Cardiology Exam Flashcards
total cholesterol high
> 240
triglycerides high
200-500
HDL low
<40
LDL high
> 100
triglycerides very high
> 500
triglycerides borderline
151-199
total cholesterol borderline
200-240
total cholesterol normal
<200
when to screen healthy adults for cholesterol
every 5 years starting at 45 (f) and 35 (m)
when to screen diabetic adults
at 20 years if other risk factors
when to use a high intensity statin
CAD, LDL>190 or TG>500, diabetes (over 50 or multiple risk factors), >20% CV risk calculator
when to use a moderate intensity statin
all diabetes 40-50 without other risk factors, between 7.5 and 20% CV risk calculator
when to consider statins (no firm recommendation)
over 75 with CAD or DM, under 40 with diabetes, between 5 and 7.5% CV risk calculator
Contraindications to statin use
active liver disease, pregnancy
adverse effects of statins
myopathy, rhabdo, increased LFTs, increased A1C, cognition
what about niacin, omega-3, fibrate for hyperlipidemia
not recommended
what is ezetimibe
inhibits cholesterol absorption at small intestine
when to consider bile acid sequestrants
ezetimibe intolerant and TG<300
when to use PCSK9 inhibitors
very high-risk patients
lipid lowering effect of high-intensity statins
decrease LDL by 50%
lipid lowering effect of moderate intensity statins
30-50%
parasympathetic cardiac receptor
M2
parasympathetic bronchial smooth muscle receptor
M3
sympathetic vasodilation for skeletal muscle receptor
B2
sympathetic receptor for renin release
B1
toxicities of parasympathomimetics
bradycardia, bronchospasm
atropine mechanism of action
competitive antagonist of muscarinic receptors
can atropine cross BBB
yes
atropine toxicity
parasympatholytic effects (dry mouth, tachycardia), sedation, delirium, hyperthermia, flushing
what is PO atropine
oxybutinin
what is an alpha 1 and alpha 2 agonist used for hypotension
phenylephrine
what is isoproterenol
B1 B2 agonist used to stimulate the heart in AV block
what is dobutamine
B1 agonist used to increase cardiac output in heart failure
what is the only sympathomimetic used to treat hypertension and why
clonidine (alpha 2 agonist)
what cardiac biomarker other than troponin is sometimes used and why would it be used
CK-MB: levels return to normal faster than troponin so it is useful for re-infarction
when do troponin levels rise
4 hours after infarction
when do troponin levels peak
24 hours
when do CK-MB levels rise
6-12 hours
how long do troponin levels stay elevated
7 days
elements of Virchow’s triad
hypercoagulable state, endothelial damage, stasis
class 1 antiarrhythmics
1a procainamide, 1b lidocaine, 1c flecainide
class 1 antiarrhythmics mechanism
fast sodium channel blockers
class 2 antiarrhythmics mechanism
beta blockers
class 3 antiarrhythmics mechanism
potassium channel blockers
class 4 antiarrhythmics mechanism
calcium channel blockers
nonspecific beta blocker
propranolol
cardioselective beta blocker
metoprolol/atenolol/esmolol
class 3 antiarrythmic prototype
amiodarone
class 4 antiarrhythmic prototype
verapamil
labetalol/carvedilol mechanism
alpha 1 and nonselective beta blocker
what are non-dihydropyridines used for and what are they called
antiarrhythmics, verapamil/diltiazem
what are dihydropyridines used for and what are they called
antihypertensives, nifedipine, amlodipine
what types of arrhythmias are calcium channel blockers used for
supraventricular
what tissues do class I and class III antiarrhythmics affect
atrial and ventricular myocytes
most common cause of aortic stenosis <70 y.o
bicuspid valve
most common cause of aortic stenosis >70 y.o
degenerative (calcific)
murmur of aortic stenosis
systolic ejection murmur (crescendo-decrescendo)
causes of acute aortic regurg
infective endocarditis, aortic dissection, trauma, prosthetic valve dysfunction
causes of chronic aortic regurg
bicuspid, aortic root dilatation, rheumatic disease, connective tissue disease
blood pressure on aortic regurg
wide pulse pressure
murmur of aortic regurg
diastolic decrescendo
most common cause of chronic mitral regurg
degenerative changes
most common causes of acute mitral regurg
myxomatous mitral valve with chordal rupture, papillary rupture 2/2 AMI, infective endocarditis
most common etiology of mitral stenosis
rheumatic disease
4/6 murmur
loud with thrills
5/6 murmur
can hear with steth partly off chest
6/6 murmur
can hear with steth completely off chest
when is auscultation used with pt in left lateral decubitus position
S3, S4, mitral stenosis (using bell)
S3
occurs right after S2
S4
occurs right before S1, blood hitting a noncompliant ventricle
heart sound just before the carotid pulse
S1
characteristics of restrictive cardiomyopathy
normal EF but severe systolic dysfunction and concentric hypertrophy
hypertrophic cardiomyopathy murmur
dynamic systolic ejection murmur that increases with increased preload and increased afterload
what causes concentric hypertrophy
chronic pressure overload (HTN, aortic stenosis)
what causes eccentric hypertrophy
chronic volume overload (aortic regurg, dilated cardiomyopathy)
