mitral and tricuspid valves closing
.Systolic events tend to occur at the same time as the carotid pulse
. Loudest at the apex.
The S1 is muffled when there is an increased amount of tissue between the
heart and the stethoscope, as occurs with pleural effusion, pericardial
effusion, emphysema, pneumothorax, and obesity.
Conditions associated with a loud S1 include the following:
Increased transvalvular gradient (MS, TS, atrial myxoma)
Increased force of ventricular contraction (tachycardia, hyperdynamic
states [ie, anemia, fever, thyrotoxicosis, exercise, inotropic agents])
Shortened PR interval - Tachycardia, preexcitation syndromes (ie,
Wolff-Parkinson-White [WPW] syndrome)
Conditions associated with diminished intensity of S1 include the following:
Inappropriate apposition of the AV valves
(ie, mitral regurgitation [MR], tricuspid regurgitation [TR], dilated
cardiomyopathy)
Prolonged PR interval (ie, bradycardia, heart block, digitalis toxicity)
Decreased force of ventricular contraction
(ie, cardiomyopathy, myocarditis, myxedema, myocardial infarction [MI])
Increased calcification of the AV valve
(ie, calcific MS, postirradiation)
Increased distance from the heart
(ie, obesity, emphysema, pleural effusion, pericardial effusion)
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SO , S1 CAN BE HELPFUL FOR EVALUTING THE SEVERITY OF VALVULAR
LESION.
.
• The second heart sound
.Closure of the aortic and pulmonary valves at end of systole.
.Follows the apical impulse and carotid pulsation.
. Best heard at the upper left sternal edge using the
diaphragm of the stethoscope.
A2 is best heard at the aortic area (second right intercostal space); P2 is best
heard at the pulmonary area. S2 is a high-pitched sound heard best with the
diaphragm of the stethoscope. The intensity depends on valvular factors, the
transvalvular gradient, mechanical factors, and size of the great vessels.
The intensity of A2 is increased in Systemic hypertension,
Coarctation of the aorta,
Aortic aneurysm,
Thin individuals,
and when the aorta is closer to the anterior chest wall as may occur with
tetralogy of Fallot and transposition of the great arteries (TGA).
The intensity of A2 is decreased with decreased aortic diastolic pressure ( AR),
with improper valvular apposition ( AR or aortic dissection), calcific immobile
valves ( calcific aortic stenosis [AS]), and decreased systemic arterial pressure.
The intensity of P2 is increased with pulmonary arterial hypertension
Split S2
Normally, the aortic valve closes slightly before the pulmonary valve. This
difference is more pronounced with inspiration due to increased RV stroke
volume.
The fixed-split S2- ASD, right heart failure
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Third Heart Sound
The third heart sound (S3) is a low-pitched, early diastolic sound audible during
the rapid entry of blood from the atrium to the ventricle. When arising from the
LV, it is best audible at the apex with the patient in left lateral decubitus position
with breath held at end expiration. When it is of RV origin, S3 is best audible at
the left lower sternal border or the xiphoid with the patient in supine position.
These are best heard with the bell of the stethoscope. Conditions associated with
pathological S3 include the following:
A. Systolic and/or diastolic ventricular dysfunction
1. Ischemic heart disease
2. MR or TR
3. Sysetmic and pulmonary hypertension
4. Acute aortic regurgitation
5. Chronic AR with systolic dysfunction
B.Hyperkinetic states - Anemia, fever, pregnancy, thyrotoxicosis, AV fistula
C.Volume overload - Renal failure
Fourth Heart Sound
The fourth heart sound (S4) is a late diastolic sound that corresponds to late
ventricular filling through active atrial contraction. It is a low-intensity sound
heard best with the bell of the stethoscope. When of LV origin, S4 is best heard at
the apex with the patient in the left lateral decubitus position at end expiration.
