Cards

Front 1

Fick principle

Back 1

CO = rate of O2 consumption / (Arterial O2 - Venous O2)

Front 2

MAP

Back 2

2/3 DBP + 1/3 SBP

Front 3

SV affected by

Back 3

CAP
Contracility
Afterload
Preload

increases in anxiety, exercise (early), pregnancy

Front 4

Myocardial O2 demand

Back 4

Increased by increase in:
1. Afterload
2. Contractility
3. HR
4. Heart size (increased wall tension)

Post-MI, O2 demand decreased by:
1. Nitrates (preload)
2. ACEI (preload and afterload)
3. BB (contractility)

O2 demand is met by INCREASE IN CORONARY BLOOD FLOW (not by increase in O2 extraction bc always 100%)

Front 5

Nitroglycerin

Back 5

VeNodilator
decreases preload (EDV)

Front 6

Hydralazine

Back 6

Vasodilator
decreases Afterload (Arterial)

Front 7

ACEI/ARB

Back 7

Decrease both preload and afterload

Front 8

Resistance

Back 8

P = Q*R
R = 8*viscosity*length/(pi*r4)

Resistance is directly proportional to viscosity and inversely proportional to radius^4

*arterioles account for most of TPR (regulate capillary flow)

Front 9

Wide splitting

Back 9

PS or RBBB

Front 10

Paradoxical Splitting

Back 10

AS or LBBB
(delayed LV emptying)
inspiration: earlier P2 and later A2 move CLOSER to one another (eliminating the split)

Front 11

Dicrotic notch

Back 11

Win-Kessel effect: increased pressure in aorta due to elasticity: allows for diastolic filling of coronaries

Front 12

Fixed splitting

Back 12

ASD

Front 13

Aortic area

Back 13

Systolic murmurs:
AS
Flow murmur
Aortic valve sclerosis

Front 14

Pulmonic area

Back 14

Systolic murmur:
PS
Flow murmur (ASD: increased flow thru pulm valve, no murmur from flow across ASD; can also cause a diastolic rumble across TV and with progression, PR due to dilatation of pulm a.)

Front 15

Tricuspid area

Back 15

Holosystolic:
TR
VSD

Diastolic:
TS
ASD (diastolic rumble across TV)

Front 16

Mitral area

Back 16

Systolic:
MR
Diastolic:
MS

Front 17

Left sternal border

Back 17

Systolic:
HCM

Diastolic:
AR
PR

Front 18

Left lateral decubitus

Back 18

Listen for:
MS
MR
S3
S4

Front 19

Aortic Stenosis

Back 19

Causes:
1. Bicuspid (after 40-60yo)
2. Senile or degenerative (70-90yo)
3. Chronic rheum
4. Unicuspid
5. Syphilis

**Ejection Click

Angina, syncope, CHF

Front 20

Pulsus parvus et tardus

Back 20

pulses weak compared to heart sounds; can lead to syncope

Front 21

VSD

Back 21

holosystolic, harsh-sound murmur; loudest in tricuspid area

**same as TR (must look at clinical case)

Front 22

MVP

Back 22

most common valve lesion

*LATE systolic crescendo murmur with midsystolic click due to sudden tensing of chordae tendinae

loudest at S2

can predispose to endocarditis if you have mitral regurg with it

Causes;
1. myxomatous degeneration
2. rheumatic fever
3. chordae rupture

**enhanced by maneuvers that decrease venous return (standing, valsalva)

Front 23

AR

Back 23

wide pulse pressure, bounding pulses, head bobbing

cause:
1. aortic root dilation (marfans, syphilis)
2. bicuspid aortic valve
3. rheumatic fever
4. aortic aneurysm

Front 24

MR

Back 24

radiates to axilla

causes:
1. ischemic heart disease
2. MVP
3. LV dilation
4. endocarditis
5. rheumatic heart disease

Front 25

TR

Back 25

radiates to right sternal border
causes:
1. RV dilation
2. endocarditis
3. Rheum fever

Front 26

MS

Back 26

**opening snap: due to abrupt halt in leaflet motion in early systole

2/2 rheumatic fever
can cause LA dilation

Front 27

Rheumatic Heart Disease

Back 27

early lesion:
MVP

late lesion:
MS

M > A > T (uncommon)

JONES:
Joints (migratory polyarthritis)
Heart: valve, pericarditis
Nodules
Erythema marginatum; ESR
St. Vitus' dance (chorea)

Aschoff bodies: granuloma with giant cells, fibrinous necrosis
Anitschkow's cells: activated histiocytes
ASO titers
A.B. to M protein (bacterial and human epitope homology; type 2 hypersensitivity)

Front 28

Cardiac vs. Skeletal

Back 28

GAP between cardiac and skeletal muscle:
1. Gap junction electrically couple cardiac myocytes
2. Automaticity of nodal cells due to If channels
3. CICR during the plateau of action potential

