Cardio USMLE Flashcards by Mani Yavi

pregnant woman in 3rd trimester has normal BP when standing and sitting. When supine BP drops to 90/50.
what is the dx?

compression of the IVC

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35 y/o man has high BP in arms and lowBP in his legs.

what is the dx

coarction of teh aorta

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5 y/o boy presents weith a systolic murmur and a wide fixed split S2. what is the dx

ASD

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During a game a young football player collapses and dies immediately. What is the most likely type of cardiac dz

hypoertrophic cardiomyopathy

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pt has a stroke after incurring multiple long bone fractures in trauma stemming from a MVA. What caused the infarct

fat emboli

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elderly woman presents with a headache and jaw pain. labs show elevated ESR. what is teh dx

temporal arteritis

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80 y/o man presents w/ systolic crescendo-decrescendo murmur. What is the most likely cause?

aortic stenosis

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Man starts a medication for hyperlipidemia. He then develops a rash, pruritis, and GI upset. What drug was it

Niacin

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Pt developes a cough and must discontinue captopril. What is a good replacement drug and why doesn’t it have the same side effects?

losartan, an angiotensin II receptor antagonist, does not increase bradykinin as captopril does.

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What are the 3 sx inside the carotid sheath

1) Internal jugular Vein (lateral)
2) Common carotid Artery (medial)
3) Vagus Nerve (posterior)

mneu: VAN

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In the majority of cases, the SA and AV nodes are supplied by this carotid artery?

Right coronary artery

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80% of the time the Right coronary artery is “dominant”, suppplying the left ventricle via the _________ branch

Posterior descending artery

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cardiac output =

SVxHR

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During exercise, CO ↑ initially as a result of an ↑ in ____. After prolonged exercise, CO ↑ as a result of an ↑ in ____.

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Mean argerial Pressure (MAP)=
give 2 equasions:
1) CO, TPR
2) systolic, diastolic

1) CO x TPR

2) 1/3 systolic +2/3 diastolic

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CO=

rate of O2 consumption, aa O2 content, vv O2 content

rate of O2 consumption
_______________________
aa O2 content-vv O2 content

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Pulse pressure =

systolic, diastolic

systolic-diastolic

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pulse pressure ≈

stroke volume

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SV=
(2 equasions)
1) CO, HR
2)EDV,ESV

1) =CO/HR

2) =EDV-ESV

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Coronary Artery Anatomy [pic]

1) Right Coronary aa (RCA)
2) Left main coronary aa (LCA)
3) Circumflex artery (CFX)
4) Left anterior descending aa (LAD
5) Posterior descending aa (PD)
6) Acute marginal aa

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Stroke volume is affected by what 3 things

mneu: SV CAP

Contractility, Afterload, and Preload

mneu: SV CAP

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↑Preload →__SV

↑

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↑Afterload→ __SV

↓

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↑contractility→ __SV

↑

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SV ___ in anxiety, exercise, & pregnancy

↑

a failing heart has a ___ SV

↓

Contractality (and SV), ____ with catecholemines

↑

Contractality (and SV), ____ with ↑ intracellular Ca++

↑

Contractality (and SV), ____ with ↓ extracellular sodium

↑

Contractality (and SV), ____ with digitalis

↑

Contractality (and SV), ____ with β1 blockade

↓

Contractality (and SV), ____ with heart failure

↓

Contractality (and SV), ____ with acidosis

↓

Contractality (and SV), ____ with hypoxia/hypercapnea

↓

Contractality (and SV), ____ with Ca++ channel blockers

↓

Myocardial demand is ___ by ↑ afterload (diastolic BP)

↑

Myocardial demand is ___ by ↑ contractility

↑

Myocardial demand is ___ by ↑ heart rate

↑

Myocardial demand is ___ by ↑ heart size

↑

ventricular EDV

Preload

Systolic arterial pressure

afterload

proportional to peripheral resistance

afterload

``` venous dialators (e.g. nitroglycerine) ↓ _______ (preload or afterload) ```

preload

``` vaso dialators (e.g. hydralazine) ↓ _______ (preload or afterload) ```

afterload

______ ↑ w/ exercise, ↑ blood volume, exitement (sympathetics) (preload or afterload)

Preload

Starling Curve: Force of _______ is proportional to initial length of cardiac mm fiber (preload)

contraction

contraction state of the myocardium is ____ by circulating catecholamines (+,-)

contraction state of the myocardium is ____ by digitalis | +,-

contraction state of the myocardium is ____ by sympathetic stimulation (+,-)

contraction state of the myocardium is ____ by pharmacologic depressants (+,-)

contraction state of the myocardium is ____ by loss of myocardium (MI) (+,-)

EF= (give 2 equasions) 1) SV, EDV 2) EDV, ESV, EDV

1) SV/EDV | 2) EDV-ESV/EDV

this is an index of ventricular contractility

EF is normally > ___%

Place condition on the Starling curve [pic p.219]

1) exercise 2) CHF + digitalis 3) CHF

(driving Pressure)ΔP= | Q (flow) ,R (resistance)

Q x R

Resisitance (R) = Give 2 equasions: 1)ΔP(driving pressure),flow(Q) 2)n(viscosity), length(l), radius (r)

