Week 4 (Acute Coronary Syndrome and Arrhythmias) Flashcards

Question

How does arteriosclerotic vascular disease cause death?

Answer 1

**Sudden death** **MI** **Stroke** **Renal failure** **Peripheral vascular disease** Note: interventions to decrease modifiable risk factors can ameliorate many manifestations of vascular diseases

Answer 2

**Arteriolosclerosis** refers to **arterioles**; can be **hyperplastic** type (onion skinning) or **hyaline** type (most impt in kidneys) **Atherosclerosis** refers to **elastic** and **large arteries**; basic lesion is the **atheroma**

Answer 3

**Vulnerable** plaque: **large** lipid core, **thin** fibrous cap, **inflammation** **Stable** plaque: **small** lipid core, **thick** fibrous cap, **not** much inflammation

Answer 4

**Unstable angina**: no ST elevation; thrombus occluding vessel **partially** **NSTEMI**: non ST elevation myocardial infarction; thrombus occluding vessel **partially** or completely (rare); either NQMI or Qw MI **STEMI**: ST elevation myocardial infarction; thrombus occluding vessel partially (rare) or **completely**; either NQMI or Qw MI

Answer 5

**Pharmacologic**: **widely available, quickly administered**, less effective, bleeding risk Percutaneous coronary intervention (**PCI**): limited availability, treatment delay, **more effective, lower bleeding risk**

Answer 6

**Coronary thrombosis**

Answer 7

**Fibrinolytic** therapy (lytics, or inappropriately thrombolytics): **streptokinase**, **alteplase** (recombinant tPA), **tenecteplase** (TNK-tPA); for **STEMI** only, never NSTEMI! **Antithrombin** therapy: unfractionated heparin (**UFH**), low molevular weight heparin (enoxaparin - **Lovenox**), heparin pentasaccharide analogue (**fondaparinox** - Arixtra) **Antiplatelet** therapy: aspirin (**ASA**), **clopidigrel** (**Plavix**) or Prasugrel, **G2b3a** **inhibitors** (**Abciximab**, eptifibatide)

Answer 8

Lytic agents differ by dosing and kinetics **Tenecteplase** (TNK-tPA) is a genetically engineered, multiple point mutant of **tPA** with **longer plasma half-life** allowing for a single **IV bolus** injection; also 14x more **fibrin** **specific** and 80x higher **resistance** to **inhibition** by **plasminogen activator inhibitor 1** Indications for fibrinolytics: STEMI within 12-24 hours if PCI not possible within 120 min of medical contact), severe PE, clotted catheters (low doses) Catalyze formation of serine protease **plasmin** from plasminogen Major complication = **bleeding** Contraindications: recent major surgery, **stroke**, bleeding (GI), aneurysm, **pericarditis**, CNS tumor

Answer 9

1) Thrombus might **fall apart** and **microembolize** 2) Lytics only affect fibrin-rich part of thrombus, leaving **platelet-rich part untouched** 3) Fibrinolysis generates raised concentrations of **free thrombin** and activates platelet aggregation (opposite of what you're tyring to do!)

Answer 10

Most **commonly** **used** First **IV bolus** then **IV** **infusion** **Increases PTT 1.5-2x** control (50-70 sec); adjust drip to this--need to balance between thrombosis and bleeding so must **monitor PTT** Use for **48 hours** during ACS, give **with fibrinolytic** therapy in setting of STEMI Use **protamine** to reverse the effect of heparin; but protamine difficult to use, people don't know how to...can create its own bleeding problems Effective across ACS spectrum, during PCI/CABG

Answer 11

Easier to use but more contraindications Excellent bioavailability (IV and SC) Stable anticoagulant effect (**don't need to monitor**!) Use **48 hours** to duration of hospitalization **Decrease** the dose in **renal** **failure** **Cannot reverse** LMWH Useful for all ACS; more effective than UFH in PCI but reversal a problem; not used in CABG Increases risk of **bleeding** in patients **over 70** receiving **fibrinolytics** (use UFH instead)

Answer 12

Excellent bioavailability; SC injection Stable anticoagulant effect, **no A/C monitoring** Use **48 hours** to duration of hospitalization **Contraindicated** in **renal** **failure** **No available reversal** agent Similar to LMWH for NSTEMI and UFH for STEMI Used in **PCI** but not in CABG **No platelet interaction** (won't cause HIT like UFH will)

Answer 13

Variety of molecules (**argatroban, hirudin, bivalirudin**) Anticoagulant effect, A/C **monitoring** needed **Decrease** dose in **hepatic** dysfunction (argatroban) and **renal** failure (hirudin and bivalirudin) **No reversal** agent, effect dissipated by clearance Generally equivalent to UFH for NSTEMI, possibly less bleeding risk in certain situations (with GP2b3a?) **Doesn't cause HIT**: effective alternative to UFH

Answer 14

**IV bolus**: UFH, LMWH **IV Infusion**: UFH, argatroban **SC injections**: LMWH, fundaparinox (UFH less common)

Answer 15

**Bleeding**! **UFH**: bleeding reduced by **monitoring** **PTT**; heparin-induced thrombocytopenia (**HIT**, due to **platelet aggregation** leading to paradoxical thromboembolism; test for Heparin Abs) **LMWH/fondaparinox**: monitoring of anti factor Xa units (currently not practical but will be soon!) **DTI**: monitor PTT

Answer 16

**Clopidogrel**, prasugrel, ticagrelor: block ADP receptor (P2Y12) **Aspirin** blocks COX so can't make TxA2, so now can't induce conformational change in platelet to make it sticky **G2b3a** **inhibitors**: IV abciximab, IV eptifibatide, IV tirofiban **G2b3a inhibition** targets **final common pathway** of platelet aggregation; but barely better than placebo... Complications: **bleeding**, inappropriate dosing in **renal** **insufficiency**, **platelet** **transfusions** necessary for bleeding complications

