Cardiovascular Disorders Flashcards
most common site of coronary artery occlusion
left anterior descending artery
heart region supplied by left anterior descending artery
anterior wall of left ventricle
heart region supplied by LAD septal branch
anterior 2/3 of interventricular septum
heart region supplied by left coronary circumflex branch
left atrium, posterolateral left ventricle
heart region supplied by right coronary posterior descending branch
inferior wall of left ventricle, posterior 1/3 of interventricular septum
heart region supplied by right coronary marginal branch
right atrium, right ventricle
heart region supplied by right coronary nodal branches
SA and AV nodes
gold standard for identifying coronary artery disease
coronary aniography
next step when exercise stress test is equivocal
nuclear exercise test with thallium-201 or technetium-99m-sestamibi during exercise testing
second line when comorbidities prevent exercise stress test
pharmacologic stress testing with dobutamine
age to begin screening for hyperlipidemia
men after age 35
women after age 45
goal LDL for patients at high risk for CAD
< 100 mg/dL
goal LDL for patients with 2+ risk factors for CAD
< 130 mg/dL
goal LDL for patients with 0-1 risk factors for CAD
< 160 mg/dL
HMG-CoA reductase inhibitors
acts on liver
decreases LDL and triglycerides
increases HDL
SE: myositis, increases LFTs
ezetimibe
cholesterol absorption inhibitor acts on intestines
decreases LDL
SE: myalgias, increases LFTs
gemfibrozil, fenofibrate
stimulates lipoprotein lipase in blood
decreases LDL and triglycerides
increases HDL
SE: myositis, increases LFTs
cholestyramine, colestipol, colesevelam
bile acid sequestrants in GI tract
decreases LDL
increases triglycerides
SE: bad taste, abdominal discomfort
niacin
acts on liver
decreases LDL, triglycerides
increases HDL
SE: flushing, nausea, pruritis, insulin resistance, gout, paresthesias, increases LFTs
vessels most commonly used for CABG
saphenous vein
internal mammary artery
pharmacotherapy for unstable angina
aspirin and clopidogrel (if no PTCA) GP IIb/IIIa (if PTCA) oxygen nitroglycerin heparin beta-blockers
time limit for thrombolysis in MI
12 hours
use t-Pa or urokinase
cardiac enzyme to evaluate immediate re-infarct
CPK-MB
decreases in 2-3 days
risk reduction medications after MI
low dose ASA clopidogrel beta-blockers ACE inhibitors K-sparing diuretics HMG-CoA reductase inhibitors exercise, smoking cessation, and dietary modifications
V2, V3, V4 infarction
anterior infarction
LAD artery
V1, V2, V3 infarction
septal infarction
LAD artery
II, III, aVF infarction
inferior infarction
posterior descending or marginal branch
1, aVL, V4, V5, V6
lateral infarction
LAD or circumflex artery
V1, V2
posterior infarction
posterior descending artery
first degree heart block
PR > 0.2 seconds
asymptomatic
caused by increased vagal tone or functional conduction impairment
second degree mobitz I heart block
progressive PR lengthening until skipped QRS
asymptomatic
caused by his bundle conduction defect, drug effects (beta-blockers, digoxin, calcium channel blockers), or increased vagal tone
adjust medications, consider pacemaker if symptomatic bradycardia is present
second degree mobitz II heart block
randomly skipped QRS without changes in PR interval
usually asymptomatic
caused by infranodal conduction problem in bundle of his or purkinje fibers
can progress to third degree heart block
treat with ventricular pacemaker
third degree heart block
no relationship between P waves and QRS complexes
syncope, dizziness, hypotension
absence of conduction between atria and ventricles
treat with ventricular pacemaker and avoid medications affecting AV conduction
next step of management in congenital heart disease with early cyanosis
prostaglandin E
medication that closes PDA
indomethacin
6 week old infant has signs of left heart failure and EKG shows left-sided MI
anomalous origin of the left coronary artery
most common vasculitis
temporal arteritis
defects of tetrology of fallot
VSD, pulmonary stenosis, RVH, overriding aorta
management for DVT in patient with high likelihood of falling
IVC filter
management of peripheral vascular disease
smoking cessation, glucose and lipid control, exercise
cilostazol, statins, aspirin
indications for operating on AAA
greater than 5.5 cm
growing more than 0.5 cm in 6 months
mechanism of PSVT
accessory conduction pathways through AV node
treatment for ventricular tachycardia
hemodynamically stable: amiodarone or lidocaine
hemodynamically unstable: cardioversion
treatment for paroxysmal noctural dyspnea
acute: nitroglycerin
chronic: furosemide
drug that blocks ventricular remodeling s/p myocardial infarction
ACE-inhibitor
periumbilical systolic-diastolic bruit
renal artery stenosis
abdominal systolic bruit
more classically associated with AAA
blood pressure discrepancy in coarctation of the aorta
if coarctation is distal to the subclavian artery: upper extremity pressure is higher than lower extremity pressure
