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USMLE Step 1: Things I Cannot Remember > Cardiovascular > Flashcards

Cardiovascular Flashcards

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USMLE® Step 1 flashcards
1
Q

What is used to treat primary (essential) hypertension?

A
  1. Thiazide diuretics
  2. ACE inhibitors
  3. ARBs
  4. Ca2+ channel blockers (dihydropyridines)
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2
Q

What is used to treat hypertension w/ heart failure?

A
  1. Diuretics
  2. ACE inhibitors/ARBs
  3. β-blockers (compensated heart failure)
    • used cautiously in decompensated heart failure
    • contraindicated in cardiogenic shock
  4. Aldosterone antagonists
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3
Q

What is used to treat hypertension w/ diabetes mellitus?

A
  1. ACE inhibitors/ARBs
    • protective against diabetic nephropathy
  2. Ca2+ channel blockers
  3. Thiazide diuretics
  4. β-blockers
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4
Q

What is used to treat hypertension in pregnancy?

A
  1. Hydralazine
  2. Labetalol
  3. Methyldopa
  4. Nifedipine
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5
Q

Which Ca2+ channel blocker is used to treat subarachnoid hemorrhage?

A

Nifedipine - prevents cerebral vasospasm

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6
Q

Which Ca2+ is used to treat hypertensive urgency/emergency?

A

Clevidipine

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7
Q

Which nitrate has the highest oral bioavailability?

A

isosorbide mononitrate

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8
Q

What HTN drug can cause cyanide toxicity?

A

Nitroprusside

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9
Q

Which anti-arrythmic drugs can lead to heart failure?

A

Negative inotropes:

  1. Ca2+ blockers (especially non-dihydopyridines)
  2. β-blockers
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10
Q

What increases stroke volume?

A

SV CAP

  • Increase contractility, prelodad
  • Decrease afterload
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11
Q

How do calculate MAP?

A
  • MAP = CO x total peripheral resistance (TPR)
  • MAP = 2/3 diastolic pressure + 1/3 systolic pressure
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12
Q

What is the physiology of normal splitting?

A

Inspiration ⇒ ↓ intrathoracic pressure ⇒ ↑ venous return ⇒ ↑ RV filling ⇒ ↑ RV stroke volume ⇒ ↑RV ejection time ⇒ delayed closure of pulmonic valve

  • ↓ pulmonary impedance ( ↑ capacity of pulmonary circulation) also occurs which contirbutes to delayed closure of the pulmonary valve
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13
Q

Causes of:

  1. Wide splitting
  2. Fixed splitting
  3. Paradoxical splitting
A
  1. Wide splitting (conditions that delay RV filling)
    • pulmonic stenosis, RBBB
  2. Fixed splitting (pulmonic closure is greatly delayed)
    • ASD (L to R shunt ⇒ ↑ RA & RV volumes ⇒ ↑ flow thru pulmonic valve)
  3. Paradoxical splitting​ (delay in aortic valve closure)
    • aortic stenosis, LBBB (P2 occurs before delayed A2)
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14
Q

Bedside maneuvers:

Inspiration

A

↑ intensity of right heart sounds

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15
Q

Bedside maneuvers:

Hand grip

A
  1. ↑ intensity of MR, AR, VSD murmurs
  2. ↓ intensity hypertrophic cardiomyopathy murmurs
  3. MVP: later onset of click/murmur
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16
Q

Bedside maneuvers:

Valsava (phase II), standing up (↓ preload)

A

↓ intensity of most murmurs (including AS)
↑ intensity hypertrophic cardiomyopathy murmur
MVP: early onset of click/murmur

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17
Q

Bedside maneuver:

Rapid squatting (↑ venous return, ↑ preload)

A
  1. ↓ intensity hypertrophic cardiomyopathy murmur
  2. ↑ intensity of AS murmur
  3. MVP: later onset of click/murmur
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18
Q

Speed of conduction ⇒

A

Purkinje fibers > atria > ventricles > Av node

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19
Q

Pacemaker activity ⇒

A

SA node > AV node > Bundle of His/Purkinje fibers

20
Q

List the Right -to -Left Shunts:

A
  1. Patent Truncus Arteriosus
  2. Transposition of the Great Vessels
  3. Triscupid Atresia
  4. Tetralogy of Fallot
  5. Total Anomalous Pulmonary Venous Return
21
Q

List the Left-to-Right shunts:

A
  1. Ventricular Septal Defect
  2. Atrial Septal Defect
  3. Patent Ductus Arteriosus
  4. Eisenmenger Syndrome
22
Q

What are the waves for the jugular venous pulse (JVP)?

