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386 Cards in this Set
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- 3rd side (hint)
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Define sinus rhythm.
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P before every QRS and QRS after every P.
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Normal axis on EKG.
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upright QRS on leads I and aVF
(means 0 to 90 degrees) |
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Define left-axis deviation EKG.
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upright QRS in I and downward in aVF
(up to -30 degrees is considered normal variant) |
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Define right-axis deviation.
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down QRS in I and up on aVF
(up to +105 degrees is considered a normal variant) |
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EKG Intervals
Normal PR and QRS |
PR
120 - 200 msec QRS < 120 msec |
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EKG Intervals
AV Block |
PR > 200 msec
or P with no QRS afterward |
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EKG Intervals
LBBB |
QRS > 120 msec
one R wave in V1 wide, tall R in I, V5 and V6 A mnemonic to remember the ECG changes is WiLLiaM MaRRoW i.e. with Left bundle branch block there is a W in V1 and a M in V6 and with a RBBB there is a M in lead V1 and a W in lead V6 |
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EKG Intervals
RBBB |
QRS > 120 msec
RSR' complex (rabbit ears) qR or R morphology with a wide R wave in V1 QRS pattern with a wide S in I, V5 and V6 A mnemonic to remember the ECG changes is WiLLiaM MaRRoW, i.e. with Left bundle branch block there is a W in V1 and a M in V6 and with a RBBB there is a M in lead V1 and a W in lead V6 |
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EKG Intervals
Long QT Syndrome What is this? |
QTc > 440 msec
predisposes to v tach |
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Ischemia / Infarction
Ischemia changes on EKG |
new inverted T waves
poor R-wave progression in the precordial leads ST depression and elevation |
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EKG CHANGES
Transmural Infarct |
significant Q waves
(> 40 msec or more than 1/3 of the QRS amplitude) ST elevations T-wave inversions |
Q waves represent no electrical activity
myocardial tissue has undergone scarring in that area |
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Chamber Enlargement
EKG Changes Right Atrial Enlargement |
P PULMONALE
P-wave amplitude in II is > 2.5 mm -------------- P Pulmonale causes Peaked P waves P Mitrale causes M-shaped P waves |
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Chamber Enlargement
EKG Changes Left Atrial Enlargement |
width of P-wave in II > 120 msec
or terminal negative deflection in V1 > 1mm in amplitude and > 40 msec in duration notched P waves can frequently be seen in II -------------- P Pulmonale causes Peaked P waves P Mitrale causes M-shaped P waves |
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Chamber Enlargement
EKG Changes LVH |
ONE CRITERIA
amplitudes of S in V1 + R in V5 or V6 > 35 mm ALTERNATE CRITERIA amplitude of R in aVL + S in V3 > 28 mm in men or > 20 mm in women |
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Chamber Enlargement
EKG Changes RVH |
right-axis deviation
and R in V1 > 7 mm |
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Define JVD and what it means.
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> 7 cm above sternal angle
suggests: RH failure pulm HTN volulme overload tricuspid regurg pericardial disease |
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What does hepatojugular reflux suggest?
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fluid overload
impaired RV compliance |
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Define Kussmaul's sign and what it suggests.
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Kussmaul's sign
increase in JVP with inspiration suggests: RV infarction postop cardiac tamponade tricuspid regurg constrictive pericarditis |
similar to hepatojugular reflex
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Physical Examination of Murmurs
Systolic or Diastolic Aortic Stenosis |
systolic murmur
harsh systolic ejection murmur that radiates to the carotids |
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Physical Examination of Murmurs
Systolic or Diastolic Mitral Regurgitation |
systolic murmur
holosystolic murmur that radiates to the axilla or carotids |
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Physical Examination of Murmurs
Systolic or Diastolic Mitral Valve Prolapse |
systolic
midsystolic or late systolic murmur with preceding click |
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Physical Examination of Murmurs
Systolic or Diastolic Flow Murmur |
very common
does not imply cardiac disease |
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Physical Examination of Murmurs
Systolic or Diastolic Aortic Regurgitation |
diastolic
an early decrescendo murmur |
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Physical Examination of Murmurs
Systolic or Diastolic Mitral Stenosis |
diastolic
mid to late low pitched murmur |
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What does an S3 gallop suggest?
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dilated cardiomyopathy
(floppy ventricle) mitral valve disease (often normal in younger pts and in high-output states like pregnancy) |
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What does an S4 gallop suggest?
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HTN
diastolic dysfunction (stiff ventricle) aortic stenosis (often normal in younger pts and in athletes) |
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What does pulmonary edema suggest?
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left heart failure
(fluid "backs up" into the lungs) |
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What does peripheral edema suggest?
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RH Failure
and Biventricular Failure (fluid "backs up" into the periphery) peripheral venous disease constrictive pericarditis tricuspid regurgitation hepatic disease lymphedema others: nephrotic syndrome hypoalbuminemia drugs |
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PERIPHERAL PULSES
What does increased peripheral pulses mean? |
compensated aortic regurgitation
coarctation (arms > legs) PDA |
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PERIPHERAL PULSES
What does decreased peripheral pulses mean? |
peripheral arterial disease
late-stage heart failure |
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PERIPHERAL PULSES
What is pulsus paradoxus and what does it suggest? |
decreased systolic BP with inspiration
pericardial tamponade asthma and COPD tension pneumothorax foreign body in airway |
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PERIPHERAL PULSES
What is pulsus alternans and what does it suggest? |
alternatiang weak and strong pulses
cardiac tamponade impaired LV systolic fxn poor prognosis |
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PERIPHERAL PULSES
What is pulsus parvus et tardus and what does it suggest? |
weak and delayed pulse
aortic stenosis |
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Management options for atrial fibrillation.
ABCD |
Anticoagulate
B-blockers to control rate Cardiovert/Calcium channel blockers Digoxin |
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Risk factors for CHF.
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CAD
HTN cardiomyopathy valvular heart disease diabetes |
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CHF
Systolic vs Diastolic Dysfxn Define systolic dysfxn. |
EF < 50%
and increased LV EDV |
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What is the mechanism of systolic dysfxn?
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inadequate LV contractility or increased afterload
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How does the heart compensate for systolic dysfxn?
