Week 4 (Acute Coronary Syndrome and Arrhythmias)

Question 1

Types of arteriosclerosis

Answer 1

Arteriosclerosis

Monkeberg’s Medial Calcific Sclerosis

Atherosclerosis

Question 2

Layers of normal artery

Answer 2

Adventitia

Media

Internal elastic lamina (IEL)

Lumen

Question 3

2 types of arteriolosclerosis

Answer 3

Hyperplastic type: onion skinning

Hyaline type: most impt in kidneys

Question 4

Atherosclerosis

Answer 4

A disease of elastic and large muscular arteries in which the basic lesion is the atheroma (a fibrofatty plaque within the intima, having a core of lipid and covering a fibrous cap)

Leading cause of death in industrialized nations

Death results from occlusion or rupture of arteries

Prevalence close to 100% in industrialized countries

Question 5

Gross types of arterial plaques

Answer 5

Fatty streak

Fibrous plaque

Complicated plaque

Question 6

Fatty streak

Answer 6

Lipid-laden macrophages

Smooth muscle cells

Few lymphocytes

Little extracellular lipid

Fine meshwork of collagen and elastic fibers

Question 7

Relationship of fatty streak to raised plaque in atherosclerosis

Answer 7

Both contain lipid

Racial groups with more streaks have fewer plaques

Distribution of lesions in aorta are very different

Mouths of intercostal arteries usually free of streaks but develop raised plaques

Fatty streaks most often posterior-midline and proximal aorta

Raised plaques are usually anterior and lateral and in distal aorta

Note: some people say fatty streak evolves into atherosclerosis but must take this with a grain of salt

Question 8

Characteristics of regions with adaptive intimal thickening

Answer 8

Abundant smooth muscle cells and matrix

Increased turnover of SMCs and endothelial cells

Increased permeability

Increased concentration of low density lipoproteins

Low shear stress and/or high wall tensile stress

Question 9

Relationship between adaptive intimal thickening (AIT) and atherosclerosis

Answer 9

Advanced atherosclerotic lesions often form first in regions with AIT: in coronary, renal and carotid arteries, and aorta

Hence, these are designated as atherosclerotic-prone regions

However, advanced atherosclerotic lesions are not confined to regions with AIT

Question 10

Fibrous plaque

Answer 10

Smooth muscle cells

Macrophages

Other leukocytes

Prominent connective tissue stroma with collagen, elastic tissue, proteoglycans, intra and extracellular lipids, with a fibrous cap over central lipid core

Question 11

Complicated plaque

Answer 11

Only type of plaque that is clinically significant

Fibrous plaque which has undergone calcification, ulceration, hemorrhage, thrombosis

Question 12

Susceptible sites for atherosclerosis?

Answer 12

Abdominal aorta and iliac arteries

Proximal coronary arteries

Thoracic aorta, femoral and popliteal arteries

Internal carotid arteries

Vertebral, basilar and middle cerebral arteries

Question 13

Evolution of plaque rupture

Answer 13

Plaque fissure can lean to healed fissure, buried thrombus, plaque larger (contributes to progression of atherosclerosis)

Plaque fissure can lead to mural intraluminal thrombus and intra-intimal thrombus <–> occlusive intra-luminal thrombus (= ruptured plaque; this is what ruptures and is the cause of >75% of MIs)

Question 14

Vulnerable plaques and patients definitions

Answer 14

Vulnerable, high-risk and thrombosis-prone plaque: synonyms to describe plaque at increased risk of thrombosis and rapid stenosis progression

Inflamed thin-cap fibroatheroma (TCFA): an inflamed plaque with a thin cap covering a lipid-rich, necrotic core; thought to be a high risk, vulnerable plaque

Vulnerable patient: patient at high risk to experience cardiovascular ischemic event due to a high atherosclerotic burden; high risk, vulnerable plaques and/or thrombogenic blood

Question 15

Different types of vulnerable plaque as underlying cause of acute coronary events (ACS) and sudden cardiac death (SCD)

Answer 15

Rupture-prone

Ruptured/healing

Erosion-prone (more in women who are on OCP or smokers)

Eroded (with mural thrombus on erosion)

Vulnerable plaque with intra-plaque hemorrhage

Vulnerable plaque with calcified nodule (area of Ca near area with no Ca makes susceptible to rupture)

Critically stenotic vulnerable plaque

Note: any of these plaques can rupture!