Answer 17

Percutaneous coronary intervention (**PCI**): preferred mode of reperfusion; balloon angioplasty with stenting, clot retrieval systems Coronary artery bypass graft surgery (**CABG**): complete revascularization, arterial conduits; rarely used acutely Neither PCI nor CABG treats underlying disease and patients still at risk for recurrent MI Patients must be treated with **same drug regimen** for PCI and CABG that they receive for fibrinolytic therapy

Answer 18

**Beta** **blockers**: use **within 24 hours** of presentation of ACS; reduce ischemia, reduce MVO2, reduce infarct size, reduce reperfusion injury, reduce rupture, reduce remodeling, reduce ischemic triggers, reduce SNS effects on cAMP (target muscle and arrhythmias) **ACEI/ARBs**: use **within 24 hours** of presentation of ACS; reduce rupture, prevent heart failure, reduce remodeling Fish oil: not used anymore! **Nitrate**: for dilating coronary arteries; non-significant reduction in mortality Calcium channel blockers: for dilating coronary arteries; some trials show increase in mortality Coronary care units: arrhythmia monitoring/detection, defibrillators

Answer 19

Antiplatelet therapy: **ASA** 81mg enteric coated/day; **clopidogrel** 75mg/day added to ASA or in place of ASA if ASA intolerant **Beta** **blocker**: metoprolol, atenolol, carvedilol if low EF and heart failure RAAS: **ACEI**, **ARB** if ACEI intolerant; **aldosterone antagonists** if low EF and on ACEI **Statin**: LDL \<\< 70mg/dL

Answer 20

Widespread failure of adequate tissue **perfusion** that leads to **cell** **injury** and **death** **Signs** of shock: **hypotension, tachycardia, abnormal mental status, decreased urine output**

Answer 21

Class I: no clinical signs of heart failure Class II: **crackles**, **S3** gallop and **elevated** **JVP** Class III: frank **pulmonary edema** Class IV: cardiogenic shock--**hypotension** (systolic \<90) and evidence of **peripheral** **vasoconstriction** (oliguria, cyanosis, sweating)

Answer 22

**Cardiogenic** shock due to **pump** **failure**: cardiac function impaired with **inadequate cardiac output**, elevated filling pressures and systemic vascular resistance **Cardiogenic** shock due to **extracardiac/obstructive**: cardiac output is impaired by **hemodynamic obstruction to outflow** **Hypovolemic** shock (GI bleed): **preload is inadequate** with low filling pressures **Neurogenic** shock (stroke): vascular tone is inadequate with **low SVR** and filling pressures **Septic** shock (sepsis): decreased vascular tone and contractility with **low SVR**

Answer 23

**Pump** **failure**: acute **MI**, end stage **heart failure,** post-cardiac arrest, acute fulminant **myocarditis** **Obstruction**: hypertrophic **cardiomyopathy** with severe outflow obstruction, severe **valvular obstruction** (critical aortic or mitral stenosis), pericardial **tamponade**, massive **PE**, **pneumothorax** **Valve** **failure**: aortic dissection with **aortic insufficiency** or tamponade, acute severe aortic or **mitral regurgitation** Refractory sustained **tachyarrhythmias** and **brady arrhythmias** **Toxic-metabolic**: beta blocker or CCB **overdose**, severe **acidosis**, severe **hypoxemia**

Answer 24

Of people who get to the hospital after acute MI (remember 50% of people die of arrhythmias before they get to hospital), **cardiogenic shock** is **leading** cause of **death** Only **50%** of people with cardiogenic shock will **survive to discharge** Half of shock deaths are **within 48 hours** of onset of MI Classic teaching is that shock occurs when 40% of LV is irreversibly damaged Almost always due to **LV failure**! Second most common cause of cardiogenic shock in AMI is mitral regurg (due to papillary muscle rupture)

Answer 25

**Older** **Female** **Prior MI** **Diabetes** **Anterior MI** (called "motor" of the heart)

Answer 26

**Cardiac index** (CO that is indexed for body surface area): **\< 1.8-2** L/min/m2 Sustained systolic arterial **hypotension \< 80-90 mm** **PCWP** \> 18-20 **Urine output \<20 ml/hr** These numbers are usually present in cardiogenic shock but don't always mean cardiogenic shock

Answer 27

**Organ perfusion requires** **resistance** to blood flow to maintain arterial pressure, and can **get** **vasodilation** in shock **Obstruction** of **microvasculature** by **leukocytes** and **platelets** and activation of **coagulation** system with fibrin deposition and **microthrombi** --\> occlusion of microvessels

Answer 28

Maintain mean **circulatory pressure** Maximize **cardiac performance** Redistribute **perfusion to most vital organs** Optimize **unloading of oxygen to tissues**

Answer 29

Stimulation of **SNS** (but this is bad because vasoconstriction **increases** **afterload** which is not good for ischemic heart) Release of **vasoconstricting hormones**: angiotensin II, vasopressin, epi, NE **Increased unloading of O2** (provoked by local acidosis, pyrexia, increased RBC 2,3-BPG) You're trying to compensate for loss of pump function but these things are **bad**!

Answer 30

Systemic and regional **vasoconstriction** and microvascular dysfunction **decreases blood flow** to splanchnic, renal, muscular beds causing **ischemic** **injury**: **Renal**: **ATN** and anuria, inability to excrete K+ and H+, **acidosis** **Hepatic**: centrolobular ischemia and **necrosis**, impaired **drug** **metabolism**, decreased **clotting** **factors** **Skeletal** **muscle**: anaerobic metabolism and **lactic acidosis** **Vasculature**: ischemia and cytokines lead to **capillary leak**

Answer 31

**WBC elevated** with **left** shift (more immature WBC just like in infection): indicates general inflammatory state Rising **BUN** and **creatinine** Elevated **hepatic** **transaminases** (AST and ALT elevated because of hepatic injury from poor perfusion) Lactic acid levels elevated (**anion gap acidosis**) because of poor perfusion, anaerobic respiration **Hypoxemia** and **metabolic** **acidosis**, which may be compensated by **respiratory alkalosis** Cardiac **biomarkers** markedly elevated (troponin, CK-MB?)