What happens in the long run? |
HYPERTROPHY and VENTRICULAR DILATION
(Frank-Starling law) compensation fails leading to increased myocardial work and worsening systolic fxn |
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CHF
Systolic Dysfxn Early Signs Progression Late Signs |
EARLY
exertional dyspnea PROGRESSION orthopnea paroxysmal nocturnal dyspnea (PND) LATE rest dyspnea |
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Physical Examination
CHF Systolic Dysfxn |
parasternal lift
elevated and sustained LV pulse S3/S4 gallop JVD peripheral edema |
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Diagnostic W/U
CHF Systolic Dysfxn |
mostly a clinical workup
CXR shows cardiomegaly cephalization of pulmonary vessels pleural effusions vascular congestion interstitial edema prominent hila Echo shows decreased EF ventricular dilation Labs BNP > 500 pg/mL inc creatinine decreased sodium in later stages EKG usually nondiagnostic, but could help point to: AF old MI LVH sign of long-standing HTN |
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Acute Tx
CHF Systolic Dysfxn |
DIURESE
thiazides loops ACEIs or ARBs Do not start beta-blockers during decompensated CHF, start after the patient is euvolemic |
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Acute Pulm Congestion Tx
CHF Systolic Dysfxn |
LMNOP
Lasix Morphine Nitrates Oxygen Position (upright) |
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Chronic Tx
CHF Systolic Dysfxn |
PREVENT HEART REMODELING AND DECREASE MORTALITY
beta-blockers ACEIs/ARBs (avoid CCBs) MAINTAIN VOLUME STATUS (to prevent vol overload) restrict sodium and fluids diuretics (loops, thiazides) DECREASE MORTALITY RISK low-dose spironolactone |
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Tx for EF < 35%
CHF Systolic Dysfxn |
ICD
Implantable Biventricular Cardiac Defibrillator |
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Tx for pts unresponsive to maximal therapy
CHF Systolic Dysfxn |
mechanical LV assist device
cardiac transplantation |
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Left vs Right Sided CHF
Name 5 Left Sided Signs |
left-sided S3/S4 gallop
b/l basilar rales pleural effusions pulm edema orthopnea / paroxysmal nocturnal dyspnea |
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Left vs Right Sided CHF
Name 5 Right Sided Signs |
right-sided S3/S4 gallop
JVD hepatojugular reflex hepatomegaly / ascites peripheral edema |
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CHF
Comparison of systolic vs diastolic dysfunction. For Systolic: Age Comorbidities Physical Exam CXR EKG/echo |
AGE
< 65 COMORBIDITIES DCM valvular heart disease PE displaced PMI S3 gallop CXR pulm congestion cardiomegaly EKG/ECHO Q waves EF < 40% |
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CHF
Comparison of systolic vs diastolic dysfunction. For Diasystolic: Age Comorbidities Physical Exam CXR EKG/echo |
AGE
> 65 COMORBIDITIES restrictive or hypertrophic cardiomyopathy renal disease HTN PE sustained PMI (ie you feel pulse for a longer duration of time) S4 gallop CXR pulm congestion normal heart size EKG/ECHO LVH EF > 55% |
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Define non-systolic dysfxn.
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decreased ventricular compliance with normal systolic function
impaired relaxation of ventricles or impaired passive filling |
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Mechanisms of non-systolic dysfxn.
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IMPAIRED RELAXATION
ischemia aging hypertrophy IMPAIRED FILLING scarring from prior MI restrictive cardiomyopathy |
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Echo of non-systolic dysfxn.
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LV end-diastolic pressure is up
cardiac output is normal EF normal or increased |
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What history is associated with non-systolic dysfxn?
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stable angine
unstable angina SOB dyspnea on exertion arrythmias MI heart failure sudden death |
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Tx
Non-Systolic Dysfxn |
FIRST LINE
diuretics MAINTAIN RATE AND BP CONTROL beta-blockers ACEIs/ARBs CCBs (digoxin is not useful) |
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SIDE EFFECTS
loop diuretics |
ototoxicity
hypokalemia hypocalcemia dehydration gout |
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SIDE EFFECTS
thiazides |
hypokalemic metabolic alkalosis
hyponatremia HYPERGLUC hyperGlycemia hyperLipidemia hyperUricemia hyperCalcemia |
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SIDE EFFECTS
K+-sparing agents |
hyperkalemia
gynecomastia sexual dysfxn |
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SIDE EFFECTS
carbonic anhydrase inhibitors |
hyperchlormeic metabolic acidosis
neuropathy NH3 toxicity sulfa allergy |
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SIDE EFFECTS
osmotic agents |
pulm edema
dehydration |
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When are osmotic agents contraindicated?
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contraindicated in anuria and CHF
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Causes of sinus bradycardia.
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normal response to cardiovascular conditioning
sinus node dysfxn EXCESS MEDS beta-blocker ccb |
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Signs and Sx
Sinus Bradycardia |
asymptomatic
lightheadedness syncope chest pain hypotension |
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Tx
Sinus Bradycardia |
asymptomatic
no tx atropine to increase HR pacemaker for definitive tx in severe cases |
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Cause of first-degree AV block.
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can occur in normal individuals
assoc with increased vagal tone and with beta-blockers or CCBs |
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Signs and Sx
First-Degree AV Block |
asymptomatic
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EKG findings
1st Degree AV Block |
PR > 200 msec
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Tx
1st Degree AV Block |
none necessary
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Causes of 2nd degree AV block, Mobitz Type 1.
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DRUGS
digoxin beta-blockers CCBs increased vagal tone right coronary ischemia or infarction |
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Signs and Sx
2nd degree AV block, Mobitz Type 1 |
usually asymptomatic
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EKG Findings
2nd degree AV block, Mobitz Type 1 |
Progressive PR lengthening until a dropped beat occurs
the PR interval then resets |
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Tx
2nd degree AV block, Mobitz Type 1 |
stop offending drugs
atropine as indicated |
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Causes
2nd degree AV block, Mobitz Type 2 |
fibrotic disease of the conduction system
acute, subacute or prior MI |
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Signs and Sx
2nd degree AV block, Mobitz Type 2 |
occasionally syncope
frequent progression to 3rd degree AV block |
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EKG Findings
2nd degree AV block, Mobitz Type 2 |
unexpected dropped beat without a change in PR interval
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Tx
2nd degree AV block, Mobitz Type 2 |
pacemaker
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Mechanism behind 3rd degree AV block (complete).
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no electrical communication between atria and vetricles
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Signs and Sx
3rd degree AV block (complete) |
syncope
dizziness acute heart failure hypotension cannon A waves |
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EKG Findings
3rd degree AV block (complete) |
no relationship between P and QRS complexes
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Tx
3rd degree AV block (complete) |
pacemaker
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Signs and Sx
Sick Sinus Syndrome / Tachy-bradycardia Syndrome |
depends on brady or tachy
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Tx
Sick Sinus Syndrome / Tachy-bradycardia Syndrome |
this is the most common indication for pacemaker placement
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Causes
Premature Ventricular Contraction |
ectopic beats arise from ventricular foci
assoc with: hypoxia electrolyte abnorm hyperthyroidism |
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Signs and Sx
Premature Ventricular Contraction |
usually asymptomatic
may lead to palpitations |
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EKG Findings
Premature Ventricular Contraction |
early, wide QRS not preceded by a P wave
PVCs are usually followed by a compensatory pause |
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Tx
Premature Ventricular Contraction |
treat the underlying cause
if symotpmatic: give beta-blockers or other antiarrhythmics |
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Cause of V Tach.
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assoc with:
CAD MI structural heart disease long QT |
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Signs and Sx
V Tach |
nonsustained VT is often asymptomatic
sustained VT can lead to: palpitations hypotension angina syncope VF death |
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EKG Findings
V Tach |
3 or more consecutive PVCs
wide QRS in a regular rapid rhythm may see AV dissociation (AV block) |
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Tx
V Tach |
cardioversion and antiarrhythmics
(eg amiodarone, lidocaine, procainamide) |
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Cause
V Fib |
assoc with:
CAD structural heart disease cardiac arrest / asystole |
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Signs and Sx
V Fib |
syncope
absence of blood pressure pulselessness |
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EKG Findings
V Fib |
totally erratic wide-complex tracing
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Tx
V Fib |
immediate electrical cardioversion
ACLS protocol |
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Cause
Torsades de pointes |
assoc with:
long QT syndrome proarrhythmic response to meds hypokalemia congenital deafness alcoholism |
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Signs and Sx
Torsades de pointes |
sudden cardiac death
typically assoc with: palpitations dizziness syncope |
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EKG Findings
Torsades de pointes |
polymorphous QRS
VT with rates btw 150-250 bpm |
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Tx
Torsades de pointes |
give magnesium initially and cardiovert if unstable
correct hypokalemia withdraw offending drugs |
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What is dilated cardiomyopathy characterized by?