Question 16

New AHA classification for coronary artery lesions

Answer 16

DON’T NEED TO KNOW THIS CLASSIFICATION

Coronary artery at lesion-prone location: adaptive thickening (smooth muscle)

Type II lesion: macrophage foam cells

Type III lesion (preatheroma): small pools of extracellular lipid

Type IV lesion (atheroma): core of extracellular lipid

Type V lesion (fibroatheroma): fibrous thickening

Type VI lesion (complicated lesion): thrombus, fissure and hematoma

Question 17

Atherogenesis: factors involved in initiation and/or progression of atherosclerosis

Answer 17

Lipid deposition (most important factor because if low lipid levels, no atherosclerotic disease)

Degeneration/aging: dead theory

Mutation/neoplasia: dead theory

Inflammation: lots of hype

Hemodynamic factors: sheer stress plays role in where atherosclerosis develops

Endothelial dysfunction (caused by hemodynamic factors): increase permeability and allow lipids to get into vessel from bloodstream

Thrombosis

Lipid infiltration starts process but pathogenesis of atherosclerosis not adequately explained by any one of above factors (but lipid infiltration starts the process)

Question 18

Proposed steps in evolution of atherosclerotic plaques

Answer 18

Endothelial dysfunction–increased permeability

Penetration of plasma lipids into arterial wall: LDL gets into walls and gets oxidized; oxidized LDL is very inflammatory and toxic to the vessel

Monocyte conversion to macrophages, which take up lipids to make foam cells which causes inflammation to get more stromal deposition until get atherosclerosis

Smooth muscle cell migration/proliferation

Complications: calcification, ulceration, hemorrhage, thrombosis, aneurysm formation, rupture

Question 19

Risk factors for atherogenesis

Answer 19

Age, gender, FH

HTN, cigarette smoking, DM, obesity (contraversial about obesity in itself), hypothyroidism, gout

Fibrinogen level, lipid level, diet, sedentary lifestyle, personality, environmental facotrs (air pollution, infection)

Question 20

Inflammatory markers of disease

Answer 20

Current consensus is that atherosclerosis is primarily an inflammatory disease; elevation of these markers associated with increased risk of event

CRP: acute phase reactant (statins reduce CRP)

Fibrinogen: acute phase reactant

Soluble CD40 ligand (sCD40L): proinflammatory cytokine

WBCs: contain myeloperoxidas (MPO)

MPO

VCAM-1, ICAM-1

Question 21

Role of oxidants

Answer 21

Oxidation of LDL is primary event in atherogenesis

SOD, an antioxidant, is expressed in regions of laminar flow

NO, which has antioxidant properties, inhibits VCAM gene expression by inhibiting NFkB

Myeloperoxidase, present in neutrophils and monocytes, generates oxidants and contributes to LDL oxidation in the plaque

However, trials evaluating anti-oxidants as a single potential preventative intervention have been negative

Question 22

Link between risk factors and inflammation

Answer 22

Diabetes mellitus: glucose enhances glycation and thereby the inflammatory properties of LDL

Hypertension: not directly inflammatory, but ATII is

Obesity: controversial alone, but contributes to DM and HTN; adipose tissue is associated with increased cytokine production that create a systemic pro-inflammatory state

Smoking: causes oxidants to form that directly oxidize LDL

Infection: all trials of antibiotics negative

Question 23

Possible biomarkers for CV disease

Answer 23

Not sure how any of these work though!

Inflammation: IL-6, myeloperoxidase, soluble CD40 ligand

Oxidative stress: oxidized LDL

Altered lipids: lipoprotein(a), low-density lipoprotein particle size

Altered thrombosis: tPA/plasminogen activator inhibitor 1, fibrinogen, homocysteine, D-dimer

Question 24

Complications of atherosclerosis

Answer 24

Aneurysms and ruptures are due to destruction of media beneath complicated plaques

Ulceration may lead to atheroemboli, plaque hemorrhage and superimposed thrombosis

Abnormal vessels within the plaque may lead to hemorrhage

The pathogenesis of plaque ulceration, fissures, and hemorrhage leading to luminal thrombosis is unknown

Question 25

How does arteriosclerotic vascular disease cause death?

