CARDIOVASCULAR

Normal Heart Sounds

S1: LUB

  • caused by the closure of AV valves (mitral, tricuspid)

  • loudest at the APEX of the heart (midclavicular, 5th intercostal space)

  • marks the end of diastole, the beginning of systole

S2: DUB

  • caused by the closure of semilunar valves (aortic, pulmonic)

  • loudest at the BASE of the heart (R sternal border, 2nd instercostal space)

  • marks the end of systole, the beginning of the diastole

  • S2 splits on inspiration: wide, fixed splitting of S2 is caused by R bundle branch block (RBBB)

  • S2 is louder with a pulmonary embolism

Abnormal Heart Sounds

S3

  • caused by a rapid rush of blood into a dilated ventricle

  • occurs early in diastole, right after S2

  • heard best at the apex with the bell of the stethoscope

  • associated with HF (heart failure); may occur before crackles

  • ventricular gallop, “Kentucky”

  • also caused by:

    • pulmonary HTN and cor pulmonale

    • mitral, aortic, or tricuspid insufficiency

S4

  • caused by atrial contraction of blood into a noncompliant ventricle

  • occurs right before S1

  • best heard at the apex with the bell of the stethoscope

  • a/w myocardial ischemia, infarction, HTN, ventricular hypertrophy, and aortic stenosis

  • atrial gallop, “Tennessee”

Pericardial Friction Rub

  • d/t pericarditis, a/w pain on deep inspiration

  • may be positional

Murmurs

  • valvular disease

  • septal defects (atrial or ventricular)

Blood Pressure and Pulse Pressure

  • pulse pressure = systolic - diastolic

  • normal pulse pressure = 40-60 mmHg (i.e. 120/80)

  • systolic BP = indirect measurement of the cardiac output and stroke volume

    • decrease in systolic pressure with little change or an increase in diastolic pressure = narrowing in pulse pressure

      • seen most often with severe hypovolemia or a severe drop in cardiac output (i.e. 100/78)

  • diastolic BP = indirect measurement of the systemic vascular resistance (SVR)

    • a decrease in diastolic pressure that widens pulse pressure may indicated vasodilation, a drop in SVR

      • often seen in sepsis, septic shock (i.e. 100/38)

  • diastole is normally 1/3 longer than systole

  • coronary arteries are perfused during diastole

Valvular Heart Disease

  • stenosis or insufficiency of heart valves

  • systole: ejection, high pressure

  • diastole: filling, low pressure

  • causes of valvular heart disease:

    • coronary artery disease (CAD), ischemia, acute MI

    • dilated cardiomyopathy

    • degeneration

    • bicuspid aortic valve; genetic

    • rheumatic fever

    • infection

    • connective tissue diseases

  • murmurs of insufficiency (regurgitation) occur when the valve is closed

    • can be acute or chronic

  • murmurs of stenosis occur when the valve is open

    • chronic issue, develops over time

  • systolic murmurs: lub…shhhb…dub

    • semilunar valves are OPEN during systole

      • aortic stenosis

      • pulmonic stenosis

    • AV valves are closed during systole

      • mitral insufficiency

        • will cause large, giant V-waves on the pulmonary artery occlusion tracing if the patient has a pulmonary artery catheter

      • tricuspid insufficiency

    • ventricular septal defect (VSD) = common with acute MI —> can result in a systolic murmur

      • heard at the left sternal border, 5th intercostal space

  • diastolic murmurs: lub…dub…shhhb

    • semilunar valves are closed during diastole

      • aortic insufficiency

      • pulmonic insufficiency

    • AV valves are open during diastole

      • mitral stenosis is a/w atrial fibrillation d/t atrial enlargement that occurs over time

      • tricuspid stenosis

  • Key Points:

    • mitral insufficiency occurs when mitral valve is closed (murmurs occurs) —> mitral valve is closed during systole

    • mitral stenosis occurs when mitral valve is open (murmur occurs) —> mitral valve is open during diastole

    • aortic insufficiency occurs when aortic valve is closed —> aortic valve is closed during diastole

    • aortic stenosis occurs when the aortic valve is open —> aortic valve is open during systole