1) =ΔP/Q | 2) 8nxl/Πr(^4)

viscosity depends mostly on _______

hematocrit

increased ______ in: 1) Polycythemia 2) Hyperproteinemic states (e.g., multiple myeloma) 3) hereditary spherocytosis

viscosity

resistance is ________ to viscosity | proportional or inversely proportional

proportional

resistance is ________ to the radius to the 4th power | proportional or inversely proportional

inversely proportional

cardiac and vascular fx curves [pic p.219]

1) (+) inotropy 2) (-) inotropy 3) (↑) blood volume 4) (↓) blood volume

cardiac cycle image [p. 220]

1) isovolumetric contraction 2) aortic valve opens 3) ejection 4) aortic valve closes 5) isovolumetric relaxation 6) mitral valve opens 7) ventricular filling 8) mitral valve closes

Name the phase of the cardiac cycle: | period between mitral valve closure and aortic valve opening.

isovolumetric contraction

Name the phase of the cardiac cycle: period of highest O2 consumption

isovolumetric contraction

Name the phase of the cardiac cycle: period between aortic valve opening and closing

systolic ejection

Name the phase of the cardiac cycle: period between aortic valve closing and mitral valve opening

isovolumetric relaxation

Name the phase of the cardiac cycle: period just after mitral valve opening

rapid filling

Name the phase of the cardiac cycle: period just before mitral valve closure

slow filling

name the heart sound: mitral and tricuspid valve closure

name the heart sound: aortic and pulmonary valve closure

name the heart sound: at the end of rapid ventricular filling

name the heart sound: high atrial pressure/stiff ventricle

this heart sound is associated w/ dilated CHF

this heart sound AKA "atrial kick" is associated with a hypertrophic ventricle

Jugular venous pulse waves: | a wave

Atrial contraction

Jugular venous pulse waves: c wave

RV Contraction (tricuspid valve bulging into atrium)

Jugular venous pulse waves: v wave

increaseed atrial pressure due to filling against closed tricuspid Valve

jugular venous distention is seen in ___________

right heart failure

when the aortic valve closes before the pulmonic this heart sound abnormality results

S2 splitting

S2 splitting is increased upon ________

inspiration

Paradoxical splitting (S2 split increasd upon expiration is associated with what?

aortic stenosis

cardiac mm contraction is dependent on extracellular ________, which enters the cells during plateau of action potential and stimulates ______ release from the cardiac mm sarcoplasm reticulum.

calcium calcium calcium induced calcium release

In contrast to skeletal mm, cardiac mm action potential has a plateau, which is due to ____ influx.

Ca+

In contrast to skeletal mm, cardiac nodal cells ________ depolarize, resulting in automaticity

spontaneously

In contrast to skeletal mm, cardiac myocytes are electrically coupled to each other by ________

gap junctions

myocardial action potential occurs in atrial and ventricular myocytes and ________

perkinje fibers

In a myocardial action potential, this phase is the rapid upstroke, when voltage gated Na+ channels open

phase 0

In a myocardial action potential, this phase is the initial repolarization-inactivation of voltage0gated Na+ channels. Voltage gated K+ channels begin to open

Phase 1

In a myocardial action potential, this phase is the plateu--Ca++ influx through voltage-gated Ca++ channels balances K+ efflux. Ca++ influx triggers another Ca++ release from sarcoplasmic reticulum and myocyte contraction.

phase 2

In a myocardial action potential, this phase is the rapid repolarization--massive K+ efflux due to opening of voltage-gated slow K_ channels and closure of voltage gated Ca++ channels.

Phase 3

In a myocardial action potential, this phase is the resting potential--high K+ permeability through K+ channels.

phase 4

Pacemaker action potentials occur where

SA & AV nodes

In a pacemaker action potential this phase is the upstroke phase--it involves opening of voltage-gated Ca++ channels. These cells lack fast voltage-gated Na+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

phase 0

In a pacemaker action potential this phase, the plateau is absent.

phase 2

In a pacemaker action potential this phase, the slow diastolic depololarization results in membrane potential spontaneously depolarizing as Na+ conductance increases. This accounts for automaticity of SA and AV nodes. The slope of this phase in the SA node determines the heart rate. ACh decreases and catecholamines increasee the rate of diastolic depolarization decreasing or increasing heart rate respectively.

phase 4

electrocardiogram: atrial depolarization

P wave

electrocardiogram: conduction delay through AV node (normally <200 msec)

PR segment

electrocardiogram: vetricular depolarization (normally < 120 msec)

QRS complex

electrocardiogram: mechanical contraction of the ventricles

QT interval

electrocardiogram: ventricular repolarization

T wave

electrocardiogram: | atrial repolarization is masked by _______

QRS complex

electrocardiogram: isoelectric, ventricles depolarized

ST segment

electrocardiogram: These waves caused by hypokalemia

U wave

this syndrome is caused by an accessory conduction pathway from atria to vetricle (bundle of kent), bypassing AV node. As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave on ECG. May result in reentry current leading to supraventricular tachycardia [image p.223]

Wolff-Parkinson-White syndrome

This ECG tracing has a chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes (pic. p 224)

Atrial fibrillation

This ECG tracing has a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the "sawtooth" appearance of the flutter waves. (pic. p 224)

Atrial flutter

In this condition PR interval is prolonged (>200 msec). Asymptomatic. (pic. p 224)

1st degree AV block.

