Cardiac H&P PDF

Cardiac and History/Physical L. Michael Waters, DO, FACOFP, FAAFP Chair of Primary Care PCOM-GA Original by: Bruce Kornberg, DO and Dave Adelstein, DO Learning Outcomes History Ellicit an accurate medical history from a patient. List the...

Cardiac and History/Physical L. Michael Waters, DO, FACOFP, FAAFP Chair of Primary Care PCOM-GA Original by: Bruce Kornberg, DO and Dave Adelstein, DO Learning Outcomes History Ellicit an accurate medical history from a patient. List the contributing risk factors for the patient's reason to visit the physician. Create a differential diagnosis that causes the associated history. Physical Demonstrate how the physical examination of the patient’s cardiovascular system correlates to his cardiac history in helping to determine a diagnosis. List those physical findings that rule in favor or against the differential diagnosis of the patient. Correlate the patient’s diagnosis with physical findings. Choose the proper treatment in order to bring symptomatic relief to the patient.  Cardiovascular History-Taking A thorough history is vital for the diagnosis of patients with issues such as chest pain, heart failure symptoms, palpitations or syncope. The cardiovascular history may also provide important insight into patients' cardiac status, and their risk of future cardiovascular disease in the future.  Presenting Complaint The first step is to ask the patient why they presented with their current issue. Common cardiovascular symptoms include: Chest pain → concerning for coronary ischemia infarction, though there are a wide variety of causes of chest pain. Dyspnea (shortness of breath) → a common symptom of heart failure Palpitations → a sensation of fast, slow or irregular heart beats Presyncope/syncope → the feeling of fainting, or being about to faint Peripheral edema → a classic symptoms of heart failure Lower limb pain  History of Presenting Complaint When asking for more information about a patient’s symptoms, start by asking general questions such as “could you please tell me more about that”, and then narrow down the questions as more information is provided. Generally speaking, the following questions are a good starting point for any type of pain, and may be useful in gaining information about other symptoms (SOCRATES/ OLD CAARTS): Site → localized or generalized; unilateral or bilateral Onset → sudden or gradual, and what the situation was (e.g. following trauma) Character → sharp, dull, burning or pressure-like Radiation → e.g. down the arm or across the back Associated symptoms → e.g. fevers, nausea / vomiting, bony pain Timing → duration of symptoms, frequency of episodes, changes through the day Exacerbating & alleviating factors → e.g. exacerbation with exertion and alleviation with rest Severity → on a scale of 1 to 10, with 10 being the worst  Past Medical History Ask about any medical conditions the patient has previously been diagnosed with, the management of these conditions, and any complications they may have. Common cardiovascular conditions include: Ischemic heart disease Arrhythmia → e.g. atrial fibrillation, atrial flutter, Wolff-Parkinson-White syndrome Heart failure Pulmonary hypertension Cardiomyopathy Peripheral vascular disease Rheumatic heart disease Valvular disease → e.g. aortic stenosis, aortic regurgitation, mitral regurgitation Congenital heart disease Hx of inflammatory diseases, gout and cancer Eclampsia and pre-eclampsia  Past Medical History Ask about any cardiac risk factors that may be present, such as: Diabetes mellitus Hyperlipidemia Hypertension Chronic kidney disease Obesity Ask about any cardiac devices that may be present, such as pacemakers or defibrillators.  Medication History Ask about what medications the patient takes regularly, what they take them for, and what side effects they have had. Some cardiovascular medications include: Antiarrhythmics Antihyperlipidemics Antihypertensives Diuretics Vasodilators Also meds that increase risk by causing heart damage Nexium and other anti-acid medications Doxyrubicin/Adriamycin cancer meds  Family History Ask about family history of cardiac disease, such as ischemic heart disease, cardiomyopathies or arrhythmias. Also ask about any sudden cardiac death that may have occurred in the family. Risk Factors any hyperlipidemia, diabetes, Hx Rheumatic heart disease (Streptococcal Dz.)  