Answer 32

**MI** causes **sytolic** **dysfunction** which causes **decreased CO and SV** which causes **decreased systemic perfusion**, compensatory **vasoconstriction**, even more myocardial dysfunction and death Decreased CO and SV also cause **hypotension**, **decreased coronary pressure**, which causes **ischemia**, more myocardial dysfunction and death **Diastolic** **dysfunction** causes **increased LVEDP**, **pulmonary congestion, hypoxemia, ischemia** then more myocardial dysfunction and death ALSO, newly discovered, MI causes **inflammation** which increases inflammatory **cytokines**, iNOS, NO, peroxynitrite, **vasodilation** and **decreased** **SVR** which causes **decreased systemic perfusion** and **coronary perfusion pressure** **Vasodilation** usually "wins" in those who **die**

Answer 33

If **cardiac power** is high, less likely to die Cardiac power = cardiac index x MAP

Answer 34

Compared with classic hypotensive shock, patients in **cardiogenic** **shock** who had **higher** **power** despite same EF, CI and PCWP had **lower** **mortality** In other words, ability to **vasoconstrict** was essential, presumably to **maintain flow** to **cerebral** and **coronary** circulations by shunting away from non-essential circulations

Answer 35

**Fever** Elevated **WBC** **Low SVR** despite vasopressors Elevations in **body** **temp**, WBC, complement, interleukins, **CRP**, **NO** levels, potentially leading to generation of **peroxynitrite** Documented at outset before sepsis could develop

Answer 36

**Direct** **inhibition** of **contractility** **Suppression** of mitochondrial **respiration** **Reduces catecholamine** responsivity **Proinflammatory** effects Induces systemic **vasodilation** NOS inhibitors or knockouts better tolerate MI

Answer 37

**Cardiogenic** shock: low MAP, high RA, high PCWP, **low CI**, **high SVR** (to compensate for low CI), or low SVR if vasodilation "wins" and this is bad? **Septic** shock: low MAP, normal RA, normal PCWP, **high CI** (to compensate for low SVR), **low SVR**

Answer 38

Treat the **underlying** **cause** (usually LV failure form coronary artery occlusion) --\> **revascularize**! Medical treatment is just a means of **transporting** patient to **cath** **lab** or **OR**, but main idea is to **maintain BP** (increase afterload), **increase** **contractility** to increase SV, mechanical support, reduce preload if BP will tolerate, right heart catheterization to guide treatment

Answer 39

Medical treatment is just a means of transporting patient to cath lab or OR: **Maintain BP** (increase afterload): **vaosconstrictors** (**NE** best, DA, epi) **Increase contractility** to increase SV: inotropic agents like **dobutamine**, epi, **milrinone** but caution if patient vasodilated **Mechanical support**: intra-aortic balloon pump, mechanical assist device, mechanical ventilation if necessary to correct hypoxia/acidemia Apply **defibrillator**/pacing pads **Reduce preload** if BP will tolerate (because if PCWP high then can't oxygenate, need to bring it down): **nitroglycerine, furosemide** Right heart **catheterization** to guide treatment

Answer 40

**Hemorrhage** **Infection** Excess **negative** **inotropic** or **vasodilator** medication **Hyperglycemia/ketoacidosis**

Answer 41

Warm and dry: no congestion, good perfusion (well compensated) Warm and wet: congestion but good perfusion Cold and dry: no congestion but low perfusion Cold and wet: congestion and low perfusion Evidence of **low** **perfusion**: narrow **pulse** **pressure**, sleepy/**obtunded**, **low** serum **Na+**, **cool extremities**, **hypotension** with ACEI, renal dysfunction Signs/symptoms of **congestion** (**elevated** **PCWP**): **orthopnea/PND**, **JV** **distension**, hepatomegaly, **edema**, **rales** (rare in chronic heart failure), elevated estimated PA systolic, valsalva square wave

Answer 42

Diuretics if low perfusion and congestion (cold and wet) Vasodilators if low perfusion and **congestion** (counterintuitive, but because you're lowering LVEDP and because you're in heart failure, you're on right most downward sloping part of curve?): **nitroprusside** because more arterial than nitroglycerin, **dobutamine** (increases contractility by beta 1 but also vasodilates by beta 2), **milrinone** (phosphodiesterase inhibitor so SM stays relaxed) Use inotropic drugs if no congestion? But don't use them much because have to do invasive hemodynamic monitoring (swan-gantz) if use them and this has complications

Answer 43

Use **diuretics** and **vasodilators** when you can to decrease congestion and MvO2 If you have to, use inotropes (increases MvO2, bad!) and assist devices while you think about what definitive therapy to use (heart transplant perhaps)

Answer 44

**No**!! Useful for **short-term stabilization** but routine use in decompensated HF is detrimental

Answer 45

**Ventricle** myocyte AP is **longer**, has longer plateau **Atrium** myocyte AP is shorter, has **shorter** plateau and therefore **atrial tachycardia can be faster** than ventricular tachycardia because there is a shorter refractory period

Answer 46

**Beta 1** receptors stimulated and increase **cAMP** to **open more Na+ funny channels** so phase 4 of SA node AP has **steeper** slope so depolarization and AP happens sooner and **HR is faster**

Answer 47

**ACh** acts on **M2** **receptors** to **close more Na+ funny channels** so phase 4 of SA node AP is **shallower**/slower and **HR is slower** **Adenosine** has similar mechanism? **Parasympathetic** stimulation **opens resting K+ channels** as well to let K+ out and make depolarization **even slower**/more shallow

Answer 48

Cells with automaticity can **depolarize** **themselves** to threshold voltage to generate a spontaneous action potential, and can be **pacemakers** **SA** **node**: native pacemaker and fires at **60-100 bpm** **AV** **node**: latent pacemaker would fire at 50-60 bpm **Purkinje** **fibers**: latent pacemaker would fire at 30-40 bpm

