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236 Cards in this Set

  • Front
  • Back
What's in the carotid sheath?
Vein- internal jugular (lateral)
Artery- Common carotid (medial)
Nerve- Vagus (posterior)
What provides the blood supply for the SA and AV nodes?
RCA- 80%
What does the RCA provide the circulation for?
inferior portion of the left ventricle via the posterior descending
A pregnant woman in the 3rd trimester has normal bp when standing and sittling, but when lying down, bp drops to 90/50, why?
compression of the IVC
a 35 y/o man ha s high bp in arms and low pression in his legs
coartaction of the aorta
A 5 y/o presents with systolic murmur and wide, fixed split S2, what is it?
A football player collapses and dies, what is the most likely cause?
hypertrophic cardio myopathy
Pt. has a stroke after multiple long bone fractures, why?
fat emboli
elderly woman with headache and jaw pain with elevated ESR?
temporal arteritis
80 y/o w/ systolic crecendo decrescendo, what is causing the murmur?
aortic stenosis
A man starts a medication for hyperlipidemia. He gets pruritus, and GI upset, what was the drug?
Patient witha cough must disconinue captopril. What should the drug be replaced with?
Losartan, ARB. No, increase in bradykinin, no SEs
What does the LAD supply?
the ant. Right and left ventricle and intraventricular septum
What does teh posterior descending artery supply?
IV septum and left ventricle
What does the truncus arteriosus become?
aorta and plulmonary trunk by formation of the aroticopulmonary septum
What does the bulbus cordis form?
conus arteriosus (smooth part of the right ventricle) and aortic vestibule (smooth part of the left ventricle)
What is the aortic vestibule?
the smooth part of the left ventricle
What is the conus arteriosus?
the smooth part of the right ventricle
What are the CV abnlties in Marfan's?
aortic root dilation, Aortic Aneurysm, aortic regurgitation, mitral valve prolapse.

Rx- Beta blocker
What does the sinus venosus form?
sinsus venarum (smooth part of the right atrium), coronary sinus, and oblique vein of the left atrium
How do you calculate Cardiac Output?
What is the Fick principle?
CO=rate of 02 consumption/arterial 02 content - venous O2 content
How do you calculate MAP?
MAP=1/3systolic +2/3diastolic
How do you calculate pulse pressure?
How do you calculate Stroke Volume?
How does CO increase in excercise?
initially, CO increases due to SV, after prolonged excercise, SV increase from an increase in HR
What happens to diastolic filling if HR is too high?
In what pathologic rhythm does this happen in?
filling is incomplte and CO decreases.
happens in V-tach
What are the major variables in Cardiac Output?
Stroke Volume affected by:
SV increases when CP goe up and when A goes down.
What increases the contractility?
1. Catecholamines- increase Ca2+
2. Increases in intracellular Ca2+
3. Decrease in extracellular Na+
4. Digitalis (increases intracellular Na+, leaing to increase in Ca2+)
What decreases contractility?
1. B1 blockade
2. Heart failure
3. Acidosis
4. Hypoxia/hypercapnia
5. Ca2+ channel blockers
6. ACh from vagus decreases Ca in the atrium
When does SV increase?
anxiety, exercise, preggers
When is myocardial 02 increased?
Increased afterload
increased contractility
increased hr
increased heart size (from wall tension)
When does preload increase?
exercise (a little)
Increased blood volume
excitement (symps)
preload pumps up the heart

Preload=ventricular EDV= Right atrial pressure
What is the afterload equivalent to?
systolic arterial pressure
proportional to peripheral resistance.
what makes up the thick filaments of the saromere?
what makes up the thin filaments of the sarcomere?
actin, troponin, tropmyosin
What is the role of T-tubules?
invaginate cells at the Z-lines and carry action potentials into the cell interior
- better developed in the ventricles
- form dyads with the sarcoplasmic reticulum
What are the steps to muscle contraction?
AP flows, Ca enters, triggers release of Ca from SR (dependant on how much Ca there is)
- this binds to troponin C, moves tropomyosin out of the way, no more inhibition of myosin and actin.
What are two situations that result in higher contractility from increased Ca.
1- Positive staircase. Increased HR = incrased force as Ca builds over a few beats
2- post-extrasystolic potentiation- beat occurs afer an extrasystolic beat has icnreased fource of contraction.
What is phospholamban?
regulates the pump of the SR. when phosphorylated, more Ca2+ is released.
What is the mechanism of digitalis?
blocks the Na/K ATPase-> increase Na, less of an Na gradient.
an Na/Ca pump turns on and brings Ca into the cell to get Na out.
How do you calculate the ejection fraction?
EF is a measure of contractility
EV is about 55% when normal.
What is the relationship between velocity, blood flow, and x-sectional area?
Aorta has a small x-sectional area compared to the capillaries. higher velocity
What is the relationship between flow, pressure and resitance?
R=driving pressure/Q=8n(viscosity)xlength/(pi)r4

