Cardio Flashcards
What does the trucus arteriosus become?
ascending aorta and pulmonary trunk
Timeframe of eryhtropoiesis in fetus/newborn
Yolk sac 3-10 wk
Liver 6wk-birth
Spleen 15-30wk
Bone marrow 22wk-adult
Different between fetal and adult hemoglobin
fetal=alpha2gamma2 subunits
adult=alpha2beta2 subunits
fetal has much higher affinity for oxygen
What molecules can impact the ductus arteriosus?
prostaglandins E1/E2 keep ductus arteriosus open
Indomethacin helps close PDA
What are SA and AV nodes supplied by usually?
R coronary artery
When do the coronary arteries fill with new blood?
During diastole
When aortic valve closes and blood is pushed backwards into the sinuses in the valves
Sx of L atrial hypertrophy
dysphagia/hoarseness
Molecules increasing contractility of the heart (4)
catecholamines
increased intracellular Ca2+
decreased extracellular Na+
Digitalis
Causes of decreased contractility of the heart (5)
Beta1 blockade (blockers)
heart failure
acidosis
hypoxia/hypercapnea
nondihydropyridine Ca2+ channel blockers
Results of venodilators on the heart
decrease preload
i.e. nitroglycerin
Result of vasodilators on the heart
decrease afterload
i.e. hydralazine
Biggest determinant of blood viscosity
hematocrit
During cardiac cycle, when is most oxygen consumed by the heart?
isovolumetric contraction
b/t closure of mitral and opening of aortic
What is the S1 heart sound?
mitral/tricuspid valve closure
What is the S2 heart sound?
aortic and pulmonic valve closures
What is the S3 heart sound?
rapid ventricular filling in early diastole
more common in dilated ventricle
What is the S4 heart sound?
atrial kick from high atrial pressure
assc with ventricular hypertrophy
from L atrium pushing against stiff LV wall
What causes wide splitting of heart sounds?
delaying of R ventricle emptying
from R bundle block/pulmonic stenosis
What causes fixed splitting of heart sounds?
From atrioseptal defects
due to increased flow through pulmonic valve
What causes paradoxical splitting of heart sounds?
delaying of L ventricle emptying
i.e. aortic stenosis/L bundle block
What heart sounds does inspiration excentuate?
R heart sounds
What heart sounds does expiration excentuate?
L heart sounds
What heart sounds does hand grip/increase systemic vascular resistance excentuate?
MR, AR, VSD, MVP
What heart sounds does valsalva/decreased venous return excentuate?
MVP, hypertrophic cardiomyopathies
What are systolic heart sounds?
aortic/pulmonic stenosis
mitral/tricuspid regurg
ventricular septal defect
What are diastolic heart sounds?
aortic/pulmonic regurg
mitral/tricupsid stenosis
Sound/cause of mitral/tricuspid regurg
Holosystolic, high pitched
from MVP, LV dilation, ischemic heart disease for mitral
R ventricular dilation for tricuspid
Rheumatic fever/endocarditis can cause either
Sound/cause of aortic stenosis
Crescendo-decrescendo after ejection click
radiates to carotids/heart base
bicuspid aortic or calcific aortic stenosis
Sound of ventricular septal defect
holosystolic, harsh murmur
Sound/cause of mitral valve prolapse
late systolic crescendo murmur with midsystolic click
from myoxmatous degen/Rheumatic fever/chordae rupture
Sound/cause of aortic regurg
high pitched, blowing diastolic decresecendo
from aoritc root dilation/bicupsid aortic/endocarditis/rheumatic fever
Sound/cause of mitral stenosis
delayed rumbling in late diastole
often from rheumatic fever
Sound of a patent ductus arteriosus
continuous machine like murmur
Cause of plateau in ventricular AP
balance of K+ and Ca2+ crossing the membrane
eventually K+ overtakes and decreases the AP by exiting more quickly than Ca2+ enters
Phases/actions of a ventricular AP
Phase 0-upstroke/Na+ channels open
Phase 1-inactivation of Na+ channels/K+ channels open
Phase 2-Ca2+ influx/K+ efflux causes plateau
also Ca2+ causes SR Ca2+ release and myocyte contraction
Phase 3-massive K+ efflux and closure of Ca2+ channels
Phase 4-resting potential/K+ high permeability
Phases/actions of SA/AV node action potentials
Phase 0-upstroke/Ca2+ channels open (Na+ fast inactivated due to less negative RMP)
Phase 2-no plateua
Phase 3-inactivation of Ca2+ channels/efflux of K
Phase 4-spontaneous depolarization of membrane due to increased Na+ conductance
What is the P wave on ECG?
atrial depolarization
What is PR interval on ECG?
conduction delay through AV node (less than 200ms)
What is the QRS complex on an ECG?
