Cardiology Review

From Iusmicm

Contents 1 Cardiology Review 1.1 In Utero Circulation 1.2 Physical Exam Stuff 1.3 Concepts

Cardiology Review

In Utero Circulation

• The physiological differences in utero:
  • The pulmonary vessels are under large pressure (because there's no air in the lungs) so they have much higher resistance.
  • We don't need to get much oxygen to the lungs because it only has to supply the pulmonary tissue, not get oxygenated.
  • The blood coming into the right atrium is the oxygenated blood.
    • Recall that the oxygenated blood comes from the umbilicus which dumps into the IVC such that the right atrium receives half-oxygenated blood and half-non-oxygenated (from the SVC).

• What must be achieved by in utero circulation:
  • Both sides of the heart must pump blood so that the cardiac tissue can develop.

• In utero shunts as the solution:
  • So that the right heart can develop (pump blood) even in the face of very high pressures (resistance) in the pulmonary arteries, the ductus arteriosus allows blood leaving the right ventricle (via the pulmonary arteries) to shift to the aorta. The ductus arteriosus becomes the ligamentum arteriosus.
  • So that the left heart can develop (pump blood) even when there is very little return from the pulmonary veins (recall that there is high resistance and low flow in the in utero lungs), the formaen ovale allows blood to shift from the RA to the LA.

• Changes upon the first breath:
  • The resistance drops, the flow to the lungs increases, LA pressure increases as more blood is returned from the pulmonary tissue, the foramen ovale closes.
  • Increased pulmonary return at the LA results in increased pressure at the LV and the aorta, thus preventing shunting from R to L at the ductus arteriosus.

• In utero and adult structures:
  • Foramen Ovale: Fossa Ovalis
  • Umbilical Vein: Ligamentum teres
  • Ductus Arteriosum: Ligamentum arteriosum

• Here's a great explanation.
• Here's a simple explanation, too.

Physical Exam Stuff

• The cardinal symptoms of cardiovascular disease are: chest pain (angina), dyspnea, orthopnea, paroxysmal (a sudden worsening of symptoms) nocturnal dyspnea, edema, palpitations, and syncope.

• NY Heart Association Classification:
  • Class I- No dyspnea
  • Class II- Dyspnea on more than usual activities (able to climb 2 flights/ walk 2 blocks)
  • Class III- Dyspnea on less than usual activities (unable to climb 2 flights/ 2 blocks)
  • Class IV- Dyspnea at rest or with any activity

• Wide pulse pressure (aortic regurgitation, anemia, thyrotoxicosis, pregnancy)
• Narrow pulse pressure (aortic stenosis, severe LV dysfunction, severe volume depletion, mitral stenosis, shock of any cause)
• Blood pressures:
  • Normal < 120/80
  • PreHTN: 120-139/80-90
  • Stage 1 HTN: 140-159/90-99
  • Stage 2 HTN: 160+/100+

• Pulsus parvus et tardus and Corrigan's manifest from aortic issues and are the exact opposite in cause and nature.
• Pulsus parvus et tardus: Severe aortic stenosis
  • Slow upstroke
  • Low amplitude
  • Small pulse pressure
• Corrigan's pulse (Waterhammer): Severe aortic regurg
  • Rapid upstroke
  • High amplitude
  • Wide pulse pressure

• Pulsus paradoxus: pericardial tamponade, constriction, obstructive lung disease, large PE, and RV infarction
  • Exaggeration of the normal inspiratory fall in systolic blood pressure during inspiration.

• JVP:
  • JVP is an estimate of right atrial pressure / volume.
  • The JVP waveform can hint at cardiac pathology, too.
  • Large V waves = severe tricuspid regurg.

• Murmur intensity:
  • Grade I: Not immediately audible
  • Grade II: Heard with each cardiac cycle but not loud
  • Grade III: Loud murmur without a thrill
  • Grade IV: Loud murmur with a thrill
  • Grade V: Very loud murmur
  • Grade VI: May be heard with stethoscope off the chest
• Murmurs from the right heart are more intense during inspiration and murmurs from the left heart are louder on expiration.
• Increase LV volume: squatting, isometric hand grip, phenylephrine
• Decrease LV volume: standing, valsalva maneuver, amyl nitrate
• HCM and MVP are two murmurs for which these volume-changing maneuvers are important for auscultation:
  • HCM (hypertrophic cardiomyopathy) murmur gets louder with decreased LV size.
  • MVP (mitral valve prolapse) murmur gets earlier and longer with decreased LV size.

