Cardiovascular Concepts PDF

​ Norma Heart Sounds ○​ S1 or “Lub” ​ Caused by the closure of AV Valves (Mitral and Tricuspid) ​ Loudest at Apex/Mitral Area (Midclavicular, 5th intercostal space) and marks the end of diastole and the beginning of systole. ○​ S2 or “Dub”...

​ Norma Heart Sounds ○​ S1 or “Lub” ​ Caused by the closure of AV Valves (Mitral and Tricuspid) ​ Loudest at Apex/Mitral Area (Midclavicular, 5th intercostal space) and marks the end of diastole and the beginning of systole. ○​ S2 or “Dub” ​ Caused by closure of Semilunar Valves (Aortic and Pulmonic) ​ Loudest at the Base/Aortic Area (Right Sternal Border, 2nd intercostal space) and marks the end of systole and the beginning of diastole. ​ S2 sounds can split on inspiration ​ Wide, fixed splitting is caused by a Right Bundle Branch Block ​ S2 is louder with a pulmonary embolism ​ Abnormal Heart Sounds ○​ S3 ​ This is caused by a rush of blood into a dilatted ventricle. ​ Occurs early in diastole and right after S2. ​ Best heard at the Apex/Mitral area with the Bell. ​ This is associated with heart failure and may occur with crackles. ​ Ventricular Gallop, think “Kentucky” ​ Other Causes: ​ Pulmonary Hypertension or Cor Pulmonale ​ Mitral, Aortic, or, Tricuspid insufficiency ○​ S4 ​ Caused by atrial contraction of blood into a noncompliant ventricle. ​ This occurs right before S1 and is best heard at the Apex/Mitral area with the bell. ​ Associated with Myocardial ischemia, infarction, hypertension, ventricular hypertrophy, and aortic stenosis. ​ Atrial gallop, think “Tennessee” ○​ Pericardial Friction Rub ​ Due to pericarditis and is associated with pain on deep inspiration. ​ May be positional. ​ Blood Pressure and Pulse Pressure ○​ Pulse pressure is the difference between systolic and diastolic pressures. ​ Normal is 40-60mmHg ○​ Systolic blood pressure is an indirect measurement of cardiac output and stroke volume. ​ A decrease in systolic blood pressure with little change or an increase in diastolic pressure is narrowing pulse pressure. ​ This is most often seen with severe hypovolemia or a severe drop in cardiac output.  ○​ Diastolic blood pressure is an indirect measurment of systemic vascular resistance (SVR) ​ A decrease in diastolic pressure that widens pulse pressure may indicate vasodilation and/or a drop in SVR. ​ This is commonly seen in septic shock. ​ Diastolic pressure is typically 1/3rd of systolic ​ Coronarie arteries are perfused during diastole. ​ Valvular Heart Disease ○​ There are 4 heart valves and each of them may be affected by stenosis or insufficiency (regurgitation). ○​ Basics about the heart ​ Normal heart tones, S1 and S2, are due to valve closures. ​ Valves open and close based on pressure changes above and below the valves. ​ When the pressure chamber above the valve is higher than below the valve, the valve opens. ​ When the pressure drops in the chamber above the valve and the pressure is greater below the valve, the valve closes. ​ Systolic: ejection, high pressure ​ Diastolic: filling, low pressure ​ Diastole is one-thirds longer than systole because it needs time to fill. ​ Coronaries are perfused during diatole. ​ Why do cardiac output and blood pressure drop with tachyarrhythmias? ​ Less filling time leads to less cardiac output. ○​ Causes of Valvular Disease ​ Coronary Artery Disease, Ischemia, or Acute Myocardial Infarction ​ Dilated cardiomyopathy ​ Degeneration ​ Bicuspid aortic valve (this is genetic) ​ Rheumatic fever ​ Infection ​ Connective Tissue disease ○​ Murmurs ​ Murmurs of INSUFFICIENCY (regurgitation) occur when the valve is closed. ​ Can be acute or