Cardiac Pathophysiology
Electrocardiogram (Lilly, Chapter 4)
I.
II.
III.
IV.
V.
Basic Principles
a. Depolarization – shows an upward deflection on the EKG indicating that the current of
positive charges is going towards the reference electrode
b. Repolarization – shows a downward deflection in the EKG indicating that the current of
positive charge is flowing away from the reference electrode
c. Note: in the normal human heart, the deflection on repolarization is upright, indicating the
direction of repolarization is actually opposite that of depolarization. I.e. if the depol happens
from base to apex, then the repolarization, which would normally show a downward
deflection on the EKG, must happen from apex to base. This makes sense, because AP’s in
endocardial cells (the first to become stimulated) are much longer than epicardial cells (the
last to become stimulated), thus reversing the expected pattern of depol/repol
Lead reference system
a. Limb Leads – I, II, III (use the L mnemonic)
b. Bipolar Leads – aVR, aVL, aVF (right, left, femur)
c. Precordial Leads – measure the heart’s impulses in the direction perpendicular to the frontal
plane – V1-V6
Reading the EKG –
a. Voltage Calibration – 1mV signing should be 10 large boxes. Sometimes that is changed,
such that the 1mV tracing is 5 boxes (if hypertrophy is so large that the tracing goes off the
page)
b. Rhythm – sinus if:
i. Each QRS preceeded by a P, each P is followed by a QRS, P waves are upright in I,
II, and III, and PR interval (see below) is greater than 3 small boxes
ii. Keep in mind sinus tachy and bradycardias
c. Rate – Use the mnemonic of 300, 150, 100, 75, 60, 50 for each large box. Otherwise, each
large box is 0.2 s, each small box is 0.4s and five boxes is 1s
d. Intervals
i. PR – one large block (increased in 1st degree AV block)
ii. QRS – ½ large block (BBB, ectopic beats, toxicity, hyperkalemia)
iii. QT – difficult b/c it varies w/ HR
e. Axis – Should be upright in leads I and II (-30 to 90 degrees). Can also use I and aVF. Use
the other leads to determine whether it is right axis or left axis deviation
P wave abnormalities – best visualized in lead II (parallel to flow from SA to AV)
a. P wave is normally biphasic in lead V1. RA shows upward deflection in the anterior
direction, followed by LA showing downward deflection posteriorly
b. LA enlargement shows up as a largely biphasic V1 with a large LA downstroke following the
upward deflection of the RA
c. RA enlargement is just the opposite
QRS abnormalities
a. Ventricular Hypertrophy –
i. big QRS in corresponding leads
ii. axis deviations toward the larger ventricle
b. BBB’s
i. RBBB – initial depolarization of the septum, and left ventricle is normal so you see
small R wave in V1, and small Q wave in V6. However, as the RV finally receives a
signal, it transmits a widened, asynchronous impulse showing up as a second R (R’)
wave over V1 and an S wave to V6
ii. LBBB – septal depolarization doesn’t happen, so NO R wave in V1 (you get Q
instead) or Q wave in V6. You actually see the opposite because the right bundle
takes precedence and you get signal toward the L instead of the R. Again, as LV
catches up, you get a widened and late impulse that shows up as a second R wave
over V5/V6
c.
Myocardial Infarction
i. Pathologic Q wave (small ones are normal in V6 and aVL) – deep and wide,
precordial leads designate location of infarct. Pathophysiologically, the reason for
the Q wave is that the lead over the infarcted tissue is detecting viable tissue on the
other side of the heart
ii. In the case of a posterior wall MI, you get large V1 and V2’s. This can be
differentiated from RVH by the lack of right axis deviation
iii. ST segment elevation – occurs because infarcted tissue directly below the lead
changes the baseline so that the ST segments appear elevated or depressed due to
diastolic leak of potassium either away or towards the lead depending on the depth of
the infarct. I.e. in the case of an MI, K+ leak occurs away from the lead, which shifts
the baseline lower (positive charge moving away from the lead) and shifts up the ST
segment in relative terms. In the case of a subendocardial ischemic event, K+ leak
goes from endocardium towards the lead, leading to baseline shift and therefore a
relative drop in the ST segment
Myocardial Ischemia/Stable Angina
Ischemia is defined as the state of the heart in which myocardial oxygen demand exceeds the body’s ability
to supply the heart with oxygen
I.
