Fa - Cardio

Front 1

LCX (left circumflex) supplies:

Back 1

L and posterior walls of LV

Front 2

LAD supplies:

(3)

Back 2

1. ant. 2/3 of IV septum

2. ant. papillary muscle

3. ant. surface of LV

Front 3

PDA (off RCA) supplies:

(2)

Back 3

1. post. 1/3 of IV septum

2. post. walls of BOTH ventricles

Front 4

acute marginal artery (off of RCA) supplies:

(1)

Back 4

RV

Front 5

the SA and AV nodes are usually supplied by:

Back 5

RCA

Front 6

coronary artery occlusion most commonly occurs in the:

Back 6

LAD

- then RCA, then LCX

Front 7

when does coronary blood flow peak?

Back 7

in early diastole

Front 8

the most posterior part of the heart is the:

Back 8

LA

- enlargement can cause dysphagia (compresses esophagus) or hoarseness (~recurrent laryngeal nerve off of vagus)

Front 9

MAP =

(equation)

Back 9

CO x TPR = 2/3 DP + 1/3 SP

Front 10

Pulse Pressure =

Back 10

SP - DP

Front 11

PP is increased in:

(4)

Back 11

1. hypertrophy

2. aortic regurg

3. ob. SA

4. exercise (transient)

Front 12

PP is decreased in:

(4)

Back 12

1. aortic stenosis

2. cardiogenic shock

3. cardiac tamponade

4. advanced HF

Front 13

during the late stage of exercise, CO is maintained by:

Back 13

HR only

- SV plateaus

Front 14

when HR increases, diastole is:

Back 14

preferentially shortened

=> less filling time

=> dec. CA

check FA - CA?

Front 15

***SV increases with:***

(3)

Back 15

1. inc. contractility

2. inc. preload

3. DEC. AF

Front 16

SV also increases in:

(3)

Back 16

1. anxiety

2. exercise

3. preg.

Front 17

***contractility increases with:***

(4)

Back 17

1. cat's
(inc. Ca2+ pump at sarco retic.)

2. inc. Ca2+

3. dec. extracellular Na+
(=> dec. activity of Na+/Ca2+ xch. => Ca2+ stays in the cytoplasm)

4. Digitalis
(blocks Na+/K+ => inc. intracellular Na+ => Na/Ca xch. => inc. intracell. Ca2+)

check - cross-reference with FA

Front 18

contractility decreases with:

(6)

Back 18

1. B1 block
(dec. cAMP)

2. HF with systolic dysfunction

3. acidosis

4. DCM

5. hypoxia/hypercapnea (dec. PO2/inc. PCO2)

6. non-dihydro Ca2+ chan blockers

Front 19

myocardial O2 demand is increased by:

(4)

Back 19

1. inc. AF
(proportional to arterial pressure)

2. inc. contractility

3. inc. HR

4. inc. ventricular diameter
(=> inc. wall tension)

Front 20

preload = EDV; it decreases with:

Back 20

decreased venous tone

- venodilators like nitroglycerin dec. venous tone

Front 21

AF ~~

Back 21

MAP

Front 22

ACEI's and ARB's dec. BOTH:

Back 22

preload AND AF

(they dec. volume and prevent vasoconstriction)

Front 23

EF ~~ ventricular contractility; nl EF >=

Back 23

55%

Front 24

EF is ______________ in systolic HF, and __________ in diastolic HF

Back 24

decreased in systolic HF,

NORMAL in diastolic HF

Front 25

viscosity depends mostly on:

Back 25

hematocrit

Front 26

viscosity is inc'd in:

(3)

Back 26

1. polycythemia

2. hyper-proteinemic states
(e.g. MM)

3. non-hereditary spherocytosis

Front 27

viscosity is decreased in:

Back 27

anemia

Front 28

inotropy =

Back 28

change in contractility that => change in CO

Front 29

2 examples that cause positive inotropy:

Back 29

1. cat's

2. Digoxin

(inc. contractility => inc. CO)

Front 30

2 examples of neg. inotropy:

Back 30

1. uncompensated HF

2. narcotic OD

(=> dec. contractility => dec. CO)

Front 31

venous return ~~

(2)

Back 31

1. blood volume

2. TPR

Front 32

relationship of venous return to blood volume:

Back 32

venous return proportional to blood volume

(also to sympathetic activity)

Front 33

relationship of venous return to TPR:

Back 33

dec. TPR = inc. in venous return

dTPR ~~ change in SLOPE of venous return

(x-intercept stays put if CO increases to offset dec. in TPR)

- TPR and slope are INVERSELY proportional

Front 34

PR interval ~~

Back 34

conduction b/w atria and ventricles

Front 35

QT interval ~~

Back 35

mechanical contraction of the ventricles

Front 36

U wave:

(3)

Back 36

1. pathogenic

2. right after T wave

3. caused by hypoK+, bradycardia

Front 37

ranking of speed of conduction by area of the heart:

Back 37

Purkinje > atria > ventricles > AV node

Front 38

speed of conduction of Pacemakers:

