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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Pericarditis

A

S+S

  • Sudden sharp/ stabbing substernal chest pain
  • Sob + tachycardia
  • Radiates along trapezius ridge, pericardial rub.
  • Pain worse with inspiration or laying flat.
  • May have recent hx of fever + URTI sx, or occur within 1-2 days of an MI

Investigations
- ECG: ST elevation + PR depression across almost all leads

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2
Q

Aortic Dissection

A

S+S

  • Abrupt onset of severe, sharp, or “tearing” chest pain
  • Radiates to abdomen.
  • Associations: back pain, syncope, stroke, MI, cardiac tamponade, sudden death
  • Pulse differential (weaker pulse on 1 side) (high spec low sens)

Investigations
- Wide mediastinum on CXR, then image the aorta via CT, MRI, trans-eso ECHO, or aortic root angio

Tx

  • Ascending aorta or aortic arch - surgical ER
  • Distal to the subclavian artery - pharmacologically (dec BP)
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3
Q

Pulmonary Embolism (PE)

A

S+S

  • Acute pleuritic chest pain, dyspnea, sometimes cough + hemoptysis
  • Sinus tachycardia, tachypnea, wheezing

Investigations

  • ECG: sinus tachy, non-specific ST + T wave changes, and sometimes P pulmonale, RAD, RBBB, RVH.
  • Well’s score risk assessment: s+s, sinus tach, immobilization/ surgery, previous venous thromboembolism, malignancy, etc
    • -> If Well’s is LOW, can r/o with D-dimer
  • Gold std is pulmonary angiogram, but CT PE is great.

Tx

  • Complete obstruction + hemodynamically unstable –> thrombolysis
  • Otherwise, IV LMWH or unfractionated heparin for anticoagulation
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4
Q

Valvular Disease - Aortic Stenosis

A

S+S

  • Dec CO, so: exertional chest pain/ syncope, dyspnea, palpitations
  • Crescendo-decrescendo murmur

Investigations
- Transthoracic ECHO

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5
Q

Valvular Disease - Aortic Regurgitation

A
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6
Q

Valvular Disease - Mitral Stenosis

A

Etiology
- 50% from rheumatic fever. Also congenital, calcification.

Pathophys
- L heart backup -> Phtn -> sob, LAE, a.fib +/- thrombus

S+S

  • Mild: inc S1 (valve is further apart when slams shut).
  • Severe: dec S1 (doesn’t move).
  • Opening snap (stiff MV opening)

Tx

  • Diuretics for vascular congestion
  • Slow HR (B-blocker, CCB, or digoxin) if afib
  • Chronic anti-coag if MS + afib, abx prophylaxis (turbulent flow + rheumatic fever)
  • Valve repair or replacement if severe
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7
Q

Valvular Disease - Mitral Regurgitation

A

Etiology
- Rheumatic fever, annular calcification, endocarditis, HCM, papillary muscle dysfunction, LV dilation

Pathophys

  • Acute: inc P of LA -> helps prevent further regurg, but also backs up into pulmonary system
  • Chronic: inc LA compliance overtime -> less pulmonary backup, but dec forward CO -> LVH/ dilation to compensate

S+S

  • Acute: pulmonary congestion/ edema
  • Chronic/ Severe: sx of dec CO (dizzy, weak, fatigue), sob, orthopnea, POD, RHF from LHF, S3
  • Pansystolic blowing murmur

Tx

  • Acute: diuretics to dec pulmon edema, vasodilators to dec forward resistance
  • Chronic: vasodilators less helpful
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8
Q

Valvular Disease - Mitral Valve Prolapse

A
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9
Q

Valvular Disease - Tricuspid

A
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10
Q

Stable Angina

A

Categories

  • Typical: substernal chest pain + worse with exertion/ stress + relief with rest or nitro
  • Atypical: 2 of the 3 components
  • Non-cardiac: 0 to 1 of the 3 components

Myocardial Ischemia

  • O2 demand > supply
  • Myocardial O2 demand: HR, systolic BP/ afterload, myocardial contractility, LV wall stress/ LV EDV/ preload, myocardial mass
  • Myocardial O2 supply: coronary blood flow, perfusion pressure