Answer 25

Sudden death

MI

Stroke

Renal failure

Peripheral vascular disease

Note: interventions to decrease modifiable risk factors can ameliorate many manifestations of vascular diseases

Question 26

Arteriolosclerosis vs. atherosclerosis

Answer 26

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

Question 27

Vulnerable plaque vs. stable plaque

Answer 27

Vulnerable plaque: large lipid core, thin fibrous cap, inflammation

Stable plaque: small lipid core, thick fibrous cap, not much inflammation

Question 28

Acute coronary syndromes

Answer 28

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

Question 29

Reperfusion strategies for STEMI

Answer 29

Pharmacologic: widely available, quickly administered, less effective, bleeding risk

Percutaneous coronary intervention (PCI): limited availability, treatment delay, more effective, lower bleeding risk

Question 30

What is responsible for acute coronary syndromes?

Answer 30

Coronary thrombosis

Question 31

Pharmacologic approach to acute coronary syndrome

Answer 31

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)

Question 32

Fibrinolytics (lytics, or incorrectly called thrombolytics)

Answer 32

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

Question 33

Why are thrombolytics not good enough?

Answer 33

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!)

Question 34

Unfractionated heparin (UFH) in acute coronary syndrome

Answer 34

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

Question 35

LMWH in acute coronary syndrome

Answer 35

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)

Question 36

Fondaparinux in acute coronary syndrome

Answer 36

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)

Question 37

Direct thrombin inhibitors (DTIs) in acute coronary syndrome

Answer 37

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

Question 38

Routes of administration for antithrombin agents

Answer 38

IV bolus: UFH, LMWH

IV Infusion: UFH, argatroban

SC injections: LMWH, fundaparinox (UFH less common)

Question 39

Complications of thrombin inhibition

Answer 39

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

Question 40

Antiplatelet therapy for acute coronary syndrome

Answer 40

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

Question 41

Mechanical revascularization

Answer 41

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

Question 42

Medications for acute coronary syndrome

Answer 42

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

Question 43

Preparation for discharge after ACS

Answer 43

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

Question 44

What is shock?

Answer 44

Widespread failure of adequate tissue perfusion that leads to cell injury and death

Signs of shock: hypotension, tachycardia, abnormal mental status, decreased urine output

Question 45

Killip classification of shock severity

Answer 45

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)

Question 46

Etiology of shock

Answer 46

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

Question 47

Additional cardiovascular-related causes of shock

Answer 47

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

Question 48

Cardiogenic shock in AMI

Answer 48

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)

Question 49

What kinds of patients with AMI are prone to shock

Answer 49

Older

Female

Prior MI

Diabetes

Anterior MI (called “motor” of the heart)

Question 50

Classical hemodynamics in cardiogenic shock

Answer 50

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

Question 51

Other than pump failure (decreased CO), what else is a problem in shock?

Answer 51

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

Question 52

Goals of autoregulatory compensation when cardiac output falls

Answer 52

Maintain mean circulatory pressure

Maximize cardiac performance

Redistribute perfusion to most vital organs

Optimize unloading of oxygen to tissues

Question 53

Key mechanisms of compensation in cardiogenic shock

Answer 53

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!

Question 54

Extracardiac effects of cardiogenic shock

Answer 54

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

Question 55

Common lab findings in shock

Answer 55

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?)

Question 56

Downward spiral of cardiogenic shock

Answer 56

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

Question 57

How can we predict who is going to survive cardiogenic shock?

Answer 57

If cardiac power is high, less likely to die

Cardiac power = cardiac index x MAP

Question 58

Importance of vasoconstriction

Answer 58

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

Question 59

Systemic inflammatory response in patients with AMI and shock

Answer 59

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

Question 60

NO and peroxynitrite

Answer 60

Direct inhibition of contractility

Suppression of mitochondrial respiration

Reduces catecholamine responsivity

Proinflammatory effects

Induces systemic vasodilation

NOS inhibitors or knockouts better tolerate MI

Question 61

Hemodynamics in cardiogenic shock vs. septic shock

Answer 61

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

Question 62

Treatment for cardiogenic shock in AMI

Answer 62

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

Question 63

Medical treatment until you can get patient to cath lab or OR

Answer 63

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

Question 64

Complicating factors in cardiogenic shock

Answer 64

Hemorrhage

Infection

Excess negative inotropic or vasodilator medication

Hyperglycemia/ketoacidosis

Question 65

Assessment of hemodynamic status

Answer 65

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

Question 66

Therapies of cardiogenic shock due to chronic advanced heart failure

Answer 66

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

Question 67

Current treatment of acute decompensated heart failure

Answer 67

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)

Question 68

Is it good to use vasoconstrictors and inotropes in decompensated heart failure?