• Prosthetic heart valves:
  • Complications include endocarditis (initially high risk, then decreases), structural failure, thromboembolism, bleeding w/ anticoagulation.
  • Don't replace valves in state I and stage II; it doesn't really decrease mortality.
  • Indicators for sx:
    • Symptomatic severe valvular disease
    • Asymptomatic severe valvular disease with evidence of LV dysfunction
    • Asymptomatic severe mitral valve disease with evidence of significant pulmonary HTN
    • Asymptomatic moderate to severe valvular disease when performing other cardiac surgery
    • Asymptomatic, normal LV function but repairable valve?
  • Class I indications:
    • History of CAD, chest pain, or other evidence of ischemia
    • Patients at risk of concurrent CAD:
      • Men > 35 years old
      • Post-menopausal women
      • Pre-menopausal women > 35 with coronary risk factors
    • Patients in whom an autograft (Ross procedure) will be performed

• Sudden changes in otherwise stable valve disease pt often due to: atrial arrythmia onset, endocarditis, progression of disease (chordal rupture on valve), ischemic heart disease.

• Coronary artery disease: abnormal narrowing, ectasias, or occlusion or coronary vessels.
• Coronary heart disease: coronary artery disease with symptoms (angina, MI, HF).

• Metabolic syndrome = 3 of:
  • HTN (>=130/85)
  • Abdominal obesity (>40 cm in men, >35 cm in women)
  • HDL < 40
  • TAGS >= 150
  • Fasting glucose >= 100
• Associated with inflammation, coagulation issues, and progression to DM

• Cardiac stress testing:
  • The major focus is risk stratification: how many vessels involved?, how much tissue at risk?, how severe?, LV function?
  • Contraindications: unstable symptoms, severe/symptomatic aortic stenosis, uncontrolled HTN, decompensated CHF, uncontrolled arrhythmias, uncooperative pt
  • Without imagine: 68/77 (sens/spec); with imaging: 83/84%.
  • Dobutamine is the drug of choice for pharmacologic stressing.
  • Target heart rate is 85% of predicted.
  • METs estimate the oxygen consumption (as it is hard / expensive to measure directly); 6-10 mets is average functional capacity
  • ST segment depression is dx of ischemia
  • ST segment elevation is leads w/o Q waves is dx of ischemia
  • High risk stress test results:
    • inability to complete stage II
    • angina at <6 METs
    • < 80% (120) HR achieved
    • fall in BP > 10 mmHg
  • High risk EKG findings:
    • ST depression:
      • >= 2 mm (espeically downsloaping)
      • at < 6 METs
      • in multiple leads
      • lasting > 5 min of recovery
      • more is worse, earlier is worse, longer is worse, and more leads is worse.
    • ST elevation >= 1mm (in lead w/o Q waves)
    • Sustained ventricular tachycardia
  • High risk MPI findings:
    • multiple areas of defects
    • large defect in LAD area
    • transient ischemic LV dilation
    • increased lung uptake
    • abnormal LV fxn
  • High risk echo findings:
    • Wall motion abnormalities in multiple coronary territories
    • Large, inducible wall motion abnormalities in one territory
    • LV dysfunction (EF < 35%)
  • Indications for imaging (echo or MPI-myocardial perfusion imaging):
    • Unable to exercise
    • Abnormal baseline EKG (LBBB, LVH, pacer, WPW, ST depression > 1 mm, digoxin tx)
    • Known CAD (prior infarct, cath, etc.)