Etiology

  • Most commonly CAD
  • Also coronary vasospasm, aortic stenosis, HOCM, systemic arterial htn, tachyarrhythmias, hyperthyroid, anemia, polycythemia

Investigations

  • ECG, ECHO, MIBI, stress test
  • CT angio, coronary angio (gold std for CAD dx)

Tx

  • Risk factor modification
  • Meds are key: anti-anginal (B-blocker, CCB, nitrates), vascular protection (anti-platelets, statins, ACE-I)
  • PCI if meds fail- inc quality of life + dec angina, but doesn’t dec mortality
  • CABG for severe/ extensive CAD, dec mortality* with L main stenosis, 3 vessel disease, and 2 vessel disease including LAD
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11
Q

Coronary Artery Disease (CAD)

A
  • 94% = typical angina

Risk Factors

  • Assess 10 yr CAD risk with Framingham Risk Score
  • Smoking, dyslipidemia, DM, sedentary, bad diet, family hx
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12
Q

Pharmacology - Beta Blockers

A
  • 1st line for most chronic stable angina
  • Dec mortality* after MI. Esp metoprolol, carbedolol, bisoprolol.

Pathophys
- Dec HR, dec myocardial contractility, dec BP –> dec myocardial demand –> dec angina severity + frequency

Contraindications
- Severe reactive airway disease, severe bradycardia, decompensated HF

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13
Q

Pharmacology - Calcium Channel Blockers (CCB)

A
  • 2nd line after B-blockers

Pathophys
- Vasodilate (dec BP), inc coronary blood flow, dec myocardial contractility
- Non-dihydropyridine (verapamil, diltiazem - greater effect on myocardial contractility/ conduction)
VS dihydropyridine (greater effect on vasodilation - can use in HF, and can combo with B-blockers)

Contraindications

  • Short acting nifedipine (inc MI risk)
  • Non-dihydro with HF, bradycardia, or B-blockers
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14
Q

Pharmacology - ACE-inhibitors (ACE-I)

A
  • Best for pts with HF + dec LV EF
  • Dec mortality* + in high-risk pts
  • Ex: catopril

S/E/ contraindications

  • Kinins cause chronic cough in 20% –> switch to ARB
  • Teratogenic. Do NOT use in pregnancy
  • HyperK
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15
Q

Pharmacology - Nitrates

A

Pathophys

  • Dilate epicardial coronary vessels, inc venous capacitance, dec preload –> dec myocardial demand
  • Will help sx, but need to combo with hydralazine

Contraindications
- Phosphodiesterase-5 inhibitor (ex: sildenafil)

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16
Q

Pharmacology - Thienopyridine derivatives

A
  • Ex: clopidogrel
  • 2nd line after aspirin, or for recent stent placement, or ACS
  • $$
17
Q

Blood Pressure Equations

A

BP = Cardiac Output (CO) x Total Peripheral Resistance (TPR)

  • -> CO = Heart Rate (HR) x Stroke Volume (SV). (5L)
  • -> SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV). (60-100 mL).
  • -> SV determined by contractility, preload, afterload
18
Q

Heart Failure - Categories

A
  1. Systolic dysfunction/ Dec EF
    - Abnormal ventricular emptying, but normal filling
    - -> Dec contractility: CAD (MI/ transient ischemia), volume overload (AR, MR), DCM, or
    - -> Inc afterload: severe AS, severe htn
  2. Diastolic dysfunction/ Preserved EF
    - Abnormal diastolic relaxation or ventricular filling, but can pump out what there is
    - LVH, hypertrophic/ restrictive cardiomyopathy, fibrosis, transient ischemia, pericardial tamponade/ constriction
  • Can only distinguish via ECHO
  • Can have combo - doesn’t fill AND doesn’t pump well
  • About 50/50 each, and both have similar prognosis
19
Q

Frank-Starling Relationship

A
  • Inc myocardial stretch, inc preload, inc force of contraction
20
Q

Heart Failure - Investigations & Tx

A

Investigations

  • ECG, lytes, liver + kidney fncn, CBC.
  • Sometimes: thyroid fncn, tests for cardiomyopathy, BNP