Answer 68

No!!

Useful for short-term stabilization but routine use in decompensated HF is detrimental

Question 69

Difference between ventricle myocyte AP and atrial myocyte AP

Answer 69

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

Question 70

How does NE, epi action on beta 1 increase HR?

Answer 70

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

Question 71

How do ACh and adenosine decrease HR?

Answer 71

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

Question 72

Which cells have automaticity?

Answer 72

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

Question 73

What is the relationship between single cell AP and ECG?

Answer 73

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

Question 74

Tachyarrhythmia

Answer 74

Abnormal rhythm that is fast

Question 75

Mechanisms of tachyarrhythmia formation

Answer 75

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

Question 76

Increased automaticity of latent pacemakers

Answer 76

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

Question 77

Premature atrial complex (PAC)

Answer 77

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

Question 78

Multifocal atrial tachycardia

Answer 78

Three separate foci of ectopic rhythms coming from different parts of atria

Hypoxemia (lung disease) can make this worse

Question 79

Triggered activity

Answer 79

An AP may trigger abnormal depolarizations that lead to extra heart beats or tachyarrhythmias

First AP leads to oscillations of membrane voltage called afterdepolarizations

Question 80

Early vs. delayed afterdepolarization

Answer 80

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

Question 81

Clinical significance of early afterdepolarizations

Answer 81

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

Question 82

How can antipsychotic drugs cause prolonged QT?

Answer 82

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)

Question 83

How can you tell if QT is prolonged?

Answer 83

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

Question 84

Torsades de Pointe

Answer 84

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

Question 85

Delayed afterdepolarizations

Answer 85

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

Question 86

Clinical significance of delayed afterdepolarization

Answer 86

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

Question 87

Altered impulse conduction as mechanism of tachyarrhythmia

Answer 87

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

Question 88

2 requirements for reentry

Answer 88

1) Unidirectional block
2) Slow retrograde conduction velocity

Question 89

Wolff-Parkinson White syndrome (WPW)

Answer 89

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

Question 90

Desired drug effects to eliminate rhythms caused by increased automaticity

Answer 90

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

Question 91

Classes of anti-arrhythmic drugs

Answer 91

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)

Question 92

Common side effects of anti-arrhythmics

Answer 92

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

Question 93

What is dangerous about antiarrhythmics in general

Answer 93

They are actually all proarrhythmics

We don’t really know exactly which channels will be modulated

Question 94

Supraventricular tachcardia

Answer 94

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

Question 95

AV nodal reentrant tachycardia (AVNRT)

Answer 95

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

Question 96

Presenting features of AVNRT

Answer 96

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

Question 97

AVNRT treatment

Answer 97

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

Question 98

IV adenosine

Answer 98

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

Question 99

Atrial flutter

Answer 99

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

Question 100

Clinical significance of aflutter

Answer 100

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)

Question 101

Clues to DDx of SVT

Answer 101

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

Question 102

Short-term treatment for SVT

Answer 102

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

Question 103

Carotid sinus massage

Answer 103

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)

Question 104

Atrial fibrillation

Answer 104

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

Question 105

Clinical presentation of afib

Answer 105

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)

Question 106

Initial workup for afib

Answer 106

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

Question 107

CHADS2 score

Answer 107

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

Question 108

Stroke prevention with anticoagulation in patients with afib

Answer 108

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)

Question 109

Who to electrically cardiovert in afib?

Answer 109

If hemodynamically unstable

If first episode of atrial fibrillation

If infrequent episodes that do not spontaneously convert back to normal sinus rhythm

Question 110

What do you do if afib has lasted for longer than 48 hours (or unknown amount of time)

Answer 110

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

Question 111

Rate control for afib

Answer 111

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!

