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random step studying > cardio > Flashcards

cardio Flashcards

1
Q
  1. CO
  2. Fick principle
  3. MAP
  4. PP
  5. SV
  6. EF
A
  1. SV x HR
  2. CO = rate of O2 consumption/PaO2 - PvO2
  3. MAP = CO x TPR = 2/3 diastolic P + 1/3 systolic P
  4. PP= systolic - diastolic P (proportional to SV
    1. increase PP in hyperthyroidism, aortic regurg, arteriosclerosis, obstructive sleep apnea, exercise
  5. SV = EDV-ESV
    1. SV increases with increasing contractility + preload, pregnancy
    2. decreases with increasing afterload, acidosos/hypoxia/hypercapnia
  6. EF = SV/EDV (normal > 55%)
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2
Q

PV loops and cardiac cycle

  1. Isovolumetric contraction
  2. Sysolic ejection
  3. isovolumetric relaxation
  4. ventricular filling
A
  1. period between mitral valve closing and aortic valve opening (R wall of box)
  2. period between aortic valve opening and closing (roof of box)
  3. period between aortic valve closing and mitral valve opening (L wall of box)
  4. period between mitral valve opening and closing (floor of box)
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3
Q

PV loops

  1. increased contractility
  2. increased afterload
  3. increased preload
A
  1. increased SV, increased EF, decreased ESV (yellow)
  2. increased arotic pressure, decreased SV, increased ESV (blue)
  3. increased SV (pink)
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4
Q

Heart sounds

  1. S1
  2. S2
  3. S3
  4. S4
A
  1. mitral and tricuspid valves closing
  2. aortic and pulmonic valves closing
  3. rapid ventricular filling
    • associated with increased filling P – mitral regurg, CHF, dilated cardiomyopathy, normal in kids and pregnancy
    • after S2 (early diastole)
  4. high atrial P
    • associated with ventricular hypertrophy
    • before S1 (late diastole)
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5
Q

Jugular venous pulse

A
  • a wave = atrial contraction
  • c wave = RV contraction (closed tricuspid valve bulges into atrium)
  • x descent = atrial relaXation + downward displacement of closed tricuspid vavle during vent contraction
  • v wave = increased rate atrial pressure due to filling against closed tricuspid valve
  • y descent = blood flow from RA to RV

**remember this is all on the R side of the heart

“At Carter’s X-ing, Vehicles Yield”

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6
Q
  1. normal splitting
  2. wide splitting
A
  1. inspiration –> drop in intrathoracic P –> increased venous return to RV –> increased RV SV and ejection time –> delayed closure of pulmonic valve
  2. seen in condition that delay RV emptying (pulmonic stenosis, RBBB) –> an exaggeration of normal splitting
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7
Q
  1. fixed splitting
  2. paradoxical splitting
A
  1. seen in ASD (L–> R shunt –> increased RA and RV volumes -> very delayed flow through pulmonic valve
  2. seen in conditions that delay LV empyting (AS, LBBB) – normal order of valve closure is reversed so that P2 occurs before dealyed A2 –> therefore on inspiration P2 closes later and moves closer to A2 thereby paradoxically eliminating the split
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8
Q

bedside maneuvers

  1. inspiration
  2. hand grip
  3. valsalva
  4. rapid squatting
A
  1. increases intensity of R heart sounds (increases R atrial filling)
  2. increase intensity of L heart sounds (MR, AR,VSD) bc it increases systemic vascular resistance
  3. increase intensity of hypertrophic cardiomyopathy (decreases venous reture to R heart –> decreased preload and afterload)
  4. increased intensity of AS murmur and MVP (increased venous return, increased preload and increased afterload with prolonged squatting)
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9
Q

Heart murmurs

  1. MR and TR
  2. AS
  3. VSD
  4. MVP
A

all systolic murmurs (between S1 and S2)

  1. holosystolic, high-pitched “blowing murmur” -- mitral enhanced by hand grop and squatting (increase TPR); tricuspid enhances by inspiration (increased RA filling)
  2. Crescendo-decrescendo systolic ejection murmur – radiates to carotids; weak pulses –> syncope, angina, dyspnea on exertion
  3. holosystolic harsh-shounding murmur (newborns)
  4. midsystolic click (due to sudden tensing of chordae tendinae) –> higher risk of infective endocarditis
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10
Q