Driving Pressure=MAP-RAP

When is viscosity increased?
Hyperproteinemic states (multiple myeloma)
Hereditary spherocytosis
What is the relationship between resistance, viscosity and radius of the blood vessel?
R is directly proportional to visc.
R is inversly proportional to r4
Explain R in series vs. R in parrallel
1/R=1/R1 + 1/R2
example- renal, hepatic, other.

artery, arteriole, capillary
arterioles provide the greatest resistance
What changes cause turbulent flow?
Increased blood velocity (narrowed vessel)
Decreased viscosity (anemia, decreased hematocrit)
What is the equation for capacitance?

greater capacitance in veings.
decreases with age.
decreased capacitance = increases in pulse pressure.
What increases mean systemic pressure/right atrial pressure?
MAP increases with:
increase in blood volume or decreased venous compliance (blood shifted from veins to arters)
What decreases mean systemic pressure?
decrease in blood volume or an increase in venous compliance
What determines the slope of the venous return?
resistance of the arterioles
Increas in TPR rotates counter-clockwise (lowers venous return/slope)
What changes the CO curve?
What is stroke work?
work a heart performs on each beat.
Work = pressure x sv
What happens in Isovlumetric contraction?
period between mitral valve closure and aortic valve opening (high O2 consumption)
What are the phases of the cardiac cycle?
Isovolumentric contraction
systolic ejection
Isovolumetric relaxation
Rapid filling
slow filling
When does the S3 occur?
end of rapid filling
usually in a dilated ventricle
What causes an S4?
stiff ventricle or high atrial pressue. comes with the atrial kcick in hypertrophic ventricle (hypertension)
How does preload change the pressure-volume loop?
It moves the bottom right to the rightand up a little. Systole occurs at a greater volume
How does an increased afterload change the volume loop?
decreases the stroke volume
EDV moves up.
More pressure is needed for ejection
How does increased contractility change the volume loop?
bigger curve on top
lower EDV
now real change in pressure
What do the following correspond to:
a wave
c wave
v wave
a wave- atrial contraction
c wave- RV contraction (tricuspid bulges into the atrium)
v wave- passive filling
What causes paradoxical S2 splitting?
Aortic stenosis (takes longer to get the blood out)
What are some differences between cardiac and skeletal muscle?
1. Cardiac muscle action potential has a plateau
2. Cardiac nodal cells spontaneously depolarize- automaticity
3. Cardiac myocytes are coupled by gap junctions.
What is the effect of K on the cardiac ap?
conductance of K determines resting membrane potential.
Inward current brings + charge into cell and epolarizes
outward current takes + out of the cell and hyperpolarizes
Go through the cardiac ap, Phase 0-4 (not in the SA node)
Phase 0- Rapid upstroke (voltage gated Na)
Phase 1- brief initial repol by K channels open
Phase 2- plateau- Ca2+ influx through voltage gated Ca2+ channels balances the K+ efflux. Triggers Ca release from Sarcoplasmic reticulum and myocyte contraction.
Pase 3- rapid repolarization. opening of slow K+ channels and closure of Ca2+ channels.
Phase 4=resting potential- high K+ permeability
Go through how the pacemaker action potential is different
Phase 0- upstroke- opening of Ca channels. no fast na channels. slow conduction velocity. AV uses to prolong conduction to ventricles.
Phase 2 plateau does not exist
Phase 4- has slow diastolic depolarization. If has a depol current
What changes the funny current?
ACh decreases and catecholamines increase the rate of diastolic depolarization.
What do the following correspond to?
P wave
PR segment
QRS complex
QT interval
T wave
ST segment
U wave
P- atrial depol
PR- conduction delay through the aV node (<200 msec)
QRS complex- ventricular depol (<120 msex)
QT interval- mechanical contraction of the ventricles
T wave- ventricular repol
ST segment- isoelectric, ventricles depolarized
U wave- hypokalemia
What happens in Wolf-Parkinson-White syndrome?
Accessory conduction pathway from atria to ventricle (bundle of Kent. Bypassing AV node. As a result, ventricles begin to partially depolarize earlier, gives rise to delta wave on ECG. can cause supraventricular tachycardia. Afib is really bad.
What ECG changes occur in afib?
chaotic, irregularly irregular. no discrete p waves
What ECG changes occur in atrial flutter?
rapid succession of identical, back to back atrial depol waves. sawtooth looking flutter waves
What ECG changes occur in 1st degree AV block?
prolonged PR- asymptomatic
What ECG changes occur in 2nd degree, type 1 AV block?
Progressive lenthening of th ePR-> dropped beat.
What are the ECG changes in 2nd degree, Mobitz type II AV block?
No PR change
can be 2:1 block (2ps for 1Q)
may progress to 3rd degree
What are the ECG changes in 3rd degree AV block?
atria and ventricles beat independantly
What happens in the baroreceptor reflex?
How can a physician physically manipulate it?
where is it located?
is it fast or slow?
hypotention-> decrease in pressure-> decrease in stretch-> decrease in firing-> increase in symps and decrease in effecrent paras-> increase in HR, contractility, BP and vasoconstriction