Tx (pretty much only for systolic dysfunction)

  • Diet Na >2g/ day, fluid ARB if ACE-I causes cough.
    • -> Hydralazine + isosobide dinitrate if hyperK + renal insufficiency. Also works better for black ppl.
  • Add B-blocker if euvolemic and no recent clinical deterioration. (Carvedilol, metoprolol).
  • Sometimes add aldosterone blocker for advanced HF. (Spironolactone = aldost antagonist + weak diuretic).
  • Finally, may add hydralazine + isosobide dinitrate or digoxin.
  • Mortality benefit: ACE-I, ARB, B-blockers, aldosterone blockers. (Not diuretics, not inotropes, ie digoxin/ digitalis). ICD, CRT, transplant.
  • Implantable Cardioverter-Defibrilator (ICD): NYHA 2 or 3, optimal med tx, life expectancy >1yr
  • Bi-ventricular pacing: NYHA 3 or 4, EF>= 35%, QRS >120msec
21
Q

Natriuretic peptides

A
  • Atrial Natriuretic Peptide (ANP): released from atria when it is stretched
  • B-type natriuretic peptide (BNP): released from pathologic hearts when myocardium is under hemodynamic stress/ stretched.
    • -> Inc BNP (>100pg/mL) correlates with inc HF prognosis/ dec severity. Best for use in an ACUTE setting.
    • -> Other reasons for inc BNP: acute MI, PE, CKD, old age, female. Dec by obesity.
  • Fncn: diuretic, excrete Na + H2O, vasodilate, inhibit renin, oppose angio II effects on aldost + ADH
  • Act as a compensatory mechanism in heart failure, but often not enough
22
Q

Heart Failure - Clinical Picture

A

Left Heart

  • Etiology: IHD/ MI, htn, aortic/ mitral valve disease, myocardial disease
  • S+S: soboe*, orthopnea, PND
    • -> Diaphoresis, tachycardia, tachypnea, pulmonary crackles, loud P2, S3 (systolic dysfunction), S4 (diastolic dysfunction), mitral regurg
    • -> Other: dec mental status, dec urine output, fatigue + weakness (from dec perfusion to brain, kidney, muscles)
    • -> Decompensated: dusky + diaphoretic

Right Heart

  • Etiology: most commonly L HF, then chronic lung disease. Also RV MI, PE, 1° pulmonary htn, pulmonic valve stenosis, ARDS
  • S+S: wt gain then peripheral edema, RUQ discomfort (hepatomegaly), inc JVP
    • -> S3, S4, tricuspid regurg
23
Q

Orthopnea

A
  • Harder to breath when lay flat, relieved from sitting up
  • Pathophys: redistribution of intravascular blood from the gravity-dependent portions of the body (abdomen, lower extremities) toward the lungs after lying down.
  • # of pillows the pt sleeps on is a hint
24
Q

Paroxysmal Nocturnal Dyspnea (PND)

A
  • Severe breathlessness that wakes the pt from 2-3 hrs after going to bed.
  • Pathophys: lower extremity interstitial edema is gradually reabsorbed into the circulation after lying down –> expansion of intravascular volume –> inc venous return to heart + lungs
25
Q

Heart Failure - Classification

A

NHYA
I: No limitation of physical activity.
II: Slight limitation, sob + fatigue w moderate exertion (quickly walking upstairs)
III: Marked limitation, sob w minimal exertion (slowly walking upstairs).
IV: Severe limitation, sx at rest.

26
Q

Cardiomyopathy - Dilated (DCM)

A
  • Dilatation + impaired contraction of LV or LV+RV

Etiology
- Idiopathic > myocarditis > ischemic > peripartum > toxic.