When of RV origin, it is heard best at the left lower sternal border. Maneuvers
that increase the preload increase the intensity of S4 by increasing the separation
of S4 from S1.
Active atrial contraction is necessary for the generation of S4. Thus, S4 is not
audible with atrial fibrillation or flutter.
Some of the conditions associated with S4 include the following:
Ventricular hypertrophy - LV hypertrophy (systemic hypertension,
hypertrophic cardiomyopathy, AS); RV hypertrophy (pulmonary
hypertension, pulmonary stenosis [PS])
Ischemic heart disease - Acute MI,angina
Ventricular aneurysm
Hyperkinetic states that cause forceful atrial contraction
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Both S3 and S4 need to be differentiated from splitting of the normal heart
sounds. With splitting, the heart sounds are high pitched and best audible
with the diaphragm, whereas the S3 or S4 are low-pitched sounds best audible
with the bell of the stethoscope
Is there any audible sound other than heart sounds?
MURMURS
1.‘‘Inching’’ the stethoscope (i.e., slowly dragging it from site to site)
can be the best way to avoid missing important findings.
2. From MA TO TA THEN PA OT AA or THE REVERSE AA.
3. Murmurs are common in MA AND AA THAT IS LEFT SIDE.
Definition:
The production of murmurs results from turbulent flow across valves. Three main
factors have been attributed to cause a murmur:
(1) high flow rate through normal or abnormal orifices
(2) forward flow through a constricted or irregular orifice or into a dilated vessel or
chamber, (3) backward or regurgitant flow through an incompetent valve.
When evaluating a heart murmur, it is important to know the timing of the
murmur in the cardiac cycle, the location, the duration, character, configuration,
radiation, aggravating maneuvers, and diminishing maneuvers.
Types of murmurs:
1.Systolic (holosystolic, early/middle/late systolic)
2.Diastolic (early/middle/late) or
3.Continuous (ie, present in both systole and diastole).
All diastolic murmurs and any systolic murmur above grade 2
in severity requires further evaluation with echocardiography.
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TIME
The timing of the murmur is determined by palpating the carotid pulse while
listening to the murmur. The carotid upstroke corresponds to the onset of
systole.
LOCATION
This is the area of the heart where the murmur is heard the loudest.
While auscultating, one should concentrate on the apex, pulmonary
area, tricuspid, and aortic areas, in addition to the axilla, base of the
heart, and left fourth ICS for evidence of radiation of murmur.
INTENSITY:
The intensity of the murmur depends on the volume of blood flow
across the valve and the pressure gradient across which the blood
flow occurs.
What is the Levine system for grading the intensity of murmurs?
The intensity or loudness of a murmur is traditionally graded by the
Levine system from 1/6 to 6/6. Increased intensity usually reflects
increased flow turbulence. Thus, a louder murmur is more likely to be
pathologic and severe.
Grade I - Heard in a quiet room by an expert examiner
Grade II - Heard by most examiners
Grade III - Loud murmur without thrill
Grade IV - Loud murmur with a thrill
Grade V - Thrill with a very loud murmur audible with stethoscope placed
lightly over the chest
Grade VI - Thrill with a very loud murmur audible even with the stethoscope
slightly away from the chest
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Quality/character:
Different murmurs have different qualities, such as
harsh, blowing, rumbling, musical.
Pitch:
This can be high or low pitched depending on the frequency of the
murmur. The high-pitched sounds are best audible with a diaphragm
and the low-pitched sounds with the bell.
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Radiation:
Murmurs tend to radiate to certain specific areas that are often characteristic of a
particular murmur. The murmur of MR radiates to the axilla or base of the heart,
depending on which leaflet is involved. In the case of AS, the murmur radiates in
the direction of the jet of turbulent blood (ie, radiates to the carotids). Similarly,
the aortic regurgitant murmur tends to radiate along the left sternal border.
Configuration:
This corresponds to the shape of murmur intensity over time. It can be a plateau,
decrescendo, crescendo-decrescendo, or crescendo murmur.