chronic ​ Murmurs of Stenosis occur when the valve is open ​ This will always be chronic, develops over time ​ Never acute ○​ Systolic Murmurs ​ Lub….Shhhb….Dub ​ Semilunar Valves are OPEN during systole ​ Aortic Stenois or Pulmonic Stenosis  ​ AV Valves are CLOSED during systole ​ Mitral Insuffciency ○​ Will cause large, V waves on the pulmonary artery occlusion tracing if the patient has a pulmonary artery catheter. ​ Tricuspid Insuffciency ​ Ventricular-septal defect (VSD), is common with an acute MI and may result in a systoplic murmur. ​ This is heard on the left sternal border, 5th intercostal space ○​ Diastolic Murmurs ​ Lub….Dub….Shhhb ​ Semilunar Valves are CLOSED during diastole ​ Aortic insufficiency (AI) ​ Pulmonic Insuffciency (PI) ​ AV Valves are OPEN during diastole ​ Mitral stenosis is associated with atrial fibrillation dur to atrial enlargement that occurs overtime ​ Tricuspid stenosis ○​ Murmur Summary ​ Mitral Insufficiency occurs when the mital valve is closed (Murmur occurs). When is the mitral valve closed? ​ Systole ​ Mitral Stenosis occurs when the mitral valve is open (Murmur occurs). When is the mitral valve open? ​ Diastole ​ Aortic Insufficiency occurs when the aortic valve is closed. When is the aortic valve closed? ​ Diastole ​ Aortic Stenosis occurs when the aortic valve is open. When is the aortic valve open? ​ Systsole ​ If you can picture what the aortic valve is doing, the pulmonic is doing the same. If you can picture when the mitral valve is doing, the tricuspid is doing the same. ​ Does a murmur due to VSD happen during systole or diastole? ​ During ejection or systole. ○​ Murmurs associated with acture MI ​ The mitral valve is attached to the left ventricle wall by the papillary muscles and the chordae tendineae. Myocardial ischemia or infarction can affect the mitral valce function and lead to acute mitral valve regurgitation. ​ Papillary muscle dysfunction (Grade I or II), loudest at Apex/Mitral area ​ Papillary muscle rupture (Grade V or VI), loudest at the apex/mitral area. ​ This is a SURGICAL EMERGENCY!  ​ Ventriculat septal defect ​ Sternal Border, 5th intercostal space. ​ Acute Coronary Syndrome ○​ Risk Factors for Coronary Artery Disease ​ Non-Modifiable Risk Factors ​ Age, sex, family history, and genetics ​ Modifiable Risk Factors ​ Smoking, atherogenic diet, alcohol intake, physical activity, dyslipidemias, hypertension, obesity, diabetes, metabolic syndrome ○​ Spectrum of Ischemic Heart Disease ​ Asymptomatic coronary artery diseas (CAD) ​ Stable angina, chest pain with activity, predictable, lesions are usually fixed and calcified ○​ Acute Coronary Syndrome ​ Due to platelet-mediated thrombosis ​ Can result in sudden cardiac death ​ Multiple Types: ​ Unstable angina ○​ Chest pain at rest, unpredictable, may be relieved with nitroglycerin, troponin negative, ST depression, or T-wave inversion on the ECG. ​ Non-ST Elevation Myocardial Infarction (NSTEMI) ○​ Troponin positive, ST depression, T-wave inversion on the ECG, unrelenting chest pain ​ ST Elevation Myocardial Infarction (STEMI) ○​ Troponin positive, ST elevation in 2 or more contiguous leads, unrelenting chest pain. ​ Variant or Prinzmetal’s Angina ○​ A type of unstable angina associated with transient ST segment elevation. ○​ Due to coronary artery spasm with or without atherosclerotic lesions. ○​ Occurs at rest and may be cyclic (same time each day) ○​ May be precipitated by nicotine, ETOH, cocaine ingestion ○​ Troponin’s will be negative ○​ Nitroglycerin (NTG) administration results in relief of chest pain and ST’s return to normal ○​ Management of Acute Chest