if coarctation is proximal to the subclavian artery: right arm pressure higher than left arm pressure
indications for class IA anti-arrhythmics
PSVT, Afib, Aflutter, Vtach
quinidine, procainamide
indications for class IB anti-arrhythmics
Vtach
lidocaine, tocainide
indications for class IC anti-arrhythmics
PSVT, Afib, Aflutter
flecainide, propafenone
indications for beta-blockers used as anti-arrhythmics
PVC, PSVT, Afib, Aflutter, Vtach
propanolol, esmolol, metoprolol
indications for K-channel blockers
Afib, Aflutter, Vtach (not bretylium)
amiodarone, sotalol, bretylium
indications for calcium channel blockers used as anti-arrhythmics
PSVT, MAT, Afib, Aflutter
verapamil, diltiazem
drug used in PSVT that activates K-channels and decreases intracellular cAMP
adenosine
first drug that should be administered when coronary artery event is suspected
aspirin to prevent platelet aggregation
situational syncome
autonomic dysregulation that may occur when an older man is micturating or coughing
treatment for prolonged QT
asymptomatic: propranolol
symptomatic: propranolol plus a DDD pacemaker (dual chamber)
treatment for pulseless electrical activity
initiate CPR followed by epinephrine or vasopressin
treament of asymptomatic young patient with no other health problems and CHADS2 score of 0
aspirin
CHADS2 score
congestive heart failure - 1 hypertension - 1 age > 75 - 1 diabetes mellitus - 1 stroke - 2
causes of pulsus paradoxus
cardiac tamponade, tension pneumothorax, and severe asthma
treatment of unstable patient with Afib
immediate cardioversion
treatment of stable patient with Afib
< 48 hours: cardioversion
> 48 hours: 3-4 weeks of rate control and antiocogulation prior to cardioversion
mechanism of dipyramidole infused myocardial perfusion scanning
dipyramidole is a vasodilator, diseased vessels are already maximally dilated, so dipyramidole vasodilates non-disease vessels and draws even more blood away from diseased vessels
treatment for aortic regurgitation
afterload reduction with ACE-inhibitor or nifedipine, severe cases should undergo valve replacement
ranking of lifestyle modifications for high blood pressure
weight loss DASH diet dietary sodium exercise alcohol intake
smoking has little effect on hypertension but does contribute to heart disease
treatment of cocaine-induced STEMI
PTCA or thrombolysis
aspirin, nitrates appropriate, avoid beta-blockers which will allow unopposed alpha-activity and further vasoconstriction
pulsus parvus et tardus
decreased pulse amplitude and delayed pulse upstroke seen in aortic stenosis
mechanism of decreased preload in cardiac tamponade
pericardial fluid pressure exceeds ventricular pressure and inhibits ventricles from expanding and filling properly
drug of choice in patient with stable angina and hypertension
beta-blocker
mixed venous oxygen concentration in hypovolemic shock
decreased from increased oxygen extraction by hypoperfused tissue
mixed venous oxygen concentration in septic shock
normal from hyperdynamic circulation and improper distribution of the cardiac output
mechanism by which nitroglycerin relieves angina
dilaiton of veins decreases preload and stretching of myocardial muscle
it is actually unclear if nitroglycerin increases coronary blood flow in diseased patients although it performs this function in healthy coronary vessels, so this is not the major way angina is relieved
metabolic abnormalities found in hyperaldosteronism (conn’s syndrome)
low renin, high aldosterone
high sodium, low potassium, high bicarbonate (metabolic alkalosis)
pansystolic murmur at the apex with radiation to the axilla days to months after a myocardial infarction
ventricular aneurysm
papillary muscle rupture occurs 3-7 days after
normal right atrial pressure
4-6 mmHg
normal pulmonary artery pressure
25/15 mmHg
normal PCWP
6-12 mmHg
right atrial pressure > 10 mmHg
pulmonary artery systolic pressure > 40 mmHg
diagnostic criteria for massive pulmonary embolism
unstable angina pharmacotherapy if no percutaneous intervention is planned
aspirin, clopidogrel
unstable angina pharmacotherapy if percutaneous intervention is planned
gp IIb/IIIa inhibitor
intranodal or bundle of His conduction problem
second degree mobitz I heart block
infranodal conduction problem
second degree mobitz II heart block
absence of conduction between atria and ventricles
third degree heart block
AV nodal reentry anomaly
PSVT
treatment: adenosine, carotid massage, valsalva maneuver
AV reentry (not through the node, through accessory pathway)
wolff-parkinson-white
treatment: amiodarone, procainamide
treatment of hemodynamically stable ventricular tachycardia
amiodarone
complication of esophageal dilation
esophageal rupture, penumomediastinum, and mediastinitis
causes of mediastinitis
iatraogenic procedure, boerrhave tear
biliary side effect of gastric bypass surgery
increased risk of gallstones