Myocardial Oxygen Supply – coronary perfusion occurs during diastole, so perfusion pressure
can be measured by aortic end-diastolic pressure
a. Oxygen carrying capacity
b. Coronary Blood flow – depends on the perfusion pressure and the resistance of coronary
vasculature to blood
i. External compression – during cardiac cycle, the epicardial and subendocardial
vessels are typically compressed during systole
ii. Unlike most tissues, the heart cannot increase O2 extraction, and so must rely on
increasing blood flow. This is accomplished by dilation of major resistance
vessels
iii. Mediators such as Adenosine, NO, prostacyclin, endothelium-derived
hyperpolarizing factor, endothelin-1 (a constrictor)
iv. Neural control – sympathetic receptors (alpha and beta-2) both promote
vasodilation. Balance between alphas and betas and above factors that mediate
total tone
II.
Myocardial Oxygen Demand
a. Wall Stress – causes an increase in O2 demand because increased force pulling
myocardial cells apart requires energy to withstand. Increased diameter in the case of
MR or AI causes increased wall stress. Increased ventricular pressures also increase wall
stress. Finally, compensatory hypertrophy works to reduce wall stress because force is
spread out over a larger mass
b. Heart Rate – a higher rate means more energy utilized
c. Contractility – increasing the force of contraction increases the demand for O 2
III.
Pathophysiology of Ischemia – myocardial ischemia is a result of fixed vessel narrowing and
abnormal vascular tone from the damaged endothelium
a. Fixed Vessel Narrowing
i. Usually, the distal, smaller vessels are the first to become stenotic and occluded.
The larger resistance vessels are usually plaque free and are able to adapt when
necessary. Thus the significance of vessel narrowing depends on the extent to
which distal arteries are occluded
ii. Any greater than 60% occlusion may cause progressively worse downstream
ischemia – first on exertion, then at rest
b. Endothelial Cell Dysfunction
i. Inappropriate Vasoconstriction – because endothelial derived factors (NO,
prostacyclin, etc) are not released, the catecholamines are unopposed and
vasoconstriction occurs
IV.
V.
VI.
VII.
VIII.
IX.
X.
ii. Platelet Aggregation – platelet derived anti-thrombotic factors (prostacyclin) is
not released and local hypercoagulability occurs. Furthermore, because of the
impaired function of the endothelium, the factors secreted by platelets
(thromboxane, ADP, serotonin) go unopposed
Non CAD causes of Myocardial Ischemia
a. Decreased aortic perfusion pressure – hypotension or aortic regurgitation
b. Decrease in O2 carrying capacity from anemia
c. Extreme myocardial demand from aortic stenosis
Consequences of Ischemia
a. Immediately, there is decreased contraction, resulting in flow backup and pulmonary
congestion (dyspnea)
b. Stunned myocardium – in times of prolonged ischemia, there is a reversible change in
which the heart will still lack full contractile function, but will eventually recover
c. Hibernating myocardium – chronic ventricular dysfunction even though irreversible
damage has not yet occurred
Stable Angina
a. Fixed obstructive plaques in one or more coronary arteries
i. Symptoms directly correlated to degree of occlusion
ii. When myocardial demand goes up, not enough reserve to compensate, leading
to transient ischemia
iii. With endothelial dysfunction, vessels may paradoxically constrict in response to
stress due to catecholamine alpha adrenergic stimulation unopposed by
endothelial derived factors
iv. Stable threshold vs. Variable threshold angina – i.e. does the angina occur after
the same activity always or only sometimes?