Carotic massage- increase in pressure-> increased stretch-> decrease in HR

located at bifurcation of the carotid artery.

fast neural mechanisms.

set point is 100mmHg
How does the renin-angiotensin-aldosterone system regulate bp?
slow, hormonal mechanism
adjusts blood volume

less renal perfusion-> renian release by the JG cells

angiotensin-> production of aldosterone and vasoconstricion
How do the aortic arch and corotid sinus reach the brain?
aortic arch- via the vagus
carotid sinus- via the glossopharyngeal
both go to the medulla

aortic arch only rsponds to an increase in bp.
How do chemoreceptors function?
Peripheral- respond to a decrease in Po2, increase in Pco2, and decrease in pH

Central- pH and Pco2. Response to cerebral ischemia-> increase in symp outflow. vasoconstriction (can be life-threatening)
Cushing reaction- increase in ICP compresses vessels-> increase symps. dangerous
ADH is secreted
What organ has the largest share of the CO?
What organ has the highes blood flow per gram of tissue?
How does the heart take in more O2?
increased flow for more 02, not by extraction
What is the role of ANP?
released from the atria when atrial pressure is increased.
- relaxation of the vascular smooth muscle
- exretion of Na and water
- inhibs renin
what crosses capillaries through water-filled clefts?
water, glucose, amino acids

liver and intestine, the clefts are huge to allow passage of protein
What is the equation of starling florces in capillary fluid movement?
fluid movement=Kf[(Pc-Pi)-(PIc-PIi)]
Heart Failure- increase Pc
Nephrotic syndrome, liver failure- decrease PIc
Toxins, infections, burns- increase permeability
lymphatic blockage- increase in PIi
How does the Heart autoregulate blood flow?
local metabolites- hypoxia, adenosine, NO
How does the brain autoregulate blood flow?
local metabolites- CO2 (pH)
How do the kidneys autoregulate blood flow?
Myogenic and tubuloglomerulo feedback
How do the lungs autoregulate blood flow?
Hypoxia causes vasoconstriction. (unique)
How does skeletal muscle autoregulate blood flow?
Local metabolites: lactate, adenosine, K+
very important in exercise

at rest, symps play a strong role
How does skin autoregulate blood flow?
Sympathetics- temperature control - not very local
What is the role of prostacyclin?
what is the role of thromboxane A2 in bp?
what is the role of Prostas E and F in bp?
E- dilate
F- constrict
What are the effects of bradykinin on the vasculature?
arteriole dilatation venous constriction.
What are the effects of histamine on the vasculature?
arteriolar dilation and veous constriciton.
Increased Pc and increased filtration. local edema
What are some causes of Right to Left shunts?
The three Ts
1. Tetralogy of Fallot- most common cause of early cyanosis
2. Transposition of great vessels
3. Truncus arteriosus

cause blue babies- (early cyanosis) kids may squat to increase venous return.
What are the frequent causes of Left-to-Right shunts?
1. VSD- most common congenital cardiac abnlty
2. ASD- low S1, wide, fixed split S2
3. PDA- close with indomethcin

increased pulm resistance due to arteriolar thickening.
progressive pulm htn. R->L (eisenmenger's syndrome)