Progressive lenthening of the PR interval until a beat is "dropped" (a P wave not followed by a QRS complex). Usually asymptomatic. (pic. p 224)

2nd degree AV block | Mobitz type I (Wenckebach)

On ECG shows dropped beats that are not preceded by a change in the length of the PR interval. These abrupt, nonconducted P waves result in a pathologic condition. It is often found as a 2:1 block, where there are 2 P waves to 1 QRS response. May progress to 3rd degree block.(pic. p 225)

Mobitz type II AV block

In this condition, the atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate. Usually treat with pacemaker.

3rd degree AV block (complete)

completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation. (pic. p 225)

Ventricular Fibrillation

________receptor transmits via vagus nn to medulla (responds only to increase blood pressure)

aortic arch receptor

________ receptor transmits via glossopharyngeal nn to medulla

carotid sinus

decreased firing by aroreceptors during hypotension results in an increase in efferent ________ firing

sympathetic

In a carotid massage, the increased pressure on carotid aa results in increased stretch and ____ in heart rate

decrease

Peripheral chemoreceptors in the carotid and aortic bodies respond to (3 things)

decreased PO2 (<60mmHg), increased PCO2 and decreased pH of blood

Central chemoreceptors respond to what changes (2)

changes in pH and Pco2 (not Po2)

This chemoreceptor is responsible for Cushing reaction, response to cerebral ischemia, response to increase intracranial pressure leads to hypertension (sympathetic response) and bradycardia (parasympathetic response)

Central chemoreceptor

This orgen gets the largest share of systemic cardiac output

liver

this organ gets the highest blood flow per gram of tissue

kidney

this orgen has a large arteriovenous O2 differnece. Increased O2 demand is met by increased coronary blood flow, not by increased extraction of O2.

heart

this is a good approximation of L atrial pressure and measured with a Swan-Ganz catheter

Pulmonary capillary wedge pressure

blood flow is altered to meet demands of tissue

autoregulation

Name the organ regulated by the local metabolites: | O2 adenosine, NO

heart

Name the organ regulated by the local metabolites: | CO2 (pH)

brain

Name the organ regulated by the local metabolites: Myogenic and tubuloglomerular feedback

kidneys

Name the organ regulated by the local metabolites: hypoxia causes vasoconstriction

lungs

_______ vasculature is unique in that hypoxia causes vasoconstriction (in other organs hypoxia causes vasodilation)

pulmonary

Name the organ regulated by the local metabolites: lactate, adenosine, K+

skeletal mm

Name the organ regulated by the local metabolites: sympathetic stimulation most important mechanism--temp control

skin

______ forces determine fluid movement by osmosis throug capillary membranes

starling

moves fluid out of capillary

P(c) capillary pressure

moves fluid into capillary

P(i) interstitial fluid pressue

moves fluid into capillary

π(c) plasma colloid osmotic pressure

moves fluid out of capillary

π(i) interstitial fluid colloid osmotic pressure

net filtration pressure=Pnet=

[Pc-Pi)-(πc-πi)] capillary pressure -interstitial pressure - plasma colloid osmotic presure - interstitual fluid colloid osmotic pressures

Kf=

filtration constant (capillary permeability)

excess fluid outflow into interstitium

edema

edema is commonly caued by ___ capillary pressure (give example)

↑ P(c) | Heart failure

edema is commonly caued by ___ plasma protiens(give example)

↓π(c) plasma proteins | nephrotic syndrome, liver failure

edema is commonly caused by ___ capillary permeability (give example)

↑Kf | infections, burns

edema is commonly caued by ___ interstitial fluid colloid osmotic pressure (give example)

↑ πi lymphatic blockage

right-to-left shunts (early cyanoisis) "blue babies"

3 Ts Tetrology Transposition Truncus

Children with this type of shunt may squat to increase venous return

right to left shunts

Right-to Left shunts (early cyanosis) - "blue babies"

1) Tetrology of fallot 2) Transposition of great vessels 3) Truncus arteriosis The 3 Ts

children with this type of shunt may squat to increase venous return.

right to left shunt

Left to right shunts (late cyanosis) - "blue kids"

1) VSD 2) ASD 3) PDA

this is the most common cause of early cyanosis

tetralogy of fallot

this is the most common congenital cardiac anomaly

VSD

this congenital heart dz manifests itself with a loud S1 and a wide, fixed split S2

ASD

this congenital heart defect is closed with indomethacin

PDA

give the frequency of occurance with PDA VSD ASD

VSD>ASD>PDA

Uncorrected VSD, ASD or PDA leads to progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from L to R to R to L, which causes late cyanosis (clubbing & polycythemia). [pic p. 228]

eisenmenger's syndrome

Tetrology of Fallot [pic. p 228]

1) Pulmonary stenosis 2) RVH 3) Overiding aorta (overides VSD) 4) VSD mneu: PROVe

most important determinant for prognosis of tetrology of fallot

pulmonary stenosis

ON x-ray TOF looks ________

boot shaped

give the frequency of occurance with PDA VSD ASD

VSD>ASD>PDA

Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)leading to separation of systemic and pulmonary circulations.