A
  • a wave: atrial contraction
    • absent in a-fib
  • c wave: RV contraction
    • closed tricuspid valve bulging into atrium
  • x descent: atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
    • absent in tricuspid regurgitation
  • v wave: inc right atrial pressure due to filling (“villing”) against closed tricuspid valve
  • y descent: RA emptying into RV
23
Q

Brugada syndrome

  • Inheritance:
  • Epidemiology:
  • EKG findings:
  • Risks:
  • Treatment:
A
  • Inheritance:
    • autosomal dominant
  • Epidemiology:
    • most common in asian males
  • EKG findings:
    • pseudo-right bundle branch block and ST elevations in V1-V3
  • Risks:
    • inc. risk of ventricular tachyarrthymias and SCD
  • Treatment:
    • implantable cardioverter-defribrillator (ICD)
24
Q

What are the causes of drug-induced prolonged QT?

(hint: Anti-“ABCDE”)

A
  • Anti-Arrhythmics (class IA, III)
  • AntiBiotics (e.g. macrolides)
  • Anti “C“ychotics (e.g. haloperidol)
  • AntiDepressants (e.g. TCAs)
  • AntiEmetics (e.g. ondansetron)
25
Q

What is the most common type of ventricular pre-excitation syndrome?

A

Wolf-Parkinson-White syndrome

26
Q

What is the lab indicator for heart failure?

A

BNP

  • released by ventricular myocytes in response to inc. tension
  • longer 1/2 life than ANP
  • very good negative predictive value
27
Q

How do organs react to hypoxia?

A
  • hypoxia in pulmonary vasculature ⇒ vasoconstriction
    • so only well-ventilated areas are perfused
  • hypoxia in other organs ⇒ vasodilation
28
Q
  • Aortic arch ⇒
  • Carotid sinus ⇒
  • Baroreceptors ⇒
  • Chemoreceptors ⇒
A
  • Aortic arch ⇒ transmits via vagus nerve (CN 10) to solitary nucleus of medulla (responds to Δ BP)
  • Carotid sinus (at carotid bifurcation) ⇒ transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to Δ BP)
  • Baroreceptors ⇒ respond to stretch (see page 286 of first aid)
  • Chemoreceptors ⇒
    • Peripheral: respond to Δ PO2, PCO2, and pH of blood
    • Central: respond to Δ in interstitial brain pH and PCO2 and are influenced by PaCO2
29
Q
  • What is Cushing reaction?
  • What contributes to this reaction?
A
  • Cushing reaction: HTN, bradycardia, respiratory depression
  • Baroreceptors:
    • ↑ intracranial pressure constricts arterioles ⇒ cerebral ischemia ⇒ ↑ pCO2 and ↓ pH ⇒ central reflex sympathetic ↑ in perfusion pressure (HTN) ⇒ ↑ stretch ⇒ peripheral reflex baroreceptor induced bradycardia
30
Q

In mitral stenosis, what happens to the PCWP?

A

PCWP > LV diastolic pressure

31
Q

Causes of edema:

  1. capillary pressure
  2. plasma proteins
  3. capillary permeability
  4. interstitial fluid colloid osmotic pressure
A
  1. ↑ capillary pressure
    • e.g. HF
  2. ↓ plasma proteins
    • e.g. nephrotic syndrome, liver failure
  3. ↑ capillary permeability
    • e.g. toxins, infections,, burns
  4. ↑ interstitial fluid colloid osmotic pressure
    • e.g. lymphatic blockage
32
Q

What are the signs of hyperlipidemia?

A
  1. Xanthomas:
    • Plaques or nodules composed of lipid-laden histiocytes in skin, especially on eyelids (xanthalasma)
  2. Tendinous xanthoma
    • lipid deposits in tendon, especially Achilles
  3. Corneal arcus
    • lipid deposits in cornea
    • common in elderly (arcus senilis)
    • appears earlier in life in hypercholesterolemia
33
Q

Define arteriosclerosis:

A

hardening of arteries, w/ arterial wall thickening and loss of elasticity

Two types:

  1. Arteriolosclerosis
  2. Monckeberg (medial calcific stenosis)
34
Q

Arteriolosclerosis vs. Monckeberg (medial calcific sclerosis)

A
  1. Arteriolosclerosis
    • Common
    • affects small arteries and arterioles
    • Two types:
      • hyaline → thickening of vessel walls in essential HTN and diabetes
      • hyperplastic → “onion skinning” in severe HTN w/ proliferation of smooth muscle
  2. Monckeberg (medial calcific sclerosis)
    • Uncommon
    • affects medium-sized arteries
    • calcification of elastic lamina of arteries → vasular stiffening w/o obstruction
    • “pipestem” appearance on x-ray
    • does not obstruct blood flow; intima not invloved
35
Q

Define atherosclerosis:

A

Disease of elastic arteries, large and medium-sized muscular arteries

  • form of arteriosclerosis caused by buildup of cholesterol plaques
  • very common
36
Q