Pain ​ Stat ECG, done and read within 10 minutes ​ Allows categorization to STEMI, NSTEMI/Unstable Angina, or No Acute Change ​ Allows risk stratification to high, medium, or low ​ Aspirin ​ Give ASAP; is chewed; improves morbidity and mortality ​ Anticoagulant ​ Heparin or Enoxaparin ​ Antiplatelet Agents ​ Clopidogrel (Plavix) ​ Abciximab (Reopro) ​ Eptifibatide (Integrilin) ​ Tirofiban (Aggrastat) ​ Beta Blockers ​ Unless ACS is due to cocaine ​ Use cardioselective sich as metoprolol (Lopressor) ○​ Do not use non-cardioselective such as propranolol ​ Contraindications include hypotension, bradycardia, use of phosphodiesterase inhibitor drugs such as sildenafil (viagra) ​ Treat Pain ​ Nitroglycerin ​ Morphine ​ History, risk factor assessment ​ Lab assessment ​ Cardiac biomarkers, lipid profiles, CBC, electrolytes, BUN, creatinine, magnesium, PT, PTT ​ ECG Lead Changes and Location of Coronary Artery Disease ​ Changes in II, III, aVF - Right Coronary Artery, Inferior LV ​ Changes in V1, V2, V3, V4 - Left Anterior Descending, Anterior LV ​ Changes in V5, V6, I, aVL - Circumflex, Lateral LV ​ Chnages in V5, V6 - Low Lateral LV ​ Changes in I, aVL - High Lateral LV ​ Changes in V1, V2 - Right Coronary Artery, Posterior LV ​ Changes in V3R, V4R - Right Coronary Artey, Right Ventricle Infarct ​ Differentation of the Types of Actue MI ​ Inferior MI ○​ Associated with Right Coronary Artery Occlusion ○​ ST elevation in II, III, and aVF ○​ Reciprocal changes in lateral wall (I, aVL). ○​ Associated with AV conduction disturbances: 2nd degree Type I AV block, 3rd degree AV block, sick sinus syndrome, and sinus bradycardia. ○​ Development of systolic murmur: Mitral valve regurgitation secondary to papillary muscle rupture (posterior papillary muscle has only one source of blood supply - the RCA). ○​ Tachycardia is associated with an inferior MI - leads to higher mortality.  ○​ Associated with Right Ventricle infarct and posterior MI ○​ Use Beta Blockers and Nityroglycerin with CAUTION ​ Right Ventricle (RV) Infarct ○​ The Right coronary artery, which supplies the inferior wall of the left ventricle, also supplies the right ventricle, therefore about 30% of inferior wall MI patients also have a right ventricular (RV) infarct. ○​ Size of the infarct will determine symptoms ○​ A right sided ICG may demonstrate ST Chnages ○​ Signs/Symptoms ​ JVD at 45 degree , High CVP, hypotension, usually clear lungs, bradyarrhythmias ​ ECG with ST elevation in V3R, V4R ○​ Treatment ​ Fluids ​ Positive Inotrope ○​ Avoid ​ Preload reducers like nitrates or diuretics ​ Caution with beta blockers, often cannot give initially due to hypotension. ​ Anterior MI ○​ Associated with Left Anterior Descening Occlusion ○​ ST elevation in V1-V4: pericordial leads and V leads ○​ Reciprocal changes (ST depression) in inferior wall (II, III, aVF) ○​ May develop 2nd degree Type II AV Block or RBBB ​ The LAD supplies the common bundle of HIS, RBBB is an ominous or worrying sign ○​ Development of systolic murmur: possible ventricular septal defect ○​ Higher mortality than an Inferior MI: Heart Failure ​ Lateral MI ○​ ST Elevation in V5, V6 (Low Lateral) ○​ ST Elevation in I, aVL (High Leteral) ○​ Generally involves the left circumflex ​ Treatment of STEMI ​ Determine onset of infarct, if symptoms < 12 hours the goal is REPURFUSION ○​ Percutaneous coronary intervention (PCI) - standard is door-to-ballon within 90 minutes ○​ Fibrinolytic drug therapy - standard is door-to-drug within 30 minutes ​ Elgibility Criteria  ○​ ST Elevation in 2 or more contiguous leads or new onset Left Bundle Branch Block ○​ Onset of chest pain