Answer 49

ECG is the **sum** of single APs For example, add up all **SA node** and **atrial** APs and that gives you your **P wave** Add up all **ventricular** myocyte APs and that gives you your **QRS** **ST** **segment** happens during **phase 2 of depolarization** (plateau) **T wave** is **phase 3** of ventricular myocyte AP (repolarization) Note, you don't see atrial repolarization because its "T wave" is hidden because less muscle of atria and also happens during QRS when ventricle is depolarizing so is hidden

Answer 50

**Abnormal** rhythm that is **fast**

Answer 51

Altered impulse formation: **enhanced automaticity** (increased automaticity of **SA** **node**, of **latent** **pacemakers**, or abnormal **atrial** and **ventricular** **myocytes** that usually do not have pacemaker activity obtain it) Altered impulse formation: **triggered** **activity** (**early afterdepolarizations, delayed afterdepolarizations**) **Altered impulse conduction**

Answer 52

If it beats **faster** than intrinsic SA node rhythm, it will take over! **Ectopic beat** **Ectopic rhythm** because of high **catecholamies**, **hypoxemia**, **ischemia**, electrolyte disturbances (**hypokalemia**, **hypomagnesemia**), **digitalis** If **ischemic tissue blocks pathway** from SA node to ventricular tissue, can have abnormal pacemaker in ventricle that causes V-tach or PVCs

Answer 53

Beat originates from **one area of atrium** that is misbehaving and firing more than it should P wave of this beat is a little weird (wider, taller) because came from different place in atrium

Answer 54

**Three separate foci** of ectopic rhythms coming from different parts of atria **Hypoxemia** (lung disease) can make this **worse**

Answer 55

An AP may trigger **abnormal** **depolarizations** that lead to **extra heart beats** or **tachyarrhythmias** First AP leads to oscillations of membrane voltage called **afterdepolarizations**

Answer 56

**Early** **afterdepolarization**: can occur from **phase 2** (most Na+ channels inactivated still so this is caused by inward **Ca2+ current** depolarizing; must be more Ca2+ in than K+ out because these are usually balanced in phase 2) or can occur from **phase 3** (membrane is more negative now and Na+ channels recovered so **Na+ influx** is what causes depolarization) --\> **PVC**, and if happens again and again can get **Torsades de Pointe** **Delayed** **afterdepolarization**: arises from resting potential; before gap junction gets to it, cell decides to depolarize early for some reason

Answer 57

More likely to develop with conditions or medications that prolong the action potential duration: **inherited long QT syndrome, hypomagnesemia, hypokalemia, antipsychotics, amiodarone** Many meds prolong AP by blocking K+ so **K+ cannot get out** during phase 3 to repolarize = longer QT interval/AP Associated with **Torsades de Pointes**

Answer 58

Antipsychotics **bind rectifyer K+ channel** that is supposed to let K+ out to repolarize --\> K+ cannot exit cell and cell **cannot repolarize** as well Note: other medications that cause prolonged QT interval are type IA and III antiarrhythmics (**amiodarone**), antipsychotics (**haloperidol**), antiemetics (**ondansetron**) and antibiotics (**azithromycin**)

Answer 59

Remember, beginning of QRS to end of T 1) If QT inverval **more than half RR** interval 2) Cheat and look at **QT corrected** and if over **450** is long and if over **500** then at risk for early afterdepolarization/Torsades de Pointes

Answer 60

**Polymorphic ventricular tachycardia** characterized by shifting **sinusoidal** waveforms (looks like DNA strand/party streamer) Not tolerate hemodynamically, person may **faint** Can progress to **V-fib** Treatment includes **magnesium sulfate**

Answer 61

Appear shortly **after repolarization** is complete (**phase 4**) Occur in states of **high intracellular Ca2+**: sympathetic stimulation (including pressors), digoxin, catecholaminergic polymorphic VT (DA leads to more Ca2+ out of SR with each squeeze) Intracellular Ca2+ accumulation activates **Cl- currents** or the **Na/Ca exchanger** (Ca2+ out but 3Na+ in creates + charge inside) resulting in **brief inward currents**

Answer 62

Seem with marked **catecholamine stimulation** Can cause idiopathic ventricular tachycardias in otherwise **structurally normal** hearts Can cause atrial and ventricular tachycardias associated with **digitalis** toxicity

Answer 63

**Reentry**: anatomic pathway (WPW, AVNRT, atrial flutter), around scar tissue, "functinal" reentry (no anatomic obstacle or scar Electric impulse **circles** **repeatedly** around **specific path** Atria and/or ventricles are depolarized at **abnormally** **fast** rate each time the impulse circles its path **Most common mechanism** for arrhythmia Usually happens around a scar in ventricle

Answer 64

1) Unidirectional block 2) Slow retrograde conduction velocity

Answer 65

Born with **extra strip of muscle** across **tricuspid** or **mitral** valve and lets impulse go straight from **atrium to ventricles**, skipping AV to delay impulses going down to ventricles During **normal sinus rhythm** in WPW have no re-entry; early depolarization of ventriclea via accessory pathway leads to shortened PR interval and appearance of delta waves; wider QRS because when gets to ventricles, conducts myocyte to myocyte If **premature atrial depol**, get atrioventricular reentrant tachycardia (**AVRT**): bundle of kent and AV node form electrical loop of reentry; premature atrial contraction gets to BK earlier than expected when BK is refractory so impulse goes **down AV node** but by the time it gets to BK in ventricle, **BK is ready to depol again** and electricity can travel up BK to cause a **MACRO reentry circiut**; get retrograde P waves because BK is being used for retrograde conduction back through atria **(P wave inverted)** WPW well tolerated in young patients but is risk if patient deteriorates into afib Long-term management: **radiofrequency** **cathether** **ablation** has success of over 95%; otherwise treat with antiarrhythmic that slows accessory pathway coduction