Concepts

Disorder	Symptoms	Signs	Auscultation	EKG	Diagnosis	Treatment	Note
Bicuspid aortic valve	<symptoms>	<signs>	systolic ejection click	<ekg>	<dx>	sx replacement;	can dev stenosis, regurg, or both; increased risk of endocarditis and aortic disease (type a aneurysm, coarctation, dissection)
Complete heart block	<symptoms>	Cannon A waves	<ausc>	<ekg>	<dx>	<tx>	<note>
Benign murmur	none	none	Grade I-II, early peaking, systolic ejection murmur	normal	no ekg or pe abnormalities, no symptoms	none	<note>
Aortic stenosis	angina (reduced flow with increased muscle), syncope, heart failure	pulsus P&T; sustained PMI; S4+	SEM at RUSB (radiating to carotids and apex), later the peak, more severe	evidence of LVH	symptoms, signs, EKG, echo / doppler (LVH), cath (pressure gradient b/w LV and aorta)	sx:AVR / TAVI (indx: 1: severe, symptomatic; 2: severe, asymptomatic with LV systolic dysfunction; 3: severe, asymptomatic, another sx)	<70 (bicuspid > rheumatic > calc), >70 (calc > bicuspid > rheumatic)
Aortic valve sclerosis	<symptoms>	<signs>	early peaking SEM at RUSB	<ekg>	<dx>	<tx>	2-fold increased risk of cardiac event; may progress to aortic stenosis
Aortic regurgitation	forceful heart beat, angina, heart failure	wide pulse pressure (Corrigan's): pulsations at nails (Quinke's), head bobbing (deMusset's), femoral bruit (Duroziez's); soft s1; lateral / hyperdynamic PMI;	3 murmurs: high pitched, decrescendo, immediate diastolic murmur; early peaking systolic ejection murmur; delayed, diastolic, low-pitched, apical murmur; systolic ejection click (if bicuspid); 'pistol shot' over femoral (Traube's)	<ekg>	ECG (LVH, ST-T changes); Echo (LV wall thick, LV function, aortic root dimension, regurg); contrast aortography; cardiac MRI; grading is by volume / fraction regurged, regurgitant orifice size, and LV size	sx: AVR (+/- aortic root replacement; indx: 1: severe, symptomatic regurg, 2: severe, asymptomatic w/ LV dysfunction, 3: severe, asymptomatic, another sx); vasodilators (for non-sx pts)	diastolic murmur heard best leaning forward, holding expiration;
Acute Aortic regurgitation	edema, cardiogenic shock	no lateral PMI (LVH hasn't had time), no wide pulse pressure (LV compensation hasn't had time)	<ausc>	no LVH evidence (hasn't had time)	<dx>	emergent AVR	usually caused by endocarditis, type A dissection, or trauma
Mitral valve regurgitation	congestive heat failure (elevated PCW pressure, pulm HTN), palpitations, arterial thromboembolism	lateral / dyanamic PMI; elevated JVP; parasternal heave (LA enlargement)	soft s1; apical, holosystolic murmur (radiating to axilla); loud P2; S3	<ekg>	Echo (LV / LA size, LV function, pulm pressure, severity of MR); invasive hemodynamics; contrast ventriculography; cardiac MRI; severity based on regurg vol / fraction, orifice size, LV / LA size	sx: MV repair > replacement (indx: 1: severe symptomatic regurg, 2: severe asymptomatic regurg w/ LV fxn < 60%, 3: severe, asymptomatic regurg with ESD > 4cm); rx: diuretics (control CHF), anticoag (if atrial arrhythmias)	pulm HTN may be irreversible; complications (LV systolic dysfxn, atrial arrhythmias, arterial thrombo, endocarditis)
Acute Mitral valve regurgitation	pulm edema, cardiogenic shock	<signs>	non-holo, soft murmur	<ekg>	<dx>	hemodynamic support (intra-aortic balloon pump, IV vasodilators, dobutamine), mechanical ventilation, emergent mitral valve replair / replacement	<note>
Mitral valve prolapse	chest pain, palpitations	thoracic cage abnormalities	mid-systolic click; late systolic regurgitation; use dynamic auscultation;	<ekg>	<dx>	<tx>	associated with connective tissue disorders; LV EF should be > 60%
Mitral stenosis (rheumatic!)	CHF, fatigue, palpitations (atrial arrythmias), arterial thromboemboli	reduced carotid upstroke (narrow pulse pressure, advanced cases); elevated JVP; parasternal heave (if RV hypertrophy); "tapping" PMI (palpable S1)	opening snap (high pitched, early diastole, closer to S2 = more severe); delayed diastolic murmur (increased by increased venous return); loud S1; loud P2 (if pulm HTN)	<ekg>	severity graded by MV opening area and pressure gradient	slow HR (allow for LV filling; beta / Ca-channel blockers, digoxin); reduce LA / PCW pressure (diuretics); anticoag (if atrial arrhythmias); sx: valvuloplasty (contraindications are: severe mitral regurg, LA thrombus, calcified / immobile valve), MVR	just like MV regurg: pulm HTN may be irreversible; complications (LV systolic dysfxn, atrial arrhythmias, arterial thrombo, endocarditis)
