Flashcards in Cards Deck (165):
Patient with TIA/stroke in setting of thromboembolic disease (DVT) should be suspicious for what?
VSD most commonly occurs where?
3 main conotruncal abnormalities
Transposition of great vessels, TOF, persistent truncus arteriosus
Valves are formed from what structures?
Median umbilical ligament
Medial umbilical ligaments
Ligamentum teres hepatis (contained in falicform ligament)
What closes PDA?
Indomethacin (decrease prostaglandin)
Supplies posterior 1/3 of interventricular septum, posterior walls of ventricles, and posteromedial papillary muscle
Posterior descending/interventricular artery (PDA)
Supplies anterior 2/3 of interventricular septum, anterolateral papillary muscle, and anterior surface of left ventricle. Inferior wall of LV forms diaphragmatic heart surface
Left anterior descending (LAD)
Supplies lateral and posterior walls of left ventricle, anterolateral papillary muscle
Left circumflex coronary artery (LCX)
supplies right ventricle
Right (acute) marginal artery
What usually supplies SA/ AV node
Ricght coronary artery
Right dominant circulation
85% of individuals (PDA arises from RCA)
Left dominant ciruclation
8% individuals (PDA arises from LCX)
7% individuals (PDA arises from both LCX and RCA)
Where does coronary artery occlusion most commonly occur?
Two most important factors involved in coronary blood flow autoregulation and what do they regulate
NO-regulates large coronary artery + Pre-arteriolar vessels
Adenosine-regulates small coronary arteriolar vessels
Enlargement of what part of the heart can cause dysphagia/hoarseness?
Most coronary venous blood drains into
Coronary sinus of right atrium
Where does desceining aorta lie in regard to esophagus and left atrium?
Posterior to both allowing visualization of descending aorta via transesophageal echocardiography
3 specific factors differentiating heart ciruclation from blood flow provided to skeletal muscle and viscera
1) Heart muscle perfused during diastole consuming only 5% of CO
2) Myocardial oxygen req is very high (resting 75-80% and while at work around 90% and this extraction does not occur at this level anywhere else in body)
3) coronary flow regulated by metabolic factors (adenosine causes vasodilation and decreased vascular resistance)
Most common cause of early cyanosis
What other congenital heart anomaly do patients with persistent truncus arteriosus have?
Most common congenital cardiac defect?
How is ASD different than patent foramen ovale?
ASD has septae missing tissue while PDA has tissue that is unfused
What does tricuspid atresia require for viability?
Both ASD and VSD
Most important prognostic factor in TOF?
What is the consequence of PDA?
Late cyanosis in lower extremities (differential cyanosis) and not upper extremities because PDA after major branches of aorta that feed the upper extremities. Due to late on set reversal of shunt flow from left to right to right to left.
Alcohol rexposure in utero (fetal alcohol syndrome)
VSD (important cause), PDA, ASD , TOF
AV septal defect (endocardial cushion defect), VSD ASD (ostium primum ASD)
Infant of diabetic mother
Trasposition of great vessels
MVP, thoracic aortic aneurysm and dissection
Prenatal lithium exposure
Bicuspid aortic valve, coarctation of aorta
Supravalvular aortic stenosis
22q 11 syndromes
Truncus arteriosus, TOF
Valvular obstruction due to cardiac rhabdomyomas
Most common heart tumor
Metastasis from breast, lung, melanoma, lymphoma
Most frequent cardiac tumor in children
Rhabdomyomas (associated with tuberous sclerosis)
Most frequent cardiac tumor in adults
Growth factor avidly produced by myxomas?
CO=rate of O2 consumption/arterial O2-venous O2 content
Mean arterial pressure
CO*TPR or 2/3 SBP*1/3DBP
Systolic pressure-diastolic pressure
2 variables pulse pressure is related to
Directly related to SV and inversely related to capacitance
Contractility is a function of what?
La place law
4 factors that require increase myocardial oxygen demand
Increase contractility, increase afterload, increase heart rate, increase diameter of ventricle
What accounts for most TPR an what accounts for most blood storage capacity?