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LV dilation
decreased EF |
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Causes of dilated cardiomyopathy.
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mostly are secondary causes of:
alcohol myocarditis postpartum drugs (doxorubicin, AZT, cocaine) endocrinopathies (thyroid dysfunction, acromegaly, pheochromocytoma) infection (coxsacakievirus, HIV, Chagas, parasites) genetic nutritional defects (wet beriberi) |
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What are the 2 most common causes of DCM?
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ischemia
long-standing HTN |
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The symptoms of DCM are most similar to sx of what other disease?
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CHF
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Physical Exam
DCM |
displacement of PMI
JVD S3/S4 gallop mitral/tricuspid regurgitation |
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Diagnostic workup for DCM.
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Echo is diagnostic
EKG shows nonspecific ST-T changes low-voltage QRS sinus tachy ectopy LBBB CXR enlarged, balloon-like heart and pulm congestion |
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Tx
DCM |
address the underlying etiology
Tx CHF sx: diruetics ACEIs/ARBs beta-blockers avoid CCBs in heart failure |
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Why should you avoid CCBs in heart failure?
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some drugs have a deleterious effect in pts with HF with systolic dysfxn
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Differentiate Between:
Dilated vs Hypertrophic vs Restrictive Whats the major abnormality in each condition? |
Dilated
impaired contractility Hypertrophic impaired relaxation Restrictive impaired elasticity |
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Differentiate Between:
Dilated vs Hypertrophic vs Restrictive LV cavity size (end diastole) |
Dilated
very increased Hypertrophic decreased Restrictive increased |
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Differentiate Between:
Dilated vs Hypertrophic vs Restrictive LV Cavity Size (End Systole) |
Dilated
very increased Hypertrophic very decreased Restrictive increased |
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Differentiate Between:
Dilated vs Hypertrophic vs Restrictive EF |
Dilated
very decreased Hypertrophic normal or increased Restrictive normal or decreased |
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Differentiate Between:
Dilated vs Hypertrophic vs Restrictive Wall Thickness |
Dilated
decreased or variable Hypertropihc very increased Restrictive increased or variable |
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What causes S3 and what does it suggest?
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S3 is the sound of blood bouncing around in the ventricle as a result of inflowing blood crashing into from the atria
another way of saying: an S3 gallop signifies rapid ventricular filling in the setting of fluid overload and is assoc with HF and DCM it suggests HF |
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What causes S4 and what does it suggest?
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S4 is the sound of turbulent blood caused by the atria contracting forcibly against a stiff or hypertrophic ventricle
it is assoc with stiffness of the ventricle like hypertrophic CM (and any disease that causes stiffness) |
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What are the main characteristics of hypertrophic cardiomyopathy?
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impaired LV relaxation and filling due to thickened ventricular walls
(non-systolic dysfxn) hypertrophy involves interventricular septum, leading to LV outflow tract obsxn and impaired ejection of blood |
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What is the genetic form of hypertrophic cardiomyopathy?
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HOCM
which is autosomal dominant in 50% of HOCM pts |
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Two main causes of marked hypertrophic cardiomyopathy.
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aortic stenosis
hypertension |
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Signs and Sx
Hypertrophic Cardiomyopathy |
syncope
dyspnea palpitations angina sudden cardiac death |
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Physical Exam
Hypertrophic Cardiomyopathy |
sustained apical impulse
S4 gallop systolic ejection crescendo-descrendo murmur that increases with decreasing preload (eg valsalva maneuver, standing) and decreases with increasing preload (eg passive leg raise) |
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Diagnostic w/u of Hypertrophic Cardiomyopathy.
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echo is diagnostic and shows asymmetrically thickened septum and dynamic obsxn of blood flow
EKG shows LVH CXR left atrial enlargement 2nd to MR |
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Tx
Hypertrophic Cardiomyopathy |
beta-blockers are initial therapy
CCBs are second-line if surgery is an option: dual-chamber pacing partial excision or alcohol ablation of myocardial septum ICD placement mitral replacement AVOID INTENSE ATHLETIC COMPETITION AND TRAINING |
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What are the main characteristics of Restrictive Cardiomyopathy?
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decreased elasticity of myocardium leading to impaired diastolic filling
no significant systolic dysfxn (normal or near-normal EF) |
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What are the main causes of Restrictive Cardiomyopathy?
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INFILTRATIVE DISEASE
amyloidosis sarcoidosis hemochromatosis Scarring Fibrosis (2nd to radiation) |
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Signs and Sx
Restrictive Cardiomyopathy |
both left and right-sided HF
right-sided sx dominate JVD peripheral edema |
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Diagnostic w/u for Restrictive Cardiomyopathy.
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Echo is key for diagnosis
rapid early filling near-normal EF CXR/MRI/cardiac cath are helpful for characterization (eg sarcoid, amyloidosis) cardiac bx may reveal fibrosis or evidence of infiltration EKG LBBB low voltages seen in amyloidosis |
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Tx
Restrictive Cardiomyopathy |
tx options limited and palliative for the most part
cautious use of diuretics for fluid overload vasodilators to decrease filling pressure |
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Major risk factors for CAD.
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age (M>45, F>55)
male gender increased LDL decreased HDL DM HTN fam hx of premature CAD (m<55, F<65) smoking PAD |
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Signs and Sx
CAD |
stable and unstable angina
SOB dyspnea on exertion arrhythmias MI heart failure sudden death |
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Name 4 CAD equivalents.
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DM
symtomatic CAD PAD AAA |
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Classic triad of angina.
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substernal chest pain
precipitated by stress/exertion relieved by rest/nitrates |
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What is the underlying cause of angina?
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myocardial ischemia
(O2 supply and demand mismatch) |
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What is Prinzmetal's angina?
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angina that is caused by vasospasm of the coronary vessels, not by carotid plaques like in stable/unstable angina
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Cardiac enzymes in Prinzmetal's angina.
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PrinzMETAL's angina doesnt MEDDLE with enzymes.
it does have ST elevation, just no cardiac enzyme elevatino |
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Clinically silent MIs can be seen in which pts?
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women
diabetics elderly post-heart transplant pts |
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What two drugs have been shown to have a mortality benefit in the tx of angina?
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ASA
beta-blockers |
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Besides classic triad, what other sx in angina?
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pain radiates
SOB NV diaphoresis lightheadedness |
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Physical Exam
Angina |
PE is generally unremarkable
look for carotid or peripheral bruits to suggest atherosclerosis and HTN |
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How to diagnose CAD?
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exercise stress test with EKG monitoring showing ST changes
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Acute Tx
angina |
ONAM
ASA O2 IV nitro IV morphine Also: IV beta-blockers CCBs ACEIs |
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Chronic TX
Angina |
nitrates
ASA beta-blockers CCBs (second-line agents for symptomatic control only) RISK FACTOR REDUCTION smoking cholesterol HTN |
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What's the main idea behind the cause of ACS?
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plaque disruption
vasospam that leads to acute myocardial ischemia |
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Define unstable angina.