Tricuspid regurgitation	peripheral edema; fatigue; atrial arrythmias	elevated JVP (prominent V waves); parasternal heave (RV dilation); ascities; pulsatile liver	loud P2 (w/ pulm HTN); low pitched, holosystolic murmur (at LSB); S3 (at LSB)	<ekg>	<dx>	diuretics; anticoag (for atrial arrythmias); sx: annuloplasty	mild versions can be normal
Tricuspid stenosis	fatigue, systemic congestion (edema, ascites, etc.)	elevated JVP (with prominent A waves); hepatomegaly	opening snap (LSB); delayed, diastolic murmur (LSB)	<ekg>	<dx>	sx: valvuloplasty (note that regurg may or may not use sx but stenosis always does)	use A wave to distinguish from regurg; usually due to rheumatic fever
Infectious endocarditis	constitutional (fever, chills, weight loss, night sweats); cardiac (CHF, conduction abnormalities); peripheral embolisms; musculoskeletal complaints	Janeway lesions (non-blanching, palms, soles; embolic); Osler nodes (painful, palpable nodules, finger / to pulp; immunologic); Roth spots (retinal hemorrhages, central clearing; immunologic); splinter hemorrhages; labs (normocytic anemia, abn urinalysis, elevated ESR / CRP, presence of rheumatoid factor, elevated BUN / Cr)	murmurs	<ekg>	bacteremia (Staph a., Strep v., HACER); echocardiogram evidence; new murmur; Duke criteria (2/0 or 1/3 or 0/5; major: positive blood culture, endocardial (TEE > TTE) involvement; minor: predisposing condition, fever, vascular phenom, immunologic phenom, other positive blood culture)	oral hygeine maintenance; antibiotics (4-6 weeks); sx (indx: class III-IV, paravalv extension, persistent infections, difficult pathogens, recurrent emboli, prosthetic valve involvement); prophylactic antibx (prosthetics, previous endocarditis, CHD, transplants, dental, respiratory tract, infected cutaneous, not GI/GU)	Staph > Str. viridans; atypicals are HACER; IVDU and HIV association; complications (CHF, emboli, infection spread)
Acute pericarditis	pleuritic pain (sharp, stabbing, worse on inspiration / supine, better leaning forward, radiates to left trap); fever; malaise; dyspnea; URI symptoms	sinus tachycardia; fever	friction rub (triphasic / biphasic; listen when upright and forward)	sinus tachycardia; diffuse concave ST elevations; PR depression	get CBC, chemistries, CXR, echo, autoimmune serology, pericardiocentesis	rx: aspirin (high dose), NSAIDs, colchicine, corticosteroids; pericardiocentesis; hemodialysis (if uremic)	usually viral (coxsackie, echo, adeno, influ, HIV); TB, bacteria, cancer, and radx, too; complications (pericardial effusion / tamponade, constrictive pericarditis (late), relapse)
Pericardial effusion, tamponade	CHF (but with clear lungs); right heart failure (edema, increased JVP);	cardiomegaly on CXR; tachypnea; hypotension; elevated JVP (loss of y descent); pulsus paradoxus (Kussmaul)	<ausc>	sinus tachycardia, low voltage, electrical alternans (swinging heart / axis)	ECG; CXR; emergent echo; right heart catheterization	medical emergency; IVF (temporizing); NO diuretics / vasodilators; vasopressors; pericardiocentesis; pericardial window	causes: acute pericarditis, radx, malignancy,
Constrictive pericarditis	right heart failure (systemic congestion: edema, ascites, hepatomegaly; fatigue; dyspnea)	"square root RA pressure curve"; elevated JVP (prominent X & Y descents); Kussmaul's; pericardial knock (early diastole)	<ausc>	low voltage, ST and T wave changes	EKG; CXR (pericardial calcifications); CT (pericardial thickening); cardiac MRI; echo; simultaneous hemodynamics (equal LV and RV diastolic pressures)	diuretics; pericardial stripping	cause: idiopathic / viral, post-MI, radx; often misdiagnosed as cirrhosis;
Aortic dissection	abrupt onset of severe (worst ever) pain in chest or back (ripping, tearing, migrating); focal neurologic deficits; syncope; pulm congestion; tamponade (pulsus paradoxus, elevated JVP)	unequal brachial BPs; tachycardia; pulse deficits;	soft S1	often normal; sometimes shows new onset MI; often non-specific ST-T change	CXR (wide mediastinum, abnormal aortic contour); CT (for typing: A/B) > MRI > TEE > aortogram;	beta-blockers (reduce dP/dt); Ca-channel blockers (alternative to b-blocker); vasodilators (after b-blocker); analgesia (narcotics); intubation; no fibrinolytics; type A: sx; type B: bp control via b-blocker, sx if complicated	risk factors (chronic HTN: smoking, cocaine; connective tissue disorders: marfans, ehlers-d; inflammation: giant cell, Takayasu, syphillis); cystic medial damage -> intimal tear; difficult dx;