Back 38

SA > AV > bundle of His/Purkinje

Front 39

features of Torsades:

(2)

Back 39

1. a ventricular tachy

2. can progress to V-fib

Front 40

a long QT interval predisposes to:

Back 40

Torsades

Front 41

causes of Torsades:

(3)

Back 41

1. QT-interval prolonging drugs
(see below)

2. dec. K+

3. dec. Mg2+

Front 42

Some Risky Meds Can Prolong QT:

Back 42

Sotalol

Risperidone

Macrolides

Chloroquine

Protease inhibitors (-navirs)

Quinidine (class Ia, III)

Thiazides

Front 43

congenital long QT syndrome =

Back 43

disorder of myocardial repol

Front 44

congenital long QT syndrome increases the risk of:

Back 44

sudden cardiac death due to Torsades

Front 45

2 kinds of congenital long QT syndrome:

Back 45

1. Romano-Ward syndrome

2. Jervell and Lange-Nielsen syndrome

Front 46

2 features of Romano-Ward syndrome:

Back 46

1. AD

2. pure cardiac phenotype
(no deafness)

Front 47

2 features of Jervell and Lange-Nielsen syndrome:

Back 47

1. AR

2. ~~ Torsades AND sensorineural deafness

Front 48

WPW syndrome =

Back 48

m.c. ventricular pre-excitation syndrome

Front 49

WPW pathophys:

Back 49

electrical signal bypasses AV node via the abnly-fast bundle of Kent

=> ventricles begin to partially depol. earlier

=> shortened PR interval, characteristic delta wave

Front 50

WPW may result in:

Back 50

REENTRY CIRCUIT

=> supra-V-tach

Front 51

features of a-fib:

(3)

Back 51

1. irregularly irregular

2. **NO discrete P waves**

3. irregularly-spaced QRS complexes

Front 52

a-fib => inc. risk for:

Back 52

atrial stasis, => thromboembolic stroke

Front 53

tx of a-fib =

(3)

Back 53

1. rate control

2. anticoags

3. cardioversion
(reset to nl rhythm via electricity or drugs)

Front 54

features of atrial flutter:

(2)

Back 54

1. rapid succession of back-to-back atrial depol waves

2. => sawtooth appearance

Front 55

tx of a-flutter:

(3)

Back 55

1. catheter ablation (definitive)

2. conversion to sinus rhythm: class IA, IC, or III antiarrhythmics

3. rate control: B- or Ca2+ chan. blocker

Front 56

features of V-fib:

(2)

Back 56

1. **completely erratic** rhythm with **no identifiable waves**

2. fatal w/o immediate CPR and defib.

Front 57

3 features of 1st-degree AV block:

Back 57

1. prolonged PR interval (>200 msec)

2. benign, asymp

3. NO tx nec.

Front 58

two 2nd-degree AV blocks:

Back 58

1. Mobitz type I / Wenckenbach

2. Mobitz type II

Front 59

features of Mobitz type I / Wenckenbach:

(4)

Back 59

1. progressive lengthening of the PR interval...

2. ...until a beat (i.e. QRS) is dropped
(P wave NOT followed by QRS

3. reset

4. usually asymp

Front 60

features of Mobitz type II:

(3)

Back 60

1. 2:1 pattern
(2 P waves followed by QRS)

2. NO lengthening of PR interval

3. may progress to 3rd-degree block

Front 61

tx of Mobitz type II =

Back 61

pacemaker

Front 62

features of 3rd-degree / complete AV block:

(3)

Back 62

1. atria and ventricles beat independently of each other

2. atrial rate is faster than the ventricular rate

3. pot.ly caused by Lyme dz

Front 63

tx of 3rd-degree AV block =

Back 63

pacemaker

Front 64

mechanism/effects of ANP:

(6)

Back 64

1. constricts efferent arterioles,

2. dilates afferent arterioles ==> Na+/H2O into urine

(^via cGMP^)

3. inhibits Na+ reabsorption at collecting tubule

4. inhibits renin secretion

5. restricts aldo secretion at the adrenal glands

6. vasodilates

=> aldo escape

Front 65

3 features of BNP:

Back 65

1. released from VENTRICULAR myocytes

2. in response to inc. tension of ventricles

3. longer half-life than ANP

Front 66

BNP blood test is used to dx:

Back 66

HF

Front 67

name of recombinant BNP drug:

Back 67

Nesiritide,

for HF

Front 68

2 ways to stimulate carotid sinus firing:

Back 68

1. inc. BP

2. carotid massage (mechanical pressing)

Front 69

3 effects of stimulating carotid sinus baro r's:

Back 69

1. vasodilation

2. dec. HR/contractility

3. dec. BP

Front 70

aortic arch baro r's respond ONLY to:

Back 70

inc. BP

- carotid baro r's respond to both inc. AND dec. in BP

Front 71

peripheral chemo r's are found in:

(2)

Back 71

carotid bodies,

aortic body

Front 72

**peripheral chemo r's are stimulated by:**

(3)