treatment: ursodeoxycholic acid prophylactically for 6 months after surgery
somatic pain
sharp, localized pain
visceral pain
generalized, crampy pain
referred pain
visceral fibers enter spinal cord at the same location as somatic fibers and brain misinterprets visceral pain as somatic
wide fixed splitting of second heart sound
atrial septal defect
normal PCWP pressure
6-12 mmHg
normal right atrial pressure
4-6 mmHg
normal pulmonary artery pressure
does not exceed 25/15 mmHg
treatment of hemodynamically unstable PSVT
cardioversion or calcium channel blocker
treatment of stable PSVT
carotid massage or valsalva maneuver
pharmacotherapy: beta-blocker or CCB
treatment for wolff-parkinson-white
amiodarone or procainamide
NO adenosine
progressive PR lengthening until dropped QRS
second degree mobitz I heart block
randomly skipped QRS without changes in PR interval
second degree mobitz II
when is pacemaker indicated in heart bock
second degree mobitz II and third degree
only indicated in mobitz I if there is symptomatic bradycardia present
several ectopic foci in the atria that discharge automatic impulses
usually asymptomatic
multifocal atrial tachycardia
treatment: CCB or beta-blockers acutely, catheter ablation of surgery to eliminate abnormal pacemakers
causes of PVCs
hypoxia, abnormal serum electrolytes, hyperthyroidism, caffeine use
what do PVCs look like
early and wide QRS without preceding P waves
treatment of PVCs
none if patient is healthy, beta-blocker in patients with CAD
treatment for atrial flutter
rate control with CCB, beta-blockers, cardioversion if unable to be controlled with medication, and catheter ablation to remove ectopic focus
treatment for torsades de pointes
magnesium sulfate
treatment for stable ventricular tachycardia
procainamide or amiodarone
amiodarone is drug of choice in patients with CHF
treatment for symptomatic bradycardia
atropine
most frequent physical exam finding of CHF
S3 sound
kerley B lines
increased marking of lung interlobular septa caused by pulmonary edema
indication for K-sparing diuretics in congestive heart failure
reduce cardiac hypertrophy caused by aldosterone
treatment for pericarditis
NSAIDs, colchicine
pericardiocentesis for large effusions
hemodialysis for uremic pericarditis
cardiac catherization shows equal pressure in all chambers
chronic constrictive pericarditis
causes of cardiac tamponade
pericarditis, chest trauma, LV rupture following MI, or dissecting aortic aneurysm
treatment for cardiac tamponade
immediate pericardiocentesis
harsh blowing holosystolic murmur radiating from apex to axilla
mitral regurgitation
widely split S2
mitral regurgitation
midsystolic click
mitral regurgitation
opening snap after S2
mitral stenosis
diastolic rumble
mitral stenosis
loud S1
mitral stenosis
widened pulse pressure
aortic regurgitation
bounding pulses
aortic regurgitation
diastolic decrescendo murmur
aortic regurgitation
late diastolic rumble
aortic regurgtation
crescendo-decrescendo systolic murmur
aortic stenosis
weak S2
aortic stenosis
dual stroke carotid pulse, systolic murmur, S4
hypertrophic obstructive cardiomyopathy
treatment for hypertrophic obstructive cardiomyopathy
beta-blockers, CCBs
pacemaker or partial septal excision
treatment for mitral regurgitation
arterial vasodilators if symptomatic (nitroprusside)
prophylactic antibiotics for increased infection risk
treatment for aortic regurgitation
decrease afterload with ACE-inhibitors, CCBs, or nitrates
treatment for aortic stenosis
beta-blockers
diuretics to decrease preload
treatment for bacterial endocarditis
4-6 weeks IV antibitoics
beta-lactam plus an aminoglycoside
antibiotic prophylaxis before surgery or dental work
heart sounds you may hear with hypertension
loud S2, possible S4
causes of thoracic aortic aneurysms
marfan’s syndrome, ehlers-danlos, and syphilis
most common location of aortic aneurysm
abdominal below the renal arteries
anti-hypertensive used in migraine headaches
beta-blockers
aortic dissection: stanford A v. stanford B
stanford A: ascending aorta, requires emergency surgery
stanford B: distal to left subclavian, treat medically with nitroprusside, beta-blockers
wide fixed split S2, systolic ejection murmur at upper left sternal border
atrial septal defect
loud pumonic S2, systolic thrill
ventricular septal defect
loud S2, bounding pulses at birth
patent ductus arteriosus
accompanied by a “machinery” murmur
risk factors for transposition of the great vessels
diabetic mother
apert’s syndrome, down syndrome, cri-du-chat, trisomy 13, trisomy 18
cardiac pathologies with “boot-shaped” heart on imaging
hypertrophic obstructive cardiomyopathy
tetralogy of fallot
persistent truncus arteriosus
treatment for tetralogy of fallot
prostaglandin E to maintain PDA, propranolol, morphine, knee-to-chest positioning during cyanotic episodes
treatment of mediastinitis
surgical debridement and prolonged antibiotic therapy
prophylactic treatment for long QT syndrome
propranolol