Transposition of great vessels

Transposition is not compatable with life unless a _____is present to allow adequate mixing of blood [pic p. 229]

shunt (e.g. VSD, PDA or patent foramen ovale)

transposition of great vessels is due to failure of the _________ septum to spiral

aorticopulmonary

this type of coarction of aorta is aortic stenosis proximal to insertion of ductus arteriosus (preductal)

infantile INfantile: IN close to the heart

this type of coarction of aorta is aortic stenosis is distal to ductus arteriosus (postductal) it is associated with notching of the ribs, hypertension in upper extremities, weak pulses in lower extremities.

adult type aDult: Distal to Ductus

Coarction of aorta has a male: female ratio of ____

3:1

what is best way to diagnose coartation of aorta

femoral pulses on pysical exam

In fetal period, shunt is right to left. In neonatal period, lung resistance decreases and shunt becomes L to R w/ subsequent RVH and failure. [pic p. 229]

patent ductus arteriosis

______ is used to closed a PDA

indomethacin

______ is used to keep a PDA open, which may be necessary to sustain life in conditions such as transposition of the great vessels

PGE

Congenital cardiac defect associations: | 22q11

truncus arteriosus, tetralogy of Fallot

Congenital cardiac defect associations: | Down syndrome

ASD, VSD

Congenital cardiac defect associations: | Congenital rubella

septal defects, PDA

Congenital cardiac defect associations: | Turners syndrome

coarctation of aorta

Congenital cardiac defect associations: | Marfan's syndrome

aortic insufficiency

Congenital cardiac defect associations: Offspring of diabetic mother

transposition of great vessels

Hypertension

BP >140/90

HTN risk factors

increase age, obesity, diabetes, smoing, genetics, blck>white>asians

90% of hypertension is this kind

essential

essentail hypertention is related to either one of these two factors

increased CO or TPR

10% of HTN is mostly secondary to ______ dz

renal

this type of HTN is severe and rapidly progressing

malignant

HTN predisposes pts to (give 3)

athrosclerosis, stroke, CHF, renal failure, retinopathy, & aortic dissection

Hyperlipidemia signs: | Plaques in blood vessel walls

Atheromata

Hyperlipidemia signs: | plaques or nodules composed of lipid-laden histocytes in the skin, especially the eyelids

Xanthoma

Hyperlipidemia signs: lipid deposits in the tendon, esp. the achilles

Tendinous xanthoma

Hyperlipidemia signs: lipid deposit in cornea, nonspecific (arcus senilis)

corneal arcus

This type of arteriosclerosis is in the media of the arteries, esp radial or ulnar. Usually benign.

Monckeberg

This type of arteriosclerosis is hyalin thickening of small arteries in essential hypertension. Hyperplastic "onion skinning" in malignant hypertension.

Arteriolosclerosis

This type of arteriosclerosis is when fibrous plaques and atheromas form in intima of arteries

atherosclerosis

this is a disease of elastic arteries and large and medium sized mm arteries (image 79)

atherosclerosis

risk factors for atherosclerosis

smoking, hypertension, dbts, hyperlipidemia, family hx

progression of atherosclerosis complex atheromas, fatty streaks, proliferative plaque

fatty streaks to proliferative plaque to complex atheromas

complications of atherosclerosis (give 3)

aneurisms, ischemia, infarcts, peripheral vascular dz, thrombus, emboli

most common location of atherosclerosis

abdominal aorta> coronary artery>popliteal artery>carotid artery

symptoms of atherosclerosis

angina, claudication, but can be asymptomatic

CAD narrowing >75%

angina

retrosternal chest pain with exertion , mostly secondary to atherosclerosis

stable angina

chest pain occurring at rest secondary to corony artery spasm

prinzmetal's variant (unstable angina)

worsening of chest paiin due to thrombosis but no necrosis

unstable/crescendo angina

most often acute thrombosis due to coronary artery atherosclerosis. Results in myocyte necrosis

myocardial infarction

death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrythmia

sudden cardiac death

progressive onset of CHF over many years due to chronic ischemic myocardial damage

chronic ischemic heart dz

infarcts occuring in loose tissues with collaterals, such as lungs, intestine, or follwing reperfusion

red (hemorrhagic) infarcts REd=REperfusion

infarcts occur in solid tissues with single blood supply, such as brain, heart, kidney and spleen.

pale infacts

give order of highest frequency of coronary artery occlusion CFX, LAD, RCA

LAD>RCA>CFX

symptoms of MI (give 4)

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm or jaw, shortness of breath, fatigue, adrenergic symptoms.