Front 29

Resting membrane potential

Back 29

depends on what is freely permeable

K+: -90mV (cardiac) -75 (skeletal)
Na+: +55mV
Ca2+: +20mV

Front 30

Speed of conduction

Back 30

PAVA:
Purkinje > atria > ventricles > AV node

Front 31

WPW

Back 31

accessory conduction pathway from atria to ventricle: bundle of Kent, bypassing AV node

**delta wave: ventricles depolarize earlier

*may result in reentry leading to SVT

Tx: NOT adenosine
amio or procainamide

Front 32

Atrial Fibrillation

Back 32

Tx:
new: synchronized cardioversion
old: must anticoagulate first (24-48h)

chronic:
rate control: BB, CCB, Dig
Rhythm: amio, sotalol

Front 33

AFlutter

Back 33

Tx:
IA
IC
III

Front 34

Complete heart block

Back 34

Lyme disease
Congenital Lupus

Tx: pacemaker

Front 35

ANP

Back 35

Aldo
Natriuresis
Peripheral vasodilation

released from atria in response to increased blood volume and atrial pressure

*activate guanylate cyclase --> cGMP --> periph vasodilation

-constricts efferent renal arterioles and dilates afferent arterioles (increase GFR) --> diuresis, natriuresis

kidney: decreases renin secretion
adrenals: decrease aldo secretion

Front 36

Aortic arch

Back 36

transmits vis vagus n. to medulla

Baroreceptor: responds to INCREASE in BP

Chemoreceptor: responds to decreased PO2 (<60), increased PCO2, and decreased pH

Front 37

Carotid sinus

Back 37

transmits vis glossopharyngeal n. to solitary nucleus of medulla

Baroreceptor: responds to decrease AND increase in BP

in hypotension: increase efferent symp firing, decrease efferent parasymp firing --> vasoconstriction, HR, contractility, BP

carotid massage: increase afferent baroreceptor firing --> decrease HR

Carotid body (chemoreceptor):
responds to decrease in PO2, increase in PCO2, decrease in pH

Front 38

Central chemoreceptor (brain)

Back 38

responds to changes in pH and PCO2 of brain interstitial fluid --> influenced by arterial CO2

Cushing reaction:
1. increase ICP constricts arterioles --> cerebral ischemia -->sympathetic outflow (vasoconstriction) -->
HTN & tachycardia

2. Carotid baroreceptor causes reflex bradycardia

3. Increased ICP affects breathing area of brain stem --> irregular breathing

Front 39

Cushing Triad

Back 39

1. HTN (with wide pulse pressure)
2. Bradycardia
3. Respiratory depression

Front 40

BNP

Back 40

released by ventricles in response to vol overload (dx CHF)

*in LVH --> change in gene transcription --> upregulate fetal proteins from atrial and vent myocytes --> release ANP and BNP in response to vol overload

Front 41

Autoregulation of heart

Back 41

vasodilation when decreased O2, increased adenosine (low energy molecule), increased NO

Front 42

Autoreg of brain

Back 42

CO2 and pH

Front 43

Autoreg of lungs

Back 43

hypoxia causes VASOCONSTRICTION so only well-ventilated areas are perfused

Front 44

Autoreg of Skeletal muscle

Back 44

lactate, adenosine, K+

Front 45

Autoreg of skin

Back 45

sympathetic stimulation --> temperature control

Front 46

Capillary fluid exchange equation

Back 46

Net fluid flow = Pnet * Kf (filtration constant = capillary permeability)

Pnet = (Pc - Pi) - (plasma osmotic - interstitial osmotic)

Front 47

Causes of edema

Back 47

1. Increased capillary pressure (heart failure: congestion)
2. Decreased plasma osmotic pressure: decreased plasma proteins (nephrotic syndrome, liver failure)
3. Increased interstitial osmotic pressure (lymphatic blockage- proteins stuck in interstitium)
4. increased Kf: (toxins, infxn, burns, sepsis- bradykinin, histamine)

Front 48

NItric Oxide

Back 48

Most important mediator of coronary vasc dilation in large arteries and prearteriolar vessels

synthesized from Arg & O2 by endo cells --> increase cGMP --> activates myosin phosphatase --> smooth muscle relaxation (myosin)

Front 49

Eisenmenger's

Back 49

uncorrected L--> R shunt causes RVH and progressive pulm HTN --> shunt goes from R to L causing late cyanosis


*get lower extremity cyanosis in PDA

Front 50

TOF

Back 50

PROV
1. Pulmonary stenosis
2. RVH
3. Overriding aorta
4. VSD

boot-shaped heart

Front 51

R --> L shunts

Back 51

3 caused by abnormal neural crest migration:
1. TOF
2. TA
3. TGA

supposed to migrate into truncal and bulbar ridges of TA and bulbis cordis and grow, spiraling to separate A&P arteries

Front 52

Coarc of aorta

Back 52

Infantile: preductal; seen in Turner's

Adult: postductal; associated with bicuspid AV; have notching of ribs, HTN in upper extremities, weak pulses in lower extremities

can result in AR

Front 53

Kartagener's

Back 53

situs inversus

Front 54

Tuberous sclerosis

Back 54

cardiac rhabdomyomas

Front 55

Friedrich's

Back 55

HCM

Front 56

DiGeorge

Back 56

TA, TOF, interrupted aortic arch

Front 57

Downs

Back 57

Septal defects: ASD, VSD, etc.