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chest pain that is:
new onset accelerating (ie occurs with less exertion, lasts longer, or is less responsive to meds) occurs at rest different from stable angina by pt history MEANS PLAQUE INSTABILITY MEANS IMPENDING INFARCTION |
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Contrast unstable angina and NSTEMI.
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NSTEMI = necrosis
marked by elevations in trop I and CK-MB without ST elevations UNSTABLE ANGINA only suggests impending infarction |
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Labs and EKG
Unstable Angina |
no elevations in cardiac enzymes
EKG shows ST elevations |
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Labs and EKG
NSTEMI |
elevations in Trop I and CK-MB
no ST elevations on EKG |
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Risk Stratification in NSTEMI and UA.
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risk stratification by Thrombolysis in Myocardial Infarction (TIMI)
used to categorize a patient's risk of death and ischemic events and provides a basis for therapeutic decision making |
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When risk-stratifying pts, what TIMI score indicates high risk and out of how many total points?
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more than 3 out of 7 total
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TIMI
History (4) and Presentation (3) |
HISTORY
Age > 65 > 3 CAD risk factors Known CAD (stenosis > 50%) ASA use in past 7 days PRESENTATION severe angina (> 2 episodes within 24 hrs) ST deviation > 0.5mm + cardiac marker |
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What is the best predictor of survival in STEMI pts?
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LV EF
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EKG
STEMI |
ST Elevations
LBBB RECIPROCAL CHANGES IN POSTERIOR WALL INFARCTS ST depression and dominant R waves in V1-V2 |
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Sequence of EKG changes in STEMI.
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Peaked T Waves -->
ST elevation --> Q Waves --> T-wave inversion --> ST normalization --> T normalization |
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What is the most sensitive cardiac marker for STEMI?
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Troponin I
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Define the CK Index.
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CK-MB/Total CK ratio
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How long does it take for Trop I and CK-MB to rise following chest pain?
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up to 6 hrs
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What are the ST Abnormalities in inferior MI?
What vessels are involved? |
ST elevations in II, III, aVF
RCA/PDA LCA Right Coronary / Posterior Descending Left Coronary Artery |
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What other workup should you do to evaluate an inferior MI?
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obtain a right-sided EKG to look for ST elevations in the RV
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What are the ST Abnormalities in anterior MI?
What vessels are involved? |
ST elevations in V1-V4
LAD and diagonal branches |
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What are the ST Abnormalities in lateral MI?
What vessels are involved? |
ST elevation in I, aVL, V5-V6
LCA Left Coronary Artery |
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What are the ST Abnormalities in posterior wall MI?
What vessels are involved? |
ST depression in V1-V2 (anterior leads)
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What other workup can you do to evaluate for posterior wall MI?
|
obtain posterior EKG leads V7-V9 to assess for ST elevations
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Common causes of chest pain.
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GERD
angina esophageal pain musculoskeletal d/o (costochondritis, trauma) pneumonia |
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Acute Tx
STEMI What if the pt is in HF? |
O2
nitrates ASA morphine beta-blockers clopidogrel If pt is in HF or cardiogenic shock, do not give beta-blockers, instead give ACEIs provided the pt is not hypotensive. THEN EMERGENT ANGIOGRAPHY AND PCI WITHIN 90 MINUTES |
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If PCI cannot be performed within 90 minutes, what next?
|
if there are no contraindications to thrombolysis (eg hx of hemorrhagic stroke or recent ischemic stroke, severe HF, or cardiogenic shock) and the pt presents within 3 hrs of chest pain onset ...
thrombolysis with tPA, reteplase or steptokinase |
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Long-term tx for STEMI.
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ASA
ACEIs beta-blockers high-dose statins clopidogrel (if PCI was performed) |
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Modifiable risk factors in STEMI treatment.
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diet
exercise smoking cessation |
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STEMI COMPLICATIONS
Most common event |
arrhythmia
lethal arrhythmia is the most frequent cause of death |
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STEMI COMPLICATIONS
Other common events |
reinfarction
LV wall rupture VSD pericarditis papillary muscle rupture (MR regurg) LV aneurysm mural thrombi |
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What is Dressler's syndrome?
|
autoimmune process occurring 2-10 wks post-MI
F pericarditis pleural effusion leukocytosis inc ESR |
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What complications generally occur on the first day after a STEMI?
|
heart failure
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What complications generally occur 2-4 days after MI?
|
arrhythmia
pericarditis |
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What complications generally occur 5-10 days after MI?
|
LV wall rupture
(acute pericardial tamponade causing electrical alternans, pulseless electrical activity) papillary muscle rupture (mitral regurg) |
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What complications generally occur weeks to months post-MI?
|
ventricular aneurysm
(CHF, arrhythmia, persistent ST elevation, mitral regurg, thrombus formation) |
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Define dyslipidemia.
|
HDL < 40 mg/dL
LDL > 130 mg/dL Triglycerides > 150 mg/dL Total Cholesterol > 200 mg/dL |
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Indications for CABG are UnLimiTeD.
ULTD |
Unable to perform PCI (diffuse disease)
Left main coronary artery disease Triple-vessel disease Depressed ventricular fxn |
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Causes of dyslipidemia.
|
obesity
DM alcoholism hypothyroidism nephrotic syndrome hepatic disease Cushing's syndrome OCP use high-dose diuretic familial hypercholesterolemia |
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Signs and Sx
Dyslipidemia |
no specific signs or sx
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Physical Exam
Dyslipidemia |
extremely high triglycerides or LDL may have:
xanthomas (eruptive nodules in the skin over tendons) xanthelasmas (yellow fatty deposits in the skin around eyes) lipemia retinalis (creamy appearance of retinal vessels) |
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Diagnostic w/u for dyslipidemia.
|
fasting lipid profile for pts > 35 or > 20 yo with CAD risk fators
repeat q 5 yrs or sooner if lipid levels are elevated DIAGNOSIS Total choles > 200 on 2 separate occasions is diagnostic of hypercholesterolemia LDL > 130 or HDL < 40 is diagnostic of dyslipidemia even if total choles < 200 |
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Tx
Dyslipidemia |
FIRST INTERVENTION
12-week trial of diet and exercise in a pt with no konwn atherosclerotic vascular disease |
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Name 4 CAD risk equivalents.
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symptomatic carotid artery disease
peripheral arterial disease AAA diabetes *An HDL > 60 counts as a "negative" risk factor and removes 1 risk factor from the total score |
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3 RISK CATEGORIES
CAD or CAD Risk Equivalents 2+ risk factors 0-1 risk factor For the 1st category, what is the LDL goal, when do you start lifestyle modification and drug therapy? |
GOAL
< 100 mg/dL or < 70 LIFESTYLE MOD when LDL > 100 mg/dL ADD DRUG THERAPY when LDL > 100 mg/dL |
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3 RISK CATEGORIES
CAD or CAD Risk Equivalents 2+ risk factors 0-1 risk factor For the 2nd category, what is the LDL goal, when do you start lifestyle modification and drug therapy? |
GOAL
< 130 mg/dL LIFESTYLE MOD when LDL > 130 DRUG when LDL > 130 |
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3 RISK CATEGORIES
CAD or CAD Risk Equivalents 2+ risk factors 0-1 risk factor For the 3rd category, what is the LDL goal, when do you start lifestyle modification and drug therapy? |
GOAL
LDL < 160 mg/dL LIFESTYLE MOD when LDL > 160 mg/dL ADD DRUG when LDL > 190 |
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Define HTN.