Social History It is important to understand any patient’s social situation when taking their history. This includes key aspects such as their occupation (or previous occupation, if retired), living situation, mobility and ability to perform activities of daily living. Of particular importance in the cardiovascular history is a patient’s diet and exercise history. When taking a nutritional history, ask about the number of meals the patient eats per day, any snacking in between, and what they would eat on a usual day. This can provide valuable information about a patient’s cardiovascular risk, particularly in an obese or diabetic patient. In assessing a patient’s exercise history, ask about the amount of time they spend exercising as well as what type of exercise they perform. A sedentary lifestyle is a strong risk factor for cardiovascular disease.  Substance History Smoking is a major risk factor for atherosclerotic disease. Ask about how long a patient has smoked for, how many cigarettes they smoke per day, and how long since they quit (if appropriate). Ask about alcohol intake, as alcohol is an important risk factor for hypertension, dilated cardiomyopathy and atrial fibrillation. Ask how many drinks the patient has per week, what type of drinks, and whether they have considered cutting down their intake if heavy. Finally, ask about recreational drug use, and particularly intravenous drug use: this is an important risk factor for infective endocarditis. However a hx. Of cocaine and amphetamines can cause cardiac damage. Up to 25% of all non-fatal MIs in ages of 18-45 are associated with Cocaine usage. History and physical differentiate the DIAGNOSIS History and physical differentiate the DIAGNOSIS  Physical Examination of the Cardiovascular System Physical Examination Cardiovascular System General Examination Arterial Pulse - brachial, carotids, peripheral Jugular Venous Pressure ○ The heart Inspection Palpation Percussion Auscultation  Cardiovascular System General Examination Walking and Gait Sitting or Lying Orthopnea Cyanosis (central or peripheral), anemia, jaundice Fever and embolic signs Right heart failure (JVP, dependent edema, hepatomegaly, ascites, pleural effusions) Left heart failure (dyspnea, tachypnea, orthopnea, cough, basal crepitations) Pulmonary disease Systemic Disease: thyrotoxicosis, scleroderma, lupus erythematosus, etc. Physical findings of CV disease Xanthelasma Frank’s sign Poor dentition  Left Heart Failure Elevated LVEDP L. Atrial Pressure (LAP) Periph.Venous Pr (PVP) Pulmonary Congestion Cough Dyspnea Orthopnea Tiredness and Lethargy Common causes of left side cardiac failure? HTN,CAD and Heart attack Left Heart Failure Symptoms Dyspnea (breathlessness) o Common in CV disorders, especially L. ventricular failure (due to pulmonary edema) Pulmonary edema --- result of elevated pulmonary capillary hydrostatic pressure Dyspnea on exertion in early stages of LHF (SOB or difficulty breathing) As progresses, occurs at rest (orthopnea) Orthopnea (breathlessness while flat) o Will see pt have difficulty breathing while lying down o Cause --- Blood pooling in pulmonary circulation (coming from extremities and abdomen) Leads to increased left atrium pressure and pulmonary capillary hydrostatic pressure Paroxysmal Nocturnal Dyspnea (PND) o Pt woken from sleeping breathless o Similar mechanism to orthopnea, but since sensory awareness is decreased while asleep, pulmonary edema can become severe Blood tinged sputum Elevated pulmonary capillary "wedge" pressure (PCWP) Most common cause of right heart failure is ???? Left Heart disease  Arterial Pulse Radial Artery 1. Heart Rate: (60-100) 2. Rhythm: a. Regular b. Irregular - Sinus arrhythmia, P wave present c. Occasional - Premature beats, dropped beats, irregular d. Total- atrial fibrillation S1 correlates with the carotid and radial artery