Answer 66

1) **Reduce** **slope** of phase 4 automatic cells: beta blocker 2) Make diastolic potential more negative (**hyperpolarize**) 3) Make **threshold** potential **less negative** (CCB, Class I antiarrhythmics) 4) **Shorten AP** duration to prevent early afterdepolarization 5) **Correct conditions of Ca2+ overload** to prevent delayed afterdepolarizations 6) **Decrease conduction in the reentry circuit** to the point where it fails 7) **Increase refractory period** within the reentrant circuit (propagating impulse will run into unexcitable tissue!) 8) **Suppress premature beats** that can initiate reentry

Answer 67

**Class I**: blocks **Na+** channels, predominantly reduces max velocity of **upstroke of AP (phase 0)** **Class IA**: intermediate potency blockade; increase AP duration; use for Afib, Aflutter, **PSVT**, VT = **quinidine, procainamide, disopyramide** **Class IB**: least potent blockade; decrease AP duration; use for VT, digitalis-induced arrhythmia = **lidocaine, tocainide, mexiletine, phenytoin** **Class IC**: most potent blockade; no change in AP duration; use for Afib and **PSVT** = **flecainide, propafenone, moricizine** **Class II**: beta blockers; use for PAC, PVC, PSVT, Afib, Aflutter, VT (**propranolol, metoprolol, atenolol**) **Class III**: K+ channel blockers to prolong AP duration; increase AP duration; VT (amiodarone and sotalol), afib, aflutter, bypass tract-mediated **PSVT** (**amiodarone, sotalol, bretylium, ibutilide**) **Class IV**: Ca2+ channel blockers; use for PSVT, afib, aflutter, multifocal atrial tachycardia (**verapamil, diltiazem**)

Answer 68

**Quinidine**: nausea, diarrhea, **cinchonism**, **tinnitus**, blurred vision, rash, thrombocytopenia, hemolytic anemia, torsades, quinidine syncope **Procainamide**: **drug-induced lupus**, rash, fever, hypotension, psycholsis, Torsades **Disopyramide**: **anticholinertic** sx (dry mouth, blurred vision, constipation, urinary retention) **Lidocaine**: peri-oral numbness, paresthesias, seizures, coma **Flecainide**: CHF and pro-arrhythmia **Propafenone**: GI, exacerbation of asthma **Amiodaron**: agranulocytosis, pulmonary fibrosis, **hepatopathy**, hyper/**hypothyroidism**, corneal deposits, skin discoloration (**blue**) Sotalol, ibutilide, dofetalide: Torsades

Answer 69

They are actually all **proarrhythmics** We don't really know exactly which channels will be modulated

Answer 70

Any tachycardia that has **origin above ventricles** (sinus tachy, ectopic atrial tachy, AVRT, AVNRT, afib, aflutter) Note: paroxysmal SVT (PSVT) is sudden onset of SVT, usually refers to AVRT and AVNRT

Answer 71

Most **common** cause of **paroxysmal supreventricular tachycardia** (65%) Substrate is **dual AV node pathways** with different effective refractory period (ERP): fast pathway with **longer ERP** and slow pathway with **shorter** **ERP** In normal person, fast pathway depolarizes tissue because gets there first then slow dies out, but in person with **premature atrial beat**, fast pathway runs into **block** (is right behind the beat that just started) in AV node so instead goes down **slow** pathway, and by the time you get down farther tissue that was refractory can now be depolarized and develop **reentry loop**

Answer 72

**Sudden onset** and **termination** of regular narrow QRS complex tachycardia **Rate 150-250** More common in women, can occur at any age May occur in **absence of organic heart disease** May produce **palpitatins, chest pain, dyspnea and presyncope** but generally well-tolerated (could just not feel well) Can't see retrograde P waves because loop so small that QRS happening same time as atrial depolarization

Answer 73

**Valsalva** (vagus stimulation) may terminate episode by causing transient AV nodal blockade **Adenosine** terminates episodes in more than 95% of patients, treatment if vagal maneuvers fail; **hyperpolarizes** cell but shortens atrial tissue refractory period, can lead to **afib** and if accessory pathway (WPW) then **vfib** can be induced **Radiofrequency** **catheter** ablation of slow limb of pathway can cure AVNRT in more than 90% of patients, with low risk for inducing complete heart block (\<2%); small risk of touching fast pathway and then whole AV node burnt and get complete heart block and need pacemaker for the rest of your life

Answer 74

**Transient AV block** is obtained Works on **A1 receptor** and **inhibits adenyl cyclase** which reduces cAMP Increasing outward flow of K+ **hyperpolarizes** cell Adenosine **shortens atrial tissue refractory period**, thus can lead to **afib** and if patient has accessory pathway (WPW), **vfib** can be induced Tachyarrhythmias that do not involve AV node as part of re-entrant circuit are not commonly converted by adenosine Adenosine often induces **ventricular asystole** for a few seconds do patients may develop chest pain or sense of impending doom If problem is **afib** or **aflutter**, adenosine with **not help**, but will get QRSs out of the way so can see better what is going on on ECG

Answer 75

**Anatomical macro-reentrant tachycardia** localized to **RA** running counter-clockwise Circuit limited anteriorly by tricuspid valve (goes up **intraatrial** **septum** then down **back wall** of atrium) Direction of impulse propagation around tricuspid annulus determines P wave morphology: if counterclockwise then negative P waves seen in inferior leads with sawtooth pattern "typical AFL" **Atrial** **rate** during AFL is usually **250-350 bpm** but **ventricular** **rate** depends on conduction down AV node and usually is 2:1 resulting in ventricular rate of 150 bpm

Answer 76

May occur in patients **with or without structural heart disease,** may be precipitated by **thyrotoxicosis**, **pericarditis**, **alcohol** ingestion, pulmonary embolism Managed same as afib (including anticoagulation) except: easier to **cardiovert**, much easier to **ablate** (can be cured 95% of the time)

Answer 77

If **abrupt** onset in **young** **person** with no other problems then **paroxysmal SVT** If **older** **patient** with **heart disease, HTN, vavlular heart disease**, the probably **afib, aflutter, multifocal atrial tachycardia** (might see LVH on EKG) If **v-tach**, will see **wide QRS complex** so can tell that's what it is, also may see **pathological Q waves**