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EITHER
systolic BP > 140 ORRRR diastolic BP > 90 mmHg based on 3 measurements separated in time |
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Risk factors for essential / primary hypertension.
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family hx of HTN or heart dis
high-sodium diet smoking obesity ethnicity (black > white) advanced age |
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Signs of end-organ damage in HTN.
(List out by organ.) |
BRAIN
stroke dementia EYE cotton-wool exudates hemorrhage HEART LVH KIDNEY proteinuria CKD |
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What do renal bruits signify?
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renal artery stenosis
it signifies that renal artery stenosis is the cause of HTN |
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In HTN, what is the single most effective lifestyle modification?
|
weight loss
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What is the BP goal in HTN and DB pts?
(Give 2 answers.) |
HTN PTS
< 140 / < 90 mmHg DB PTS < 130 / < 80 |
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Which tx for HTN has shown to decrease mortality in uncomplicated HTN?
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diuretics
ACEIs beta-blockers |
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Periodically test for end-organ complications including renal complications, in pts with HTN.
What test would you use for evaluating renal damage? |
SERUM
BUN, Cr URINE urine protein to creatinine ratio (this is a better estimate of proteinuria) |
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Periodically test for end-organ complications including cardiac complications, in pts with HTN.
What test would you use for evaluating cardiac damage? |
any test that evaluates for the heart
EKG shows evidence of hypertrophy |
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Treatment for HTN.
ABCD |
ABCD
ACEIs/ARBs Beta-blockers CCBs Diuretics |
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Causes of secondary HTN.
CHAPS |
Cushing's syndrome
Hyperaldosteronism (Conn's Syndrome) Aortic coarctation Pheochromocytoma Stenosis of renal arteries |
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Tx
Stage 1 HTN (140-160/90-100) |
Thiazides diuretics
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Tx
Stage 2 HTN (>160/100) |
two-drug combo
thiazide + ACEI/ARB, beta blocker or CCB |
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Side Effects
HMG-CoA Reductase Inhibitors |
increased LFTs
myositis warfarin potentiation |
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Effect on Lipid Profile
HMG-CoA Reductase Inhibitors |
decreases LDL and triglycerides
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Example Meds
HMG-CoA Reductase Inhibitors |
atorvastatin
simvastatin lovastatin pravastatin rosuvastatin |
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Side Effects
Lipoprotein Lipase Stimulators (Fibrates) |
GI upset
cholelithiasis myositis increased LFTs |
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Effect on Lipid Profile
Lipoprotein Lipase Stimulators (Fibrates) |
decreases triglycerides
increases HDL |
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Mechanism of Action
Lipoprotein Lipase Stimulators (Fibrates) |
increases lipoprotein lipase leading to increased VLDL and triglyceride catabolism
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Example Meds
Lipoprotein Lipase Stimulators (Fibrates) |
Gemfibrozil
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Side Effects
Cholesterol absorption inhibitors |
diarrhea
abdominal pain angioedema |
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Effect on Lipid Profile
Cholesterol absorption inhibitors |
decreases LDL
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Mechanism of Action
Cholesterol absorption inhibitors |
decreases absorption of cholesterol at the small intestine brush border
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Example Meds
Cholesterol absorption inhibitors |
Ezetimibe (Zetia)
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Side Effects
Niacin |
skin flushing
(prevent with ASA) paresthesias pruritis GI upset increased LFTs |
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Effect on Lipid Profile
Niacin |
decreases LDL
increases HDL |
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Mechanism of Action
Niacin |
decreases fatty acid release from adipose tissue
decreases hepatic synthesis of LDL |
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Example Meds
Niacin |
Niaspan
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Side Effects
Bile Acid Resins |
constipation
GI upset LFT abnormalities myalgias can decrease absorption of other drugs from small intestine |
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Effect on Lipid Profile
Bile Acid Resins |
decrease LDL
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Mechanism of Action
Bile Acid Resins |
binds intestinal bile acids, leading to decreased bile acid stores and increases catabolism of LDL from plasma
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Example Meds
Bile Acid Resins |
cholestyramine
colestipol colesevelam |
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Treatment of Essential HTN in Specific Populations
List the drugs for uncomplicated HTN. |
Diuretics
Beta-blockers ACEIs |
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Treatment of Essential HTN in Specific Populations
List the drugs for CHF. |
Diuretics
Beta-blockers ACEIs/ARBs Aldosterone blockers |
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Treatment of Essential HTN in Specific Populations
List the drugs for Diabetes. |
Diuretics
Beta-blockers ACEIs/ARBs CCBs |
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Treatment of Essential HTN in Specific Populations
List the drugs for Post-MI. |
Beta-blockers
ACEIs/ARBs Aldosterone Blockers |
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Treatment of Essential HTN in Specific Populations
List the drugs for CKD. |
ACEIs/ARBs
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Treatment of Essential HTN in Specific Populations
List the drugs for BPH. |
Diuretics
Alpha1-adrenergic blockers |
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Treatment of Essential HTN in Specific Populations
List the drugs for isolated systolic HTN. |
Diuretics
ACEIs CCBs (dihydropyridines) |
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Renal artery stenosis is a cause of secondary HTN in pts < 25 and > 50.
Name the cause of renal artery stenosis for each age group above. |
< 25
Fibromuscular Dysplasia > 50 Atherosclerosis |
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How do you diagnose renal artery stenosis?
|
MRA or Renal artery doppler ultrasound
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Tx
Renal Artery Stenosis |
Angioplasty or Stenting
Consider ACEIs in unilateral disease In b/l dis, ACEIs can accelerate kidney failure by prefrential vasodilation of the efferents Open Surgery if angioplasty not effective |
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Which common medication that females take is a cause of secondary HTN? And how is this treated?
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OCP
(common in women > 35, obese women, and long-time users) discontinue it |
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Pheochromocytoma is a cause of secondary HTN.
What is the basic mechanism? What are the 3 classic sx? |
adrenal gland tumor secretes epi and norepi
SX episodic headache sweating tachycardia |
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How to diagnose pheochromocytoma?
|
urine metanephrines
plasma metanephrines |
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Tx
Pheochromocytoma |
surgical removal of tumor after tx with both alpha-blockers and beta-blockers
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What causes Conn's syndrome (hyperaldosteronism)?
What is the classic triad of sx? |
adrenal adenoma produces aldosterone
TRIAD of SX HTN unexplained hypokalemia metabolic alkalosis |
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Diagnostic w/u for Conn's syndrome (hyperaldosteronism).
|
plasma aldosteorne
renin level increased aldosterone and decreased renin suggests primary hyperaldosteronism |
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Tx
Conn's Syndrome (Hyperaldosteronism) |
surgical removal
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What causes Cushing's Syndrome?
|
pituitary tumor produces excess ACTH
or ectopic tumor adrenal adenoma/carcinoma produces cortisol exogenous steroids |
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Tx
Cushing's Syndrome |
surgical removal of tumor
removal of exogenous steroids |
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How do pts with hypertensive crisis present?
|
presents with end-organ damage
renal damage chest pain (ischemia/MI) back pain (aortic dissection) changes in mental status (hypertensive encephalopathy) |
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What causes Cushing's Syndrome?
