CCRN– Cardiac

S1 heart sound description

• “lub”

• mitral and tricuspid valves closing

• loudest at apex of heart (5th ICS)

S2 heart sound description

• “dub”

• aortic and pulmonic valves closing

• loudest at base of heart (2nd ICS)

• louder with a pulmonary embolism

which valves are the AV valves and which are the semilunar?

• AV: mitral and tricuspid

• semilunar: aortic and pulmonic

what causes S3 heart sound?

• rapid rush of blood into dilated ventricle (early diastole)

• associated with heart failure (“gallop”)

• pulmonary HTN and cor pulmonale

• mitral, aortic, or tricuspid insufficiency

right after S2

what causes S4 heart sound?

• caused by atrial contraction of blood into a noncompliant ventricle

  • "atrial kick" pushing blood into a chamber that resists filling, hits rigid wall and makes sound

• myocardial ischemia

• infarction

• HTN

• ventricular hypertrophy

• aortic stenosis

right before S1

normal pulse pressure

40-60 mmHg

what is SBP an indirect measure of

CO and SV

what is DBP an indirect measure of

SVR

what can a narrowing or widening pulse pressure represent

• narrowing: severe drop in CO or hypovolemia

• widening: vasodilation, sepsis, shock

causes of valvular heart disease

• dilated cardiomyopathy

• degeneration

• bicuspid aortic valve, genetic

• rheumatic fever

• infection

• connective tissue diseases

when do you get murmurs from stenosis vs insufficiency?

• stenosis: murmur when valve should be open

• insufficiency: murmur when valve should be closed

what type of murmurs are only chronic? (not acute)

murmurs from stenosis (occur when valve is open)

systolic murmurs

• aortic and pulmonary stenosis

• mitral and tricuspid insufficiency

• ventricular septal defect

  • most common with acute MI

diastolic murmurs

• aortic and pulmonary insufficiency

• mitral and tricuspid stenosis

  • mitral stenosis associated with a fib– causes atrial enlargement

murmurs associated with acute MI

• mitral valve regurgitation

  • attached by papillary muscles (and chordae tendineae)

• papillary muscle dysfunction or rupture

• VSD

  • septal wall has blood supply from only one major artery that can get occluded during MI with no collateral vessels

stable angina

• chest pain with activity

• predictable

• lesions are usually fixed

• hardened arteries cannot supply enough oxygen to meet heart’s increased demands during activity

unstable angina

• chest pain at rest

• unpredictable

• may be relieved with nitroglycerin

• troponin negative

• ST depression or T wave inversion

types of acute coronary syndrome

• unstable angina

• NSTEMI

• STEMI

NSTEMI characteristics/results

• troponin positive

• ST depression

• T wave inversion

• unrelenting chest pain

• blockage is usually partial

STEMI characteristics/results

• troponin positive

• ST elevation in 2 or more contiguous leads

• unrelenting chest pain

• blockage is usually occlusive

NSTEMI vs STEMI

• NSTEMI usually partial occlusion– ischemia is confined to inner layer of heart and outside layer not affected

  • because heart normally repolarizes from outwards in, the electrical vector flips

• in STEMI, all layers of the heart experience ischemia

  • potassium rapidly leaks out of dying cells and prevents full repolarization that shifts EKG baselines downwards and makes the real baseline (0) look elevated

populations with different MI symptoms and what the symptoms can be

women, diabetes, over 75

• nausea

• SOB

• extreme fatigue

• syncope, falling

• acute delirium

Variant or Prinzmetal’s angina characteristics

• type of unstable anginia

• due to coronary artery spasm with or without lesions

• transient ST elevation

• troponin negative

• occurs at rest and may be cyclic

• can be precipitated by nicotine, alcohol, cocaine

• relief with nitroglycerin

medications for acute chest pain (after EKG)

• aspirin ASAP

• anticoagulant (heparin or enoxaparin)

• antiplatelets (Plavix, abciximab, eptifibatide, tirofiban)

• beta blocker

  • except if due to cocaine

  • use cardioselective (metoprolol, not propanolol)

  • avoid in hypotension, bradycardia, or use of PDE-I

• treat pain with NTG and morphine

what areas of the heart do leads II, III, aVF correspond to?

• right coronary artery

• inferior left ventricle

what areas of the heart do leads V1, V2, V3, V4 correspond to?

• left anterior descending

• anterior left ventricle

what areas of the heart do leads V5, V6, I, aVL correspond to?

• circumflex artery

• lateral left ventricle (high and low)

what areas of the heart do leads V5, V6 correspond to?

low lateral left ventricle

what areas of the heart do leads I, aVL correspond to?

high lateral left ventricle

what areas of the heart do leads V1, V2 correspond to?

• RCA

• posterior left ventricle

what areas of the heart do leads V3R, V4R correspond to?

• RCA

• right ventricular infarct

where will you see ST elevation in an inferior MI?

• leads II, III, aVF

• associated with RCA occlusion

• reciprocal ST-depression in leads I and aVL

what are conditions associated with an inferior MI?

AV conduction disturbances:

• 2nd-degree type I AV block

• 3rd degree AV block

• sick sinus syndrome

• sinus brady

inferior MI complications

• papillary muscle rupture —> mitral valve regurgitation

• tachycardia (associated with higher mortality)

• associated with right ventricular infarct and posterior MI

  • also supplied by RCA

what should be used with caution in inferior MIs?

• beta blockers

• NTG

assessment findings for RV infarct

• JVD

• high CVP

• hypotension

• bradyarrhythmias

• usually clear lungs

where will you see ST elevation for a RV infarct?

V4R

treatments for RV infarct (and what to avoid)

• fluids

• positive inotropes

• avoid preload reducers (nitrates, diuretics)

  • stiff RV relies on increased preload to create enough stretch to generate contraction

• caution with beta blockers (hypotension)

where will you see ST elevation in an anterior MI?

associated with LAD occlusion

• V1-V4

• reciprocal ST-depression in leads II, III, aVF (inferior wall)

anterior MI complications

• 2nd degree type II AV block

• RBBB

  • LAD supplies bundle of His

• systolic murmur from ventricular septal defect

• higher mortality rate than inferior MI: heart failure

where will you see ST elevation during a lateral MI?

• V5 and V6 for low lateral

• I and aVL for high lateral

generally involves left circumflex artery

treatments for STEMI

• if less than 12 hours: reperfusion

  • PCI (within 90 min arrival)

  • fibrinolytic drug therapy (within 30 min of arrival)

reperfusion treatment for STEMI inclusion therapy

• ST elevation in 2 or more contiguous leads or new onset LBBB

• onset of chest pain less than 12 hours ago and lasted at least 30 minutes

• chest pain unresponsive to SL nitroglycerin