Answer 78

If **hemodynamically** **unstable**, do **electrical cardioversion** If **hemodynamically** **stable** with **narrow** **QRS** complex (\<120ms) try **vagal** **maneuver**, then IV **adenosine**, then IV **verapamil** (at this point may have uncovered afib or atrial tachycardia so analyze ECG further), if still nothing works try IV **procainamide**, **propafenone**, **flecainide**, **ibutilide**, or **electrical** **cardioversion** If **hemodynamically stable** with **wide** **QRS** complex try to define SVT as **STV + BBB or SVT + preexcitation**, but if not then **short-term therapy for VT**

Answer 79

**Press** firmly on carotid (at top of thyroid cartilage) for **5 seconds** to stimulate vagal loop: **afferents** stimulate **efferents** which innervate **AV node** and act like **adenosine** to **slow conduction through AV** to **break the SVT** If you have someone with aflutter but couldn't tell because too many QRSs in the way, pressure on carotid **blocks QRSs** so you can see what's going on in atria and can **diagnose aflutter** Note: listen for bruits first in carotid so don't cause stroke (usually only do this in young healthy people)

Answer 80

**Paroxysmal** afib: episodes terminate spontaneously within 1 week **Persistent** afib: fails to terminate spontaneously within 1 week **Permanent** afib: lasts more than one year The longer you're in afib the longer you'll stay and less likely to come back to sinus rhythm Need **trigger** (**ectopic** atrial **beats** arising from muscle sleeves of pulmonary veins) and **substrate** (enlarged atrium harboring **fibrosis** and inflammation; with persistence of afib atrial myocytes undergo **shortening** of their **refractory** **period**) Rate of **death** among patients with afib doubles that among patients in normal sinus rhythm **5% risk of stroke** per year and 15% of all strokes attributed to afib

Answer 81

May be **asymptomatic** (up to 25%) **Palpitations** **Dyspnea** **Fatigue** **Light-headedness** **Syncope** **Irregularly irregular** pulse on examination (because ventricles still depolarizing due to AV node stimulation down to purkinje fibers etc, but which reentrant circuit gets through to AV node is random)

Answer 82

Search for **identifiable** **causes**: **thyrotoxicosis**, **pericarditis/myocarditis, mitral stenosis** (send for surgery to fix), recent **cardiac surgery** (postop afib, usually goes away after a month), excessive **alcohol** intake, **OSA** (catecholamine surge because not breathing) 12-lead EKG, CXR, thyroid function tests, echocardiogram

Answer 83

Predicts **risk of stroke** if patient has afib **CHF** = 1 **HTN** = 1 **\>75 yo** = 1 **DM** = 1 **Prior stroke** or **TIA** = 2 Just take **aspirin** if score is **1** **Anticoagulate** if score is **2 or greater**

Answer 84

**Warfarin** to get INR 2-3 (**inhibits** **epoxide** **reductase** which usually converts oxidized vitamin K to active vitamin K so it can bind gamma glutamyl carboxylase which can carboxylate factors 2, 7, 9, 10 so they can bind Ca2+ and anticoagulate!) **Dabigatran** (oral direct **thrombin** **inhibitor**) Rivaroxaban (oral direct **factor Xa inhibitor**)

Answer 85

If **hemodynamically unstable** If **first episode** of atrial fibrillation If i**nfrequent episodes** that **do not spontaneously convert** back to normal sinus rhythm

Answer 86

Need to **look for clots** (if pt went into afib right in front of you, don't need to look for clots because wouldn't get a clot in that short a period of time) **TEE** to check LA and LA appendage for thrombus before cardioversion OR **Anticoagulation** for at least 3 weeks prior to cardioversion Still need anticoagulation after cardioversion for at least 4 weeks because can develop de novo LA thrombi after cardioversion because atria are stunned after cardioversion

Answer 87

**Beta blocker** or **CCB** is first line **Digoxin** is second line (poor HR control during exercise because when you start exercising you withdraw vagal input to heart so when sitting its ok but when get up to walk around HR up to 160 because no more vagal inhibition), used at times if BP too low for beta blocker or CCB but pt not unstable enough to require cardioversion)f Note: don't use antiarrhythmic to get sinus rhythm in people with afib because did not reduce mortality!

Answer 88

If symptoms significantly **diminishing quality of life** Some patients with HF unable to tolerate hemodynamic changes with afib Success rate is **only 50% get back to sinus rhythm** at 1 year follow up **Amiodarone** used in people with other heart problems (HF, CAD, HTN, LVH) Antiarrhythmic side effects: death, Torsades de pointes neuropathy, thyroid dysfunction, GI side effects

Answer 89

**Radiofrequency** energy or **freezing** used to destroy atrial tissue Goal is to electrically disconnect pulmonary veins from atrial substrate If already on antiarrhythmic, ablation is better than adding another antiarrhythmic Indicated for **symptomatic** patients in whom **medical** **therapy is ineffective**, not just those who don't want to be on anticoagulation, costs $25K, complications include perforation with tamponade, phrenic nerve injury, esophageal injury (arterioesophageal fistula, get food in heart and infection!), stroke, pulmonary vein stenosis

Answer 90

Can present with **afib** or **aflutter** with rates up to **300 bpm** Can lead to **vfib** and **cardiac** **arrest** even in otherwise **young and healthy patients** Can have **rapid** **conduction** of **atrial arrhythmias** down conduction tract leading to vfib Giving **AV nodal blocking agents** (beta blocker or CCB) during episodes of atrial tachycardia can push conduction down bundle of kent accessory tract (increasing ventricular rate, **bad**!) **Procainamide** is drug of choice to rate control afib or aflutter in setting of WPW because **blocks** conduction via **BK** also! May need to **cardiovert** immediately if very fast rhythm not hemodynamically tolerated