Evolution of MI

  • Commonly occluded arteries:
  • Symptoms:
  • 0 - 4 hours
  • 4 - 24 hours
  • 1 - 3 days
  • 3 - 14 days
  • 2 weeks - several months
A
  • Commonly occluded arteries: LAD > RCA > circumflex
  • Symptoms: diaphoresis, n/v, severe retrosternal pain, pain in lt. arm and/or jaw, SOB, fatigue
  • 0 - 4 hours: (none)
    • arrhythmia, HF, cardiogenic shock
  • 4 - 24 hours: (early coagulative necrosis, wavy fibers, neutrophils appear, reperfusion injury)
    • arrhythmia, HF, cardiogenic shock
  • 1 - 3 days: (extensive coagulative necrosis, acute inflammation w/ neutrophils)
    • postinfarct fibrinous pericarditis
  • 3 - 14 days: (macrophages and granulation tissue)
    • Free-wall rupture → tamponade; papillary muscle rupture → mitral regurgitation; interventricular septal rupture due to macrophage-mediated structural degradation
    • LV pseudoaneurysm (risk of rupture)
  • 2 weeks - several months: (complete contracted scar)
    • Dressler syndrome, HF, arrythmias, true ventricular aneurysm (risk of mural thrombus)
37
Q

Causes of dilated cardiomyopathy:

(hint: ABCCCD)

A
  • Alcohol abuse
  • wet Beriberi
  • Cocksakie B virus myocarditis
  • chronic Cocaine use
  • Chagas disease
  • Doxorubicin/Daunorubicin
  • Other causes: hemochromatosis, sarcoidosis, peripartum cardiomyopathy (pregnant women)
38
Q

Findings in HF:

  • Systolic dysfunction:
  • Diastolic dysfunction:
A

Heart failure: dyspnea, orthopnea, fatigue; rales, JVD, pitting edema

  • Systolic dysfunction:
    • reduced EF, ↑ EDV ⇒ ↓ contractility often 2/2 ischemia/MI or dilated cardiomyopathy
  • Diastolic dysfunction:
    • preserved EF, normal EDV ⇒ ↓ compliance often 2/2 myocardial hypertrophy
39
Q

Right HF most often results from ….

Isolated right HF is usually due to ….

A

Right HF most often results from left HF

Isolated right HF is usually due to cor pulmonale

40
Q

List the vasculitides:

  1. Large vessel vasculitis
  2. Medium vessel vasculitis
  3. Small vessel vasculitis
A
  1. Large vessel vasculitis
    • Temporal arteritis
    • Takayasu arteritis
  2. Medium vessel vasculitis
    • Polyarteritis nodosa
    • Kawasaki disease
    • Buerger disease (thromboangitis obliterans)
  3. Small vessel vasculitis
    • Granulomatosis w/ polyangitis (Wegener)
    • Microscopic polyangitis
    • Eosinophilic granulomatosis w/ polyangitis (Churg-Strauss)
    • Henoch-Schönlein purpura
41
Q

Temporal (giant cell) arteritis

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:
A
  • Epidemiology:
    • elderly females
  • Presentation:
    • unilateral headache, jaw claudication,
    • may lead to opthalmic artery occlusion → blindness
    • associated with polymyalgia rheumatica
  • Pathology:
    • affects branches of carotid artery
    • focal granulomatous inflammation
    • ↑ ESR
  • Treatment:
    • high dose steroids prior to temporal artery biopsy to prevent blindness
42
Q

Takayasu disease

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:
A
  • Epidemiology:
    • asian females < 40 yrs old
  • Presentation:
    • “Pulseless disease” (weak UE pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
  • Pathology:
    • Granulomatous thickening and narrowing of aortic arch and proximal great vessels
    • ↑ ESR
  • Treatment:
    • corticosteroids
43
Q

*Polyarteritis nodosa

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:
A
  • Epidemiology:
    • young adults
    • Hepatitis B (+) in 30% of patients
  • Presentation:
    • fever, weight loss, malaise, headache
    • GI: abdominal pain, melena
    • HTN, neurologic dysfunction, cutaneous eruptions, renal damage
  • Pathology: Type III Hypersensitivity
    • renal and visceral vessels not pulmonary vessels
    • immune complex mediated
    • transmural inflammation of arterial wall w/fibrinoid necrosis
    • innumerable renal microaneurysms and spasm on arteriogram
  • Treatment:
    • corticosteroids, cyclophosphamide
44
Q

Kawasaki disease

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:
A
  • Epidemiology:
    • Asian children < 4 yrs old
  • Presentation: CRASH and burn
    • Conjuctival injection, Rash (polymorphous → desquamating), Adenopathy (cervical), Strawberry tongue (oral mucositis), Hand/foot changes (edema, erythema), fever
  • Pathology:
    • may develop coronary artery aneurysms
  • Treatment:
    • IV Ig and aspirin
45
Q

Beurger disease (thromboangitis obliterans)

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:
A
  • Epidemiology:
    • heavy smokers, males < 40 yrs old
  • Presentation:
    • intermittent claudication → gangrene, autoamputation of digits, superficial nodular phlebitis
    • Raynuad phenomenon often present
  • Pathology:
    • segmental thrombosing vasculitis
  • Treatment:
    • smoking cessation

USMLE Step 1: Things I Cannot Remember (16 decks)

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