Blue Kids- late cyanosis
What is Eisenmenger's syndrome?
uncorrected VSD, ASD, or PDA leads to progressive pulm hypertension. Pulm resistance increases and the L->R becomes R->L. Late cyanosis (clubbing, polycythemia)
Breakdown Tetralogy of Fallot
What is the defect?
What are the buzzwords
what is the cause?
PROVe it exists
Pulm stenosis- determines prognosis
Overriding aorta (overides VSD)

Bootshaped heart, cyanotic spells
anterosuperior displacement of the infundibular septum.
Breakdown the transposition of the great vessels
What is the defect?
How does it evolve?
RV connects to aorta and LV connects to the pulmonary trunk
is not compatable with life unless there is a shunt too.
Caused by a failure of the aorticopulmonary septum to spiral
What are the differences between infantile and adult type coartation of the aorta?
Infantile- aortic stenosis proximal to the insertion of ductus arteriosus (preductal).

Adult- stenosis is distal tothe ductus (postductal). Notching of the ribs, htn in upper extremities, weak pulses in lower

INfantile: IN close
aDult- Distal to Ductus
M:F 3:1
Break down PDA:
what's the defect
what keeps it open?
when do you want to keep it open?
PDA in fetal period, shunt is R->L adn normal. In neonatal, lung resistance decreasesa nd shunt becomes L-> R with RVH and failure. Machine-like murmur. Patency is maintained by PGE and low O2.

PGE used in transposition of the great vessels
What genetic defect is truncus arteriosus and tetrology of fallot associated with?
22q11 syndromes
What genetic defect is ASD and VSD associated with?
What heart defects does congenital rubella cause?
septal defects, PDA
What genetic defect is coartaction of the aorta associated with?
Turner's syndrome
What genetic defect is aortic insufficiency associated with?
What congenital heart defect can occur in the offspring of a diabetic mother?
transposition of the great vessels
What is the difference of stable, unstable and prinzmetal angina?
stable- comes on with exertion, relieved by rest and NO
Untstable- prolonged and even at rest. MI real soon
Prinzmetal- vasospasm causes angina at rest
what immune cells are not involved in MIs?
lymphocytes and plasma cells
What are the major complications of the heart post MI? (7)
Arrhytmia- most common cause of death in first several hours after infarction
Pump failure- can lead to CHF or shock. dependant on size and location of lesion. also pulm edema
Myocardial rupture- w/in first 4-7 days. Death from cardiac tamponade
Ruptured papillary muscle
Mural thrombosis- thrombus formation on the endocardium
Ventricular aneurysm
Fibrinous pericarditis
Dressler's syndrome- autoimmune phenomenon that causes fibrinous pericarditis.
What are the manifestations of chronic ischemic heart disease?
Progressive onset of CHF over many years from chronic ischemic damage.
What is Monckeberg arteriosclerosis?
medial calcific sclerosis- >50, radial and ulnar arteries.
ring-like calcifications
no obstruction of flow. pipestem arteries.
What is arteriolosclerosis?
hyaline thickening in small arteries and arterioles- kidnesy
htn and dm.
What is the difference between hyaline arteriolosclerosis and hyperplastic?
hyaline- thickening of walls. in kdneys it is benign nephroscleorsis- w/ HTN

Hyperplastic- onionskin thickening of arteriolar walls. W/ necrotizing arteriolitis.
This is malignant nephrosclerosis with melignant HTN.
What is atherosclerosis?
fibrous plaques (atheromas) in the intima of arteries.
What are some common sites of atherosclerosis?
Abdominal Aorta > Coronary artery > popliteal artery > carotid

Proximal portions of the coronary arteries
larger branches of carotids
circle of Willis
large vessels of the lower extremities
renal and meseteric arteries.
What are the parts of a plaque in atherosclerosis?
core- central core of cholesterol, esters, macrophages, foam cells, calcium, necrotic debris
cap- subendothelial cap of smooth muscle, foam cells, fibrin and other coag proteins. Collagen, elastin, gags, proteoglycans

develop from fatty streaks.
What can cause problems with plaques?
Ulceration, hemorrhage, calcification
Thrombus formation at the sight-> obstruction
What are teh concequences of atherosclerosis?
ischemic heart disease
Ischemic bowel disease
peripheral vascular occlusive disease- gangrene, claudication
renal arterial ischemia with 2ry HTN.
What are some risk factors in atherosclerosis?
gender (M>W)
Obesity, physical inactivity, type A, hyperuricemia, hyperhomocysteinemia, methylene tetrahydrofolate reductase mutations, lipoprotein A, chlamydia pneumoniae and OCs.
What are the Insudation, Encrustation/thrombogenic, and monoclonal hypotheses of atherosclerosis?
Insudation- infiltration of the intima with lipid and protein is the 1ry event.
Encrustation- organization of repeated mural thrombi on the intimal surface leads to buidl up of plaques.
Monoclonal- smooth muscle migration and prolifereation is the same as tumor growth.
What is the current concept of atherosclerosis?
Injury of endothelium is the 1ry event
- injury by hyperchol, injury, htn, immun, toxin, virus or other