Variant Angina and Silent Ischemia
a. Variant or Prinzmetal’s angina refers to vasospasm as the source of angina which occurs
at rest often due to early atherosclerotic changes
b. Silent Ischemia – occurs often in the presence of symptomatic stable angina, but is
unrecognized by the patient. Use a Holter monitor to truly test
Differential Diagnosis of intermittent chest pain
a. Cardiac – myocardial ischemia, pericarditis
b. Gastrointestinal – GERD, ulcers, esophageal spasm, biliary colic
c. Musculoskeletal – costochondritis, cervical radiculopathy
Diagnosis
a. EKG – shows acute ST segment depressions, but may be normal between episodes
b. Stress Test –
i. considered positive if EKG changes are found or angina is experienced
ii. considered very positive if EKG changes occur in 1st three minutes, ST
depression is deep, systolic dysfunction causes a drop in systolic BP, ventricular
arrhythmias develop, or the patient cannot exercise for more than two minutes
c. Nuclear Exercise – nuclear labeling of myocardial perfusion during exercise
d. Exercise Echo
e. Pharmacologic Stress testing – give dobutamine and see what happens
f. Coronary Angiography – the “gold standard” for diagnosing CAD, it does not really tell
you how vulnerable the plaques are to thrombose
Treatment – increase myocardial O2 supply and decrease demand
a. Medical Treatment of Acute Angina – venodilation with nitrates reduces venous return to
the heart cause decreased wall stress via preload (lower R)
b. Medical treatment of recurrent ischemic episodes
i. Nitrates prior to vigorous activity
ii. B-Blockers – reduce myocardial oxygen demand by decreasing chronicity and
contractility (note: not used in decompensated LV dysfunction – CHF)
iii. Ca++ channel blockers –
1. dihydropyridines (nifedipine, amlodipine)– vasodilators that 1)
decrease oxygen demand via preload 2) decrease oxygen demand via
2.
afterload (arterial dilation) and 3) increase myocardial supply via
coronaries
Nondihydropyridines (verapamil, diltiazem) are also vasodilators but
not as potent. These also have antianginal effects via chronotropic and
contractile effects
Drug
Dihydropyradine (nifedipine)
Non-dihydropyradine (verapamil, diltiazem)
c.
d.
Vasodilatory
+++
+
Contractility
+
+++
Chronotropy
+
+++
Treatment to prevent MI and death
i. Antiplatelets – Aspirin, clopidogrel
ii. Lipid-lowering
iii. ACE inhibitors
Revascularization – only if patient does not respond to medical management
i. PTCA has high ~50% chance of restenosis
ii. PTCA w/ stent has much better outcome
iii. CABG, which often have poor patency rates -especially veins such as saphenous
Valvular Heart Disease (Chapter 8, Lilly)
I.
II.
Rheumatic Fever – inflammatory condition involving heart, skin, and connective tissue
a. Pathogenesis of ARF remains unclear, but direct bacterial colonization of the heart does
not happen. Mechanism appears to be elaboration of bacterial toxin or autoimmune
cross-reactivity with some Ag
b. Histology shows “Aschoff body,” an area of focal fibrinoid necrosis surrounded by
inflammatory cells (lymphs, plasma, and MO’s)
c. While RF can affect all layers of myocardium, the most devastating effects occur in the
valvular endothelium
Mitral Valve Disease
a. Mitral Stenosis – almost always a result of RF
i. Pathology – fibrous thickening of the leaflets, with fusion at the commissures
and thickening of the chordae
ii. Pathophysiology – due to the increased resistance from which the LA must
overcome, there is increases in LA pressure and LV stroke volume may be
diminished despite normal pressures
1. High LA pressures get passively transmitted to pulmonary capillary
pressure causing pulmonary edema
2. Pulmonary edema can result in two types of pulmonary HTN
a. Passive – in response to increased backflow
b. Reactive – medial hypertrophy and intimal fibrosis of the
pulmonary vasculature which 1) prevents pulmonary
congestion but 2) causes increases in RV/RA pressures
3. Chronic LA enlargement leads to atrial fibrillation
4. Finally, relative stagnation of blood may predispose to
thromboembolus
iii. Clinical Manifestations –
1. Dyspnea either on exertion or at rest depending on severity
2. Occasionally, MS may present as the complications, AF, thrombus,etc
3. On PE, palpation may reveal an RV “heave”, increased S1 sound due to
slamming shut of non-compliant valves
4. Major feature is the opening snap of MS, thought to be due to the
sudden tensing of the chordae and leaflets on opening followed by low
frequency decrescendo murmur
5. Echo shows stenotic leaflets
iv. Treatment
III.
