cardio Flashcards
1
Q
- CO
- Fick principle
- MAP
- PP
- SV
- EF
A
- SV x HR
- CO = rate of O2 consumption/PaO2 - PvO2
- MAP = CO x TPR = 2/3 diastolic P + 1/3 systolic P
- PP= systolic - diastolic P (proportional to SV
- increase PP in hyperthyroidism, aortic regurg, arteriosclerosis, obstructive sleep apnea, exercise
- SV = EDV-ESV
- SV increases with increasing contractility + preload, pregnancy
- decreases with increasing afterload, acidosos/hypoxia/hypercapnia
- EF = SV/EDV (normal > 55%)
2
Q
PV loops and cardiac cycle
- Isovolumetric contraction
- Sysolic ejection
- isovolumetric relaxation
- ventricular filling
A
- period between mitral valve closing and aortic valve opening (R wall of box)
- period between aortic valve opening and closing (roof of box)
- period between aortic valve closing and mitral valve opening (L wall of box)
- period between mitral valve opening and closing (floor of box)
3
Q
PV loops
- increased contractility
- increased afterload
- increased preload
A
- increased SV, increased EF, decreased ESV (yellow)
- increased arotic pressure, decreased SV, increased ESV (blue)
- increased SV (pink)
4
Q
Heart sounds
- S1
- S2
- S3
- S4
A
- mitral and tricuspid valves closing
- aortic and pulmonic valves closing
- rapid ventricular filling
- associated with increased filling P – mitral regurg, CHF, dilated cardiomyopathy, normal in kids and pregnancy
- after S2 (early diastole)
- high atrial P
- associated with ventricular hypertrophy
- before S1 (late diastole)
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”
6
Q
- normal splitting
- wide splitting
A
- inspiration –> drop in intrathoracic P –> increased venous return to RV –> increased RV SV and ejection time –> delayed closure of pulmonic valve
- seen in condition that delay RV emptying (pulmonic stenosis, RBBB) –> an exaggeration of normal splitting
7
Q
- fixed splitting
- paradoxical splitting
A
- seen in ASD (L–> R shunt –> increased RA and RV volumes -> very delayed flow through pulmonic valve
- 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
8
Q
bedside maneuvers
- inspiration
- hand grip
- valsalva
- rapid squatting
A
- increases intensity of R heart sounds (increases R atrial filling)
- increase intensity of L heart sounds (MR, AR,VSD) bc it increases systemic vascular resistance
- increase intensity of hypertrophic cardiomyopathy (decreases venous reture to R heart –> decreased preload and afterload)
- increased intensity of AS murmur and MVP (increased venous return, increased preload and increased afterload with prolonged squatting)
9
Q
Heart murmurs
- MR and TR
- AS
- VSD
- MVP
A
all systolic murmurs (between S1 and S2)
- holosystolic, high-pitched “blowing murmur” -- mitral enhanced by hand grop and squatting (increase TPR); tricuspid enhances by inspiration (increased RA filling)
- Crescendo-decrescendo systolic ejection murmur – radiates to carotids; weak pulses –> syncope, angina, dyspnea on exertion
- holosystolic harsh-shounding murmur (newborns)
- midsystolic click (due to sudden tensing of chordae tendinae) –> higher risk of infective endocarditis
10
Q
Heart murmurs
- AR
- MS
- PDA
A
- diastolic: early diastolic decrescendo murmur; wide pulse pressure, bounding pulses and head bobbing
- diastolic: opening snap (leaflets stuck together than snap open) –> late diastolic murmur
- continous (blood always flowing through PDA) machine-like murmur; loudest at S2
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)
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)
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)
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
15
Q
- A fib
- A flutter
- V fib
A
-
irregularly irregular w/ no discrete p waves –> atrial stasis and thromboembolic stroke
- can cardiovert new onset, but not older onset bc if clot formed it will be thrown (anticoag 1st)
- rapid succession of identical atrial depolarization waves (“sawtooth” appearance)
- completely erratic rhythm w/ no identifiable waves –> CPR and defibrilliation ASAP
16
Q
- 1st degree AV block
- 2nd degree: Mobitz 1 and 2
- 3rd degree
A
- prolonged PR (>200 ms) – benign and asymptomatic
- 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
- 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
- Truncus arteriosus
- Transposition of the great vessels
- Tricuspid atresia
- Tetralogy of Fallot
- 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
- Anterior Wall
- Anteroseptal
- Anterolateral
- Lateral wall
- 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
- 1st dose orthostatic hypotension
- ototoxic (esp with aminoglycosides)
- Cyanide toxicity
- dry mouth, sedation, severe rebound HTN
- reflex tachy
- avoid in PTs with sulfa allx
- angioedema
- drug-induced lupus
- hypercalcemia, hypokalemia
- hyperkalemia
A
- alpha blockers (prazosin)
- loops
- nitroprusside
- clonidine
- nitrates, hydralazine, dihydropyridines (any vasodilators)
- loops and thiazides
- ACEI and ARBs
- hydralazine
- thiazides
- 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
- hydralazine
- Nitroglycerin, dinitrate, isosorbide
A
- increase cGMP –> smooth mm relaxation (vasodilates arterioles –> reduces afterload)
- use: 1st line tx for HTN in pregnancy, severe HTN
- toxicity: compensatory tachy, Lupus
- 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
- statins
- Niacin
- bile acid resins
- ezetimibe
- fibrates
A
- best at decreasing LDL – hepatotoxicity and rhabdomyolysis
- best at increasing HDL – red, flushed face and hyperuricemia (precipates gout attacks)
- 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
- blocks absorption of cholesterol at SI brush border
- best at decreasing TG (hi TG can lead to acute pancreatitis) – myositis (esp with statins), hepatotoxicity
- clofibrate, gemfibrozil, fenofibrate
24
Q
cardiac glycosides
A
- inhibit Na/K ATPase –> inhibition of Na/Ca antiporter –> increase intracell Ca –> + inotropy and stimulation of vagus nerve –> decrease HR
- uses: CHF (increase contractility), Afib (decrease conduction through AV node and SA node depression
- 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
- mortality benefit in CHF
- acute HF
A
- ACEI/ARBs, Spironolactone, Metropolol/Carvedilol
- spironolactone inhibits the negative cardiac remodeling effect on aldo on the heart
- symptomatic relief: diuretics, nitrates, digoxin
- LMNOP: loops, morphine, nitrates, O2, Pressors and positioning
26
Q
- Class I antiarrhythmics
- Class II
A
- 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
- Beta-blockers
- decrease SA and AV nodal activity, decrease slope of phase 4 in nodal tissue
27
Q
- Class III antiarrhythmics
- Class IV
A
- 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
- Ca channel blockers (non-dihydros) – Verapamil, diltiazem
- work at phase 0 on nodal cells
- toxicity: constipation, flushing, edema
28
Q
- Adenosine
- Mg2+
A
- increase K+ efflux –> hyperpolarize cells –> flat-lines people for 10-15 s
- DOC in abolishing SVT
- flushing, hypotension, chest pain
- effective in Torsades and dig toxicity