How long ago did the MI occur? Occluded artery but no visable change by light microscopy

2-4 hours

How long ago did the MI occur? Gross: dark mottling; pale with tetrazolium stain. Micro: coagulative nocrosis. coagulation bands visable. release of contents of necrotic cells into bloodstream and the begining of neutrophil emigration.

after 4 hrs. 1st day

How long ago did the MI occur? Gross: hyperemic border; central yellow-brown softening. Micro: outer zone (ingrowth of granulation tissue), macrophages, & neutrophils

5-10 D

How long ago did the MI occur? Gross: grey-white Micro: scar complete

7 weeks

dx of MI what is gold standard in the 1st 6 hrs

ECG

This lab test rises after 4 hours and is elevated for 7-10D.

troponin I

this lab test is more specific than other protein markers

troponin I

This is predominantly found in myocardium but can also be relased from skeletal mm

CK-MB

This is nonspecific and can be found in cardiac, liver and skeletal mm cells

AST

ECG changes include ST elevation which indicates

transmural infarct

ECG changes include ST depression which indicates

subendocardial infarct

ECG changes include pathological Q waves

transmural infact

This MI complication is the most important cause of death before reaching hosptial; it is common in the 1st few days

cardiac arrhythmia

This MI complication results in pulmonary edema

LV failure

This MI complication has a high risk of mortanilty and occurs when there is a large infarct

cardiogenic shock

Rupture of ventricular free wall, interventricular septum, or paillary mm, usually occurs _____ post MI

4-10D

This MI complication of an MI results in decreased CO, a risk of arrythmia, and embolus from mural thrombus

aneurism formation

this MI complication is also known as a friction rub and occurs 3-5 D post MI

fibrinous pericarditis

This MI complication is an autoimmune phenomenon resulting in fibrinous pericarditis, several weeks post-MI

dresslers syndrome

This is the most common cardiomyopathy (90%)

dialated (congestive) cardiomyopathy

In dialated (congestive) cardiomyopathy ________ dysfunction ensues

systolic

In this type of cardiomyopathy, the heart looks like a baloon on chest x-ray

dialated (congestive) cardiomyopathy

etiology of dialated (congestive) cardiomyopathy

``` Alcohol Beriberi Coxsackie B Cocaine Chagas dz Doxorubicin peripartum hemochromatosis ```

this type of cardiomyopathy often involves an asymetric enlargement of the intraventricular septum

hypertrophic cardiomyopathy

In hypertrophic cardiomyopathy ______ disfunction occurs

diastolic

hypertrophic cardiomyopathy is a __________ trait, and 50% are familial

autosomal dominant

This is a very common cause of sudden death in young athletes.

hypertrophic cardiomyopathy

What are the heart sound findings with hypertrophic cardiomyopathy

loud S4, apical impulses, systolic murmur

How do you tx hypertrophic cardiomyopathy

Beta blocker

major causes of this type of cardiomyopathy include sarcoidosis, amyloidoss, postratdiation fibrosis, endocarrdial fibroelastosis, and endomyocardial fibrosis (Loffler's)

restrictive/obliterative cardiomyopathy

Heart Murmurs: | holostolic, high piched "blowing murmur" loudest at apex[pic. p 234]

mitral regurgitation

Heart Murmurs: crecendo-decrescendo systolic ejection murmur following ejection click. radiates to carotids/apesx. "pulsus parvus et tardus" pulses weak compared to heart sounds [pic. p 234]

aortic stenosis

Heart Murmurs: holosystolic murmur [pic. p 234]

VSD

Heart Murmurs: Late systolic murmur with midsystolic click. Most frequent valvular lesion [pic. p 234]

mitral prolapse

Heart Murmurs: immediate high-pitched "blowing" diastolic murmur. Wide puse pressure [pic. p 234]

aortic regurgitation

Heart Murmurs: follows opening snap. delayed rumbling late diastolic murmur. [pic. p 234]

mitral stenosis

Heart Murmurs: Continuous machine like murmur. Loudest at time of S2 [pic. p 234]

PDA

most common primary cardiac tumor in adults. Usually described as a "ball-valve" obstruction in the LA

myxomas.

90% of myxomas occur in the _____

atria (mostly LA)

Most frequent primary cardiac tumor in children, associated with tuberous sclerosis

rhabdomyomas

Most common heat tumor (see color image 88)

metasteses

Given the pathophysiology tell me the symptom of CHF: | failure of LV output to increase during exercise

dyspnea on exertion

Given the pathophysiology tell me the symptom of CHF: greater ventricular end-diastolic volume

cardiac dilation

Given the pathophysiology tell me the symptom of CHF: Lv ventrical failure leads to increased pulmonary venous pressure which leads to pulmonary venous distention and transudation of fluid.

pulmonary edema (paroxysmal nocturnal dyspnea)

this CHF abnormality is associated with presence of hemosiderin-laden macrophages

pulmonary edema

Given the pathophysiology tell me the symptom of CHF: increase venous return in supine position exacerbates pulmonary vascular congestion

orthopnea (shortness of breath when supine)

Given the pathophysiology tell me the symptom of CHF: increased central venous pressure leading to increased resistance to portal flow.

hepatomegaly (nutmeg liver)

Given the pathophysiology tell me the symptom of CHF: RV failure leads to increased venous pressure which leads to fluid transudation

ankle , sacral edema

embolus types

Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor mneu: an embolus moves like a a FAT BAT

this type of emboli are associated with long bone fractures and liposuction.

fat

approximately 95% of pulmonary emboli arise from where?

deep leg veins

this type of emboli can lead to DIC, especially postpartum

amniotic fluid

this type of embolus is associated with chest pain, tachypnea, and dyspnea

pulmoary embolus

compression of heart by fluid (i.e.,blood) in pericardium, leading to decreased cardiac output and equilibration of pressures in all four chambers.

cardiac tamponade

youre pt presents with hypotension, JVD, and distant heart sounds. He shows pulsus paradoxus and ECG shows electrical alternans

cardiac tampanad

pulsus paradoxus

(exaggeration of nml variation in the systemic arterial pulse volume with respiration-- becoming weaker with inspiration and stronger with expiration)

electrical alternans

(beat to beat alterations in QRS complex height)

Symptoms of bacterial endocarditis