Aortic intramural hematoma	identical to dissection	identical to dissection	identical to dissection	identical to dissection	use imaging to differentiate from dissection (remember: CT > MRI > TEE > aortogram)	<tx>	rupture of vasa vasorum; HTN risk factor; most in descending; may progress to rupture / dissection / resorption
Aortic penetrating ulcer	identical to dissection	identical to dissection	identical to dissection	identical to dissection	imaging to diff from intramural hematoma and dissection	treat as one treats a dissection at same location (type A vs B)	deep ulceration of a plaque; usually in descending; risk of rupture
Aortic aneurysm: Ascending	usually asymptomatic (discovered incidentally); chest pain; aortic regurgitation	<signs>	aortic regurgitation (early, decrescendo diastolic murmur at LSB)	<ekg>	<dx>	control HTN (beta blockers); serial imaging for progression; sx (1: >5.5 cm, 2: >4.5cm + marfans / bicuspid, 3: symptomatic, rapid progression)	risk factors (marfans, ehlers, turner's, familial, bicuspid, aortitis, not atherosclerosis which is protective); complications (chronic aortic regurg, dissection, rupture)
Aortic aneurysm: Descending	usually asymptomatic (discovered incidentally)	<signs>		<ekg>	<dx>	control HTN (beta blockers); serial imaging for progression; sx (>6.0 cm)	risk factors (atherosclerosis which is different than ascending aneurysms; aortic dissection); complications (dissection, rupture)
Aortic aneurysm: Abdominal	usually asymptomatic (discovered incidentally); back / flank / abdominal pain; lower extremity claudication; distal embolization	<signs>	aortic regurgitation (early, decrescendo diastolic murmur at LSB)	<ekg>	<dx>	control HTN (beta blockers); serial imaging for progression; sx (>5.5 cm, expansion > 1cm/year, symptoms); assess for CAD	risk factors (atherosclerosis which is different than ascending aneurysms; smoking, family hx, HTN, dyslipidemai, db, age, male sex); complications (peripheral embolization; rupture: increases with size and rate of expansion)
Aortic coarctation	often asymptomatic (like aneurysms);	HTN (upper limbs); arm-leg pulse difference (radio-femoral delay); exertional leg fatigue;	systolic ejection click / murmur (with bicuspid); cerebral hemorrhage	LVH	CXR (rib notching from colaterals, "3" sign); echo (location, gradient, bicuspid?, aneurysm?, LVH, LV fxn); MRI; contrast aortography; severe: >15 mmHg pressure gradient	sx: percutaneous stenting	usually near the ligamentum arteriosum; strong assoc with bicuspid; assoc with aneurysm / dissection, VSD, berry aneurysms, premature CAD
Aortic atheroma	<symptoms>	<signs>	<ausc>	<ekg>	US	rx: anti-platelet, lipid lowering	plaque formation w/in aorta; complications (cerebral / peripheral emboli, esp. >=4mm, mobile, or adherent thrombus);
Atherosclerosis (Coronary Artery Disease, Myocardial Ischemia)	angina (stable / unstable; typical = substernal, exertion induces, rest / NTG relieves; class II / III: more than usual / usual activity); sudden cardiac death; dyspnea; arm / jaw / back pain; nausea; diaphoresis; fatigue;	<signs>	S4 often heard during active ischemia	Q waves (previous MI), LVH, ST andT wave changes	stress testing (assess fxnal limitations); assess LV fxn; assess modifiable risk factors (BP, BMI); labs (lipids, OGTT, chemistries, CBC);	baby ASA daily; NTG as needed; lipid lowering drugs; beta-blockers; ca-channel blockers; ACE inhibitors; long-acting nitrates; change lifestyle; CABG (indx: 1: left main > 50%, 2: 3 vessels with lower LV fxn, 3:2 vessels including proximal LAD, 4: 2+ vessels with DB)	risk factors (age, fam hx, DB, HTN, smoking, chol, BMI > 30, sedentary; chronic inflam, high hsCRP, homocystein, kidney disease, coag issues); complications (stenosis, aneurysms, embolization); 2nd causes: anemia, hypoxemia, HTN, LVH, tachycardia, thyrotoxicosis; 50+yo with angina: 93% have CAD
Prinzmetal, Vasospastic Angina	angina; diaphroesis; early morning; upon hyperventilation; other vasospasm symptoms (migraines; Raynaud's)	<signs>	ventricular arrythmia	ST elevation; ventricular arrythmia	<dx>	Ca-channel blockers; nitrates; smoking cessation	50% occur at site of plaque
Unstable angina	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
NSTEMI	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
NQMI	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
QwMI	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>
<disorder>	<symptoms>	<signs>	<ausc>	<ekg>	<dx>	<tx>	<note>