Monocytes and lipid enter subendothelium. sometiems w/ platelet adhesion. release of mitogenic factors.
Monos become foam cells when b-VLDL receptor reacts with modified LDL
What are teh mitogenic factors released in atherosclerosis?
PDGF, Fibroblast GF, epidermal growth factor, Transforming GF-Alpha.
Whaat are the signs of hyperlipidemia?
Atheromata- Plaques in vessel walls
Xanthoma- plaques or nodules of lipid-laden histiocytes in skin, especially the eyelids
Tendinous Xanthoma- lipid in tendon, especiall achilles
Corneal arcus- Lipid deposit in cornea, nonspecific (also hapens in arcus senilis)
What is the DDx of hypertension?
1ry- 90-95%- unknown cause
Renal disease
renovascular disease
1ry aldosteronism
congenital adrenal hyperplasia
Toxemia of preggers
Increased ICP
Toxic HTN- lead, cadmium
What are the determinants of Essential Hypertension?
race- black>white>asian
dietary Na
What are the long-term complications of HTN?
retinal changes
LV hypertrophy and cardiac failure
benign nephrosclerosis
ischemic heart disease, stroke, aneurysm.
aortic dissection, atherosclerosis
What is a mark of renal artery stenosis?
atrophy of affected kidney
correct HTN by surgery.
What is 1ry aldosteronism/conn syndrome?
adrenocortical adenoma or bilateral adrenal hyperplasia-> HTN. Also, increased Na and decreased K.
What are some notable drugs that can cause HTN?
Roids and amphetamines
what is different about Malignant HTN?
what is its clinical course?
what are some clinical Sx?
What happens to the kidney?
What population is most at risk?
retinal hemorrhages
LV hypertrophy
LV failure
Glomerular capillaries rupture-> flea-bitten kidney. Fibrinoid necrosis. Hyperplastic arteriosclerosis.
Young Black Males are most at risk.
What is the difference between a red and a pale infarct?
Red- loose tissues w/ collaterals (lung, intestine, or reperfusion)

Pale- solid tissues w/ singel blood supply (brain, kidney, heart, spleen)
What are the gross and microscopic changes of the heart in the first day of an MI?
No change in 1st 4 hrs.
after 4 hrs- contraction bands, necrotic cells in bloodstream and neutrophils in heart.
After 12 hrs- gross changes in color- dark mottling; pale with tetrazolium stain.
microscopic loss of nuclei, more neutrophils.
at 24 hrs- well developed changes of coag necrosis, progressive infiltration by neutrophils
What are the gross and microscopic changes of the heart in days 2-4 post MI?
Grossly yellow/hyperemia.
Inflam of surrounding tissue
Dilated vessels (hyperemia)
Muscle shows coag necrosis.
What are the gross and microscopic changes of the heart in days 5-10 days post MI?
Grossly Yellow- max at 10 days
Hyperemic boarder
Microscopically- macrophages replace neutrophils start sweeping up debris
Growth of fibroblasts. new vessels into the lesion;

Days 4-7 are most likely for myocardial rupture.
What are the gross and microscopic changes of the heart in days 7 wks post MI?
Recanalized artery, gray-white exteria
contracted scar complete
aneurysm can occur in scarred area.
Where are coronary occlusions most likely?
What are the symps of an MI?
sever retrosternal pain
pain in left arm/jaw
Shortness of breath
adrenergic symps.
How do you Dx an MI?
1st six hrs- ECG- ST elevation or depression. Q waves for transmural
Troponin I rises after 4 hrs, high for 7-10 days (more specific); strong at 12 hrs. peaks at 24 hrs.
CK-MB- week at 6 hrs. good after 12-16 hrs. not as specific. Gone at 3 days
AST- weak at 12 hrs, positive at 24 hrs, peaks at 2 days, negative at 3
LDH- Peaks at day 3 and persists.
Dilated cardiomyopathy:
what are the etiologies?
Most common
Coxsacki B
Chronic Cocaine