``` Fever Roth spots osler nodes Murmur (new) Janeway lesions Anemia Nail-bed hemorrhage Emboli ``` mneu: bacteria FROM JANE

osler nodes

tender raised lesions on finger or toe pads

Roth's spots

round white spotss on retina surrounded by hemorrhage

Janeway lesions

small erythematous lesions on palm or sole

What is the most frequently involved valve in bacterial endocarditis

mitral valve

What valve is associated with endocarditis associated with IV drug abuse

tricuspid valce

what are some of the complications associated with bacterial endocartitis (give 2)

chordae rupture glomerulonephritis supportive pericarditis emboli

acute endocarditis has a rapid onset. It results from large vegetations on previously normal valves. It is most often caused by this bug.

S. aureus (high virulence)

Subacute bacterial endocarditis has a more insidious onset. It consists of smaller vegetations on congentitally abnormal or diseased valves. It can be a sequela of dental procedures. Often caused by this bug

viridans streptococcus (low virulence)

endocarditis may also be nonbacterial and secondary to these 2 conditions

metastasis or renal failure (marantic/ thrombotic endocarditis)

In this condition, associated with lupus, vegetations develop on both sides of valve leading to mitral valve stenosis but do not embolize

libman-sacks endocarditis mneu: SLE causes LSE

Rhematic heart dz is a late consequence of pharyngeal infection with this organism

a beta hemolytic streptococci

rhematic heart dz affects heart valves in this order

mitral>aortic>>tricuspid mneu: high pressure valves associated most.