Arterial Pulse Carotid Artery NEVER PALPATE BOTH SIDES AT THE SAME TIME. At BIFURCATION if the patient needs CAROTID MASSAGE used for tachyarrythmais  Carotid pulse 120 Amplitude/Contour 80 1. Hypokinetic (weak): a. Hypovolemia b. Heart failure 120 c. Aortic Stenosis (Tardus et parvus) 80 2. Hyperkinetic (increased stroke volume): a. Fever b. Anemia c. Hyperthyroidism 120 d. Aortic regurgitation 80 e. Bradycardia f. Atherosclerosis Learning Objective #1  Amplitude/Contour: Bisferiens – HOCM and Aortic regurgitation Double systolic pulse Carotid Artery Collapsing (Corrigan’s pulse) – Aortic Regurgitation Rapid upstroke with rapid downstroke Parvus et tardus – Aortic stenosis Weak amplitude with long ejection Alternans - Heart failure (overexpressed calsequestrin) Intermittent weak/strong pulse Bigeminal - Premature beats Paradoxical - Pericardial tamponade and constrictive pericarditis Intermittent weak and strong pulse changing with inspiration and expiration Dicrotic – Cardiomyopathy, hypovolemic shock Difficult to distinguish from Bisferiens without CVP tracing Filiform – shock Thready pulse Learning Objective #1 CAROTID ARTERY AUSCULTATION Auscultate both sides of the carotid artery (BELL) Near clavicle before the bifurcation Near the jaw line for bifurcation Jugular Venous Pressure 45 degree angle  Jugular Venous Pressure Reflects: ○ Right atrial pressure is increased ○ Blood volume could be increased ○ Tricuspid valve regurgitation? ○ Diastolic events in the right ventricle Estimate CVP ○ Maximal 3 cm from sternal angle + 5 cm from atrium (right atrial pressure) Increased pressure: ○ Right sided heart failure ○ Constrictive pericarditis ○ Tricuspid stenosis (rare)/ seen with mitral stenosis ○ Obstructed Superior Vena Cava Increased intrathoracic pressure  Jugular Venous Pressure NORMAL JVP CATHETER FINDINGS Amplitude of pulsations: ○ a wave = atrial contraction ○ c wave = tricuspid valve closure ○ x descent = relaxation x ○ v wave = atrial filling ○ y descent = emptying ○ Note: A wave is the pressure of atrial contraction, P wave is the electronic voltage of the atrial contraction. ○ S-1, coincides with contraction of the ventricles, thus identifying the onset of ventricular systole and the end of mechanical diastole. ○ S-2, immediately following closure of the aortic and pulmonic valves. The vibrations of the second heart sound occur at the end of ventricular contraction and identify the onset of ventricular diastole and the end of mechanical systole. Cardiovascular Examination Aortic area --- right of the sternum at the second intercostal space. Pulmonary area --- left of the sternum at the second intercostal space. Tricuspid area --- 4th intercostal space left parasternal area. Mitral area --- apex beat (5th intercostal space mid-clavicular line). Cardiovascular Examination  Cardiovascular Examination Palpation Areas of palpation ○ Apical impulse (PMI) ○ Left sternal border/R ventricle ○ Left and right 2nd interspace ○ Epigastric area/tricuspid area feeling for ○ Thrills (vibrations/ turbulence) ○ Heaves (lift or thrust)  Cardiovascular Examination Cardiac Pulsations Point Max. Intensity (PMI), 2cm Parasternal lift Thrills/vibrations S3, S4 Dyskinesis Aneurysm Cardiovascular Examination Palpation Apical Impulse: PMI  Cardiovascular Examination Palpation Left Sternal Border - Right ventricle  Cardiovascular Examination Palpation Left Parasternal lift Right ventricular volume load ○ ASD ○ Pulmonary incompetence ○ Tricuspid incompetence → seesaw motion Right ventricular pressure load ○ Pulmonary hypertension ○ Pulmonary stenosis Left atrial lift ○ Mitral incompetence  Cardiovascular Examination Palpation 1. Left second interspace → Pulmonic: P. HTN 2. Right second interspace → Aortic: HTN 3. Epigastric area → Right ventricle in hyperinflated lungs 4. Thrills → Murmurs grade 4+ Cardiac Examination: Auscultation Areas of auscultation: ○ Aortic ○ Pulmonic ○ Left Sternal Border ○ Apex Diaphragm High pitch sound, Bell low pitch sounds  Cardiac Examination: Auscultation Lean Forward and Exhale Best to hear Aortic regurgitation Third intercostal space (Erb’s point)  Cardiac Examination: Auscultation Left decubitus position, using the bell Best to hear mitral stenosis at the 5th intercostal space, midclavicular. Low pressure gradient, mid diastolic  Cardiac Examination: Auscultation Left decubitus position, using the Diaphragm Best to hear mitral regurgitation at the 5th intercostal space, midclavicular. High pitch, large pressure gradient causing the prolapse back into atria.  