1. Prophylaxis against ARF
2. Diuretics to prevent pulmonary congestion
3. Digoxin if LV function is impaired
4. B blockers if HR is up due to conducting AF
b. Mitral Regurgitation – may result from structure, leaflets, chordae, or papillary muscles
i. Etiology
1. Myxomatous degeneration (Mitral prolapse) can lead to MR
2. Myocardial infarct of papillary muscles
3. Left ventricular enlargement, specifically dilation
ii. Pathophysiology – portion of LV systolic volume goes to low-pressure LA
1. Elevation of LA pressure and volume
2. Reduction in forward cardiac output
3. Volume related stress when regurgitant fluid comes back during
diastole
4. Acute MR – caused by ruptured papillary muscles can cause immediate
pulmonary congestion
a. Prominent v wave in the LA tracing
b. Increased LV output via the FS curve (increased EDP and
increased stroke volume)
5. Chronic MR – caused by rheumatic heart disease – LA/LV allowed to
undergo compensatory changes
a. LA becomes low-pressure sink
b. LV undergoes eccentric hypertrophy to volume overload
c. Forward output is maintained for a while
d. Eventually compensated state becomes decompensated and
heart failure occurs
iii. Clinical Manifestation
1. Acute shows pulmonary edema
2. Chronic shows low forward cardiac output
3. Holosystolic murmur radiating to the axilla
4. CXR shows increased LA and LV size
5. Echo shows increased LA and LV size as well as regurgitant flow in
Doppler Echo
iv. Treatment – augment forward cardiac output and reduce regurgitation
1. Acute MR – diuretics to relieve pulmonary congestion, nitro to reduce
forward resistance
2. Chronic MR – oral arterial vasodilators (ACE or hydralazine)
3. Surgery to repair the leaky valve before heart failure sets in
c. Mitral Valve Prolapse
i. Characterized by asymptomatic billowing of the mitral leaflets into the LA
during ventricular systole – shows myxomatous degeneration which means
dense collagen matrix is replaced by loose connective tissue
ii. Sometimes patients may reveal chest pain or palpitations due to associated
arrhythmias
iii. Clinical finding is a systolic click which is the sound of the mitral leaflet of the
chordae as they tense – sound increases with squatting
iv. Major complication is chronic progressive MR
Aortic Valve Disease
a. Aortic Stenosis – age related calcific changes of the valve – “senile” AS
i. Pathology
1. Age related – calcification of normal tricuspid valve
2. Congenital – bicuspid valve provides irregular flow and damage
ii. Pathophysiology – blood flow across the valve is obstructed
1. AS develops over a chronic course and so LV is able to compensate via
concentric hypertrophy (similar to hypertension)
2.
IV.