Systolic Dysfunction
Breakdown hypertrophic heart
asymmetric and involve the intraventricular septum. 50% are AD, familial. disorganized muscle. LV outflow obstruction

Sudden Cause of death in young athletes

Findings: loud S4, apical impulses, systolic murmur, Rx-B-blocker

Diastolic dysfunction.
Breakdown Restrictive Cardiomyopahty?
postradiation fibrosis
endocardial fibroelastosis
endomycardial fibrosis
Describe the murmur of mitral prolapse
late systolic murmur with midsystolic click. Frequent valvular lesion.
How does tricuspid stenosis differ from mitral stenosis?
tricuspid gets louder with inspiration.
What is the most common cardiac tumor?
Mets are the most common.
1ry- Myxoma- 90% occur in the LA. Ball-valve obstruction in the LA.
Rhabdomyomas are the most frequent in kids (tuberous sclerosis)
What are some causes of Aortic valve insufficiency?
Nondissecting aortic aneurysm- from cystic medial necrosis
Rheumatic- w/ mitral valve disease
Syphilitic aortitis- dilation of the aortic valve ring
What are the major causes of Left-sided heart failure?
Ischemic heart disease- MI
Aortic and mitral valvular disease
myocardial diseases- cardiomyopathis, myocarditis
What are the major causes of R-sided heart failure?
Left-sided heart failure- most common
Left-sided lesions
pulm hypertension - chronic lung disease or cors pumonale
Tricuspid or pulm valve disease.
CHF, how does it cause the following:
Dyspnea on exertion
Cardiac Dilation
Pulm edema, Paroxysmal nocturnal dyspnea
Orthopnea (SOB when supien)
Hepatomegaly (nutmeg liver)
Ankle, sacral edema
Dyspnea: Failure of LV output in exercise
Cardiac dilation: Greter vetricular EDV
Pulm edema: LV failure-> increase in pulm pressure -> pulm distension and transudation of fluid. Hemosiderine macrophages
Orthopnea- Increase in venous return in supine-> increase in pulm vasc congestion.
Hepatomegaly- Increase in venous pressure-> increase in resistance to portal flow
Ankle Edema: RV failure-> Increase in venous pressure-> fluid transudation.
Define cor pulmonale
R ventrical hypertrophy and/or dilation 2ry to lung disease or disase of pulm vasculature.

Emphysema is a frequent cuase
What are the types of embolis?
Amniotic fluid

Fat Emboli-> long bone fractures and liposuction.
Amniotic fluid emboli can cause DIC, especially post partum
PE- Chst pain, tachypnea, dyspnea
What is Virchow's triad?
Endothelial damage
What is Cardiac tamponade?
Compression of heart by fluid (blood) in pericardium, leading to decrease in CO.
Equilibrasiono of pressure in all 4 chambers
increased venous pressure
distant heart sounds
Pulsus paradoxus
ECG-> electrical alternans- beat to beat alteration of QRS complex height.
What is Libman-Sacks endocarditis?
Vegetations develop on both sides of valve-> mitral valve stenosis.
No embolis. Seen in Lupus
What is rheumatic fever
pharyngeal infection with group A B-hemolytic streptococci. Late sequelae are rheumatic heart disease- Mitra>aortic>>tricuspid.
Aschoff bodies
migratory polyarthritis
eerythema marginatum
elevated ASO

Erythema marginatum
Valvular damange
ESR increase
Red-hot joints
Subcutaneous nodules
St. Vitus dance (chorea)
What is an Aschoff body?
Granuloma w/ giant cells
found in rheumatic fever
What is an Anitschkow cell?
activated histiocyte
found in rheumatic fever
What are some causes of serous pericarditis?
SLE, Rheumatoid, infection, uremia
What are some causes of Fibrinous pericarditis?
Uremia, MI, Rheumatic fever
What are the causes of Hemorrhagic Pericarditis?
TV, malignancy (melanoma)
What are the findings in Pericarditis?
pericardial pain, friction rub, ECG changes (Diffuse ST elevations in all leads), pusus paradoxus, distant heart sounds
What is the prognosis of pericarditis?
Can resolve without scarring or lead to chronic adhesive or constrictive pericarditis.
What are the effects of 3ry syphilis on the heart?
disrupts the vasa vasora of the aorta with consequent dilation of the aorta and valve ring.
Often affects the aortic root and calcification of ascending arch of the aorta
May see calcification of the aortic root and ascending aortic arch.