Answer 91

1) Reentry around **anatomical** **path** somebody was born with (**WPW**) 2) **Scar** in myocardium that developed often from **prior** **MI** 3) **Functional** **reentry** where no pre-formed reentry path and no scar tissue but **several** **areas** of myocardium in general vicinity that have **diff abilities to conduct electricity** often seen with ischemia that has not yet led to infarction but has **altered function of ion channels** in ischemic cells --\> this can create reentry circuit

Answer 92

Premature ventricular contractions (**PVC**): is an **early** **beat** that doesn't pump much blood so **feels** like skipped beat **Ventricular** **tachycardia**: **nonsustained** (\>3 beats, \<30 sec) or **sustained** (\>30 sec); will still be **conscious** **Ventricular** **fibrillation**: just **squiggles** on EKG, **not conscious**

Answer 93

**Asymptomatic** **Palpitations** **Lightheadedness** **Syncope** **Sudden cardiac death**

Answer 94

**V-tach** is majority (62%) Bradycardia Torsades de pointes Primary v-fib

Answer 95

No, there's a **paradox** because people at **highest risk** for SCD are those with **MI, low EF, VT**, but many people that die suddenly do **NOT** have previous MI or other heart disease

Answer 96

One **PVC**, then **normal** beat, then **PVC**, then **normal** beat

Answer 97

**Monomorphic**: only one QRS morphology in an episode; the morphology in these cases can give insights into likely site of origin of VT; **scar** is common cause **Polymorphic**: multiple QRS morphologies in a single run (one example is Torsades de pointe); associated with **prolonged QT** or **ischemia**

Answer 98

Usually in patients with underlying structural heart disease: **acute ischemia, dilated cardiomyopathy**, old infarct with scar, hypertrophic cardiomyopathy, RV dysplasia **Metabolic** abnormalities: **hyperkalemia, hypomagnesemia, hypoxia** **Medication** toxicities: **antiarrhythmic** agents (proarrhythmia)

Answer 99

**Early** phase (first **48** **hours**): **2-3%** of patients with **STEMI** have v-tach within 48 hours; probably mehcanisms other than reentry; long-term **risk** of recurrence probably **low** **Late** phase (after first 48 hours have passed): probably **reentry** mechanism; long-term risk of recurrence probably **higher** than in early phase; **worse** **prognosis** than in patients without v-tach

Answer 100

If **pulseless** or **unstable**, do **cardioversion** if **v-tach** and **defibrillation** if **v-fib** **Amiodarone** is best and official drug to use Procainamide is another Na+ channel blocker to used, prolongs QRS Lidocaine blocks both open/active and inactivated Na+ channels; block rapidly reversed in diastole when channels are closed/resting; more effective in ischemia

Answer 101

**Polymorphic** v-tach associated with **QT prolongation (\>450ms)** Causes of long QT syndrome include **congenital** (**Jervell** **Lange-Nielsen** syndrome which is AR and have deafness, **Romano Ward** syndrome which is AD**); acquired** (**hypo** K, Mg, Ca, drug induced by **Class I, sotalol, amiodarone, TCAs, pentamidine, erythromycin, antihistamines, methadone**) Worst if some parts of heart have QT long and others don't **Treatment**: stop drug that prolongs QT interval, give **magnesium sulfate** IV, increase HR to **shorten QT** with temporary **pacing** or isuprel to prevent R on T, shorten QT interval with **lidocaine** or **phenytoin**

Answer 102

A depolarization during **ventricular** prolonged and heterogeneous **repolarization** promotes reentry (**QT** **interval** is vulnerable period) On T wave, heart is still recovering but then get PVC, and another PVC and some cells ready, others not The longer the QT interval the more vulnerable you are **Commotio cordis** is a **mechanical** R on T where you get chest **trauma** which induces **PVC** right at **T wave** and you **die**!

Answer 103

**Reentry**: circuit (most common in structural heart disease) **Automaticity**: enhanced or abnormal is due to increase AP **phase 4** activity **Triggered** activity: impulse initiation caused by **afterdepolarization** (either early or delayed)

Answer 104

Implantable cardioverter defibrillator (**ICD**) is best most effective treatment **Antiarrhythmic** drugs (**amiodarone**, **sotalol**) are effective in controlling sustained ventricular arrhythmias in **30-50%** of patients only! **Catheter** **ablation** with radiofrequency energy application has been curative for **specific types of v-tach**

Answer 105

**Class I**: **Na+** channel blockers **Class** **II**: **beta** blockers **Class III**: **K+** channel blockers (amiodarone, sotalol, ibutilide, dofetilide) **Class IV**: **Ca2+** channel blockers

Answer 106

**Synchronized** **shock** depolarizes myocardial tissue Makes tissue **refractory**, allowing sinus node to take control as pacemaker Exact cellular mechanism is controversial

Answer 107

**Yes!** A study showed **primary** **prevention** of first arrhythmic event by using ICDs

Answer 108

**Cardiac** **arrest** due to **v-fib or v-tach** not due to transient or reversible cause **Spontaneous sustained v-tach** **Syncope** of undetermined origin with clinically relevant, hemodynamically significant **sustained v-tach or v-fib** induced at electrophysiological study **Ischemic** or **dilated** **cardiomyopathy** with **EF \<35%**

Answer 109

**Normal** heart with triggered/automatic arrhythmia: **outflow** tract v-tach, **fascicular** v-tach; \>90% success rate **Structural** **heart** **disease** with reentrant loops: **scar** reentrant monomorphic v-tach (ischemic cardiomyopathy, nonischemic/PVC-induced cardiomyopathy, chagas disease, ARVD, hypertrophic cardiomyopathy)

Answer 110

**Fibrofatty** replacement of **RV**: triangle of dysplasia (apex, outflow, lateral annulus) Common cause of **SCD** in Veneto region of Italy Age 10-50, mean age of 30 **30% familial** with desmosome abnormalities (AD or AR Naxos disease with palmoplantar keratosis, woolly hair)

Answer 111

**Sinus node disease:** failure of impulse formation **AV conduction block**: failure of impulse propagation

Answer 112

**Syncope or pre-syncope** **Dizziness** **SOB** **Exercise intolerance** **Heart failure** **Mental confusion** **Palpitations**