Heart murmurs

  1. AR
  2. MS
  3. PDA
A
  1. diastolic: early diastolic decrescendo murmur; wide pulse pressure, bounding pulses and head bobbing
  2. diastolic: opening snap (leaflets stuck together than snap open) –> late diastolic murmur
  3. continous (blood always flowing through PDA) machine-like murmur; loudest at S2
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11
Q

ventricular AP

A
  • phase 0: rapid upstroke and depolarization (VG Na channels open) = QRS complex
  • phase 1: initial repolarization (inactivation of Na channels and K channels begin to open)
  • phase 2: plateau – Ca influx balanced by K efflux (Ca influx triggers Ca release from SR + myocyte contraction)
  • phase 3: rapid repolarization (massive K+ efflux) – class III work here
  • phase 4: resting potential (high K permeability)
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12
Q

pacemaker AP

A
  • phase 0: upstroke – Ca influx
  • phase 3: K efflux
  • phase 4: slow diastolic depolarization – spontaneous depolarization due to funny current (Na influx)
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13
Q

torsades de pointes

A
  • polymorphic Vtach characterized by shifting sinusoidal waveforms
  • long QT interval predisposes
  • caused by drugs: Sotalol, Risperidone, Macrolides, Chloroquine, Protease inhibs, Quinidine, Thiazides (Some Risky Meds Can Prolong QT)
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14
Q

Wolff-Parkinson-White Syndrome

A
  • ventricular pre-excitating syndrome –> abnormal fast accessory pway (bundle of Kent) bypasses rate-slowing AV nodes
  • characteristic delta wave (slurring of QRS)
  • tx: procainamide or amiodarone
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15
Q
  1. A fib
  2. A flutter
  3. V fib
A
  1. irregularly irregular w/ no discrete p waves –> atrial stasis and thromboembolic stroke
    1. can cardiovert new onset, but not older onset bc if clot formed it will be thrown (anticoag 1st)
  2. rapid succession of identical atrial depolarization waves (“sawtooth” appearance)
  3. completely erratic rhythm w/ no identifiable waves –> CPR and defibrilliation ASAP
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16
Q
  1. 1st degree AV block
  2. 2nd degree: Mobitz 1 and 2
  3. 3rd degree
A
  1. prolonged PR (>200 ms) – benign and asymptomatic
  2. type I: progressive lengthening of PR unitl a beat is dropped; type II: dropped beats that aren’t preceded by warning
    • no QRS following p wave
  3. A and V beat independently of each other –> atrial faster (p wave) than ventricular rate (QRS complex)
    • can see in Lyme disease
17
Q

early cyanosis (“blue babies”)

A
  1. Truncus arteriosus
  2. Transposition of the great vessels
  3. Tricuspid atresia
  4. Tetralogy of Fallot
  5. Total anomalous pulmonary venous return

*5 T’s

18
Q

Morphology of MI

A
  • 4-12 hrs: early coagulative necrosis (dark mottling) –> risk of arrhythmia, cardiogenic shock –> release of cardiac enzymes
  • end of day 1: PMNS migration, contraction bands (reperfusion injury) –> risk of arrhythmia and cardiogenic shock
  • 1st 1/2 of week 1: extensive coag necrosis, more PMNs –> risk of fibrinous pericarditis (friction rub)
  • 2nd 1/2 of week 1 to week 2: macrophages then granulation tissue (collagen III) –> yellow-brown softening –> risk of rupture (free LV wall, papillary muscles –> severe mitral regurg, interventricular septum–> VSD)
  • 2 weeks to months: contracted scar complete (gray color– collagen I) –> risk of Dressler syndrome, ventricular aneurysm
19
Q

Infarct location and corresponding leads with Q waves

  1. Anterior Wall
  2. Anteroseptal
  3. Anterolateral
  4. Lateral wall
  5. Inferior wall
A
  • V1-V4 (LAD)
  • V1-V2 (LAD)
  • V4-V6 (LAD)
  • I, aVL (lateral circumflex)
  • II, III, avF (for inFerior) – RCA

tx: MONA – morphine, O2 , nitrates, aspirin

20
Q

antihypertensives

  1. 1st dose orthostatic hypotension
  2. ototoxic (esp with aminoglycosides)
  3. Cyanide toxicity
  4. dry mouth, sedation, severe rebound HTN
  5. reflex tachy
  6. avoid in PTs with sulfa allx
  7. angioedema
  8. drug-induced lupus
  9. hypercalcemia, hypokalemia
  10. hyperkalemia
A
  1. alpha blockers (prazosin)
  2. loops
  3. nitroprusside
  4. clonidine
  5. nitrates, hydralazine, dihydropyridines (any vasodilators)
  6. loops and thiazides
  7. ACEI and ARBs
  8. hydralazine
  9. thiazides
  10. ACEI/ARB
21
Q