|
pituitary tumor produces excess ACTH
or ectopic tumor adrenal adenoma/carcinoma produces cortisol exogenous steroids |
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HYPERTENSIVE CRISIS HAS 3 DIAGNOSIS
Hypertensive Urgency Hypertensive Emergency Malignant HTN What is hypertensive urgency? |
elevated BP with mild to mod sx (HA and CP), w/o end-organ damage
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Tx
Cushing's Syndrome |
surgical removal of tumor
removal of exogenous steroids |
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HYPERTENSIVE CRISIS HAS 3 DIAGNOSIS
Hypertensive Urgency Hypertensive Emergency Malignant HTN What is hypertensive emergency? |
elevated BP w/signs of impending end-organ failure, such as:
AKI intracranial hemorrhage papilledema EKG suggests ischemia pulm edema |
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HYPERTENSIVE CRISIS HAS 3 DIAGNOSIS
Hypertensive Urgency Hypertensive Emergency Malignant HTN What is malignant HTN? |
diagnosed on the basis of progressive renal failure
and/or encephalopathy with papilledema |
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How do pts with hypertensive crisis present?
|
presents with end-organ damage
renal damage chest pain (ischemia/MI) back pain (aortic dissection) changes in mental status (hypertensive encephalopathy) |
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Tx
Hypertensive Urgencies |
oral antihypertensives
(eg beta-blockers, clonidine, ACEIs) GOAL lower BP over 24-48 hrs |
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HYPERTENSIVE CRISIS HAS 3 DIAGNOSIS
Hypertensive Urgency Hypertensive Emergency Malignant HTN What is hypertensive urgency? |
elevated BP with mild to mod sx (HA and CP), w/o end-organ damage
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Tx
Hypertensive Emergencies |
IV meds
(labetalol, nitroprusside, nicardipine) GOAL lower MAP by no more than 25% over 1st 2 hours to prevent cerebral hypoperfusion or coronary insufficiency |
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HYPERTENSIVE CRISIS HAS 3 DIAGNOSIS
Hypertensive Urgency Hypertensive Emergency Malignant HTN What is hypertensive emergency? |
elevated BP w/signs of impending end-organ failure, such as:
AKI intracranial hemorrhage papilledema EKG suggests ischemia pulm edema |
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How does pericarditis affect hemodynamics?
|
compromises cardiac output via:
tamponade constrictive pericarditis |
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HYPERTENSIVE CRISIS HAS 3 DIAGNOSIS
Hypertensive Urgency Hypertensive Emergency Malignant HTN What is malignant HTN? |
diagnosed on the basis of progressive renal failure
and/or encephalopathy with papilledema |
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|
Causes of pericarditis.
CARDIAC RIND |
CARDIAC RIND
Collagen Vascular Disease Aortic dissection Radiation Drugs Infection (TB, viral) Acute Renal Failure (uremia) Cardiac (MI) Rheumatic Fever Injury Neoplasms Dressler's Syndrome Other: SLE - autoimmune Type III hypersensitivity, reacts against heart |
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Tx
Hypertensive Urgencies |
oral antihypertensives
(eg beta-blockers, clonidine, ACEIs) GOAL lower BP over 24-48 hrs |
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Tx
Hypertensive Emergencies |
IV meds
(labetalol, nitroprusside, nicardipine) GOAL lower MAP by no more than 25% over 1st 2 hours to prevent cerebral hypoperfusion or coronary insufficiency |
|
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|
How does pericarditis affect hemodynamics?
|
compromises cardiac output via:
tamponade constrictive pericarditis |
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Causes of pericarditis.
CARDIAC RIND |
CARDIAC RIND
Collagen Vascular Disease Aortic dissection Radiation Drugs Infection (TB, viral) Acute Renal Failure (uremia) Cardiac (MI) Rheumatic Fever Injury Neoplasms Dressler's Syndrome Other: SLE - autoimmune Type III hypersensitivity, reacts against heart |
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Signs and Sx
Pericarditis |
pleuritic chest pain
dyspnea cough fever |
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Whats the pattern of chest pain in pericarditis?
|
chest pain worsen in the supine position and with inspiration
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Physical Exam
Pericarditis |
pericardial friction rub
elevated JVP pulsus paradoxus (a decreases in systolic BP > 10 on inspiration) |
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Diagnosis
Pericarditis |
CXR, EKG, Echo to r/o MI and Pneumonia
EKG diffuse ST elevations and PR depressions followed by T-wave inversions ECHO pericardial thickening or effusion |
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Tx
Pericarditis |
tx underlying cause
(steroids/immunosuppressants for SLE, dialysis for uremia) avoid corticosteroids within a few days after MI, they can predispose to ventricular wall rupture if there is tamponade, pericardiocentesis with continuous drainage pericardial effusions w/o sx can be monitored |
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Beck's Triad
Acute Cardiac Tamponade |
JVD
Hypotension Distant Heart Sounds |
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What is the mechanism of cardiac tamponade?
|
excess fluid in pericardial sac, leading to compromised ventricular filling and decreased cardiac output
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Whats the most important factor in cardiac tamponade?
|
rate of fluid formation is more than important than the size of the effusion
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|
Risk factors for cardiac tamponade.
|
pericarditis
malignancy SLE TB trauma (commonly stab wounds medial to the left nipple) |
|
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|
Signs and Sx
Cardiac Tamponade |
fatigue
dyspnea anxiety tachycardia tachypnea |
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Physical Exam
Cardiac Tamponade |
Beck's Triad
narrow pulse pressure pulsus paradoxus Kussmaul's sign (JVD on inspiration) |
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ECHO, CXR, EKG
Cardiac Tamponade |
ECHO
RA and RV diastolic collapse CXR enlarged, globular, water-bottle-shaped heart with a large effusion EKG electrical alternans |
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Tx
Cardiac Tamponade |
aggressive volume expansion with IV fluids
urgent pericardiocentesis (aspirate will be nonclotting blood) decompensation may warrant pericardial window |
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|
What is a pericardial window and what is it used for?
|
cardiac surgical procedure to create a fistula - or "window" - from the pericardial space to the pleural cavity
allow a pericardial effusion to drain from the space surrounding the heart into the chest cavity to prevent tamponade and death |
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|
Rheumatic fever affects which valve the most?
|
mitral valve > aortic valvce
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|
Mechanism of action of antihypertensive agents
Diuretics |
decreases extracellular fluid volume and thereby decreases vascular resistance
|
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|
Mechanism of action of antihypertensive agents
beta-blockers |
decreases cardiac contractility and renin release
|
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|
Mechanism of action of antihypertensive agents
ACEIs |
blocks aldosterone formation
reduces peripheral resistance salt-water retention |
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|
Mechanism of action of antihypertensive agents
ARBs |
blocks aldosterone effects,
reduces peripheral resistance and salt-water retention |
|
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|
Mechanism of action of antihypertensive agents
CCBs |
decreases smooth muscle tone and causes vasodilation
also decreases cardiac output |
|
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|
Mechanism of action of antihypertensive agents
Vasodilators |
decreases peripheral resistance by dilating arteries/arterioles
|
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|
Mechanism of action of antihypertensive agents
alpha1-adrenergic blockers |
cause vasodilation by blocking the action of norepi on vascular smooth muscle
|
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|
Mechanism of action of antihypertensive agents
centrally acting adrenergic agonists |
inhibits the sympathetic nervous system via central alpha2-adrenergic receptors
|
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|
SIDE EFFECTS
diuretics |
hypokalemia
hyperglycemia HLD hyperuricemia azotemia |
|
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SIDE EFFECTS
beta-blockers |
bronchospasm
(in severe active asthma) bradycardia CHF exacerbation impotence fatigue depression |
|
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SIDE EFFECTS
ACEIs |
cough
rashes leukopenia hyperkalemia |
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SIDE EFFECTS
ARBs |
rashes
leukopenia hyperkalemia *no cough* |
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SIDE EFFECTS
CCBs |
DIHYDROPYRIDINES
(amlodipine, nifedipine) headache flushing peripheral edema NONDIHYDROPYRIDINES (verapamil, diltiazem) decreases contractility |
|
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SIDE EFFECTS
vasodilators |
HYDRALAZINE
headache lupus-like syndrome MINOXIDIL orthostasis hirsutism |
|
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SIDE EFFECTS
alpha1-adrenergic blockers |
orthostatic hypotension
|
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|
SIDE EFFECTS
centrally acting adrenergic agonists |
somnolence
orthostatic hypotension impotence rebound HTN |
|
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CCBs
Name a few dihydropyridines |
nifedipine
felodipine amlodipine |
|
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|
CCBs
Name a few nondihydropyridines |
diltiazem
verapamil |
|
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|
what class of drugs?