Can result in aneurysm of the ascending aorta or aortic arch.
can cause aortic valve incompetence.
What are some Sx of bacterial endocarditis?
New murmur, anemia, fever, Osler's nodes, Roth's spots, Janeway lesions, splinter hemorrhages on nail bed. Valvular damage may cause new murmur.
What are Osler's nodes?
tender raised lesions on finger or toe pads
What are Roth's spots?
round white spots on retina surrounded by hemorrhage
What are Janeway lesions?
Small erythematous lesions on palm or sole
What is the most likely cause of acute bacterial endocarditis?
s. aureus- high virulence
large vegetations on previously normal valves.
What is the most likely cause of subacute bacterial endocarditis?
viridans strep (low virulence)
small vegetations on congenitally abnl or diseased valves
Sequela of dental procedures. More insidious
What are nonbacterial causes of endocarditis?
renal failure-> marantic/thrombotic endocarditis
What valve is most commonly associated with endocarditis?
Tricuspid in IV drugs
What are complications of endocarditis?
chordae rupture
suppurative pericarditis
What is FROM JANE?
Bacterial Endocarditis
Roth's spots
Osler's nodes
Janeway lesions
Nail-bed hemorrhage
What drugs can be used against HTN?
ACE Inhibitors - pril
Angiotensin II receptor inhibitors - Sartan
What type of aneurysm occurs in teh aortic root?
cystic medial necrosis.
Where does a dissecting aneurysm occur?
longitudinal intraluminal tear. Usually in the wall of the ascending aorta. Forming a second arterial lumen within the media.

pain radiates to the back
What toxin can cause an angiosarcoma?
radioactive diagnostic thorium dioxide
polyvinyl chloride
What is the mechanism of Hydralazine?
increases cGMP-> smooth muscle relaxation
Vasodilates arterioles>veins; afterload reduction
Used for severe hypertension CHF
Tox- Compensatory Tachy, fluid retention. Lupus-like syndrome
What is the mechanism of Ca channel blockers?
Block voltage-dependent L-type Ca channels of cardiac adn smooth muscle and reduce muscle contractility
vasc smooth muscle- nifedipine > diltiazem > verapamil
Heart- verapamil > diltiazem > nifedipine

Use- htn, angina, arrythmias (not nifedipine)
Tox- cardiac depression, peripheral edema, flushing, dizziness and constipation
what is the mechanism of isosorbide dinitrate?
vasodilates by releasing NO in smooth muscle causing increase in cGMP and smooth muscle relaxation. Dilate veins>>arteries, decreases preload

clinical use-angina, pulm edema. aphrodisiac and erections
Tox- tachy, hypotension, headache
Monday disease-build up of tolerance over teh week, loss on the weekend. so tachy, dizziness and headache on monday
How do Nitrates and B-blockers affect the following:
Ejection time
EDV N=down B=up both=Nochange
BP N=down B=down both=down
Contractility N=up B=down both=no effect
HR N=up B=down both=down
Ejection time N=down B=up both=none
MVO2 N=down B=down both=down down
What is the mechanism of action of cardiac glycosides?
inhibit the Na/K ATPase of the cell membrane, causes an increase in intracellular Na. Na-Ca antiport does not fuction as efficiently, causing increased intracellular Ca- +inotropy
Increased PR, decreased QT, scooping ST. T-wave inversion on ECG
Used for CHF and afib (decrease conduction at the a/v)
What are the SEs of digoxin?
Blurry yellow vision
Renal failure makes it worse
hypokalemia potentiates drugs effects
quinidine causes decreased dig clearance
What is the antidote for dig OD?
slowly normalize K
cardiac pacer
anti-dig Fab fragments
What is the mechanism of Class IA drugs?
Na channel blocker
Slows Phase 0 depol
Don't work on resting cell. Work on excited cell -> slow conductance and excitation

Increase AP duragion, Increase effective refractory period
Increase QT
What are the Class IA drugs?
Queen Amy Proclaims Diso's Pyramide