Give the symptoms of rheumatic heart dz

``` Fever Erythema marginatum Valvular damage ESR (high) Red-hot joints (polyartheritis) Subcutaneous nodules St. Vitus' dance (chorea) ``` mneu: FEVERSS

This is associated with Aschoff bodies, migratory polyarthritis, erythema marginatum, elevated ASO titers.

Rheumatic heart dz

is rheumatic heart dz immune mediated or the direct effect of bacteria

immune mediated

Associated ith Aschoff bodies and Anitschkow's cells

rheumatic heart dz mneu: think of 2 RHussians with RHeumatic heart dz (Aschoff & Anischkow)

Aschoff bodies

granuloma with giant cell

Anitschkow's cells

activated histiocytes

This condition presents with pericardial pain, friction rub, ECG changes (diffuse ST elevation in all leads) pulsus paradoxus, distant heart sounds

pericarditis

pericarditis can resolve without scarring however, scarring can lead to this

chronic adhesive or chronic constrictive pericarditis

this type of pericarditis is caused by SLE, rheumatoid arthritis, infection, or uremia

serous pericarditis

this type of pericarditis is caused by uremia, MI, rheumatic fever

fibrinous pericarditis

this type of pericarditis is caused by TB or malignancy (e.g., melanoma)

hemorrhagic

this dz disrupts the vasa vasora of the aorta with consequent dilation of the aorta and valve ring. It often effects the aortic root and results in calcification of ascending arch of the aorta

syphalitic heart dz (tertiary syphalis)

This dz can result in aneurism of the ascending aorta or aortic arch and aortic valve incompetence.

syphalitic heart dz (tertiary syphalis)

This Rx used for HTN has the adverse effect of HYPOKALEMIA, slight hyperlipidemia, hyperuricemia, lassitude, hypercalcemia, hyperglycemia

hydrochlorothiazide (diuretic)

This Rx used for HTN has the adverse effect of potassium wasting, metabolic alkalosis, hypotension, ototoxicity

loop diuretics

This sympathoplegic used in the tx of HTN has the adverse effect of dry mouth, sedation, severe rebound HTN

clonidine

This sympathoplegic used in the tx of HTN has the adverse effect of sedation, positive Coomb's test

methyldopa

This sympathoplegic used in the tx of HTN has the adverse effect of severe orthostatic hypotension, blurred vision, constipation, sexual disfunction

hexamethonium

This sympathoplegic used in the tx of HTN has the adverse effect of sedation, depression, nasal stuffiness, diarrhea

reserpine

This sympathoplegic used in the tx of HTN has the adverse effect of orthostatic and exercise hypotension, sexual dysfunction, diarrhea

Guanethidie

This sympathoplegic used in the tx of HTN has the adverse effect of 1st dose orthostatic hypotension, dizziness, headache

Prazosin

This sympathoplegic used in the tx of HTN has the adverse effect of impotence, asthma, bradycardia, CHF, AV block, sedation & sleep alterations

B blockers

This vasodialator used in the tx of HTN has the adverse effect of nausea, headache, lupus-like syndrome, reflex tachycardia, angina, salt retension

hydralazine

This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension

minoxidil

This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea

nifidipine, veripamil (constipation)

This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)

nitroprusside

This ACE inhibitor used in the tx of HTN has the adverse effect of Hyperkalemia, Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

Captopril mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

This angiotensin II receptor inhibitor has theadverse effect of fetal renal toxicity, hyperkalemia

Losartan

This vasodialator used in the tx of HTN has the adverse effect of hypertrichosis, pericardial effusion, reflex tachycardia, angina, salt retension

minoxidil

This vasodialator used in the tx of HTN has the adverse effect of dizziness, flushing, constipation, nausea

nifidipine, veripamil (constipation)

This vasodialator used in the tx of HTN has the adverse effect of cyaide toxicity (releases CN)

nitroprusside

Captopril mneu:CAPTOPRIL-Cough, Angioedema, Proteinuria, Taste changes, hypOtension, Pregnancy problems (fetal renal damage), Rash, Increased renin, Lower angiotensin II

The MOA of this drug used for severe HTN & CHF is that it increases cGMP leading to smooth mm relaxation. It vasodilates arterioles > veins resulting in a reduction of afterload

hydralazine

Toxicity of this drug for severe HTN & CHF include compensitory tachycardia, fluid retension, & lupus like syndrome

hydralazine

The druges Nifedipine, verapamil & diltiazem belong to this category

calcium channel blockers

The MOA of these drugs is that they block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce mm contractilty

calcium channel blockers

give the order of potency of the 3 CCBs (nifedipine, verapamil, diltiazem) in 1) the heart 2) vascular smooth mm

heart-verapamil>diltiazem>nifedipine vascular sm mm-- nifedipine>diltiazem>verapamil

CCBs are used in hypertension but also in these 2 conditions

angina, arrythymias (not nifedipine)

These drugs produce a toxicity of cardiac depression, peripheral edema, flushing, dizziness, & constipation

CCBs

These 2 drugs used for angina, pulmonary edema, and as an erection enhancer have a MOA of vasodilating by releasing NO in smooth mm, causing an increase in cGMP and smooth mm relaxation. They dialate vv>>arteries resulting in a decrease in preload

nitroglycerine, isosorbide dinitrate

toxicity of these drugs include tachycardia, hypotension, headache, "Monday dz" in industrial exposure, development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting intahycardia, dizziness, and headache.

nitroglycerin, isosorbide dinitrate

What are the 2 major Rxs used in the tx of antianginal therapy

nitrates & B blockers

In antianginal therapy the goal is to do what?

reduce myocardial O2 consumption.

In order to reduce myocardial O2 consumption you need to decrease 1 or more of the determinants of MVO2 which are give 2(5)

1) EDV 2) BP 3) HR 4) contractility 5) ejection time

Used for antianginal therapy Nitrates reduce _______ (preload or afterload)

preload

Used for antianginal therapy B-blockers reduce _______ (preload or afterload)

afterload

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. EDV

N (preload):↓ BB (afternoad):↑ C: no effect or ↓

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. BP

N (preload):↓ BB (afternoad):↓ C:↓

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. Contractility

N (preload):↑ (reflex response) BB (afternoad):↓ C:little or no effect

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. HR