Maneuver affect on murmur:
1.Affect of respiration
The murmurs generated from the right side of the heart increase in intensity
with inspiration by increasing the venous return to right side. ,
Murmurs arising from the left side of the heart become more prominent with
expiration as blood is forced from lung to the heart.
2.Standing up:
This causes a peripheral pooling of blood and a net decrease in venous return.
Most murmurs are thus decreased in intensity upon standing, except that of
hypertrophic obstructive cardiomyopathy (HOCM) and MVP, which become
more prominent.
3.Squatting:
Squatting causes an increase in the afterload and venous return (ie, preload).
The net effect is an increase in intensity of all the murmurs, except those
associated with MVP and HOCM, which become less prominent with
squatting.
4.Hand grip:
Hand grip is a form of isometric exercise and increases the afterload, arterial
pressure, LV volume, and LV pressure. The net effect of these changes is
complex and variable. Murmurs of MR, AR, and VSD worsen with hand grip,
while those of HOCM and MVP are less prominent.
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Cardiac cycle
As a rule , the stenosis will be evident once blood flow through the valve and the valve is
opened that with associated turbulent flow.
The 2nd
rule is the regurgitation will be evident once there is no blood flow through the
valve and valve closed
In systole, left and right ventricles contract
Aortic valve and pulmonary valves opened
Mitral and tricuspid valves closed
Aortic and pulmonary valves opened. If there is stenosis “AS/PS” , ejection systolic
murmur will be heard in aortic area/ pulmonary area which is harsh high pithched loud of
crescendo- decrescendo in configuration as blood is pumped with high amount during
systole which became more audible by sitting leaning and in full expiration in AS.
Mitral valve and tricuspid valves closed. If there is regurgitation “MR/TR”, pansystolic
murmur will be heard in mitral area and tricuspid area which is blowing and high pitched
plateau in configuration which became more audible by telt to left side in apex beat in
the expiration and radiate to left axilla in MR.
In diastole, left and rig ventricles relaxed.
Mitral and tricuspid valves opened.
Aortic and pulmonary valves closed .
Mitral and tricuspid valves opened . If there is stenosis “MS/TS”, mid diastolic murmur
will be heard in mitral area and tricuspid area which is low-pitched rumbling , best heard
with the bell of the stethoscope placed over the cardiac apex with the patient in the left
lateral position in mitral stenosis in expiration with loud S1.
Aortic and pulmonary valves closed. If there is regurgitation, “AR/PR” early diastolic
murmur will be heard in aortic area and pulmonary area which is high-pitched sound, is
decrescendo in configuration , and is most audible at the left sternal border or the right
second ICS just to the right of sternum, with the patient leaning forward at end expiration
in AR.
AS/PS = EJCETION SYSTOLIC MURMU
MR/TR = PANSYSTOLIC MURMUR
AR/PR = EARLY DIASTOLIC MURMUR
MS/TS =MID DIASTOLIC MURMUR
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Systolic murmurs;
1. Pansystolic murmur-
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
These murmurs last throughout ventricular systole. They usually start at S1 and
proceed through S2; the intensity of the murmur may overshadow both valve
closure sounds.
These murmurs are typically produced by emptying of the high-pressure
ventricle during systole into chambers that have lower pressure at that time (the
atria with MR or TR or the right ventricle in the case of VSD).
The murmur of MR is blowing and high pitched and is best heard at the apex
with radiation to the axilla or the base of the heart. It is usually plateau in
configuration. The MR murmur is increased during expiration, passive leg
raising, squatting, and handgrip and decreased in intensity with inspiration,
Valsalva, and standing. The radiation of the murmur depends on which leaflet
is involved. A murmur generated by the deformity of anterior leaflet radiates
more toward the axilla, thoracic spine, and scapula, while a murmur arising
from posterior leaflet involvement radiates to the base of the heart
Severe MR . The presence of S3
. Signs of pulmonary hypertension and right heart failure
The murmur of TR is best heard at the left lower sternal border. It is a
blowing high-pitched murmur heard that increases in intensity with
inspiration (Carvallo sign). It can result primarily from involvement of the
tricuspid valve or secondarily from pulmonary hypertension. When due to
pulmonary hypertension, it is associated with a loud P2.