What are teh SEs of quinidine?
cinchonism- headache, tinnitus
torsades from increased QT
What are the SEs of procainamide?
reversible SLE-like syndrome
What is the mechanism of Clas IB drugs?
Na channel blocker
Shortens Phase 3 repole
Decrease AP duration
Work on ischemic or depoled purkinje and ventricular tissue.
Used for acute ventricular arrythmias
dig induced arrythmias
What are the Class IB drugs?
What are the SEs of Class IB drugs?
Tox- local anesthetic. CNS stimulation/depression. CV depression.
What is the mechanism of action of Class IC drugs?
Na channel block
markedly slows Phase 0
No effect on AP
Used in V-tachs that progress to Vfib and intractable SVT.
last resort in refractory tachyarrhythmias
What are the SEs of class IC?
proarrhythmic, especially post-MI
What are class II antiarrhythmics?
decrease cAMP
decrease Ca
suppress abnl pacemeakers by decreasing slope of phase 4
AV node is crazy sensitive
What's the problem with esmolol?
short acting
What are the SEs of B-blockers?
exacerbation of asthma
cv- bradycardia, av block, chf
CNS- sedation, sleep alterations
May mask hypoglycemia
What is the mechanism of Class III drugs?
K channel blocker
prolongs phase 3 repol
increase AP duration, increase ERP
Increase QT

used when others fail
What are the class III drugs?
What are the SEs to ibutilide?
What are the SEs of bretylium?
new arrhythmia
What are the SEs of amiodarone?
Pulm fibrosis
corneal deposits
skin deposits-> photodermatitis
Neurologic effects
CV- brady, heart block, CHF
Check PFTs, LFTs, and TFTs
What is the mechanism of the Class IV drugs?
Ca channel blockers
shortens action potential
1ry effect on AV node
decreases conduction velocity
increases ERP
increases PR
prevents nodal arrhythmias
What are the SEs of Ca channel blockers?
CV- CHF, AV block, Sinus node depression
Torsades (with bepridil)
What are the Class IV drugs?
What is the role of Adenosine in Arrhythmia
Drug of choice in diagnosing/abolishing AV nodal arrhythmias
What is the role of K in arrhythmia?
Depresses ectopic pacemakers
especially in dig tox
What is the role of Mg in arrhythmia?
helps with torsades and dig tox.
Polyarteritis Nodosa:
What is the characteristic lesion of the disorder?
What does it commonly affect?
What is the typical patient?
fibrinoid necrosis with a mixed inflam infiltrate of neutrophils, eos, and monos

commonly affects the GI and kidney

young male
What does cystic medial necrosis predispose one to?
dissecting aortic aneurysm
What is Monckeberg arteriosclerosis?
Ring-like calcifications
What does wegener granulomatosis usually affect?
upper airway
What are the classic findings of an atrial-septal defect?
prominant right ventricular cardiac impulse
systolic ejection murmur
heard in pulmonic area on left sternal border
fixed splitting of S2
what is the mechanism of action of nadolol?
b1, b2
long 1/2 life
What are the heart changes by Lyme disease?
AV block
What CV effects can an albuterol OD cause?
Where is the highest ratio of wall x-section to vessel diameter?
arterioles- it's what drops the resistance
What part of the heart can impinge on the esophagus?
L atrium
What disease causes coronary artery vasculitis?
What is leukocytoclastic angiitis?
hypersensitivity angiitis
microscopic polyarteritis nodosa
smaller vessels are usually affected
Often has fragmented neutrophils
Penicillin can trigger
What is allergic granulomatosis and angiitis?
respiratory and renal systems
What is Buerger disease?
Disease of the vasculature of the extremities
What is Behcet disease?
mult-system disorder
aphthous ulcers of genetalia and mouth
What disease causes vasculitis in the coronary arteries of kids?
What disease affects the aortic arch in young asian women?
Takayasu arteritis
What happens to the density, x-sectional area, and wall/lumen ratio in arterioles and capillaries in a patient w/ HTN?
density decreases
x-section also decreases
wall thickens making the ration increase in the arterioles.
no change in capillaries.
What kind of drug is amlodipine?
Ca channel blocker
What complication post MI is likely when a scar has replaced the myocordium?
What is the strand of amyloid in amyloidosis of the heart?
AA- acute phase
found in hear disease
associated with RA
Congo Red stain
Where would you find AE amyloid?
E- endocrine
medullary carcinoma of thyroid and pancreas islet cells
Where would you find AF amyloid?
familial amyloidosis
nerves and kidneys
F-familial and old fogies
Where would you find AL amyloid?
light chain
myeloma and B-cell maligs
heart, lung, kidney, spleen and tongue
Where is the femoral vein in relationship to the artery?
venous towards the penis
Empty space
What is the response of the vasculature to anemia?
lower afterload
increase CO
lower BP
more O2 to tissues