N (preload):↑ reflex response BB (afternoad):↓ C:↓

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. Ejection time

N (preload):↓ BB (afternoad):↑ C:little or no effect

For each of the determinants of myocardial O2 consumption (MVO2). 1) Give the effect that Nitrates have. 2) that B-blockers have.3) And that Nitrates + B-blockrs have. MVO2

N (preload): ↓ BB (afternoad): ↓ C: ↓↓

CCBs: Nifedipine is similar to ________ (nitrates or B blockers); Verapamil is similar to ________nitrates or B blockers)

Nitrates | B blockers

Cardiac drugs: sites of action

1) Digitalis (-) 2) CCB (-) 3) B blockers 4) Ryanodine (+) 5) Ca++ sensitizers

This cardiac drug inhibits Na+/K+ ATP ase

digitalis

These 2 cardiac drugs inhibit on voltage gated Ca++ channels

CCBs | B blockers

This cardiac drug sensitizes Ca++ release channel in the SR

Ryanodine

These cardiac drug is a site of Ca+ interaction with troponin-tropomyosin system

Ca++ sensitizers

This cardiac glycoside has 75% bioavalibility, is 20-40% protein bound, has a half life of 40 hours and is excreted in the urine

digoxin

the MOA of this drug is that it inhibits the Na+/K+ ATPase of the cardiac sarcomere, causing an increase in intracellular Na+. Na+-Ca++antiport does not function as efficiently, casing an increase in intracellular Ca++, leading to positive inotropy.

digoxin

this drug may cause an elevated PR, a depressed QT, a scooping of ST segment, and a T-wave inversion on ECG

digoxin

The clinical uses for this drug include 1) ________ due to increased contractility 2) _______ due to decreased conduction at AV node

1) CHF | 3) atrial fibrillation

toxicity of this drug includes N/V/D. Blurry yellow vision. Arrhythmia.

digoxin

Digoxins toxicities are increased by _________(decreased excretion), _______(potentiates drug's effects) , and _________ (decreases digoxin clearance and displaces dignoxin from tissue binding sites

renal failure hypokalemia quinidine

What is the treatment for digoxin toxicity

slowly normalize K+ lidocaine cardiac pacer anti-dig Fab fragments

antiarrythmics (Class I) are _____ channel blockers

Na+

antiarrythmics (Class II) are _____ blockers

Beta

antiarrythmics (Class III) are _____ channel blockers

K+

Thhs class of antiarrhthmics are local anesthetics. They act by slow or decreasd conduction. They decrese the slope of phase 4 ddepolarization and increase threshhold for firing in abnormal pacemaker cells.

antiarrhythmics-Na+ channel blockers (class I)

antiarrhythmics-Na+ channel blockers (class I) are state dependent meaning what

they selectively depress tissue that is frequently depolarized (e.g., tachycardia

this class of antiarrhythmics has 3 subcategories A, B, & C

antiarrhythmics-Na+channel blockers (class I)

this class of antiarrythmics includes Quinidine, Amiodarone, Procainamide, Disopyramide.

Class IA mneu: Queen Amy Proclaims Diso's PYRAMID

This class of antiarrhytmics has an ↑ AP duration, ↑ effective refractory period (EERP, ↑ QT interval. It can affect both atrial and ventricular arrhythmias

This member of class IA antiarrhytmics has toxicities that include (cinchonism-headache, tinnitis, thrombocytopenia, torsades de pointes due to prolonged QT interva)

quinidine

This member of class IA antiarrhytmics has toxicities that include reverible SLE-like syndrome

procainamide

This class of antiarrythmics include lidocaine mexiletine, tocainide

IB (Na+ channel blockers)

this class of antiarrythmics acts to decrease AP duration. It effects ischemic or depolarized purkinje and ventricular tussue. It is useful in acute ventricular arrhytmias (especially post-MI) and i digitalis-induced arrhythmias.

IB (Na+ channel blockers)

This class of antiarrhytmics has toxicities that include local anesthetic effects, CNS stimulation/depression, cardiovascular depression

IB (Na+ channel blockers)

This class of antiarrhythmics includes flecainide, encainide, propafenone.

class IC (Na+ channel blockers.

This class of antiarrhythmics has no effect on AP duration. It is useful in V-tachs that progress to VF and intractable SVT. Usually used only as last result in refractory tachyarrythmias.

class IC (Na+ channel blockers.

Toxicities of this class of antiarrhythmics includes arrythmias, especially post MI (CONTRAINDICATED)

class IC (Na+ channel blockers.

This clas of antiarrythmics includes propanolol, esmolol, metroprolol, atenolol, timool.

Beta Blockers (Class II)

This class of antiarrythmics acts by ↓ cAMP, ↓ Ca+ currents, and by supressing abnormal pacemakers by ↓ slope of phase 4. The AV node is particularly sensitive resulting in increaed PR interval

B-blockers (Class II antiarrythmics)

this is the shortest acting B blocker

esmolol

Toxicities of this class of antiarrythmics include impotence, exacerbation of asthma, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). It may mask signs of hypoglycemia.

B-blockers (Class II antiarrythmics)

This class of antiarrythmics includes Sotalol, ibutilide, bretylium, & amiodarone

K+ channel blockers (class III)

This class of antiarrythmics acts by ↑ AP duration, ↑ERP. It thends to ↑ QT interval. It is used when other antiarrhythmics fail.

K+ channel blockers (class III)

This class III antiarrythmic has toxicities which include torsades de pointes and excessive beta block

sotalol

This class III antiarrythmic has toxicities which include new arrhytmias& hypotension

bretylium

This class III antiarrythmic has toxicities which include PULMONARY FIBROSIS, HEPATOTOXICITY, HYPOTHYROIDSIM/HYPERTHYROIDISM, corneal deposits, skin depsits resulting in photodermatiitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF

amiodarone mneu: remember to check PFTs, LFTs, and TFTs when using amiodarone.

This class of antiarrythmics include the drugs verapamil, and diltiazem.

Ca++ channel blockers (class IV)

The MOA of this class of antiarrythmics is primarily on AV nodal cells. They ↓ conduction velocity, ↑ ERP, ↑ PR interval.

Ca++ channel blockers (class IV)

this class of antiarrythmics is used in prevention of nodal arrhythmias (e.g., SVT)

Ca++ channel blockers (class IV)

Toxicity of this class of antiarrythmics can include constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression, & torsades de pointes.

Ca++ channel blockers (class IV)

Other antiarrythmics: this antiarrhythmic is the drug of choice in diagnosing/abolishing AV nodal arrhythmias

adenosine

Other antiarrythmics: this antiarrhythmic depresses ectopic pacemakers, especially in digoxin doxicity

K+

Other antiarrythmics: this antiarrhythmic is effective in torsades de pointes and digoxin toxiciity

Mg+