jdlevenson's version from 2015-06-21 02:59


Question Answer
Absent P waves, irregularly irregular R-R intervals and narrow QRSAFIB, most common cardiac arrhythmia. Also may see fibrillatory waves.
How does AFIB beget AFIB AFIB-> electrical remodeling of atria with development of multiple ectopic foci and re-entrant impulses within the atria, increasing the risk and chronicity of subsequent episodes.
How does AFIB affect ventriclesAV nodes have refractory period. Ventricles depend on impulses going through AV node. Majority of atrial impulses never reach ventricles in AFIB due to AV node refractoriness. Atrial excitation is chaotic, hence ventricular rate is also irregular. Remember during AF, constant state of chaotic, continuous depolarization that is independent of sinoatrial node activity.
What limits ventricular contraction rate during AFIB, ventricles or AV node?AV node. Ventricles can actually reach 300/minute during VTach.
When can purkinje fibers assume their own pacemaker activityIn severe bradycardia.
Fastest conduction velocity among cardiac tissuesPurkinje. Park At Venture Avenue. Purkinje speed is essential to ensure that contraction of ventricles procedes in bottom up fashion, towards aorta and pulmonary arteries.
Why is AV node slowest conduction velocity To allow ventricles to fill during diastole.
WPW leads to slower or faster paceFaster from the accessory pathway that bypasses the AV node and directly connects atria and ventricles
WPW triad on EKGDelta wave, widened QRS and shortened PR interval. Presents as SVT in an otherwise healthy individual.


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QRS responds to ventricular depolarization; ventricular depolarization is mediated by inward sodium movement and modulated by...Class I**.
Antiarrythmics can affect phase 4 of ventricular cells or of pacemaking cellsPACEMAKING
Which Class I drugs do not prolong QT interval?Class IC agents.
VTach/ other forms of polymorphic vtach vs Torsade de PointesTorsades always has underlying prolongation of QT.
Drugs that can lead to torsade de pointesAntiarrythmics (quinidine Ia, procainamide Ib, sotalol III and disopyramide and ibutilidide III, dofetilide III), phenothiazines and TCAs.
A. Fib and A. Flutter drugDigoxin, since it can slow conduction through AV node (Class V antiarrythmic)
Beta blockers have what effect on PRPROLONG. Reduces sinus rate, slows conduction through AV and slow rate of depolarization in general. No effect on ventricular myocyte AP; primary site is AV node and cells with automaticity. So, effect on slowing AV node and prolong phase 4 in cardiac pacemaker
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Sudden onset of palpitationsPSVT.
PSVT therapyCarotid sinus massage (prolongs AV refractory period; carotid sinus is bulge at internal carotid/ bifurcation of common carotid and is innervated by CN9), Valsalva and Adenosine
Carotid sinus, increases or decreases baroreceptor firing in response to increased pressureINCREASES -> increases PS on heart and vessels and prolongs AV node refractory period
Carotid sinus massage functionallyIncreases baroreceptor firing.
Carotid sinus location, and nerves: Dilatation of internal carotid located just above the common carotid artery. Afferent fibers from stretch receptors to a small carotid sinus nerve, Hering’s nerve, which is a branch of GLOSSOPHARYNGEAL, CN9 and go to solitary nucleus in the medulla
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Aortic arch baroreceptors locationRun with Vagus nerve and go to solitary nucleus in the medulla
Baroreceptors increase firing when there isAn increase in stretch/ arterial wall stretch/ increase in BP and they stimulate decrease CO and peripheral vasodilation
Carotid sinus syncopePeople with super sensitive carotid sinuses who may inadvertenly put external pressure on the carotid sinuses so that they baroreceptors react as if there was a systemic blood pressure increase. -> Bradycardia, hypotension and sometime ssyncope.
Refractory period of AV node or myocardium can be prolonged?Only AV node.
Recall Parasympathetic mostly slows heart by slowing conduction through AV node
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Class III drugs act on what channelK channels! Prolong potassium efflux to repolarize. They do not affect sodium or calcium channels.
Examples of Class III beyond amiodarone-tilide (2) and sotalol.
Class III drugs have what effect on QT?Prolong.