Significant pressure gradient develops between the LV and aorta,
resulting in gradients of 100mmHg
3. LA also hypertrophies due to increased diastolic pressure and provides
an LA “kick” at the end of LV systole (beneficial ~25% of SV)
4. Normal valvular orifice is 3-4 cm. Clinical significance occurs when
valve is 2cm. Moderate stenosis is 1-1.5 cm. Severe stenosis occurs at
0.8cm or less
iii. Clinical Manifestation
1. Angina –
a. Demand increased because of hypertrophy and increased wall
stress due to higher ventricular pressures
b. Decreased supply because increased diastolic pressure does
not allow for adequate filling of coronary vessels
2. Syncope on exertion due to inability to maintain cardiac output with a
fixed stenotic aortic valve
3. Congestive heart failure symptoms – increased LA pressures at the end
of diastole causing pulmonary congestion
4. Coarse, late-peaking systolic ejection murmur heard best at the right
upper sternal border
5. Weak and late carotid upstroke
6. S4 gallop
7. Echo and EKG show ventricular hypertrophy and increases pressure
gradients between the LV and the aorta
iv. Treatment
1. Severe – Valve replacement
2. Mild – endocarditis prophylaxis, avoidance of meds that may cause
hypotension and worsened forward cardiac ouput
b. Aortic Regurgitation
i. Etiology – results from either disease of the leaflets (bicuspid, RF) or dilation of
the root (Marfan’s, aneurysm)
ii. Pathophysiology – depends on size of regurgitant orifice, pressure gradient
across valve during diastole, duration of diastole
1. Acute – may cause immediate backup and increased LA pressure.
Leads to pulmonary congestion and acute SOB
2. Chronic – LV undergoes compensatory dilation and eccentric
hypertrophy
a. Widened pulse pressure due to increased systolic pressure (via
preload) and decreased diastolic pressure (via regurgitation)
b. Decreased perfusion pressure (aortic diastolic P is low) may
cause supply-side issue to the myocardium
iii. Clinical manifestations –
1. Sensation of forceful heartbeat
2. Stigmata of widened pulse pressure (“water-hammer” pulse, head
bobbing, Duroziez’s sign of capillary pulsations)
3. AR murmur best heard at right sternal border during early diastole
(blowing quality, which ends prior to S1)
4. Austin Flint murmur which is a Mitral murmur (apex) caused by high
regurgitant flow forcing the anterior mitral valve down
iv. Treatment – usually asymptomatic and have normal contractile function
1. Endocarditis prophylaxis
2. ACE inhibitors to reduce afterload
3. Ca++ channel blockers, especially nifedipine
Infective Endocarditis – classified by clinical course, substrate (native, prosthetic, IVD), or
organism
a. Pathogenesis
i. Endocardial surface injury cause platelets to adhere and a sterile thrombus forms
b.
ii. This serves as a good place for the bacteria to land because fibrin is irregular,
and it also protects the bacteria from host immune responses
iii. Bacteria get there anytime a mucosal surface is ruptured, however, only those
bacteria (~90% gram positive) that can survive can cause endocarditis
iv. Complications once bacteria have colonized include mechanical cardiac injury,
thrombotic or septic emboli, immune mediated injury
Clinical – acute shows up as a very high fever and shaking chills, subacute is a low-grade
fever with nonspecific constitutional symptoms of weight loss, fatigue, anorexia, etc
i. May find heart murmurs consistent with the appropriate valve
ii. Septic emboli may present as neurological findings if left heart is involved
iii. Specific skin findings include splinter hemorrhage and Janeway lesions on
palms and soles of the feet
Cardiomyopathies (Chapter 10, Lilly)
Classified either as dilated (ventricular enlargement with systolic dysfunction), hypertrophic (ventricular
thickening with diastolic dysfunction), or restrictive (stiff myocardium because of fibrosis)
I.
Dilated Cardiomyopathies – dilation with only mild hypertrophy
a. Etiology – genetic, toxic, metabolic, and infectious causes
i. Acute viral myocarditis may lead to DCM
1. Though to be immune related, but immunosuppression doesn’t help
2. Often due to Coxsackie group of viruses
ii. Alcoholic cardiomyopathy – EtOH impairs cellular function by inhibition
mitochondrial oxidative phosphorylation
iii. Familial forms – autosomal dominant and recessive, X-linked, mitochondrial.
