Cardiovascular Flashcards Preview

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

Flashcards in Cardiovascular Deck (45):
1

What is used to treat primary (essential) hypertension?

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

2

What is used to treat hypertension w/ heart failure?

  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

3

What is used to treat hypertension w/ diabetes mellitus?

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

4

What is used to treat hypertension in pregnancy?

  1. Hydralazine
  2. Labetalol
  3. Methyldopa
  4. Nifedipine

5

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

Nifedipine - prevents cerebral vasospasm

6

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

Clevidipine

7

Which nitrate has the highest oral bioavailability?

isosorbide mononitrate

8

What HTN drug can cause cyanide toxicity?

Nitroprusside

9

Which anti-arrythmic drugs can lead to heart failure?

Negative inotropes:

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

10

What increases stroke volume?

SV CAP

  • Increase contractility, prelodad
  • Decrease afterload

11

How do calculate MAP?

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

12

What is the physiology of normal splitting?

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

13

Causes of:

  1. Wide splitting
  2. Fixed splitting
  3. Paradoxical splitting

  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)

14

Bedside maneuvers: 

Inspiration

↑ intensity of right heart sounds

15

Bedside maneuvers: 

Hand grip

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

16

Bedside maneuvers:

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

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

17

Bedside maneuver:

Rapid squatting (↑ venous return, ↑ preload)

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

18

Speed of conduction ⇒ 

Purkinje fibers > atria > ventricles > Av node

19

Pacemaker activity ⇒ 

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

20

List the Right -to -Left Shunts:

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

21

List the Left-to-Right shunts:

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

22

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

  • 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

Brugada syndrome

  • Inheritance:
  • Epidemiology:
  • EKG findings:
  • Risks:
  • Treatment:

  • 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

What are the causes of drug-induced prolonged QT?

(hint: Anti-"ABCDE")

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

25

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

Wolf-Parkinson-White syndrome

26

What is the lab indicator for heart failure?

BNP

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

27

How do organs react to hypoxia?

  • hypoxia in pulmonary vasculature ⇒ vasoconstriction
    • so only well-ventilated areas are perfused
  • hypoxia in other organs ⇒ vasodilation

28

  • Aortic arch ⇒
  • Carotid sinus ⇒
  • Baroreceptors ⇒
  • Chemoreceptors ⇒

  • 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

  • What is Cushing reaction?
  • What contributes to this reaction?

  • 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

In mitral stenosis, what happens to the PCWP?

PCWP > LV diastolic pressure

31

Causes of edema:

  1. capillary pressure
  2. plasma proteins
  3. capillary permeability
  4. interstitial fluid colloid osmotic pressure

  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

What are the signs of hyperlipidemia?

  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

Define arteriosclerosis:

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

Two types:

  1. Arteriolosclerosis
  2. Monckeberg (medial calcific stenosis)

34

Arteriolosclerosis vs. Monckeberg (medial calcific sclerosis)

  1. Arteriolosclerosis
    • Common
    • affects small arteries and arterioles
    • Two types:
      • hyalinethickening 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

Define atherosclerosis:

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

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

36

Evolution of MI

  • Commonly occluded arteries:
  • Symptoms:
  • 0 - 4 hours
  • 4 - 24 hours
  • 1 - 3 days
  • 3 - 14 days
  • 2 weeks - several months

 

  • 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

Causes of dilated cardiomyopathy:

(hint: ABCCCD)

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

38

Findings in HF:

  • Systolic dysfunction:
  • Diastolic dysfunction:

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

Right HF most often results from ....

Isolated right HF is usually due to ....

Right HF most often results from left HF

Isolated right HF is usually due to cor pulmonale

40

List the vasculitides:

  1. Large vessel vasculitis
  2. Medium vessel vasculitis
  3. Small vessel vasculitis

  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

Temporal (giant cell) arteritis

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:

  • Epidemiology:
    • elderly females
  • Presentation:
    • unilateral headache, jaw claudication,
    • may lead to opthalmic artery occlusionblindness
    • 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

Takayasu disease

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:

  • 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

*Polyarteritis nodosa

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:

  • 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

Kawasaki disease

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:

  • 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

Beurger disease (thromboangitis obliterans)

  • Epidemiology:
  • Presentation:
  • Pathology:
  • Treatment:

  • 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