Back 72

dec. PO2 (<60)

inc. PCO2

dec. pH of blood

Front 73

central chemo r's are stimulated by:

Back 73

changes in pH and PCO2 of interstitial fluid, which are influenced by **arterial PCO2**

- r's do NOT directly respond to PO2 changes

Front 74

***inc. O2 demand is met with:***

Back 74

inc. coronary blood flow,

NOT inc. extraction of O2
(already extracting as much as it can)

Front 75

PDA ~~

Back 75

left-to-right shunt

(where blood avoids arterioles and hits pulmonary circulation instead)

- eventually, becomes R-to-L shunt, as right side has greater volume

Front 76

persistent truncus arteriosus =

Back 76

failure of truncus arteriosus to divide into pulmonary trunk and aorta

- most pts have accompanying VSD

Front 77

D-transposition of the great vessels =

Back 77

aorta leaving RV,

pulmonary trunk leaving LV (posterior)

- not compatible with life unless a shunt is present to allow mixing of blood

Front 78

tricuspid atresia =

Back 78

absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability.

Front 79

Tetralogy of Fallot =

Back 79

1. Pulmonary infundibular stenosis
(most imp. determinant of prognosis)

2. RVH
(boot-shaped heart on CXR)

3. Overriding aorta
(aorta right next to/right off of VSD, not LV)

4. VSD

Front 80

truncus arteriosus =

Back 80

failure of truncus arteriosis to divide into pulmonary trunk and aorta

~~ VSD

Front 81

S1 =

Back 81

MV and tricuspid valve closing

- loudest at mitral area

Front 82

S2 =

Back 82

aortic and pulmonary valves closing

- loudest at left sternal border

Front 83

atheroma =

Back 83

degeneration of walls of arteries, due to accumulation of fatty deposits and scar tissue

Front 84

activated mP's of an atheroma secrete ___________________ to __________________________

Back 84

metalloproteinases

to help degrade collagen

Front 85

what 2 separate features of a plaque make it liable to rupture?

(=> thrombosis, embolism)

Back 85

1. thin fibrous cap

2. rich lipid core

Front 86

endocardium is not only the innermost surface of the heart, but also forms:

Back 86

the surface of the valves

Front 87

m.c.c. of sudden cardiac death =

Back 87

V-fib

Front 88

S3:

(4)

Back 88

1. occurs immediately after S2, during diastole/ filling

2. ~~ LV systolic failure

3. ~~ blood coming into partially-filled ventricle
(e.g. mitral regurg, CHF)

4. NL in children and preg.

Front 89

S3 is best heard at:

Back 89

ventricular apex,

***esp. in lateral decubitis pos (lying down), and EXHALING completely***

(brings heart closer to chest wall)

Front 90

S4:

(3)

Back 90

1. late diastole

2. ~~ ventricular hypert

3. - HCM, HTN, Aortic Stenosis

Front 91

pathologies heard during systole:

(5)

Back 91

1. aortic stenosis

2. pulmonic stenosis

3. mitral regurg

4. tricuspid regurg

5. VSD

Front 92

pathologies heard during diastole:

(4)

Back 92

1. aortic regurg

2. pulmonic regurg

3. mitral stenosis

4. tricuspid stenosis

Front 93

jaw claudication =

Back 93

pain while chewing

Front 94

cardiac defects of 22q11:
(e.g. DiGeroge)

(2)

Back 94

1. truncus arteriosus

2. Tetralogy of Fallot

Front 95

cardiac defects of Down syndrome:

(2)

Back 95

1. septal defects (ASD/VSD)

2. AV septal defect (endocardial cushion defect)

Front 96

cardiac defects of congenital rubella:

(3)

Back 96

1. septal defects

2. PDA

3. pulm. artery stenosis

Front 97

cardiac defects of Turner syndrome:

(2)

Back 97

1. bicuspid aortic valve

2. (pre-PDA) coarctation of aorta

Front 98

cardiac defects of Marfan:

(2)

Back 98

1. MVP

2. (thoracic) aortic aneurysm and dissection

Front 99

cardiac defect from diabetic mother:

Back 99

transposition of great vessels

Front 100

3 dihydropyridine Ca2+ chan. blockers:

Back 100

1. Amlodipine

2. Nimodipine

3. Nifedipine

Front 101

2 NON-dihydro Ca2+ chan. blockers:

Back 101

1. Diltiazem

2. Verapamil

Front 102

ACEI's/ARB's are protective against:

Back 102

diabetic nephropathy

Front 103

B-blockers must be used cautiously in decompensated CHF, and absolutely contraindicated in:

(2)

Back 103

cardiogenic shock,

suspected cocaine

Front 104

eccentric hypert:

(4)

Back 104

1. Volume overload

2. => inc. LV chamber size

3. => SYSTolic dysfunction

4. = contractile dysfunction

Front 105

concentric hypert:

(4)

Back 105

1. ~~ chronic Pressure overload

2. => dec. LV chamber size,

3. => dec. compliance (STIFF)

4. = DIASTOLIC dysfunction
(can't fill as well)