CCBs

A
  • dihydros = amlodipine, nifedipine (“dipine”)
    • vascular smooth muscle
    • use: HTN, angina, Raynaud
    • toxicity: peripheral edema, flushing
  • non-dihydros= verapamil, diltiazem
    • heart mm
    • use: HTN, angina, Afib/flutter
    • toxicity: AV block, constipation
22
Q
  1. hydralazine
  2. Nitroglycerin, dinitrate, isosorbide
A
  1. increase cGMP –> smooth mm relaxation (vasodilates arterioles –> reduces afterload)
    • use: 1st line tx for HTN in pregnancy, severe HTN
    • toxicity: compensatory tachy, Lupus
  2. vasodilation: NO –> cGMP –> smooth mm relaxation (vasodilated veins–> reduces preload)
    • ​use: angina, acute coronary syndrome (best if given with BB to further decrease MVO2)
    • toxicity: reflex tachy, flushing, headache
23
Q
  1. statins
  2. Niacin
  3. bile acid resins
  4. ezetimibe
  5. fibrates
A
  1. best at decreasing LDL – hepatotoxicity and rhabdomyolysis
  2. best at increasing HDL – red, flushed face and hyperuricemia (precipates gout attacks)
  3. prevent intest reabsorption bile acids–> liver must use cholesterol to make more — GI discomfort, decreased absorption of fat-soluble vitamins
    • cholestyramine (can also bind C. diff toxin), colestipol, colesevelam
  4. blocks absorption of cholesterol at SI brush border
  5. best at decreasing TG (hi TG can lead to acute pancreatitis) – myositis (esp with statins), hepatotoxicity
    • clofibrate, gemfibrozil, fenofibrate
24
Q

cardiac glycosides

A
  1. inhibit Na/K ATPase –> inhibition of Na/Ca antiporter –> increase intracell Ca –> + inotropy and stimulation of vagus nerve –> decrease HR
  2. uses: CHF (increase contractility), Afib (decrease conduction through AV node and SA node depression
  3. toxicity: cholinergic – NVD, blurry yellow vision, AV block, hyperkalemia (inhibit Na/K ATPase)
    • factors predisposing to toxicityL renal failure, hypokalemia, verapamil, amiodarone and quinidine (decrease dig clearance
    • dirty drug with low TI = toxicity very test-able
25
Q
  1. mortality benefit in CHF
  2. acute HF
A
  1. ACEI/ARBs, Spironolactone, Metropolol/Carvedilol
  • spironolactone inhibits the negative cardiac remodeling effect on aldo on the heart​
  • symptomatic relief: diuretics, nitrates, digoxin
  1. LMNOP: loops, morphine, nitrates, O2, Pressors and positioning
26
Q
  1. Class I antiarrhythmics
  2. Class II
A
  1. Na channel blockers \
    • 1A = Disopyramide, Quinidine (cinchonism), Procainamide (Lupus-use in WPW) – increase QT
    • 1B = Lidocaine and Mexiletine – preferentially ischemic tissue; 1B is Best post-MI — shorten QT
    • 1C = Flecainide, Propafenone – 1C is Contraindicated in structural + ischemic heart disease – no effect on QT
  2. Beta-blockers
    1. decrease SA and AV nodal activity, decrease slope of phase 4 in nodal tissue
27
Q
  1. Class III antiarrhythmics
  2. Class IV
A
  1. K+ channel blockers – work at phase III (increase AP duration
    • Amiodarone (pulmonary fibrosis, hypo/hyperthyroidism, hepatoxicity, photodermatitis), Sotalol (Torsades), Ibutilide (Torsades), Dofetilide
    • need to check PFTs, LFTs and TFTs when using Amiodarone
  2. Ca channel blockers (non-dihydros) – Verapamil, diltiazem
    1. work at phase 0 on nodal cells
    2. toxicity: constipation, flushing, edema
28
Q
  1. Adenosine
  2. Mg2+
A
  1. increase K+ efflux –> hyperpolarize cells –> flat-lines people for 10-15 s
    • DOC in abolishing SVT
    • flushing, hypotension, chest pain
  2. effective in Torsades and dig toxicity

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