What is the QT interval on ECG?
mechanical contraction of ventricles
What is the T wave in an ECG?
ventricular repolarization
inversed indicates MI
What is the ST segment on an ECG?
ventricles depolarized=isoelectric
What is torsades de pointes?
ventricular tachycardia
shifting sinusoidal waveforms on ECG
Atrial fibrillation characteristics on ECG
irregularly irregular
no discrete P waves inbetween irregular spaced QRS complexes
Atrial flutter characteristics on ECG
back to back atrial depolarizations
Ventricular fibrillation characteristics on ECG
erratic rythm with no identifiable waves
What is seen on ECG with 1st degree AV block?
prolonged PR interval (over 200ms)
What is seen on ECG with type one 2nd degree AV block?
progressive lengthing of PR interval with dropped P wave
What is seen on ECG with type two 2nd degree AV block?
dropped P waves with no change in PR interval length
Stimulation of/action of atrial natriuretic peptide
increases with increased blood volume and atrial pressure
ANP causes vascular dilation and Na+ reabsorption
constricts efferent renal arterioles and dilates afferent
Nucleus involved in BP control
solitary nucleus in medulla
Cushing reaction pathway
increased ICP-> cerebral ischemia -> reflex for increased perfusion pressure -> increased stretch -> baroreceptor -> bradycardia
Eisenmenger’s Syndrome
VSD, ASD or PDA
vascular hypertrophy
shunt reverses from L/R to R/L
late cyanosis
Tetralogy of Fallot
PROVe
Pulmonary infundibular stenosis
RVH
overriding aorta
VSD
Cardiac defect assc with Turner Syndrome
Coarctation of the aorta
Cardiac defect assc with diabetic mother
What are lipid laden histiocytes in the skin?
xanthomas
Moenckeberg arteriosclerosis
calcification of media of arteries
“pipestem” arteries
Atherosclerosis
plaques forming in intima of arteries
Types of arteriolosclerosis
Hyaline from HTN or DM
Hyperplastic from malignant HTN (onion skinning)
Progression of atherosclerosis formation
MO and LDL accumulation
foam cell formation/fatty streaks
smooth m. cell migration (PDGF/FGF)
extracellular matrix deposition
plaque formation
Associations of thoracic aortic aneurysm
HTN
cystic medial necrosis
teriary syphilis
What do you see on an ECG with stable angina?
ST depression
What do you see with Prinzmetal’s variant angina on ECG?
ST elevation
ECG of a myocardial infarct
initial ST depression
progression to ST elevation
Dx of myocardial infarct
ECG within first 6 hours
cardiac troponin I rises after 4 hours
ECG of transmural infarct
ST elevation,Q waves
ECG of subendocardial infarcts
ST depression
What is Dressler’s syndrome?
autoimmune reaction resulting in fibrinous pericarditis several weeks post MI
Pathology of dilated (congestive) cardiomyopathy
sarcomeres added in series
eccentric hypertrophy
Pathology of hypertrophic cardiomyopathy
sarcomeres added in parallel
asymmetric concentric hypertrophy
Causes of obliterative cardiomyopathy (6)
sarcoidosis
amyloidosis
postradiation fibrosis
endocardial fibroelastosis
Loffer’s syndrome
hemochromatosis
Sx of bacterial endocarditis (4)
Roth’s spots (on retina)
Osler’s nodes (on finger/toe pads)
Janeway lesions (on palm/sole)
splinter hemorrhages on nail bed
Cause/sx of rheumatic fever
Caused by streptococci infection
mitral valve regurg/mitral stenosis
Aschoff bodies
Anitschkow’s cells
elevated ASO titer
ECG of acute pericarditis
widespread ST elevation or PR depression
What is Kussmaul’s sign?
increased JVP on inspiration
rather than a normal decrease
Temporal arteritis sx
unilateral headache
jaw claudication
irreversible blindness
Takayasu’s arteritis
Pulseless disease
thickening of aortic arch
in asian females less than 40 y/o
Triad of Wegener’s granulomatosis
focal necrotizing vasculitis
necrotizing granulomas in lung/airway
necrotizing glomerulonephritis
Triad of Henoch-Schonlein purpura
palpable purpura on buttocks/legs
arthralgia
abdominal pain, melena, multiple lesions of same age
Sturge-Weber syndrome sx
Port wine stain on face
ipsilateral leptomeningeal angiomatosis
seizures
early onset glaucoma
Contraindication for beta blockers
cardiogenic shock
caution must be used with decompensated CHF
Side effect of Ca+2 channel blockers
AV block/cardiac depression
MOA of hydralazine
increase cGMP-> smooth m. relaxation
reduces afterload
used for HTN
Side effect of hydralazine
compensatory tachycardia
therefore contraindicated in angina/CAD
MOA of nitroprusside
increase cGMP
release of NO
releases cyanide and can cause toxicity
MOA of fenoldopam
D1 receptor agonist
decrease BP and increase natriuresis
MOA of nitroglycerin/isosorbide dinitrate
release NO
increase cGMP
smooth m. relaxation
decreases preload
Contraindication for pindolol/acebutolol
both partial Beta agonists
contraindicated in angina
Side effects of HMG-CoA reductase inhibitors
hepatotoxicity
rhabdomylolysis
MOA of fibrates (gemfibrozil,clofibrate,bezafibrate,fenofibrate)
upregulate LPL
increasing TG clearance
Class 1A antiarrhythmics
quinidine, procainamide, disopyramide
increase AP duration
increase refractory period
increase QT interval
Class 1B antiarrhythmics
lidocaine, mexiletine, tocainide
decreases AP duration
used in ventricular arrhythmias
Class 1C antiarrhythmics
flecainide, propafenone
used in ventricular tachycardia
contraindicated post MI
prolongs refractory period in AV node
MOA of Beta blockers (class II antiarrhythmics)
derease SA/AV node activity
decreasing cAMP/Ca2+ currents
increase PR interval
Class III antiarrhythmics
amiodarone, ibutilide, dofetilide, sotalol (K+ channel blockers)
increase AP duration, ERP, and QT interval
Class IV antiarrhythmics
verapamil, diltiazem (Ca2+ channel blockers)
decrease conduction velocity
increase ERP and PR interval