Front 58

Congenital rubella

Back 58

PDA, PS, septal defects

Front 59

Infant of diabetic mother

Back 59

TGA, HCM

Front 60

Monckeberg arteriosclerosis

Back 60

calcification in MEDIA of arteries (esp radial or ulnar); benign

Front 61

Arteriolosclerosis

Back 61

hyaline thickening of small arteries in essential HTN or DM. hyperplastic "onion skinning" in malignant HTN

Front 62

Atherosclerosis

Back 62

dz of elastic arteries and large/medium muscular arteries

fibrous plaques and atheromas form in INTIMA of arteries

path:
1. endothelial cell dysfunction
2. foam cells (macs eat LDL) form fatty streaks
3. SMC migration: PDGF and TGF-beta
4. fibrous plaque
5. Complex atheromas

abd aorta > coronary > popliteal > carotid

Front 63

Aortic Dissection

Back 63

A: prox to Subclavian (tx: surgery)
B: distal; tx: BB

Front 64

Evolution of MI

Back 64

LAD > RCA> circumflex

2-4hrs:
no visible change by LM

4h-24h:
early coagulative necrosis
necrotic contents released into blood
contraction bands after 12h

2-4d:
red: hyperemia
acute inflammation
pmn emigration
extensive coag necrosis

5-10d:
yellow-brown, soft
risk for structural defects due to degradation by macs
granulation tissue

>10d:
gray-white
contracted scar bulges
risk for ventricular aneurysm

Front 65

Transmural infarct

Back 65

ST elevation
Q waves
T wave inversions

Front 66

Subendocardial infarcts

Back 66

ischemic necrosis of <50%
fewer collaterals, higher pressure
ST depression

Front 67

ECG diagnosis

Back 67

Ant wall: LAD; V1-V4 Q waves
Anteroseptal: LAD; V1-V2
Anterolateral: LCX V4-V6
Lat wall: LCX; I, aVL
Inf wall: RCA; II, III, aVF

Front 68

DCM

Back 68

Alcohol
Beriberi (wet)
Coxsackie B
Cocaine
Chagas
Doxorubicin
**Eccentric hypertrophy
Fe (hemochromotosis
peripartum

1/3 inherited: mutation in cytoskeletal proteins (dystrophin) or mito enzymes of oxidative phosphorylation --> defective force generation or transmission

Signs:
systolic dysfunction
S3
lat displaced apex

Front 69

HCM

Back 69

outflow tract obstruction bc IV septum too close to MV
50% familial, auto dom (mutation in sarcomere proteins, esp beta-myosin heavy chain)
assoc wotih Friedrich's ataxia

disoriented, tanged, hypertrophied myocardial fibers

signs:
*concentric hypertrophy
diastolic dysfunction
S4
prominent "A wave" on JVP
nl heart size
systolic murmur, syncope
Tx: BB, CCB

Front 70

RCM

Back 70

sarcoid
amyloid
postradiation
endocardial fibroelastosis (young children)
Loffler's (eosin. infiltrate)
Hemochromatosis

*diastolic dysfunction

Front 71

Acute exac of CHF:

Back 71

Tx with LMNOP:
Loop
Morphine
Nitrates
O2
Positioning/pressors (dobutamine)

*stop BB

Front 72

Chronic CHF tx

Back 72

ACEI/ARB (most effective long-term tx, inhib myocardial remodeling and decrease BP)
BB
Dig
Loop diuretic

Front 73

TV endocarditis

Back 73

S. aureus
Pseudomonas
Candida

Front 74

Libman-Sacks endocarditis

Back 74

SLE

verrucous, sterile, eosinophilic vegetations on both sides of valve
usually benign, can cause MR or MS

Front 75

Pulsus paradoxus

Back 75

Tamponade

more than 10mmHg decrease during inspiration

Front 76

Kussmaul's sign

Back 76

Pericarditis

JVD with inspiration
rapid Y descent on JVP

Front 77

Pericarditis causes

Back 77

serous:
lupus, RA
viral infxn
uremia

Fibrinous:
Dressler's
Uremia
Rheumatic fever

Hemorrhagic:
TB
Malignancy (melanoma)

Front 78

Wegener's tx

Back 78

cyclophosphamide and corticosteroids

(Cs for C-ANCA)

also the tx. for PAN

Front 79

P-ANCA

Back 79

Microscopic polyangiitis: wegener's without granulomas

CS web PAGE
Churg-Strauss:
peripheral neuropathy
asthma
granulomas
eosinophilia

Front 80

Polyarteritis nodosa

Back 80

IC-mediated transmural vasculitis with fibrinoid necrosis

*renal and visceral vessels (small and medium)

*hep B in 30%

tx: corticosteroids, cyclophosphamide