Quinidine – blocks sodium channels, phase 0 depolarization, and has some activity on phase 3 repolarization
Lidocaine – blocks in only very rapidly depolarizing cells; no effect on K; favors ischemic/depolarized or rapidly depolarizing ventricular or purkinje tissue
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Ischemia tissue is in what voltage stageDepolarized. Ib preferentially block depolarized tissue so that’s why Ib good for ischemic tissues and hence AGENT OF CHOICE FOR post-myocadrdial arrhythmias.
Management of ventricular arrhythmiasAmiodarone
Lidocaine used forVentricular, not atrial arrhythmias (though Amiodarone is number one)
Flecainide – Icprimarily sodium channels in phase 0; most USE-DEPENDENT i.e. bind avidly to the FAST Na channels responsible for Phase O depolarization blocking the inward sodium current and prolonging QRS; slowest class I to dissociate from sodium channel; effects then intensify when HR increases and there is less time between APs for medication to dissociate from the receptor. They have most DRASTIC slowing on phase 0 of depolarization of ventricular myocyte.
Use dependence? Reverse use dependence?Class Ic – use dependence; more effect when higher rate; Class III – reverse use dependence; slower the HR, the more QTc interval is prolonged
Verapamil – blocks calcium channels in av node and pacemaker cells; slows conduction through AV node and decreases contractility; most selective for rapidly depolarizing cells; do not have appreciable effect on myocyte AP
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Esmololslow phase 4 depolarization in cells with automaticity and slows conduction through av node
Digoxin and adenosine
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slow conduction through AV node
AdenosineSlows conduction through AV node and decreases automaticity by hyperpolarizing** the cells
DigoxinIncreases vagal output to the AV node and conduction system, slowing conduction in these tissues. Does not alter AP of ventricular myocyte but it does alter intracellular calcium in ventricular myocytes by blocking Na/K ATPase leading to increased intracellular calcium concentration and thus increased cardiac contractility.
Digoxin results inHyperkalemia so hypokalemia would worsen digoxin toxicity
Class I and IV raise or lower action potential thresholdRaise.
How does verapamil increase refractory periodReduces calcium influx and slows recovery of inactivated Ca channels
Verapamil can raise the threshold potential for calcium, increase refractory period and...?Decrease the amount of Calcium available for excitation-contraction coupling within cardiomyocytes, reducing myocardial contractility.
A. Fib with rapid ventricular response (AF with RVR)?CCB first and then Digoxin; both slow through AV node.
Digoxin vs Verapamil mechanismBoth slow conduction through AV node but Digoxin increases contractility whereas Verapamil decreases contractility and hence is contraindicated in patients with heart failure. Verapamil among first lines for A Fib.
Verapamil a/eFirst, second, third degree AV blocks + bradyardia (though only in 1-2% of patients) and constipation (10%) and gingival hyperplasia
Amlodipine and other dihydropyridine CCB should be not used in ACS because drops BP and then can cause reflex tachycardia, increasing oxygen consumption of myocardium
Digoxin toxicity, how does it lead to v tach and deathDelayed afterdepolarization after complete repolarization of the cardiac myocyte in states of hyperexcitability such as very high Ca that Digoxin causes or in high catecholamine states
By blocking NaK ATPase, Digoxin allows increase in intracellular Ca; how does that increase contractilityMaximal crosslinking of actin and myosin and greater contractility
Procainamide, good for suppressing arrhythmias in normal foci or abnormal foci ?Suppressing normal foci, i.e. centers of normal automaticity
Ia and III are known to prolong APD and so prolong QT interval and increase risk of Torsade de Pointes. Which drug has smallest risk of increasing risk of Torsade?Amiodarone. Thought to be because it has more homogenous effect on ventricles compared to other drugs.
Treatment of TorsadeMg Sulfate.
Congenital long QT syndromes


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Statin a/eHepatotoxicity, myalgias (not associated with increased CK) and myopathy (increased CK, especially with higher doses; defined as muscle pain with CK over 10 times normal amount)
Statins are metabolized by ...CYP450. So watch out for inhibitors like macrolides (though azithromycin weirdly does not pose a problem)
Increased risk of increased CK when statins + ...Fibrates and or niacin
Myopathy is caused bySee page 259.
Atypical depression or treatment-resistant depressionMAO-I.
Selective coronary vessel vasodilatorsAdenosine and dipyridamole, can lead to coronary steal when ischemia exists; often used to simulate coronary vasodilation that occurs during exercise.
ARBs are useful forHTN and diabetic nephropathy
ACE-I lead to accumulation of bradykin andSubstance P and prostaglandins hence cough.