In VSD with normal pulmonary arterial pressures, a holosystolic murmur can
be heard over the left lower sternal border at the level of the third and fourth
ICSs. This murmur depends on the orifice size of the septal defect. The
smaller the defect, the greater the intensity of the murmur.
24. MAGDI AWAD SASI 2013
2.Ejection systolic murmur “mid to late systole”
Aortic
o Obstructive
Supravalvular - Supravalvular AS, aortic coarctation
Valvular - AS, aortic sclerosis
Subvalvular - HOCM
o Increased flow, hyperkinetic states, aortic regurgitation, complete
heart block
o Dilatation of the ascending aorta, aortitis, atheroma
Pulmonary
o Obstructive
Supravalvular - Pulmonary artery stenosis
Valvular - Pulmonary valve stenosis
Subvalvular - Infundibular stenosis
o Increased flow, hyperkinetic states, left-to-right shunt
o
These murmurs are usually associated with ventricular outflow tract
obstruction (which can be valvular, supravalvular, or subvalvular) or an
abnormal amount of blood flow across normal valves as can happen in
hyperdynamic states (hyperthyroidism, fever, pregnancy, anemia, renal
failure).
AS/PS
The murmur associated with valvular stenosis (AS or PS) is usually a harsh murmur
which is crescendo- decrescendo in configuration and high pitched.
AS-associated murmurs are most audible at the right upper sternal border/right
third ICS with the patient in the upright position and breath held at end
expiration. In some cases, it is audible at the apex, in which case it can be confused
with the murmur of MR. Some of the findings that help delineate the murmur of
MR from that of AS include an audible S1, forceful apex, radiation to carotids,
changes with atrial fibrillation, and post-PVC accentuation. The AS murmur usually
radiates to the carotid arteries.
25. MAGDI AWAD SASI 2013
Early diastolic murmurs
Are produced by either AR or pulmonary regurgitation.
ar
The AR murmur is a soft high-pitched sound, is decrescendo in configuration, and is most
audible at the left sternal border or the right second ICS just to the right of sternum, with
the patient leaning forward at end expiration. The murmur radiates to the left lower
sternal border if it is due to primary valve disease. In patients with aortic root disease, the
murmur may radiate to the right sternal border. The murmur increases in intensity during
expiration and decreases in intensity with hand grip. The S2 is usually muffled with AR.
PR
The murmur of pulmonary regurgitation is best audible at the pulmonary area. The
character, quality, and pitch of the murmur vary depending on the presence or absence of
pulmonary hypertension. In the presence of pulmonary hypertension, it is a high-pitched,
decrescendo murmur also known as a Graham Steell murmur. S2 is usually loud in
association with pulmonary regurgitation. In the absence of pulmonary hypertension, it is a
low-pitched crescendo-decrescendo murmur.
Mid- to late diastolic murmurs
These murmurs are produced by the blood flow across stenotic AV valves.
MS produces a low-pitched, mid-diastolic, rumbling murmur with presystolic accentuation,
best heard with the bell of the stethoscope placed over the cardiac apex with the patient in
the left lateral position. S1 is loud. The murmur usually follows an OS, and the interval
between the A2 and OS is inversely proportional to the severity of obstruction.
