Week 4 (Acute Coronary Syndrome and Arrhythmias) Flashcards
Types of arteriosclerosis
Arteriosclerosis
Monkeberg’s Medial Calcific Sclerosis
Atherosclerosis
Layers of normal artery
Adventitia
Media
Internal elastic lamina (IEL)
Lumen
2 types of arteriolosclerosis
Hyperplastic type: onion skinning
Hyaline type: most impt in kidneys
Atherosclerosis
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
Gross types of arterial plaques
Fatty streak
Fibrous plaque
Complicated plaque
Fatty streak
Lipid-laden macrophages
Smooth muscle cells
Few lymphocytes
Little extracellular lipid
Fine meshwork of collagen and elastic fibers
Relationship of fatty streak to raised plaque in atherosclerosis
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
Characteristics of regions with adaptive intimal thickening
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
Relationship between adaptive intimal thickening (AIT) and atherosclerosis
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
Fibrous plaque
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
Complicated plaque
Only type of plaque that is clinically significant
Fibrous plaque which has undergone calcification, ulceration, hemorrhage, thrombosis
Susceptible sites for atherosclerosis?
Abdominal aorta and iliac arteries
Proximal coronary arteries
Thoracic aorta, femoral and popliteal arteries
Internal carotid arteries
Vertebral, basilar and middle cerebral arteries
Evolution of plaque rupture
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)
Vulnerable plaques and patients definitions
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
Different types of vulnerable plaque as underlying cause of acute coronary events (ACS) and sudden cardiac death (SCD)
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!
New AHA classification for coronary artery lesions
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
Atherogenesis: factors involved in initiation and/or progression of atherosclerosis
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)
Proposed steps in evolution of atherosclerotic plaques
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
Risk factors for atherogenesis
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)
Inflammatory markers of disease
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
Role of oxidants
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
Link between risk factors and inflammation
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
Possible biomarkers for CV disease
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
Complications of atherosclerosis
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
How does arteriosclerotic vascular disease cause death?
Sudden death
MI
Stroke
Renal failure
Peripheral vascular disease
Note: interventions to decrease modifiable risk factors can ameliorate many manifestations of vascular diseases
Arteriolosclerosis vs. atherosclerosis
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
Vulnerable plaque vs. stable plaque
Vulnerable plaque: large lipid core, thin fibrous cap, inflammation
Stable plaque: small lipid core, thick fibrous cap, not much inflammation
Acute coronary syndromes
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
Reperfusion strategies for STEMI
Pharmacologic: widely available, quickly administered, less effective, bleeding risk
Percutaneous coronary intervention (PCI): limited availability, treatment delay, more effective, lower bleeding risk
What is responsible for acute coronary syndromes?
Coronary thrombosis
Pharmacologic approach to acute coronary syndrome
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)
Fibrinolytics (lytics, or incorrectly called thrombolytics)
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
Why are thrombolytics not good enough?
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!)
Unfractionated heparin (UFH) in acute coronary syndrome
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
LMWH in acute coronary syndrome
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)
Fondaparinux in acute coronary syndrome
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)
Direct thrombin inhibitors (DTIs) in acute coronary syndrome
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
Routes of administration for antithrombin agents
IV bolus: UFH, LMWH
IV Infusion: UFH, argatroban
SC injections: LMWH, fundaparinox (UFH less common)
Complications of thrombin inhibition
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
Antiplatelet therapy for acute coronary syndrome
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
Mechanical revascularization
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
Medications for acute coronary syndrome
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
Preparation for discharge after ACS
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
What is shock?
Widespread failure of adequate tissue perfusion that leads to cell injury and death
Signs of shock: hypotension, tachycardia, abnormal mental status, decreased urine output
Killip classification of shock severity
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)
Etiology of shock
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
Additional cardiovascular-related causes of shock
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
Cardiogenic shock in AMI
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)
What kinds of patients with AMI are prone to shock
Older
Female
Prior MI
Diabetes
Anterior MI (called “motor” of the heart)
Classical hemodynamics in cardiogenic shock
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
Other than pump failure (decreased CO), what else is a problem in shock?
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
Goals of autoregulatory compensation when cardiac output falls
Maintain mean circulatory pressure
Maximize cardiac performance
Redistribute perfusion to most vital organs
Optimize unloading of oxygen to tissues
Key mechanisms of compensation in cardiogenic shock
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!
Extracardiac effects of cardiogenic shock
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
Common lab findings in shock
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?)
Downward spiral of cardiogenic shock
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
How can we predict who is going to survive cardiogenic shock?
If cardiac power is high, less likely to die
Cardiac power = cardiac index x MAP
Importance of vasoconstriction
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
Systemic inflammatory response in patients with AMI and shock
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
NO and peroxynitrite
Direct inhibition of contractility
Suppression of mitochondrial respiration
Reduces catecholamine responsivity
Proinflammatory effects
Induces systemic vasodilation
NOS inhibitors or knockouts better tolerate MI
Hemodynamics in cardiogenic shock vs. septic shock
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
Treatment for cardiogenic shock in AMI
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
Medical treatment until you can get patient to cath lab or OR
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
Complicating factors in cardiogenic shock
Hemorrhage
Infection
Excess negative inotropic or vasodilator medication
Hyperglycemia/ketoacidosis
Assessment of hemodynamic status
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
Therapies of cardiogenic shock due to chronic advanced heart failure
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
Current treatment of acute decompensated heart failure
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)
Is it good to use vasoconstrictors and inotropes in decompensated heart failure?
