Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
101 Cards in this Set
- Front
- Back
what supplies blood for the SA and AV nodes?
|
most of the time its the RCA
|
|
when do coronary arteries fill?
|
during diastole
|
|
what 3 things affect SV
|
Contractility, Afterload, preload
SV CAP |
|
how does digitalis increase contractility
|
it inhibits the Na/K pump so that intracellular Na builds up and decreases the action of the Na/Ca pump that extrudes Ca and brings in Na
|
|
how do catecholamines increase contractility
|
increase the activity of the Ca pump on the SR so that more Ca is taken up and then able to be released on the next contraction
|
|
an example of a drug that is a vasodilator and decreases the afterload
|
hydrAlAzine----decrease Afterload (Arterial)
|
|
what does the starling curve show
|
that the force of contraction is proportional to the initials length of the cardiac muscle fibers
|
|
Romano Ward syndrome
|
mutation in the K channel protein that delays Ik channel current
leads to QT prolongation |
|
Jervell and Lange-Nielsen Syndrome
|
Mutation in the K channel protein that delats the Ik channel current
leads to QT prolongation |
|
lyme disease can result in what heart condition (conduction related)
|
3rd degree heart disease
|
|
three things that the peripheral (carotid and aortic bodies) chemoreceptors respond to
|
drop in PO2, Increase in PCO2, drop in blood pH
|
|
central chemoreceptors respond to what and DO NOT respond directly to what
|
changes in ph and CO2 which are influenced by arterial CO2. DO NOT directly respond to PO2
|
|
what is the cushing reaction and what is responsible for it
|
an increase in ICP constricts arterioles leading to cerebral ischemia which lead to HTN which leads to reflex bradycardia
central chemoreceptors are responsible for it |
|
cushing triad
|
HTN, bradycardia and respiratory depression
|
|
what is the O2 extraction from blood of the heart and how does this play with an increase in O2 demand of the heart
|
the O2 extraction is 100%
so an increase in O2 demand is met by increasing the coronary blood flow not by increase the extraction (which would be impossible since its 100% duh) |
|
what are the five T's of right-to-left shunts that produce blue babies
|
Tetralogy
Transposition Truncus Tricuspid TAPVR |
|
what is the most common congenital heart defect and what is it associated with (an assoc. cause)
|
VSD
Assoc. with Fetal Alcohol Syndrome |
|
ostium primum and secundum
which is most common and which is associated with Downs |
ostium secundum is most common
primum associated with Downs |
|
what is an associated cause of a PDA (congenital cause)
|
congenital rubella
|
|
what is Eisenmengers syndrome
|
due to uncorrected VSD, ASD, or PDA that causes compensatory right ventricular hypertrophy which results in progressive pulmonary HTN. the new HTN then reverses the shunt from L to R to R to L and you get cyanosis later in life
|
|
what produces a boot shaped heart on Xray and what is it due to
|
tetralogy of fallot
d/t the R ventricular hypertrophy |
|
what is transposition of the great vessels associated with (mothers problem)
|
maternal diabetes
|
|
what are the two types of coarctations of the aorta and what are their locations
|
Infantile type----before the ducuts arteriosus....INfant IN close to heart (proximal to duct)
Adult type---after the duct...aDult, Distal to Duct |
|
what is infantile and adult coarctation assoc. with (seen on xray for adults) and what do adults present with
|
infantile associated with Turner syndrome
adult associated with NOTCHED RIBS (seen on xray) and they present with HTN in the upper extremities and weak pulses in the lower extremities |
|
what is coarctation of the aorta associated with (think of Brandon)
|
bicuspid aortic valve
|
|
hear a continuous machine like murmur? what is it
|
PDA
|
|
PDA can result in what later in life
|
cyanosis in the lower
|
|
Monckeberg vs arteriolosclerosis vs atherosclerosis
|
monckberg: calcification of the MEDIA of the arteries (NO BLOOD FLOW OBSTRUCTION)
arteriolosclerosis: HYALINE thickening of small arteries atherosclerosis: fibrous plaques and atheromas in the INTIMA of arteries |