Genes involved code for structural proteins like actin, myosin, troponin, etc
b. Pathology – all four chamber enlargement. Some concentric hypertrophy, but dilation is
out of proportion to thickening
c. Pathophysiology – ventricular dilation with decreased contractile function
i. As V function falls, F-S mechanism is recruited such that increased diastolic
volume improves SV
ii. Sympathetics increase HR and contractility, helping to buffer falls in CO
iii. As renal blood flow drops, RAS gets activated and volume retention occurs
iv. Eventually, these compensatory mechanisms backfire and you get symptoms of
CHF (pulmonary congestion, LA enlargement with AF, volume overload)
d. Clinical findings – exactly the same as Heart Failure
e. Physical Exam – exactly the same as Heart Failure
f. Diagnosis
i. ECG shows atrial and ventricular hypertrophy with a wide variety of
arrhythmias – L or R BBB’s, AF, etc
ii. Echo shows all four chambers are enlarged
iii. Cardiac Cath is performed to rule out CAD as the source of the ventricular
dysfunction
g. Treatment
i. ACE inhibitors are 1st line Tx
ii. B-blockers have been shown to increase LF ejection fraction and mortality
iii. Digitalis – may improve symptoms
iv. K+ sparing diuretics (aldosterone blockers)
v. Anti-arrhythmics – Amiodarone may help with AF and other SVT’s
vi. Anti-coagulation b/c of AF, stasis in ventricles, venous stasis, etc.
vii. Heart transplant
II.
Hypertrophic Cardiomyopathy a.k.a. IHSS results in thickened, stiffened ventricle
a. Etiology
i. Familial disease that arises as a new mutation that gets passed down via an
autosomal dominant inheritance
ii. Genes include myosin heavy chain, cardiac troponin, etc.
Pathology – asymmetric hypertrophy of the ventricles (esp. the septum ~90%)
i. Short widened myocytes that are oriented chaotically
ii. Surrounded by fibroblasts and extracellular matrix
c. Pathophysiology – significant VH which reduces diastolic function
i. May also have systolic dysfunction if upper interventricular septum is involved.
Basically, fast flow through a thickened aortic aperture may cause a low
pressure suction of the anterior mitral valve and subsequent obstruction
ii. W/O outflow tract obstruction (i.), the thickened myocardium creates an
increased diastolic pressure, which causes backup in the LA and characteristic
dyspnea on exertion
iii. w/ outflow tract obstruction, the mitral valve remains open during systole
(recall, it’s blocking the Ao aperture), causing MR. Furthermore, the outflow
obstruction provides even more impetus for LVH, which increases myocardial
demand. Note: situations which decrease the LV volume actually exacerbate the
MV outflow obstruction. I.e. Valsalva exacerbates murmur
d. Clinical Findings – Angina, syncope (arrhythmias), ventricular fibrillations and sudden
death
e. Physical Examination
i. Commonly hear an S4 sound (LA pumping into stiff LV)
ii. LV outflow obstruction results in AS-like murmur, MR murmur heard at apex
iii. Valsalva maneuver typically reduces venous return to the heart, exacerbating the
murmur – helps to differentiate between AS and HCM
f. Diagnosis – Echocardiography can show the position of the valves and thickening of the
ventricular walls
g. Treatment
i. B-Blockers reduce myocardial O2 demand by 1) decreasing HR/contractility, 2)
decreased outflow gradient by dropping contraction, 3) increase diastolic filling
time, 4) decrease frequency of ectopic beats
ii. Ca++ blockers reduce ventricular stiffness and improve symptoms. Be careful
b/c vasodilation may actually cause exacerbations of symptoms
iii. Anti-arrhythmics
iv. Implantable defibrillator – cardioverter
v. Antibiotic prophylaxis to prevent endocarditis of aortic valve
Restrictive Cardiomyopathy – less common and characterized by rigid, but not thickened
ventricle with abnormal filling but no outflow obstruction
a. Etiology – caused by fibrosis or scarring, infiltration of abnormal substance (amyloid).