Cardiac Examination: Auscultation The first heart sound (S1): ○ Closure of Mitral and Tricuspid valves  Cardiac Examination: Auscultation The first heart sound (S1): Intensity ○ Ventricular contraction rate Tachycardia-loud Bradycardia-softer Diminished ○ Chest wall thickness ○ 1st degree AV Block Thin – loud ○ M. Regurgitation Thicker- softer Widened/Splitting ○ P-R interval (Diastoli fill time) Short PR - loud ○ RBBB Long PR – soft ○ Ventricular premature beats’s ○ Valve leaflet mobility Absence Mitral stenosis ○ LBBB  Cardiac Examination: Auscultation Second heart sound (S2): ○ Closure of Aortic and Pulmonic valves  Cardiac Examination: Auscultation Second heart sound (S2): ○ Closure of Aortic and Pulmonic valves Split S2 happens during inspiration when increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect)  Cardiac Examination: Auscultation Special physiological maneuvers: Squatting: Will increase the Abdominal pressure, decreasing the blood leaving the heart and increases the amound of blood returning to the heart, (overall effect increase blood in the heart). This increased amount of blood in the heart increases turbulence. Example: Aortic regurgitation will increase. ○ Venous return increases, increased preload ○ Vascular resistance increases → LV volume increases ○ Murmurs of MVP decreases ○ HOCM decreases (hypertrophic Obstructive Cardiomyopathy) ○ A.S. increases Valsalva, Standing Take a breath, push against closed mouth and nose for 15 seconds. (constipated) This will increase the pressure in the thorax, decreasing the amount of blood flowing into the heart. Ex ○ The opposite effect, decreased L. ventricle preload  Inspiration Chest expands, diaphragm flattens, increase in volume of chest cavity the pressure decreases. Blood flows from a high pressure to low pressure, the amount of blood the right Atrium receives from the Vena Cava will increase, this will increase the volume in the right ventricle. Example: if you have a patient with Pulmonary stenosis the amount of blood getting out during systoli is higher causing more turbulence and the murmur increased. Increase in right sided flow and event (R. sided murmers increased, by increased venous return) Decrease in left sided flow and event Expiration ○ Increase in left sided flow and event (L. sided murmers increased, from increased venous return) ○ Decrease in right sided flow and event ▪ Hand Grip causes increased vascular resistance (total peripheral resistance). The heart has to work harder to eject blood from the ventricles as afterload is now increased. Since the blood is prevented from moving forward it will increase any murmurs that occur from backward flow. Examples: Aortic or mitral regurgitation or a ventral septal defect. Forward flow murmurs will decrease aortic stenosis and hypertrophic cardiomyopathy.  Murmurs on provocation!! Maneuver Murmur Valsalva or standing Increase - HOCM and MVP ↓ Preload Decreases AS, MS, MR, AR and VSD Squat Decrease – HOCM and MVP ↑ Preload and ↑ Afterload Increases – AS, AR, MR and VSD Hand grip Increase – left sided murmurs ↑ Afterload EXCEPT decreases – HOCM, AS and MVP Inspiration Increase – right sided murmurs ↑ Venous return Decreases – HOCM Expiration Increases – left sided murmurs including HOCM ↓ Venous return ↑ Afterload Learning Objective #2 Cardiac Examination: Auscultation Murmurs (heart sounds) Timing: Pitch ○ Systolic → mid, pan Quality ○ Diastolic → early, mid, late ○ Blowing Shape: ○ Harsh ○ Crescendo ○ Rumbling ○ Decrescendo ○ Plateau ○ Musical Location Changes with physiological interventions: Radiation ○ Exercise ○ Axilla ○ Standing ○ Back ○ Squatting ○ Suprasternal notch ○ Valsalva Intensity ○ 1-6 Cardiac Examination: Auscultation Ejection Sound : Left or Right Valve Stenosis Increased blood flow through the valve Arterial hypertension Dilation of the Artery Cardiac Examination: Auscultation Ejection Sound Extra Diastolic Sounds Aortic stenosis Diastolic decrescendo HOCM Aortic/pulmonary Pulmonary stenosis regurgitation Holosystolic murmurs Opening Snap Midsystolic Click ○ Mitral Stenosis Mitral Valve Prolapse  Cardiac Examination: Auscultation The third heart sound (S3): Sudden expansion of the ventricle by rapid ventricular filling. Often palpable Physiological in young people and during exercise Pathological in volume overload and heart failure  Cardiac Examination: Auscultation The fourth heart sound (S4): Sudden expansion of the ventricle (right or left) by atrial contraction Physiological in athletes and older people Pathological due to decreased compliance (right or left ventricles) Pressure overload - HTN, AS, Ischemia, Cardiomyopathies Right - Sided S4: Pressure overload (Pulm.Stenosis, Pulm. HTN) Cardiac Examination: Auscultation Ejection Systolic Sounds Ejection Sound: Aortic Stenosis crescendo/decrscendo sound  Hypertrophic Cardiomyopathy Systolic ejection murmur at Right upper sternal border Bifid apical impulse (double apical impulse) Valsalva maneuver increases the HCM murmur by decreasing venous return and worsening obstruction Frequently associated with holosystolic MR murmur at the apex Can have family history of HCM or sudden cardiac death Young patient, unexplained syncope, palpitations Most common cause of SCD ages 9-40 Murmur to left: Left and Right ventricular outflow tract stenosis (subvalvular, valvular, ring, supravalvular)  Aortic stenosis Systolic ejection murmur at right upper sternal border Murmur decreases with Valsalva and prolongs with handgrip Degree of murmur change with provocation is not substantial HOCM tends to markedly increase w/ Valsalva (makes differentiation easier at the bedside) Usually in elderly patients Learning Objective #2  Aortic stenosis vs Hypertrophic cardiomyopathy Bisferiens pulse (Biphasic/double apical pulse) S4 gallop Crescendo/Descrescendo systolic ejection murmur HOCM vs. Valvular AS Intensity of murmur HOCM AS Valsalva (↓preload, ↓ afterload) ↑ ↓ Squatting (↑ preload, ↑ afterload) ↓ ↑ Standing (↓preload, ↓ afterload) ↑ ↓ Holosystolic apical blowing murmur of mitral regurgitation  Cardiac Examination: Auscultation Ejection Systolic Sounds Midsystolic click: Mitral Valve prolapse Cardiac Examination: Auscultation Ejection Diastolic Sounds Opening Snap: Mitral or Tricuspid stenosis Severe stenosis: shorter 2-os interval Cardiac Examination: Auscultation Murmurs; Pansystolic or holosystolic Pansystolic: Mitral, Tricuspid, Regurgitation, Ventricular septal defect (harsh sound) Cardiac Examination: Auscultation Severe MR  Atrial fibrillation Irregularly irregular pulse to palpation Irregular heart rate confirmed on auscultation Variable intensity of S1 heart sound S4 heart sound is absent Frequently associated with holosystolic murmur at the apex Chief complaint of palpitations, dyspnea on exertion, chest pain or peripheral edema Family history of CVA Rate control/rhythm control Anticoagulation Learning Objective #3  Myocardial infarction Acute ischemic leads to diastolic and systolic dysfunction S4 heart sound is often present due to impaired relaxation Inferior wall ischemia can result in tethering of the posterior leaflet of the mitral valve and resultant mitral regurgitation – apical holosystolic murmur Patient can appear toxic, diaphoretic Cold limbs may be appreciated with large infarct size and shock physiology Family history of CAD or sudden cardiac death Aspirin, statin, heparin, percutaneous intervention with revascularization as clinically indicated Learning Objective #3  Question 1: A 45-year-old male presents with chest pain. He describes the pain as a crushing sensation in the center of his chest that radiates to his left arm and jaw. He is diaphoretic and nauseated. His blood pressure is 160/90 mm Hg, pulse rate is 110 bpm, and respiratory rate is 20 breaths per minute. On auscultation, you hear a