The murmur of MS is increased in intensity with expiration and maneuvers that increase
cardiac output, such as exercise. The presystolic accentuation results from atrial
contraction in late diastole and is absent in patients with atrial fibrillation. The duration of
murmur corresponds to the period in which the LA-LV diastolic pressure gradient is
maintained. This duration correlates with the severity of obstruction; the longer the
murmur duration, the more severe the MS (provided the diastolic filling time is not
shortened, as may happen in tachycardia) except in high cardiac output and pulmonary
htpertension.
D/D OF MID DIASTOLIC MURMUR:
1. Tricuspid stenosis=tricuspid area
2. Atrial myxoma- change by position
3. Austin Flint murmur- due to AR
4. Carey Coombs murmur-rhematic heart disease
26. MAGDI AWAD SASI 2013
Continuous Murmurs
PDA
Coronary arteriovenous fistula
Ruptured sinus of Valsalva aneurysm
Aortopulmonary window
Anomalous left coronary artery from the pulmonary artery
Bronchial collateral circulation
Opening Snap
The opening snap (OS) is a high-pitched diastolic sound produced by rapid
opening of the mitral valve in MS or TS. When mitral in origin, it is best heard
at the apex following the aortic sound A2, with the patient in left lateral
decubitus position.
The time difference between the A2 and OS has a diagnostic implication. The
closer the OS is to A2, the more severe the stenosis. The OS signifies when the
left atrial pressure exceeds the LV diastolic pressure and marks the beginning of
blood entry into the LV from the LA. The more severe the stenosis, the greater
the LA pressure and the lesser the LA-LV early diastolic pressure gradient,
leading to an early opening of the mitral valve. In general, the relation between
A2 and the OS depends on LV pressure at A2 closure, LA pressure at A2 closure,
and the rate of LV pressure decline.
Pericardial rub
It indicates pericardial inflammation.
• Inflammation of the pericardial membrane or pleural sac at the 3rd
and 4th
interspace at the left sternal border. Louder during inspiration
• Scratchy, like sandpaper being used, a match being struck, or leather
squeaking .
• Sound present when the epicardial & pericardial surfaces, roughened by
inflammation, slide over one another during atrial & ventricular systole &
during the passive motion of rapid ventricular filling.
27. MAGDI AWAD SASI 2013
• 3 components
– Atrial Systolic (A)
– Ventricular Systolic (V)
– Ventricular Diastolic (D)
Percardial Knock
• Sharp, high-pitched sound present in 90% or more of patients
with constrictive pericarditis
• Heard in diastole
• Occurs .09 to .12 sec after S3
• Occurs after Heart Surgery, radiation therapy, viral infection, TB
pericarditis
• Diaphragm of the stethoscope listen at the lower left sternal
border
Tumor Plops
• Clues to a Myxoma
– Cardiac silhouette on X-Ray consistent with atrial
enlargement
– An ECG showing signs of LA enlargement
– Light-headedness
– A very short presystolic murmur
– Extra sound in diastole
• Left Atrial Tumors
– Loud, low-frequency thud heard in early diastole & caused
by abrupt movements of the tumor inside the LA
– It strikes the wall of the chamber or comes to a sudden halt
as the pedicle reaches the limit its stretch
28. MAGDI AWAD SASI 2013
SUMMARY SHEET OF CVS EXAMINATION
1. INSPECTION
Chest deformity
Skin ,scars , pulsation, vessels
Respiratory movements
Accessory muscles of respiration
2. PALPATION
Trachea
Apex beat- line , space , character
Thrill- MA , TA ,PA & AA.
Heave - left parasternal
3. AUSCULTATION
Start in mitral area by diaphragm and listen for S1 ,S2 ,M
For murmur , site ,time ,radiation, character, grade ,pitch.
Tilt pt to left lateral and use the bell to here diastole in MA
Change the bell to diaphragm to auscultate axilla for PSM
Inch to TA and check S2 and ask pt to hold in inspiration
Inch to PA to hear P2 and murmurs if present
Concentrate on AA and ask pt to sit , lean ,and full expiration
Lastly check carotids by diaphragm for systolic radiation