|
what is an ebstein anomaly
|
in utero exposure to lithium (for treating bipolar) that leads to
1) apical displacement of tricuspid valve 2) decrease volume of right ventricle 3) atrialization of right ventricle |
|
what is a good predicting sign of an aortic dissection
|
tearing chest pain that radiates down the back
|
|
three types of angina
|
stable, prinzmetals variant, unstable/crescendo
hey angie (angina), whaz SUP!!!!!!!! |
|
stable angina is secondary to what and shows what on ECG and is arises d/t what
|
atherosclerosis, ST depression arises d/t exertion or emotional stress
|
|
prinzmetals variant angina is secondary to what, shows what on ECG and how do you Rx it
|
secondary to coronary spasm, ST elevation (d/t being a COMPLETE blockage), Rx with nitro or CCB
Metal rock makes you SPASM!!!!! |
|
unstable/crescendo angina cause, ECG results and Rx
|
thrombosis, but no necrosis, ST depression Rx with nitro
|
|
most commonly involved artery with a MI
|
LAD
da widow-maker!!!!! |
|
gold standard for Dx of MI in the first 6 hours
|
ECG
|
|
most sensitive and specific marker for MI?? (gold standard)
|
Troponin I
|
|
what marker can be used to Dx an MI that occurs days after an initial MI because its levels rise and fall within 1.5 days (peaking at 24hours)
|
CK-MB
|
|
what is dresslers syndrome
|
autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post MI)
|
|
most common cardiomyopathy and etiologies, systolic or diastolic
|
Dilated Cardiomyopathy (all 4 chambers enlarged), systolic
Alcohol abuse, wet Beriberi, Coxsackie B virus, Cocaine use, Chagas disease, Doxorubicin, peripartum ABCCCD and a P |
|
hypertrophic cardiomyopathy
genetics (HY), type of murmur, Rx, systolic or diastolic |
L ventricle hypertrophy, Autosomal dominant (mutations in sarcomere proteins), systolic murmur S4, Rx with B blockers or non-dihydropyridine CCBs (verapamil) diastolic
|
|
restrictive/obliterative cardiomyopathy
causes, classic ECG finding, systolic or diastolic |
sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelestosis, lofflers syndrome (pg 83 pathoma); low-voltage EKG with diminished QRS amplitude; diastolic
|
|
eccentric vs concentric hypertrophy, cause and types of cardiomyopathies assoc.
|
eccentric---volume overload, seen with aortic regurge, seen in dilated cardiomyopathy
EEEEcentric------sEEEries (fibers added in series) concentric---pressure overload, seen with aortic stenosis and systemic HTN, seen in hypertrophic cardiomyopathy; fibers added in parallel |
|
how does paroxysmal dyspnea occur in CHF
|
patient lies down, this increases venous return and exacerbates the problem
|
|
intraavleolar hemorrhage in CHF is caused by what and marked by the presence of what?
|
caused by microhemorrhages from an increase in pressure in the pulmonary capillaries rupturing them
hemosiderin-laden macrophages (heart failure cells) |
|
nutmeg liver is seen in what disease state?
|
CHF (right sided heart failure) due to an increase in central venous pressure leading to an increase resistance in portal flow.
|
|
most common cause of right sided heart failure?
|
left sided heart failure
|
|
paradoxical problem with low CO in CHF and the kidneys
|
kindeys get lower flow, this activates the RAAS system leading to an increase in Na and water retention further exacerbating the CHF problem (fluid overload)
|
|
DOC for treating CHF
|
ACE inhibitors
|
|
Sx's for bacterial endocarditis? 8 of em, and which is more common?
|
FROM JANE
Fever (most common) Roths spots Osslers nodes (tender lesions on palms and toes) Murmur Janeway lesions (nontender lesions on palms and soles) Anemia Nail-bed hemorrhage (splinter hemorrhages) Emboli |
|
bacteria causing large vegetations in endocarditis? tell me a little about it as well
|
staph auerus, HIGH virluent, common in IV DRUG USERS, TRIcuspid valve affected
dont TRI drugs!!!! |
|
bacteria causing small vegetations in endocarditis? a little about it as well
|
strep viridans, LOW virulence, sequela of dental work, MOST COMMON OVERALL,
|
|
bacteria assoc. with endocarditis that hits prosthetic valves and one that deals with the intestines (what disease specifically?)