Question 112

Indications for antiarrhythmics in afib

Answer 112

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

Question 113

Catheter ablation for afib

Answer 113

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

Question 114

Afib in setting of WPW

Answer 114

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

Question 115

Three types of reentry

Answer 115

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

Question 116

Different types of ventricular arrhythmias

Answer 116

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

Question 117

Signs and symptoms of ventricular arrhythmias

Answer 117

Asymptomatic

Palpitations

Lightheadedness

Syncope

Sudden cardiac death

Question 118

Arrhythmias causing sudden cardiac death

Answer 118

V-tach is majority (62%)

Bradycardia

Torsades de pointes

Primary v-fib

Question 119

Is it only people with MI that die of SCD?

Answer 119

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

Question 120

Bigeminy

Answer 120

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

Question 121

Monomorphic vs. poymorphic v-tach

Answer 121

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

Question 122

Substrates for v-tach or v-fib

Answer 122

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)

Question 123

Phases of V-tach during MI

Answer 123

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

Question 124

Acute treatment for v-tach and v-fib

Answer 124

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

Question 125

Torsade de pointes

Answer 125

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

Question 126

R on T

Answer 126

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!

Question 127

Arrhythmia mechanisms

Answer 127

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)

Question 128

Treatment of v-tach

Answer 128

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

Question 129

Antiarrhythmic agents

Answer 129

Class I: Na+ channel blockers

Class II: beta blockers

Class III: K+ channel blockers (amiodarone, sotalol, ibutilide, dofetilide)

Class IV: Ca2+ channel blockers

Question 130

How do ICDs work?

Answer 130

Synchronized shock depolarizes myocardial tissue

Makes tissue refractory, allowing sinus node to take control as pacemaker

Exact cellular mechanism is controversial

Question 131

Should ICDs be used in people who have never had arrhythmia but are at risk because of low EF?

Answer 131

Yes!

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

Question 132

Indications for ICD

Answer 132

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%

Question 133

Catheter ablation/radiofrequency for normal heart or structural heart disease

Answer 133

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)

Question 134

Arrhythmogenic RV dysplasia

Answer 134

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)

Question 135

2 main mechanisms of bradycardia

Answer 135

Sinus node disease: failure of impulse formation

AV conduction block: failure of impulse propagation

Question 136

Symptoms of bradycardia

Answer 136

Syncope or pre-syncope

Dizziness

SOB

Exercise intolerance

Heart failure

Mental confusion

Palpitations

Question 137

Sick sinus syndrome

Answer 137

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

Question 138

Treatment for sinus node dysfunction

Answer 138

Asymptomatic: observation and clinical follow up

Symptomatic: stop offending drugs; consider temporary or permanent pacing

Question 139

AV conduction disease

Answer 139

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)

Question 140

First degree AV “block”

Answer 140

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

Question 141

Second degree AV block: Mobitz I (Wenckebach)

Answer 141

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

Question 142

Second degree AV block: Mobitz II

Answer 142

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

Question 143

High grade second-degree AV block

Answer 143

2:1 or 3:1 or higher

3 P waves for every QRS means high grade block

Question 144

Third degree AV block

Answer 144

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)

Question 145

Physical exam findings for third degree AV block

Answer 145

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

Question 146

Acute management for third degree heart block

Answer 146

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)

Question 147

Temporary external pacer

Answer 147

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

Question 148

Indications for placing temporary pacing patches (as back up)

Answer 148

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

Question 149

Indications for actually turning on temporary pacing

Answer 149

Symptoms from bradycardia

Severe hypotension, even if asymptomatic

Ventricular arrhythmias exacerbated by slow ventricular rate

Question 150

Atropine

Answer 150

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)

Question 151

Chronotropic drugs (adrenergic)

Answer 151

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

Question 152

Temporary transvenous pacing

Answer 152

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

Question 153

Permanent pacemaker

Answer 153

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)

Question 154

Mechanisms for inducing acute thrombosis on destabilized, vulnerable plaque

Answer 154

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

Question 155

Prinzmetal’s angina

Answer 155

Extremely rare form of coronary artery vasoconstriction

Unlikely to cause MI