27
Q

Cardiomyopathy - Restrictive

A
  • Disease of ventricular myocardium usually resulting in delayed diastolic relaxation, dec compliance, inc filling pressures
  • Non-dilated ventricles

Etiology
- Amyloidosis > sarcoidosis, hemochromatosis

S+S
- Fatigue, weakness, anorexia, edema, inc JVP, hepatojugular reflux, Kussmaul sign, loud S3, regurg murmurs

28
Q

Cardiac Biomarkers

A
  • CK: rise w/i 4-8 hrs, normal in 48-72 hours
    • -> CK-MB: more specific to heart
  • cTnI/ CtnT (troponins): rise 3-5 hrs after infarct, normal after 7-10 days (I) or 10-14 days (T)
29
Q

STEMI - Thrombolytics vs PCI

A

Thrombolytics

  • Best if given 1-3 hrs after onset of chest pain
  • Risk (bleed) > benefit at 12 hrs
  • Need all 4 Indications: 1) S+S of ischemic chest pain, 2) ST elevation >1mm in >= 2 consecutive leads, 3) no contraindications, 4) <75 yrs
  • No survival benefit if cardiogenic shock or hypotensive

PCI

  • Preferred over thrombolytics (better at opening occlusions, better clinical outcome)
  • Ideal if pt presents w/i 2-3 hrs of sx and sent to the cath lab w/i 90 mins after
  • Can use if cardiogenic shock or hypotensive
30
Q

Dressler Syndrome

A
  • A late complication (ie several wks after) of an acute MI
  • Immune phenomenon w: 1) pericarditis, 2) pleuritis, and 3) fever.
  • May remit and relapse
  • Tx: anti-inflams including NSAIDS + prednisone
31
Q

Post-MI

A
  • PCI, CABG

- Stop smoking*, ASA + clopidogrel, B-blockers, ACE-I, statins –> all dec rate of events + mortality.

32
Q

Infective Endocarditis

A

Etiology/ Pathophys

  • Usually underlying cardiac lesion -> turbulent blood flow -> endothelial damage -> nonbacterial thrombotic endocarditis -> bacteria adhere during transient bacteremia -> infective vegetations
  • Orgs: usually staphylococci, streptococci, and enterococci. S aureus is v virulent and can cause infective endocarditis in normal valves, esp with IV drug users and HD pts.

Abx Prophylaxis
- Use for a procedure only if high risk of infection/ high risk of bad outcomes from endocarditis. Abx based on predicted bacteremia.

Dx

  • Risk factors: IV drugs, recent procedure associated with risk of transient bacteremia, prosthetic valve, certain cardiac abnormalities
  • Clinical + histology of valve
  • Duke criteria:
    • -> Major: microbio (typical orgs grown from 2 blood cultures, any microorg grown from persistently + blood cultures, +ve serology or 1 blood culture for coxiella burnetii), endocardial involvement (ECHO - oscillating intracardiac mass, abscess, prosthetic valve problem)
    • -> Minor: microbio (+serology or blood culture not meeting major), predisposition (heart condition, IVDU), fever, vascular (major arterial emboli, septic pulmon infarcts, myotic aneurysm, intracranial or conjuctival hemorrhage, Janeway lesions, immune (GN, Osler nodes, Roth spots, +RF)
    • -> Need 2 major OR 1 major + 3 minor OR 5 minor

S+S

  • Non-specific: fever, malaise, fatigue
  • L-sided: blind, focal weakness, localized back/ flank pain, hematuria, gangrenous skin lesions
  • Tricuspid: sob, chest pain, cough
  • P/E: new murmur, new HF, focal neuro signs, splenomegaly, derm (petechiae, splinter hemorrhages), Osler nodes, Janeway lesions.

Investigations

  • Leukocytosis, normocytic anemia, hematuria, low serum complement
  • ECG (AV block) + ECHO
  • XR: HF or septic emboli from R side
  • Blood cultures

Tx

  • Empiric tx if suspicious (after >= 3 blood cultures from separate sites)
    • -> Community-acquired: vanco + gentamicin (streptococci, staphylococci, enterococci)
    • -> Prosthetic valve: vanco + gentamicin + rifampin (multi-drug resistant bacteria - ie coagulase neg staph)
  • Surgical resection of infected valve (native + prosthetic) in certain pts
  • ECHO after tx for new baseline

(More details starting pg 220 MKSAP)

33
Q

Atrial Fibrillation

A

S+S

  • ECG: no P waves, inc rate

Medicine (22 decks)

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