Driving pressure(delta p)/flow (q)-->8nl/pir^4
Volumetric flow rate (Q)
flow velocity (v) * cross-sectional area (A)
What period of cardiac cycle is the period of highest O2 consumption
JVP absent in atrial fibrillation
JVP absent in tricuspid regurgitation
right atrial contraction
RV contraction (closed tricuspid valve bulging into atrium)
right atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
increase right atrial pressure due to filling agains closed tricuspid valve
RA emptying into RV
murmur best heard at aortic area
systolic murmur (aortic stenosis, flow murmur, aortic valve sclerosis)
murmur best heard at left sternal border
diastolic murmur (AR/PR) systolic murmur (hypertrophic cardiomyopathy)
murmur best heard at left infraclavicular region
Continuous murmur (patent ductus arteriosus)
murmur best heard at pulmonic area
systolic ejection murmur (pulmonic stenosis, flow murmur (eg. physiologic murmur))
murmur best heard at tricuspid area
pansystolic murmur (triscuspid regurgitation, VSD) diastolic murmur (tricuspid stenosis, ASD)
murmur best heard at mitral area
systolic murmur (mitral regurg) diastolic murmur (mitral stenosis)
Bedside maneuver: Inspiration
Increase intensity of right heart sounds
Increase intensity of MR, AR, VSD
Decrease intensity of HOCM
MVP: later onset of click/murmur
Valsalva, standing up
decrease intensity of most murmurs (including AS)
increase intensity of HOCM
MVP" earlier onset of click/murmur
increase intensity of AS murmur
decrease intensity of HOCM
MVP: later onset of click/murmur
Speed of conduction
SA>AV>Bundle of his/purkinje/ventricles
Normal length of PR interval
Normal length of QRS complex
ventricular depolarization, mechanical contraction of ventricles, ventricular repolarization
From start of atrial depolarization to start of ventricular depolarization
ventricular repolarization. inversion may indicate recent mi
Point in between QRS complex and start of ST segment
isoelectric, ventricles depolarized
presence of U wave is caused by what?
Drug induced causes of Torsades
Inheritance of Romano ward an jervell lange nielsen and brugada syndrome
Auto dominant and auto recessive and auto dominant
Triad of WPW
Prolonged QRS, Shorter PR interval, Delta wave
What regulates number of atrial impulses that can reach ventricle and determines ventricular contraction rate in afib?
AV node refractory period
Afib treatment for chronic Afib (>48 hours)
Antithrombotic therapy (eg warfarin), rate control (b blocker, non-dihydropyridine Ca2+ channel blocker, digoxin), rhythm control (class IC or III antiarrhythmics)
AFib treatment for new afib (
Cardioversion (used for new and not old afibb becuase cardioverision can dislodge possible clot)
Where to right/left leads in pacemakers get in the heart
Right is simple from left subclavian to SVC while left is more difficult because it goes through coronary sinus on atrioventricular groove of right atrium
1st degree AV block
PR interval >200 msec. Each PR interval is equal
Difference btwn 2nd degree Type I and Type II av block
Type I- progressive lengthening of PR interval until beat is "dropped" (P wave not followed by QRS complex)
Type II-Dropped beats are not preceeded by change in PR interal (P wave not followed by QRS complex)
Treatment of 1st, 2nd, 3rd AV block
2nd type I-none type II-pacemaker
Disease that can cause 3rd degree av block
What is recombinant form of BNP for heart failure?
Aortic arch receptor transmits through what?
Vagus nerve to solitary nucleus of medulla (responds to increase in BP)
Carotid sinus transmits through what?
Glossopharyngeal nerve to solitary nucleus of medulla (responds to decrease and increase in BP)
Method by which carotid massage decreases HR
Increase AV node refractory period
Triad of cushing reaction
hypertension, bradycardia, and respiratory depression
Describe cushing rxn.
Increase in ICP-->arteriole constriction-->cerebral ischemia-->increased pCO2+decrease pH-->increased perfusion pressure (hypertension)-->increased stretch of carotid sinus-->peripheral reflex baroreceptor induced bradycardia
Central vs peripheral chemoreceptor response
What can be used to treat paroxysmal supraventricular tachycardia in patients with no other history of heart disease?
Carotid massage (slows conduction through AV node and increase node refractory period sotpping reentrant tachycardia)
What is unique about vasculature in lungs compared to other organs in setting of hypoxia
Lung hypoxia causes vasoconstriction so that only well ventilated areas are perfused. In other organs, hypoxia causes vasodilation
Autoregulation of skeletal muscle
Exercise: lactate, adenosine, H+, K+, CO2
At rest: Sympathetic tone (alpha1 vasoconstriction, b2 vasodilation)
Autoregulation of heart
local metabolites: adenosine, NO, CO2, decreased o2
Autoregulation of brain
CO2( decrease pH)-->potent cerebral vasodilator
equation for net fluix movement Jv
4 factors causing edema with excess fluid outflow into interstitium commonly caused by:
Increase capillary pressure (increase Pc)
Decreased plasma proteins (decrease pi(C))
Increased capillary permeability (increased kf)
increased interstitial fluid colloid osmotic pressure (increase pi (i).)
4 types of xanthomas?
Eruptive xanthoma-abruptly with plasma triglyceride or lipid increase
Xanthalesma-eyelid or periorbital
Plane anthomas-appear as linear lesions in skin folds associated with primary biliary cirrhosis
In what conditions is hyaline arteriolosclerosis found?
Essential hypertension or diabetes mellitus
In what conditions is hyperplastic arteriolosclerosis found?