Many causes including scleroderma, amyloid, sarcoid, hemochromatosis, etc.
b. Pathophysiology – like HCM w/o outflow obstruction
c. Clinical Findings – signs of left and right sided heart failure are expected
d. PE – similar to CHF, however, you may see Kussmaul’s sign, which is paradoxical
worsening of JVD during inspiration, because RV can’t accommodate increased return
e. Diagnosis – Echo, EDG, CT, MRI
f. Treatment – Usually have poor prognosis – need to treat underlying cause. Must reduce
volume to prevent symptoms of CHF
b.
III.
Arrhythmias – (Chapter 11, Lilly)
Arrhythmias can be generally classified as disorders of impulse formation, impulse conduction or both.
I.
Normal impulse formation is generated by heart’s pacemaker cells in the SA node.
a. These cells are under the influence of the autonomic nervous system, which, via Badrenergic receptors increases the probability of the slow leak (phase 4) Na+ and (phase
0) Ca++ channels of being open.
b. Cholinergic stimulation does the opposite by decreasing probability of Ca++ and
increasing the probability of K+ (hyperpolarizing) channels to be open
c. Pharmacologic agents (B-blockers, atropine) take advantage of these principles
II.
III.
IV.
Altered Impulse formation
a. Escape Rhythms – when the SA node is too slow, a latent pacemaker will take over
generating an escape beat if spontaneous and an escape rhythm if chronic
b. Ectopic Rhythm – when latent pacemaker exceeds rate of SA node. Happens in
situations of high circulating catecholamines
c. Tissue Injury leads to pathologic changes in impulse formation outside of normal
conduction system – caused by leaky membranes in injury
Altered Conduction
a. Conduction Block – impulse gets blocked when it hits a region that is not excitable.
Caused by ischemia, fibrosis, and trauma and can be unidirectional or bidirectional
b. Unidirectional block and reentry – repeated depolarization of a part of tissue due to
unidirectional block
i. Unidirectional block stops impulse conduction along one limb
ii. Impulse travels down healthy end and reenters from opposite end of the
unhealthy limb
iii. If retrograde velocity is sufficiently slow to allow for the initial depolarization
(on the healthy side) to repolarize, a reentrant circuit can be established causing
an excessively high HR
c. Bypass Tracts – in some individuals there is an alternative pathway than the normal
conduction system called the bundle of Kent
i. EKG findings include a ventricular depolarization that occurs earlier than
normal (Kent conducts faster), which shows up as a shortened PR interval
ii. EKG also shows widened QRS complex and a delta wave which is a nick in the
Q upstroke
Treatment of arrhythmias
a. Bradyarryhthmia –
i. anticholinergic drugs such as atropine
ii. B1 agonists like isoproterenol
iii. Pacing –
1. Transthoracic stimulation, which stimulates the heart via a large
external patch applied to the chest
2. Transvenous – the more common type in which an electrode is
deposited directly to the SA node, AV node or the ventricles
b. Tachyarrythmias – both stop rapid beat and treat the sequelae
i. Pharmacologic – based on the cause of the increased rate
1. Increased automaticity - reduce phase 4, make diastolic potential more
negative, make the threshold less negative (last two make it harder to
reach threshold)
2. Reentry – decrease conduction velocity, increase refractory period
3. Triggered activity – shorter AP duration, correct Ca++ overload
ii. Vagotonic – carotid sinus increases vagal tone
iii. Cardioversion and Defibrillation – apply a large external current to depolarize
all of the myocytes at one time. Cardioversion is timed to the QRS to prevent
fibrillation, whereas defib, because the heart is already in fibrillation, is simply
applied
iv. Ablation therapy – if electrophysiology can localize the area of the myocardium
responsible for the tachycardia, that region can be destroyed with a catheter
Specific Types of Arrhythmias and their Treatment (Chapter 12, Lilly)
I.