Acute Coronary Syndrome (ACS)

  • risk factors:

    • non-modifiable: age, sex, fam hx, genetics

    • modificable: smoking, atherogenic diet, alcohol intake, physical activity, dyslipidemias, HTN, obesity, diabetes, metabolic syndorme

  • spectrum of ischemic heart disease

    • asymptomatic coronary artery disease (CAD)

    • stable angina, chest pain with activity, predictable, lesions are usually fixed and calficied

acute coronary syndrome

  • due to platelet-mediated thrombosis

  • may results in sudden cardiac death

  • types:

    • unstable angina: chest pain at rest, unpredictable, may be relieved with nitroglycerins, 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 angaina

    • a type of unstable angina a/w transient ST segment elevation

    • d/t coronary artery spasm with or without atherosclerotic lesions

    • occurs at rest, may be cyclic (same time each day)

    • may be precipitated by nicotine, ETOH, cocaine ingestion

    • troponin negative

    • nitroglycerin (NTG) administration results in relief of chest pain, ST’s return to normal

  • management of acute chest pain

    • STAT ECG done and read within 10 min

    • aspirin

    • anticoagulants: heparin or enoxaparin

    • antiplatelets: clopidogrel (plavix), abciximab (reopro), tirofiban (aggrastat), epifibatide (integrilin)

    • cardioselective beta blocker: metoprolol (lopressor)

      • unless ACS is due to cocaine

      • do not use non-cardioselective BB

      • contraindications: hypotension, bradycardia, use of phosphodiesterase-inhibitor drugs such as sildenafil (viagra)

    • to treat pain: nitroglycerin, morphine

    • history, risk factor assessment

      • lab assessment

      • cardiac biomarkers, lipid profile, CBC, electrolyes, BUN, Cr, magnesium, PT, PTT

  • ECG lead changes and location of CAD

    • changes in II, III, aVF → right coronary artery (RCA), inferior LV

    • changes in V1, V2, V3, V4 → left anterior descending (LAD), anterior LV

    • changes in V5, V6, I, aVL → circumflex, lateral LV

    • changes in V5, V6 → low lateral LV

    • changes in I, aVL → high laterl LV

    • changes in V1, V2 → RCA, posterior LV

    • changes in V3R, V4R → RCA, right ventricular (RV) infarct

  • types of acute MI

    • inferior MI

      • a/w right coronary (RCA) occlusion

      • ST elevation in II, III, and aVF

      • reciprocal changes in lateral wall (I, aVL)

      • a/w AV conduction disturbances: 2nd degree type I AV block, 3rd degree AV block, sick sinus syndrome (SSS), and sinus bradycardia

      • development of systolic murmur: mitral valve regurgitation (MVR) secondary to papillary muscle rupture (posterior papillary muscle has only one source of blood supply, the RCA)

      • tachycardia is a/w an inferior MI → higher mortality

      • a/w the right ventricular (RV) infarct and posterior MI

      • use beta blockers and NTG with caution

    • right ventricular (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 infarct determines symptoms

      • a right sided ECG may demonstrate ST changes

      • s/s: JVD at 45 degrees, high CVP, hypotension, clear lungs, bradyarrhythmias, ECG with ST elevation in V3R, V4R

      • tx: fluids, positive inotropes

      • avoid: preload reducers (nitrates, diuretics), caution with beta blockers (usually can’t give initially due to hypotension)

    • anterior MI

      • a/w left anterior descending (LAD) occlusion

      • ST elevation in V1-V4; precordial leads, 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) → ominous 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, I, aVF (high lateral)

      • generally involves left circumflex artery

    • treatment of STEMI

      • if s/s <12 hrs → reperfusion

        • Percutaneous coronary intervention (PCI) - standard is door-to-balloon within 90 min

        • fibrinolytic drug therapy - standard is door-to-drug within 30 min

        • eligibility criteria:

          • ST elevation in 2 or more contiguous leads or new onset left bundle branch block (LBBB)

          • onset of chest pain <12 hrs

          • chest pain of 30 min in duration

          • chest pain unresponsive to sublingual (SL) nitroglycerin (NTG)

    • treatment of NSTEMI

    • complications of acute MI