harsh systolic ejection murmur. What is the most likely diagnosis? A) Myocardial infarction B) Aortic stenosis C) Gastroesophageal reflux disease D) Anxiety attack  Rationale: The correct answer is A) Myocardial infarction. This patient's presentation is highly suggestive of an acute coronary syndrome (ACS) or myocardial infarction. The crushing chest pain that radiates to the left arm and jaw, diaphoresis, and elevated blood pressure are all classic signs of an ACS. The systolic ejection murmur may be associated with complications like mitral regurgitation, which can occur during an acute myocardial infarction. B) Aortic stenosis is incorrect because while aortic stenosis can cause chest pain, it typically does not present with radiation to the left arm and jaw, nor with diaphoresis. Also, a systolic ejection murmur in a patient with ACS is more likely due to mitral valve dysfunction than aortic stenosis. C) Gastroesophageal reflux disease (GERD) is incorrect because GERD usually presents with burning epigastric pain and regurgitation, not a crushing chest pain radiating to the arm and jaw. D) Anxiety attack is incorrect because although anxiety can cause chest discomfort, this patient's presentation is highly concerning for an ACS, and a proper evaluation for cardiac causes should be the priority.  Question 2: A 60-year-old woman with a history of hypertension and diabetes presents with bilateral lower extremity edema, shortness of breath, and paroxysmal nocturnal dyspnea. On auscultation, you hear fine crackles at the lung bases. Which condition is most likely responsible for her symptoms? A) Hypertensive emergency B) Congestive heart failure (CHF) C) Pulmonary embolism D) Chronic obstructive pulmonary disease (COPD)  Rationale: The correct answer is: B) Congestive heart failure (CHF). This patient's presentation is classic for congestive heart failure. The bilateral lower extremity edema, shortness of breath, paroxysmal nocturnal dyspnea, and fine crackles on lung auscultation are all indicative of CHF. A) Hypertensive emergency is incorrect because while hypertension may be present, the symptoms described (edema, dyspnea, crackles) are more suggestive of heart failure than a hypertensive emergency. C) Pulmonary embolism is incorrect because the classic findings for a pulmonary embolism include sudden-onset dyspnea, pleuritic chest pain, and sometimes hemoptysis. The absence of these specific symptoms makes pulmonary embolism less likely in this case. D) Chronic obstructive pulmonary disease (COPD) is incorrect because while COPD can cause dyspnea, it typically does not present with bilateral lower extremity edema and fine crackles on lung auscultation.  Question 3: A 32-year-old male presents with a racing heart, palpitations, and lightheadedness. He mentions that these symptoms have occurred multiple times over the past few weeks and often happen at rest. On examination, his pulse rate is irregular, and you note irregularly irregular heart sounds on auscultation. What is the most likely diagnosis? A) Atrial fibrillation B) Supraventricular tachycardia (SVT) C) Ventricular tachycardia D) Premature ventricular contractions (PVCs)  Rationale: The correct answer is: A) Atrial fibrillation. This patient's presentation is consistent with atrial fibrillation. Atrial fibrillation is characterized by an irregularly irregular pulse and often presents with palpitations and lightheadedness. It can occur at rest and is a common arrhythmia in young adults. B) Supraventricular tachycardia (SVT) is incorrect because SVT typically presents with a regular and rapid heart rate. The irregular pulse in this case is more suggestive of atrial fibrillation. C) Ventricular tachycardia is incorrect because this arrhythmia is usually associated with more serious symptoms, such as hemodynamic instability. The irregular pulse and relatively benign symptoms make ventricular tachycardia less likely. D) Premature ventricular contractions (PVCs) are incorrect because while PVCs can cause palpitations, they typically do not result in an irregularly irregular pulse like atrial fibrillation.