No!!
Useful for short-term stabilization but routine use in decompensated HF is detrimental
Difference between ventricle myocyte AP and atrial myocyte AP
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
How does NE, epi action on beta 1 increase HR?
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
How do ACh and adenosine decrease HR?
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
Which cells have automaticity?
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
What is the relationship between single cell AP and ECG?
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
Tachyarrhythmia
Abnormal rhythm that is fast
Mechanisms of tachyarrhythmia formation
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
Increased automaticity of latent pacemakers
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
Premature atrial complex (PAC)
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
Multifocal atrial tachycardia
Three separate foci of ectopic rhythms coming from different parts of atria
Hypoxemia (lung disease) can make this worse
Triggered activity
An AP may trigger abnormal depolarizations that lead to extra heart beats or tachyarrhythmias
First AP leads to oscillations of membrane voltage called afterdepolarizations
Early vs. delayed afterdepolarization
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
Clinical significance of early afterdepolarizations
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
How can antipsychotic drugs cause prolonged QT?
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)
How can you tell if QT is prolonged?
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
Torsades de Pointe
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
Delayed afterdepolarizations
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
Clinical significance of delayed afterdepolarization
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
Altered impulse conduction as mechanism of tachyarrhythmia
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
2 requirements for reentry
1) Unidirectional block
2) Slow retrograde conduction velocity
Wolff-Parkinson White syndrome (WPW)
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
Desired drug effects to eliminate rhythms caused by increased automaticity
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
Classes of anti-arrhythmic drugs
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)
Common side effects of anti-arrhythmics
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
What is dangerous about antiarrhythmics in general
They are actually all proarrhythmics
We don’t really know exactly which channels will be modulated
Supraventricular tachcardia
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
AV nodal reentrant tachycardia (AVNRT)
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
Presenting features of AVNRT
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
AVNRT treatment
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
IV adenosine
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
Atrial flutter
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
Clinical significance of aflutter
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)
Clues to DDx of SVT
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
Short-term treatment for SVT
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
Carotid sinus massage
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)
Atrial fibrillation
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
Clinical presentation of afib
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)
Initial workup for afib
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
CHADS2 score
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
Stroke prevention with anticoagulation in patients with afib
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)
Who to electrically cardiovert in afib?
If hemodynamically unstable
If first episode of atrial fibrillation
If infrequent episodes that do not spontaneously convert back to normal sinus rhythm
What do you do if afib has lasted for longer than 48 hours (or unknown amount of time)
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
Rate control for afib
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!
Indications for antiarrhythmics in afib
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
Catheter ablation for afib
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
Afib in setting of WPW
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
Three types of reentry
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
Different types of ventricular arrhythmias
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
Signs and symptoms of ventricular arrhythmias
Asymptomatic
Palpitations
Lightheadedness
Syncope
Sudden cardiac death
Arrhythmias causing sudden cardiac death
V-tach is majority (62%)
Bradycardia
Torsades de pointes
Primary v-fib
Is it only people with MI that die of SCD?
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
Bigeminy
One PVC, then normal beat, then PVC, then normal beat
Monomorphic vs. poymorphic v-tach
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
Substrates for v-tach or v-fib
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)
Phases of V-tach during MI
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
Acute treatment for v-tach and v-fib
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
Torsade de pointes
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
R on T
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!
Arrhythmia mechanisms
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)
Treatment of v-tach
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
Antiarrhythmic agents
Class I: Na+ channel blockers
Class II: beta blockers
Class III: K+ channel blockers (amiodarone, sotalol, ibutilide, dofetilide)
Class IV: Ca2+ channel blockers
How do ICDs work?
Synchronized shock depolarizes myocardial tissue
Makes tissue refractory, allowing sinus node to take control as pacemaker
Exact cellular mechanism is controversial
Should ICDs be used in people who have never had arrhythmia but are at risk because of low EF?
Yes!
A study showed primary prevention of first arrhythmic event by using ICDs
Indications for ICD
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%
Catheter ablation/radiofrequency for normal heart or structural heart disease
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)
Arrhythmogenic RV dysplasia
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)
2 main mechanisms of bradycardia
Sinus node disease: failure of impulse formation
AV conduction block: failure of impulse propagation
Symptoms of bradycardia
Syncope or pre-syncope
Dizziness
SOB
Exercise intolerance
Heart failure
Mental confusion
Palpitations
Sick sinus syndrome
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
Treatment for sinus node dysfunction
Asymptomatic: observation and clinical follow up
Symptomatic: stop offending drugs; consider temporary or permanent pacing
AV conduction disease
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)
First degree AV “block”
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
Second degree AV block: Mobitz I (Wenckebach)
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
Second degree AV block: Mobitz II
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
High grade second-degree AV block
2:1 or 3:1 or higher
3 P waves for every QRS means high grade block
Third degree AV block
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)
Physical exam findings for third degree AV block
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
Acute management for third degree heart block
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)
Temporary external pacer
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
Indications for placing temporary pacing patches (as back up)
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
Indications for actually turning on temporary pacing
Symptoms from bradycardia
Severe hypotension, even if asymptomatic
Ventricular arrhythmias exacerbated by slow ventricular rate
Atropine
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)
Chronotropic drugs (adrenergic)
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
Temporary transvenous pacing
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
Permanent pacemaker
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)
Mechanisms for inducing acute thrombosis on destabilized, vulnerable plaque
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
Prinzmetal’s angina
Extremely rare form of coronary artery vasoconstriction
Unlikely to cause MI