|
strep epidermidis hits prosthetic valves
strep bovis from colon cancer |
|
what is libman-sacks endocarditis
|
sterile vegetations that occur on both sides of the heart valve, assoc. with SLE
SLE causes LSE |
|
Sx's of rheumatic heart disease
|
FEVERSS
Fever Erythema marginatum Valvular damage ESR (increases) Red hot joints (migratory polyarthritis in large joints) SubQ nodules Sydenham chorea |
|
cause of rheumatic heart disease and valve most commonly involved
|
group A Beta Hemolytic strep, mitral valve
|
|
most common cause of death in the acute phase of rheumatic fever and what is seen microscopically
|
myocarditis, aschoff bodies (granuloma with giant cells) and anitschkow cells (activated histiocytes)
|
|
what is the underlying cause of rheumatic heart disease (answer is not group a strep)
|
molecular mimicry, the bacterial M protein resembles human tissue.
|
|
what leads to a "tree bark" appearance of the aorta?
|
tertiary syphilis leading to calcification of the aortic root
|
|
most common cardiac tumor in adults? in kids? associated with what in kids?
|
myxomas in adults, rhabdomyomas in kids and assoc. with tuberous sclerosis
|
|
wegeners granulomatosis: triad, sx's, marker, Rx
|
triad: focal necrotizing vasculitis, nectrotizing granulomas in LUNG and UPPER AIRWAY, nectrotizing glomerulonephritis
Sx's: hemoptysis, hematuria, perforated nasal septum c-ANCA is the strongest marker Rx with cyclophosphamide and corticosteriods |
|
p-ANCA is associated with what?
|
microscopic polyangitis and churg-strauss syndrome
|
|
what is the most common form of childhood systemic vasculitis? triad? follows what illness and results in what other systemic organ problem?
|
henoch-schonlein purpura
triad: skin, joints, GI (skin rash on butt and legs, arthralgia, intestinal hemorrhage) follows an URT infection and results in IgA nephropathy |
|
kawasaki disease, Sx's (most serious too), Rx
|
necrotizing vasculitis in kids
see: fever, conjunctivitis, "strawberry tongue", may develop coronary aneurysms (MOST serious) rx with IVIG and aspirin |
|
polyarteritis nodosa, 30% of pts are seropositive for what?
|
Hep B
|
|
Takayasu's arteritis, known as what?, what is it, Sx's
|
known as pulseless disease
is granulomatous thickening of aortic arch and/or proximal great vessels FAN MY SKIN On Wednesday Fever Arthritis Night sweats MYalgia SKIN nodules Ocular disturbance Weak pulses in upper extremities |
|
most common vasculitis affecting medium and large arteries? Sx's? population hit the most
|
Temporal arteritis (giant cell arteritis)
Sxs of TEMPoral arteritis are near TEMPles: headache, jaw claudication, impaired vision elderly females |
|
B blockers are contrindicated in what
|
decompensated CHF
|
|
Hydralazine MUT
|
moa: increase cGMP to produce relaxation of smooth muscles and arteriole vasodilation
U: 1st line for HTN in preggos, frequently given with B blocker to prevent reflex tachy T: compensatory tachy, lupus like syndrome |
|
Nifedipine, verapamil, diltiazem
class, MUT |
CCB's
M: block voltage-dependent L-type Ca channels reducing muscle contractility, for vascular smooth muscle use nifedipine, for the heart use verapamil (V for Ventricle) U: HTN, angina, arrythmias (not nifedipine), prinzmetals angina, reynauds T: cardiac depression, AV block, peripheral edema, flushing |
|
nitroglycerine, isosorbide dinitrate MUT
|
M: release NO, increase cGMP to produce smooth muscle relaxation, hit VEINS more than arteries, decrease PRELOAD
U: angina, keeping a boner T: reflex tachy, hypotension |
|
nitroprusside can cause what toxicity?