Differentse bewtween arteriolosclerosis and monckeberg (medial calcific sclerosis)
Arteriolosclerosis decreases vessel caliber and produce end organ ischemia. Monckeberg is not clinically significant because does not affect luminal caliber and blood flow
Vessels that arteriolosclerosis and monckeberg calcific sclerosis affect
Arteriolosclerosis-small arteries and arterioles
Monckeberg-medium sized arteries
Pathophys of monckeberg (medial calcific sclerosis)
Calcification of internal elastic lamina (ie media of arteries). INTIMA NOT INVOLVED
Varicose veins blood flow
From deep veins to superficial veins due to increased pressure in superificial veins causing them to dilate restricting venous outflow
What is more common in varicose veins? thromboembolism or venous stasis?
Venous stasis that can cause ulcers common in the medial malleolus
What can happen to skin in chronic venous insufficiency?
Stasis dermatitis with erythema and scaling and perogressive dermal fibrosis and hyperpigmentation.
4 modifiable risk factors for atherosclerosis
HTN, diabetes, hyperlipidemia, smoking
What is most responsible for producing intimal response in atherosclerosis?
SMC migration involves what growth factors
FGF, PDGF, TGFB
Main determinant onf whether or not a coronary artery plaque will cause ischemic myocardial injury?
RAT at which it occludes involved artery
AAA is associated with what risk factor?
TAA associated with what risk factor?
Cystic medial degeneration
What changes are seen with cystic medial degeneration?
Most common site of injury in blunt aortic rupture (traumatic aortic rupture most commonly in MVC)
Single most important risk foctor for development of intimal tears
Common location of atheroscleorisis?
EKG for stable, unstable, prinzmetal angina
ST sement depression, st segment depression, st segment elevation
What test is most sensitive for coronary artery vasospasm?
Ergonovine test by stimulating alpha-adrenergic/serotonergic receptors
What is the mechanism behind pharmacologic stress tests?
coronary steal syndrome
What determines likelinhood of plaque rupture?
plaque stability rather than size where activated macrophages in the atheroma contribute to collagen degradation by secreting metalloproteinases contributing to collagen degradation
Most common cause of sudden cardiac death
Explain CAD induced SCD
Acute plaque-->acute myocardial ischemia-->electrical instability in heart-->potentially lead to vfib
Leads with st elevations or Q waves
anteroapical (disatl LAD)
Anterolateral (LAD or LCX)
II, III, aVF
Gold standard for MI in first 6 hours
Most sensitive and specific marker for MI (gold standard)
Troponin I (rise after 4 hours after infarction and increased for 7-10 days)
Useful marker for detecting reinfarction that occurs days afterinitial MI
CKMB (because rises 6-12 hours after and levels return to normal within 48 hours)
Risk of complications and time frame
0-4 hours, 4-24 hours, 1-3 days, 3-14 days, 2weeks- 2 months
0-24 hours (arrhythmia, cardiogenic shock , heart failure)
1-3 days (Fibrinous pericarditis)
3-14 days (Ventricular pseudoaneurysm (risk of rupture), free wall rupture-->tamponade, papillary muscle rupture-->mitral regur, iv septal rupture-->VSD)
2 weeks-2 months (Dressler syntrome, HF, arrhythmias, true ventricular aneurysm)
valvular disorder in HOCM
May see mitral regurg due to impaired mitral valve closure
Cause of LV outflow obstruction in obstructive HOCM
anterior displacement of mitral valve leaflet toward hypertrophied interventricular septum
3 places where you see eccentric hypertrophy
1) aortic/mitral regurg
3) dilated cardiomyopathy
3 places where you see concentric hypertrophy
1) chronic htn
2) aortic stenosis
Mainstay treatment of CHF
drugs that decrease mortality in CHF
ACE inhibitors or ARBs, b blockers, and spironolactone
drugs that are used for symptomatic relief in CHF
thiazide or loop diuretics
drugs that improve both symptoms and mortality in select patients
Hydralazine with nitrate therapy
Difference in EF, EDV and contractility and compliance in systolic vs diastolic dysfunction
Systolic-decreased contractility, decreased EF, increased EF
Diastolic-decreased compliance, same EF, same EDV, increased LV EDP
First sign of shock
CVP, CO, SVR or Hypovolemic, cardiogenic, obstructive, and distributive shock
Hypovolemic: decreased CVP, decreased CO, increased SVR
Cardiogenic/obstructive: increased cvp, decreased co, increased SVR
Distributive: decreased CVP, increased CO, decreased SVR
tricuspid valve endocarditis associated with what 3 bugs in IV drug abuse
candida, s auereus, pseudomonas
Negative culture and bacterial endocarditits
Coxiella burnetii, bartonella, HACEK
2 manifestations of syphillitic heart disease
Aneurysm of ascending aorta or aortic arch, or aortic insufficiency (aortic regurg)
Does verapamil work on skeletal muscle?
no. no significant flux of calcium across l-type calcium channels in skeletal muscle, but significant flux in cardiac and smc.
How is ca2+ efflux established prior to myocyte relaxation?
ca2+ atpase (active transport to sequester calcium within sr to reistablish ion gradient) and Na+/ca2+ exchanger.
what type of channels cause automaticity in cardiac nodal cells?
What increases slope of phase 4 in SA node and determines HR
What decreases slope of phase 4 in SA node and decreases HR