Answer 113

Sinus node disease Can cause **sinus bradycardia** (normal esp in athletes)**, sinus arrest** (failure of sinus node discharge results in absence of atrial depol and periods of ventricular asystole)**, tachy-brady syndrome** (fibrosis in atrium causes this, may need pacemaker bc can casuse you to fall a lot)**, chronotropic incompetence** (wide QRS and sinus bradycardia during exercise because HR does not go up as it should) **Causes** of sinus node dysfunction: **medications** (beta blockers, CCBs, digitalis, antiarrhythmic drugs), **aging** and **fibrosis** of sinus node, **inflammatory** of **infiltrative** diseases (sarcoidosis, autoimmune diseases, amyloidosis), **cardiac surgery**

Answer 114

**Asymptomatic**: **observation** and clinical follow up **Symptomatic**: stop offending **drugs**; consider temporary or permanent **pacing**

Answer 115

**Conduction block** between atria and ventricles which can occur **within the AV node** or in the conduction system below AV node (**His-Purkinje system**) Prolonged AV conduction (first degree block) Intermittent AV conduction (second degree block) Mobitz I Intermittent AV conduction (second degree block) Mobitz II Absent AV conduction (third degree block)

Answer 116

**No actual block**, only **delayed conduction** PR interval **\>200ms** Almost always **asymptomatic** Requires **no therapy** but if secondary to drugs then consider stopping or changing therapy

Answer 117

**Progressive prolongation of PR** interval until a ventricular **beat** is **dropped** (P wave fails to conduct) Ventricular rate is **irregular** (groued beating) Atrial rate = 90 bpm **AV node** is most common site of Mobitz I QRS usually normal Most people have some Mobitz I during **sleep**

Answer 118

**No PR prolongation** prior to **dropped beat** Intermittent AV conduction Usually this happens below AV node in **His bundle** and **progresses** to **complete** heart block

Answer 119

**2:1 or 3:1 or higher** **3 P waves** for **every QRS** means high grade block

Answer 120

**Complete heart block** **No impulse conduction** from **atria** to **ventricles** **PR** interval is **variable** because atria and ventricles are **dissociated** but P waves alone and QRSs alone are regular QRS is generated in His bundle of Purkinje fibers and is an "escape rhythm" that is very slow Ventricular rate = 37 bpm Atrial rate = 130 bpm Caused by **malfunction** of **AV** node or **His-Purkinje** system: **infarction** (poor prognosis), **degenerative** **fibrosis** (aging), **infiltrative** **diseases** (amyloid, sarcoid), **infection** (endocarditis) involving valve ring, **calcification** of valve rings, **valve** **surgery**, **medications**, **congenital** malformation (born with third degree heart block)

Answer 121

**Cannon A waves** in **neck** from AV dissociation (when **RA contracts** against a **closed** **tricuspid** valve) **Variable** first heard sound and **intensity** of pulse secondary to variable degrees of **random AV association** and ventricular filling

Answer 122

**Eliminate** rate slowing **medications** **Bedrest** and **watchful** **waiting**/monitoring (BP permitting) **Vagolytic** drugs (**atopine**) **Chronotropic** drugs (**isoproterenol**) **Temporary** **pacing** (external pacer pads, transvenous internal catheter insertion)

Answer 123

Large chest wall electrode patches May cause discomfort from electrical impulses **Not always effective** at capturing myocardium even at max output **Temporary** option Same device used on crash cart Need to use a pulse ox or feel pulse to make sure you're **pacing** **the** **heart** and causing systole rather than just affecting muscles

Answer 124

**Asymptomatic Mobitz II** second degree AV block **Asymptomatic third degree** AV block Before **procedures** where pacing may become necessary Not necessary in 1st degree AV block or asymptomatic Mobitz I second degree AV block

Answer 125

**Symptoms** from **bradycardia** **Severe** **hypotension**, even if asymptomatic **Ventricular arrhythmias** exacerbated by **slow ventricular rate**

Answer 126

**Muscarinic blocker**, so is anticholinergic, blocks vagal output **Increases** firing of **SA** node and conduction through **AV** node Very little effect on His-purkinje system and ventricular myocardium May **improve sick sinus syndrome** temporarily but for **AV block** is only effective if block is above bundle of His (**in AV node**)

Answer 127

**Isoproterenol**: pure **beta** agonist; positive **chronotropic** and **inotropic** action; causes **vasodilation** so can reduce BP; can also **worsen** **ischemia** by increasing MvO2 **Epi** or **DA**: **beta** and **alpha** agonists (**vasoconstriction**), so can be helpful if patient is **hypotensive**

Answer 128

Inserted **percutaneously** via **internal jugular, subclavian,** or **femoral vein** Positioned under fluoroscopic guidance in **right ventricular apex** and attached to **external pulse generator** Indications: **stabilize** patients awaiting permanent pacemaker, correct **transient** **symptomatic** **bradycardia** due to drug toxicity or metabolic defect, **suppress torsades de pointe** by maintaining a rate of 85 to 100 bpm until causative factor has been eliminated

Answer 129

To relieve **symptomatic** **bradycardia** and allow pt to take a beta blocker they need for angina and HTN Done at **first** **rib** or **axillary** or cut down to **cephalic vein** Pacing lead in **RV** and in **RA** to control both atrial and ventricular rate (called **dual chamber pacemaker**)

Answer 130

In other words, things that cause thrombosis leading to majority of acute MI: **Tissue factor** release **Platelet** attraction **Thrombolysis** **inhibition** Local **vasoconstriction** (**thromboxane**, lack of prostacyclin from endothelial cells, NE bound to platelets, serotonin, loss of NO) Note: thrombosis coincides with higher circulating levels of **fibrinogen**

Answer 131

Extremely **rare** form of coronary artery **vasoconstriction** **Unlikely** to cause MI

Week 4 (Acute Coronary Syndrome and Arrhythmias) Flashcards

(155 cards)