phenoxybenzamine |
alpha1-adrenergic blockers
|
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|
what class of antihypertensive agent?
methyldopa |
centrally acting adrenergic agonists
|
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|
Define aortic aneurysm.
|
> 50% dilatation of all 3 layers of the aortic iwall
|
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|
What are aortic aneurysms most commonly associated with?
|
*atherosclerosis*
|
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|
Most abdominal aortic aneurysms originate above or below the renal arteries?
|
>90% originate below the arteries
|
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|
Risk factors for aortic aneurysm.
|
HTN
high cholesterol other vascular diseases + fam hx smoking gender (male > female) age |
|
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|
Physical Exam
AAA |
pulsatile abdominal mass or abdominal bruits
|
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|
Signs and Sx
Ruptued AAA |
hypotension
severe, tearing abdominal pain that radiates to the back |
|
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|
Diagnostic w/u for AAA.
|
All men 65-75 with a hx of smoking should be screened by ultrasound once.
|
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|
How do you determine the precise anatomy of an AAA?
|
CT with contrast
|
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|
|
At what size do you operate on a AAA?
|
DO NOTHING
< 5 cm SURGERY > 5.5 cm (abdominal) > 6 cm (thoracic) or smaller but rapidly enlarging EMERGENT SURG for symptomatic or ruptured |
|
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|
Aortic dissection is most commonly associated with what?
|
HTN
|
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|
In aortic dissection, there is a tear in what? Be specific.
|
the intima layer of the vessel
|
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|
aortic dissection is most commonly due to what?
|
hypertension
|
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|
|
the two most common sites of origin of aortic dissection are where?
|
1
above the aortic valve 2 distal to the left subclavian artery |
|
|
|
patient population
aortic dissection |
occurs more often btw 40-60 yo
m > f |
|
|
|
if a patient has a tearing chest pain (aortic dissection) but is hypotensive, what should you consider as the diagnosis instead?
|
pericardial tamponade
hypovolemia from blood loss other cardiopulmonary etiologies |
|
|
|
Physical Exam
aortic dissection |
**asymmetric pulses and BP measurements**
aortic regurg if aortic valve involved neurologic deficits seen if aortic arch or spinal arteries are involved |
|
|
|
gold standard for diagnosing aortic dissection
|
CTA
MRA if contrast CT is contraindicated |
|
|
|
Tx
aortic dissection |
manage BP and HR
(start beta-blockers before vasodilators to prevent reflex tachy) AVOID THROMBOLYTICS in case it ruptures SURGERY IF INVOLVES ASCENDING AORTA Descending tears managed with BP usually ok. |
|
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|
Tx
Ascending vs Descending Dissections |
Ascending
emergency surgery Descending manage BP |
|
|
|
Presentation of DVT
|
unilateral LE pain and swelling
|
|
|
|
Physical Exam
DVT |
Homans' sign
calf tenderness with passive foot dorsiflexion (poor sensitivity and specificity for DVT) |
|
|
|
Diagnostic w/u for DVT.
|
doppler ultrasound
spiral CT or V/Q scan for PE |
|
|
|
Tx
DVT |
ANTICOAGULATE
IV UFH or SQ LMWH followed by PO warfarin for up to 6 months IVC filters for contraindications to meds DVT ppx for hospitalized pts (stockings, SQ LMWH, compression) |
|
|
|
Define peripheral arterial disease.
|
restriction of blood of supply to extremities by atherosclerotic plaque
|
|
|
|
Presentation of PAD.
|
intermittent claudication
(reproducible leg pain that occurs with walking and is relieved with rest) as disease progresses, pain occurs at rest and affects the distal extremities |
|
|
|
Physical Exam
PAD |
dorsal foot ulcerations
(2nd to poor perfusion) CRITICAL LIMB ISCHEMIA painful, cold, numb foot |
|
|
|
Peripheral Arterial Disease
Describe Presentation/PE Aortoiliac Disease |
buttock claudication
decreased femoral pulses male impotence (Leriche's syndrome) |
|
|
|
Peripheral Arterial Disease
Describe Presentation/PE Femoropopliteal disease |
calf claudication
decreased pulses below the femoral artery |
|
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|
Peripheral Arterial Disease
Describe Presentation/PE Acute Ischemia |
most often caused by embolization from heart
acute occlusions commonly occur at bifurcations distal to the last palpable pulse may also be 2nd to cholesterol atheroembolism ("blue toe syndrome") |
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The 6 P's of acute ischemia.
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Pain
Pallor Paralysis Pulse deficit Paresthesias Poikilothermia (body temp that varies with surroundings) |
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Peripheral Arterial Disease
Describe Presentation/PE Chronic Ischemia |
lack of blood perfusion leads to:
muscle atrophy pallor cyanosis hair loss gangrene/necrosis |
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Diagnosis of PAD.
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ABI = P leg / P arm
ankle-brachial index REST PAIN ABI < 0.4 VERY HIGH ABI indicates calcified arteries |
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Surgical planning of PAD.
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arteriography
digital subtraction angiogrpahy |
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Tx
PAD |
MANAGEMENT
control DM, tobacco exercise helps develop collateral circulation IMPROVE SX WITH: ASA cilostazol thromboxane inhibitors ANTICOAGULATE anticoagulate to prevent clot formation STENT angioplasty/stenting has variable success rate SURGERY surgery/arterial bypass or amputation if conservative tx fails |
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What is lymphedema?
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disruption of lymphatic circulation that results in peripheral edema and chronic infection of extremities
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What is lymphedema a complication of?
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surgery involving LN dissection
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What is the cause of lymphedema in underdeveloped countries?
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parasitic infection
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Congenital malformation of the lymphatic system causing lymphedema.
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Milroy's disease
lymphedema in childhood |
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How do immigrants normally present with lymphedema?
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progressive swelling of b/l lower extremities w/o any cardiac abnormalities (ie filariasis)
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How do post-mastectomy pts normally present with lymphedema?
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unexplained swelling of upper extremities
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How do children normally present with lymphedema?
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progressive, b/l swelling of extremities
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Diagnostic w/u of lymphedema.
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mostly clinical
r/o cardiac and metabolic d/o |
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Tx
Lymphedema |
mostly symptom management
exercise massage therapy pressure garments to mobilize and limit fluid accumulation diuretics are ineffective and contraindicated |
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Watch out for what disease in lymphedema?