formula for ejection fraction
(EDV-ESV)/EDV
EF values for HF with mildly reduced EF
41-49%
EF values for HF with reduced EF
<40%
HF with reduced EF has what hypertrophy
eccentric
HF with preserved ejection fraction has what hypertrophy
concentric
role of SNS activation in HF
initially helps to maintain cardiac output but long-term increase in norepi levels leads to increase in afterload, fibrosis, arrhythmias
action of ACE inhibitors/ARBs/ARNIs in HF
decreases afterload and preload, decreases myocardial fibrosis
ARNI prototype
Sacubitril-valsartan
role of hydralazine-nitrate combination in heart failure
vasodilators, use in those that cannot tolerate ACE/ARB/ARNI or in conjunction with them
beta blockers for HF
metoprolol succinate, carvedilol, bisoprolol
most common cause of endocarditis
strep viridans (usually in the presence of a damaged valve) - subacute
most common cause of acute endocarditis (IV drug abuser)
staph aureus (tricuspid valve)
cause of libman-sacks endocarditis
SLE
when is BP medication recommended
130/80 and CVD risk 10% or more
pulse pressure is proportional to ____ and inversely proportional to _____
stroke volume, arterial compliance
MABP =
cardiac output x total peripheral resistance
determinants of vascular resistance
diameter, viscosity, arrangement (series vs parallel), type of flow (laminar vs turbulent)
turbulence is proportional to ____ and inversely proportional to ____
diameter/velocity, viscosity
dicrotic notch
aortic valve closes and causes a secondary pressure wave
T-wave in wiggers diagram
during reduced ejection
mitral valve closure wiggers diagram
beginning of iso. contraction
aortic valve closure wiggers
beginning of iso. relaxation
mitral valve opens wiggers
end of iso. relaxation/beginning of rapid filling
formula for EF
SV/EDV
what are the primary determinants of coronary perfusion?
aortic pressure and coronary artery compression during ventricular compression
what is the cholinergic neuron
sympathetic preganglionic
what is the adrenergic neuron
sympathetic postganglionic
preganglionic sympathetic neurotransmitter
ach
postganglionic sympathetic neurotransmitter
norepi
the systemic circulation is primarily innervated by ____ neurons
sympathetic
what do adrenergic receptors bind
norepi and epi
what do cholinergic receptors bind
ach
what is the endogenous agonist of alpha receptors
norepi
B1 receptors on cardiac myocytes are stimulated by
norepi/epi
B2 receptors in skeletal muscle are stimulated by
epi
nicotinic receptor function
mediate neurotransmission at autonomic ganglia and catecholamine release from medulla
sympathoadrenal system is mostly responsible for releasing
epinephrine
epinephrine has a higher affinity for what type of receptor
Beta
what receptor activates RAAS
B1 on juxtaglomerular cells, this releases renin
which SNS neurotransmitter is largely released via neuronal stimulation
norepi
metabolic dilators
hypoxia and adenosine
what accounts for decrease in TPR during strenuous exercise
local vasodilatory metabolites are overriding SNS
phase 0 fast response
Na channels open and there is a massive Na influx
phase 1 fast response
Na channels close and K leaks out of cell
phase 2 fast response
trigger for contraction: Ca channels open and Ca comes in while K leaks out
phase 3 fast response
Ca channels close and K continues to leak out
phase 4 fast response
Na and Ca channels are closed, -85 mv resting maintained by constant leak of K out of the cell
phase 4 slow response
Na slowly leaks into cell until threshold
phase 0 slow response
Ca channels open and Ca rushes in
phase 3 slow response
Ca channels close and K channels open, allowing K to leak out
difference in action potential between SA and AV node
in AV node, phase 4 is longer
SV formula
SV = EDV-ESV
SBP largely determined by
SV
DBP largely determined by
TPR
hypocalcemia ekg
prolonged QT
hypercalcemia ekg
shortened QT
brugada syndrome ekg
ST elevation in V1-V3 with negative T-wave
high-intensity statins
atorvastatin, rosuvastatin
statin mechanism of action
prevent cholesterol synthesis in liver
what medications are used to lower triglycerides
fibrates
EKG changes in LAD occlusion
V1-V4
EKG changes in circumflex artery occlusion
laterals
EKG changes in PDA (right-dominant)
inferiors
EKG changes in PDA (left-dominant)
laterals (branch of circumflex)
EKG changes in isolated PDA occlusion
ST depression in V1-V2
early post MI complications
arrhythmia, then free wall rupture, papillary rupture, tamponade, septal rupture
later post MI complications
CVA, aneurysm, Dresslers syndrome
goal BP for Pts over 60
150/90
goal BP for pts under 60 or DM
140/90
dx of endocarditis requires
2 major, 1 major/3 minor, or 5 minor (modified Duke criteria)
most common organism in infective endocarditis
staph aureus (vanc) strep viridans (PCN)
3 criteria for typical angina
worsens with exercise, relieved with rest/nitro, substernal chest discomfort
what counts as satisfactory workload for stress testing
4 mets or 85% of max HR
HAS-BLED high risk
> 3