Bradyarryhthmias
a. Sinus Bradycardia – slowing of the heart rhythm, not always pathologic
b. Sick Sinus Syndrome – SA node dysfunction that causes intermittent changes in CO
leading to hypotension and dizziness/syncope/neuro changes. Can be coupled with
tachycardia to due to a atrial fibrillation/flutter. I.e. atrial changes cause both a slowed
SA node and a abnormal pacemakers
II.
III.
IV.
Escape Rhythms – cardioprotective for SA node malfunction
a. Junctional rhythm is when the AV node becomes the pacemaker
b. Slowed HR with no P wave in front of the QRS
c. If the pacemaker is lower than the AV node, you get EKG findings similar to BBB’s. I.e.
pacer in the LV spreads slowly to the RV
AV Conduction abnormalitites
a. 1st Degree Block – Prolongation of PR interval due to slowed conduction; usually benign
i. Reversible causes – vagal tone, transient ischemia, drugs (digitalis, B-blockers,
non-dihydropyridine Ca++ channel blockers
ii. Structural causes – myocardial infarct, degeneration of the conduction system
b. 2nd Degree Block – two types characterized by intermittent failure of conduction
i. Mobitz Type I – each beat shows a progressively increasing PR interval until
finally a beat is skipped – usually asymptomatic and is not great cause for
concern, but pacing is sometimes necessary
ii. Mobitz Type II – Sudden, unpredictable loss of AV conduction without
preceding change in PR interval – often show widened QRS and may progress
to type III
c. 3rd Degree Block – complete failure of conduction system (AV dissociation)
i. Caused by infarction, drug toxicity, and chronic degeneration due to age
ii. No relation between P waves and ventricular contraction
iii. Often show an escape or junctional rhythm that may resemble a BBB
Tachyarrythmias
a. Supraventricular Arrhythmias
i. Sinus Tachycardia – characterized by SA node firing at a rate above 100. P
waves appear normal and vagal stimulation reduces rate
ii. Atrial Premature Beats - atrial reentry due to sympathetic stimulation and are
often non-pathologic. These beats are often blocked because they arrive while
the ventricle is refractory. If they do get through, the QRS is wide
iii. Atrial Flutter – atria are at 180 bpm or above
1. Many P waves find a refractory AV node and thus the signal is not
transmitted (e.g. 2:1 block)
2. P waves show a sawtooth pattern
3. Carotid massage and drugs that slow conduction through the AV node
alleviate probs with A. Flutter
4. Treatment includes cardioversion, burst pacing using a permanent
pacemaker, pharmacologic treatment (B-blockers, Ca++ channel
blockers, digoxin, conduction prolongers), radiofrequency catheter
ablation
iv. Atrial Fibrillation – chaotic rhythm with extremely fast atrial rate
1. Caused by chronic diseases such as hypertension, CAD, alcohol
intoxication, etct
2. Especially dangerous because stiff ventricle needs atrial contraction to
provide enough diastolic filling and because atrial contraction prevents
stasis and thrombus formation
3. Treatment is the same as that for flutter with the addition of
anticoagulants
v. Multifocal Atrial Tachycardia
1. EKG shows an irregular rhythm with multiple P waves (>3) and an
average atrial rate greater than 100
2. A flat baseline between P waves distinguishes this from AF
b. Ventricular Arrhythmias
i. Ventricular Premature Beats (PVC’s)
1. Show up as non-P wave related, widened QRS complexes that arise
from ectopic foci in the ventricles
2. When the occur in doublets or triplets, there is an increased risk
3. If symptomatic, treat with B-blockers
V.
ii. Ventricular Tachycardia
1. Very wide QRS complexes (greater than 3 small boxes)
2. Can exists as monomorphic (homogenous) or polymorphic
3. Polymorphic variety includes “Torsades de Pointes,” which can occur
due to a number of causes
iii. Ventricular Fibrillation – cause of “dropping dead” in MI
1. The only treatment is prompt ventricular defibrillation
2. Usually preceded by a period of VT
Easy Classification scheme:
a. Insert here