|
cyanide
|
|
niacin MT
|
M: decrease lipolysis in adipose tissue and decrease hepatic VLDL secretion
T: red, flushed face, hyper glycemia, hyperuricemia |
|
Bile acid resins MT
|
M: prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more
T: taste like crap and cause GI discomfort |
|
ezetimibe MT
|
M: prevent cholesterol reabsorption at small intestine brush border
T: |
|
Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate) MT
|
M: upregulate LPL to INCREASE TG clearance
T: myositis, hepatotox |
|
digoxin MUT
|
M: binds Na/K ATPase and indirectly inhibits Na/Ca pump. this increase [Ca] and increases inotropy
U: CHF, a fib, T: cholinergic (nausea, vomit, diarrhea, blurry yellow vision); ECG (increase PR, decrease QT, T wave inversion); worsened by renal failure, hypokalemia, quinidine (decreases digoxin clearance) |
|
Class IA antiarrhythmics 3 of em
MOA |
Quinidine, Procainamide, Disopyramide
the Queen PROclaims Disos Pyramide MOA: increase AP duration, increase ERP, increase QT interval |
|
Class IB antiarrhythmics 3 of em
MOA?affect what tissue? best time to use? |
Lidocaine, Mexiletine, Tocainide
I'd Buy LIDy's MEXIcan Tacos MOA: decrease AP duration hit purkinje and ventricular tissue the most Best post-MI |
|
Class IC antiarrhythmics 3 of em
no effect on what? when NOT to use? |
Flecainide, Encainide, Propafenone
Chipolte's Food has Excellent Produce No effect on AP duration Contraindicated post-MI |
|
what condition will increase the tox for all Class I antiarrythmics?
|
hyperkalemia
|
|
Class II antiarrythmics 5 of em MUT
|
propranolol, esmolol, metoprolol, atenolol, timolol
M: decrease cAMP, decrease Ca currents, decrease slope of phase 4 in abnormal pacemakers (AV node in particular) U: v tach, SVT, slow ventricles during a fib, a flutter T: impotence, exacerbate asthma |
|
Class III antiarrhythmics 5 of em
MUT |
satalol, ibutilide, bretylium, dofetilide, amiodarone (K channel blockers) BAIDS
M: increase AP duration, increase ERP, increase QT interval T: amiodarone: pulmonary fibrosis, hepatotox, hypo/hyperthyroidism BE SURE TO CHECK: PFT, LFT, TFT |
|
Class IV antiarrhythmics 2 of em
MUT |
Verapamil, diltiazem
M: decrease conductance velocity, increase ERP, increase PR interval U: Prevent nodal arrhythmias T: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression |
|
DOC for Dx'ing/abolishing SVT and duration?? (MOA too)
|
adenosine (increase K out of cell)
very short acting (15 seconds) |
|
stills murmer
|
benign pediatric murmur in kids 2-8 years old, mid-systolic murmur of musical quality heard at apex and left sternal border
|
|
a wide pulse pressure and a "blowing murmur" indicate what?
|
aortic regurg, their head may even bob
|
|
class IB works on what type of tissue best? major S/E?
|
ISCHEMIC!!!!
CNS symptoms |
|
what drug prolongs the AP duration more than any other antiarrhythmic drug?
|
amiodarone
|
|
3 classic signs of aortic dissection?
|
substernal pain radiating to the back
severe HTN asymmetric upper extremity pulses |
|
associate churg-strauss with this disease and what ANCA
|
asthma
p-ANCA |
|
what population is hit with takayasus arteritis?
|
asian females
|
|
how long does stable angina last?
|
30 seconds to thirty minutes
|
|
does hypercalcemia increase digoxin tox?
|
YES!!
|
|
digoxin hits the Na/K pump....it also stimulates something, what is it and what could that produce?
|
the vagus nerve (parasympathetics) and this could lead to AV block
|
|
remember that right upper quadrant pain in the presence of edema, venous stasis and JVD is a sign of liver congestion and thus Right sided heart failure
|
know it!
|
|
does digoxin have any effect on mortality CHF patients?
|
NOOOOO!!!!!!!
|
|
three DOC's for CHF that increase survival
|
ACE inhibitors, spironolactone, metoprolol
|
|
holosystolic "blowing" murmur is what? heard best where?
|
VSD. Tricuspid area
|
|
DOC to convert SVT??? second line drug?
|
adenosine first
Beta blocker (propranolol) second |
|
3 bugs associated with IV drug abusers with endocarditis
|
Staph areus
Pseudomonas Candida |