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cellulitis
give gram+ coverage for infection |
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Mechanism of syncope.
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cerebral hypoperfusion
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Syncope is caused by cardiac vs non-cardiac etiologies.
What are the cardiac causes? |
valvular lesions
arrhythmias PE cardiac tamponade aortic dissection |
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Syncope is caused by cardiac vs non-cardiac etiologies.
What are the non-cardiac causes? |
orthostatic/hypovolemic hypotension
neurologic (TIA/stroke) metabolic abnormalities neurocardiogenic syndromes (eg vasovagal/micturition syncope) psychiatric |
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Cardiac causes of syncope are typically associated with what 4 observations?
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very brief or absent prodromal sx
history of exertion lack of association with changes in position lack of history of cardiac disease |
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Tx
Syncope |
commonly beta-blockers for rate control
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Cardiac syncope is associated with fatal outcomes.
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1-year sudden cardiac death rates of up to 40%
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Aortic stenosis can be seen in elderly or childhood. What are the causes of both?
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elderly
just an age thing children unicuspid and bicuspid valves |
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Aortic Stenosis
Symptoms (early vs late) |
EARLY
usually asymptomatic despite significant stenosis LATE **Angina --> Syncope --> CHF --> death within 5 yrs** |
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Diagnostic w/u for aortic stenosis.
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echo
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Tx
Aortic Stenosis |
valve replacement
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Physical Exam
aortic stenosis |
pulsus parvus et tardus
(weak, delayed carotid upstroke) single or paradoxically split S2 sound systolic murmur radiating to carotids |
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Acute causes of AR.
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infective endocarditis
aortic dissection chest trauma |
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Chronic causes of AR.
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valve malformations
rheumatic fever connective tissue d/o |
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Acute sx of AR.
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rapid onset of:
pulm congestion cardiogenic shock severe dyspnea |
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Chronic sx of AR.
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slowly progressive onset of dyspnea on exertion
orthopnea PND |
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Tx
AR |
vasodilator therapy for isolated AR until sx become severe enough to warrant valve replacement
eg dihydropyridines or ACEIs |
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Diagnostic w/u for AR.
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echo
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Physical Exam
AR |
blowing diastolic murmru at LSB
mid-diastolic rumble (austin flint murmur) midsystolic apical murmur widened pulse pressure causes de Musset's sign (head bob with heartbeat) Corrigan's sign (water-hammer pulse, ie forceful pulse) Duroziez's sign (femoral bruit) |
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Most common cause of mitral valve stenosis.
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rheumatic fever
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sx of mitral valve stenosis
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PULMONARY
dyspnea orthopnea PND CARDIAC infective endocarditis arrhythmias |
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diagnostic w/u of mitral valve stenosis
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echo
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Physical Exam
mitral stenosis |
opening snap
mid-diastolic murmru at apex pulmonary edema |
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Tx
mitral valve stenosis |
SYMPTOMATIC RELIEF
anti-arrhythmics bc a fib is a complication (beta-blockers, digoxin) SEVERE CASES mitral balloon valvotomy valve replacement |
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Causes of MR.
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rheumatic fever
chordae tendineae rupture after MI infective endocarditis |
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Sx of MR
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dyspnea
orthopnea fatigue Mostly are pulm sx |
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Physical Exam
MR |
holosystoic murmur radiating to axilla
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Diagnostic w/u of MR.
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echo to show regurgitation
angio to assess severity of disease |
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Tx
MR |
antiarrhythmics
(a fib is common with LAE) decrease preload with: nitrates and diurteics SEVERE CASES valve repair/replacement for severe cases |
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Causes of sinus tachy.
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pain
fear exercise ALSO hyperthyroidism volume contraction infection PE |
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signs and sx
sinus tachy |
palpitations
sob |
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Causes of acute A Fib.
PIRATES |
Pulm disease
Ischemia Rheumatic heart dis Anemia/Atrial myxoma Thyrotoxicosis Ethanol SEpsis |
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Causes of chronic A Fib.
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HTN
CHF |
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Signs and Sx
A Fib |
often asymptomatic
SOB chest pain palpitations |
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Physical Exam
A Fib |
irregularly irregular pulse
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EKG findings
A Fib |
no discernible P waves
variable and irregular QRS |
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Tx
A Fib |
Estimate risk of stroke with CHADS2 score. (Anticoagulate if > 2)
ANTICOAGULATION if > 48 hrs to prevent CVA RATE CONTROL beta-blockers CCBs digoxin CARDIOVERSION if new onset < 48 hrs and TEE shows no LA clot or after 3-6 wks on warfarin with INR 2-3 |
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What is the cause of a flutter?
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circular movement of electrical activity around the atrium at a rate of approximately 300 times per minute
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Sx
Atrial Flutter |
usually asymptomatic
palpitations syncope lightheadedness |
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EKG Findings
Atrial Flutter |
regular rhythm
"sawtooth" appearance of P waves atrial rate 240-320 bpm ventricular rate 150 bpm |
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Tx
Atrial Flutter |
anticoagulation
rate control cardioversion as in a fib |
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Cause of multifocal atrial tachycardia.
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multiple atrial pacemakers or reentrant pathways
COPD hypoxemia |
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Sx
multifocal atrial tachycardia |
asymptomatic
at least 3 different P-wave morphologies |
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EKG Findings
multifocal atrial tachycardia |
3 or more unique P-wave morphologies
rate > 100 bpm |
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Tx
multifocal atrial tachycardia |
treat underlying d/o
RATE CONTROL and Suppression of Atrial Pacemakers verapamil or beta-blockers |
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What is the cause of atrioventricular nodal reentry tachycardia (AVNRT)?
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a reentry circuit in the AV node depolarizes the atrium and ventricle nearly simultaneously
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Sx
atrioventricular nodal reentry tachycardia (AVNRT) |
palpitations
SOB angina syncope lightheadedness |
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EKG Findings
atrioventricular nodal reentry tachycardia (AVNRT) |
rate 150-250 bpm
P wave is often buried in QRS or shortly after |
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Tx
atrioventricular nodal reentry tachycardia (AVNRT) |
cardiovert if hemodynamically unstable
carotid massage or Valsalva or adenosine can stop the arrhythmia |
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What is the cause of atrioventricular reciprocating tachycardia (AVRT)?
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an ectopic connection between the atrium and ventricle that causes a reentry circuit
seen in WPW |
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Sx
atrioventricular reciprocating tachycardia (AVRT) |
palpitations
SOB angina syncope lightheadedness (same as in AVNRT) |
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EKG Findings
atrioventricular reciprocating tachycardia (AVRT) |
a retrograde P wave is often seen after a normal QRS
a preexcitation delta wave is characteritically seen in WPW |
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Tx
atrioventricular reciprocating tachycardia (AVRT) |
(same as for AVNRT)
cardiovert is hemodynamically unstable carotid massage or valsalva or adenosine can stop the arrhythmia |
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What is the cause of paroxysmal atrial tachycardia?
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rapid ectopic pacemaker in the atrium (not sinus node)
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Sx
paroxysmal atrial tachycardia |
palpitations
SOB angina lightheadedness (same as AVNRT and AVRT) |
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EKG Findings
paroxysmal atrial tachycardia |
rate > 100 bpm
P wave with an unusual axis BEFORE each normal QRS |
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Tx
paroxysmal atrial tachycardia |
adenosine can be used to unmask underlying atrial activity
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