ACE-I can cause angioedema viaBradyinin breakdown inhibition; bradykinin can constrict veins and dilate arterioles.
Absolute contraindications to OCPPrior history of thromboembolic event or stroke; history of estrogen dependent tumor; women over 35 who smoke a lot; hypertriglyc; decompensated or active liver disease; pregnancy.
ANP and NO both increase cGMP via GC but are different in thatReceptor/ GC exists in transmembrane protein form (for ANP) and in a free cytosolic form (for NO, which can cross)
SildenafilPDE inhibitor; prevents breakdown of cGMP
PDE 3 for cAMP and PDE 5 for cGMP?
Other cell messengers: IF, PDGF – TYRK; IL-2 – autocrine; Vit D corsses cell membrane and binds to cytospolic receptors
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Platelet aggregation activated by thrombin, ADP, TXA2; however decreased byIncreased intracellular cAMP. Prevents shape change and granule release. Dipyridamole and cilostazol decrease PLT PDE.
Cilostzol effectsPLT PDE inhibitor (and so increase PLT cAMP) and also directly vasodilate arteries ;similar to aspirin in anti-PLT and vasodilates but it has shown to be stronger.
Abciximab, the monoclonal AB that inhibits PLT aggregation by targeting the PLT II/IIIa receptor, is used forProphylaxis before percutaneous coronary intervention
Intermittent claudication/ PAD?Cilostazol.
Heparin induced thrombocytopenia, treatment?Agratroban/ thrombin inhibitors.
Synthetic prostacyclin used forPulm HTN, peripheral vascular disease, and Raynaud syndrome.
Labetalol blocks alpha and beta receptors, decreasing SVR, cardiac contractility, HR, AV nodal conduction and is used forHypertensive emergency, refractory HTN, and in patients with pheochromocytoma
Short term management of severe hypertension and used in all hypertensive emergencies and particularly good for those with renal insufficiencyFenoldopam, selective D1 agonist without effect on alpha or beta receptors; activates AC and raises cAMP; vasodilation of most arterial beds, especially renal, mesenteric* and coronary. REDUCES SVR. In kidneys, improves blood flow and leads to increased sodium and water excretion/ natriuresis.
Only IV agent that improves renal perfusionFenoldopam
Drugs like beta blockers that slow AV node conduction () the PR intervalProlong. Do not affect QRS or QT interval.
Nitrates often given with () to reduce reflex tachy/ increased cardiac demandMetoprolol, Beta 1 selective.
N-AcetylcysteineAntidote to Tylenol poisoning as well as renal protective prior to administering IV iodine contrast for radiologic studies
Clopidogrel and Aspirin, which is more efficacious in preventing thromboembolic disease? Synergistic, antagonistic or redundant?Equal; synergistic.
Clopidogrel mechanismIrreversibly blocks PLT surface ADP receptors essential for PLT activation, aggregation and fibrin binding
What drug has been shown to improve mortality and morbidity in ACS patients but is not an antiplatelet agent and also must be given IVHeparin
DOC for DVT, atrial fibrillation and pulmonary thromboembolismWarfarin
Warfarin in patients deficient of protein CSkin necrosis.
Vasoconstriction does not equalIncreased perfusion.
Nitroglycerin SL; rapid onset; if swallowed, first pass metabolism in liver
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Sodium nitroprussideused only for hypertensive emergency; can cause CN tox; only available as IV*
Isosorbide dinitrate vs mononitrateDinitrate – parent compound pre-extensive first pass metabolism by glucuronidation in liver; mononitrate – activate metabolite
Constrictive pericarditis
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Amyl Nitrate inhalation causesVasodilatation, decreased BP, transient decrease in venous return and thus preload
Procainamide is metabolized via hepatic acetylation; how many get SLE (slow acetylators)20% of patients; recall anti-histone ABBs are very common in DISLE vs only 50% in other SLE patients
Lidocaine a/eNonfocal neurological signs that can be as bad as generalized seizures but usllay tremor, drowsiness,...
Permissiveness in pharm meansOne hormone allows another to exert its maximal effect; cortisol has a permissive effect on many hormones to help improve the response to a variety of stressors (cortisol increases reactivity to catecholamines for example as well as A2). Cortisol does this via upregulation of alpha 1 receptors on vascular smooth muscle cells.
Adrenal insufficiency can lead to hypotension becauseLow cortisol levels lead to less responsiveness to A2 and NE