Cardio Part 6

Front 1

Holosystolic = pansystolic =

Back 1

lasting through systole

Front 2

AF is given by:

Back 2

peak aortic pressure

"Peak aortic pressure is a surrogate for AF"

Front 3

EKG of LAE:

Back 3

negative inflection in P of v1, tiny box wide and tiny box deep

Front 4

R wave of v1 > S wave of v1 =

Back 4

RVH

Front 5

HF is characterized by:

(2)

Back 5

1. inc. preload

2. dec. contractility

Front 6

contractility =

Back 6

the degree to which muscle fibers can shorten when activated,

independent of preload and AF.

- depends on Ca2+ available

Front 7

****to treat *chronic* HFwrEF:****

(5)

Back 7

1. ACEI's (+ diuretic if edema/congestion)

2. ARB or H-ISN (if 1. not tolerated)

3. B-blocker (if deterioration or volume overload)

4. Aldosterone Antagonist (if advanced HF)

5. Digoxin (to improve QOL)

Front 8

***5 features of ACEI's:***

Back 8

1. = balanced vasodilators

2. dec. AF

3. dec. preload

4. dec. aldosterone

5. limit maladaptive remodeling

Front 9

what does lowering the AF and preload by ACEI's do?

Back 9

inc. CO

Front 10

what does decreasing aldosterone do?

Back 10

dec. intravascular volume/preload

=> dec. pulmonary congestion

Front 11

pulmonary congestion =

Back 11

engorgement of pulmonary vessels with transudation of fluid into the alveoli and interstitial spaces

Front 12

AII relationship to catecholamines:

Back 12

it increases them

Front 13

ACEI's do NOT decrease BP, b/c:

Back 13

even though they dec. TPR, the increase in CO that they cause maintains the BP

Front 14

***ACEI drugs are called:***

Back 14

" -prils"

Front 15

**diuretics are used in HF only if (3) are present:**

Back 15

PE, congestion, peripheral edema

- given with ACEI's

Front 16

like nitrates, diuretics can decrease preload significantly, and CO:

Back 16

by a bit

- again, be careful of doing that too much

Front 17

*example of a good thiazide:*

Back 17

Metalozane

Front 18

***ARB's are called:***

Back 18

" -artans"

Front 19

balanced vasodilator therapy =

Back 19

hydralazine + isodinitrate

former opens up arteries, latter opens up veins

Front 20

when is balanced vasodilator therapy used?

Back 20

when ACEI's can't be tolerated

Front 21

what do nitrates do in HF?

Back 21

dec. preload

=> dec. CO by a little

- be careful not to dec. them too much

Front 22

arterial vasodilators like hydralazine decrease:

Back 22

TPR

=> inc. SV

=> inc. CO (*new curve*)
(given with B-blockers to stop reflex tachy)

Front 23

in general: **dec. perfusion of organs** =>

(2)

Back 23

activation of RAS and cat's

=> inc. BP, CO, and venous return

=> perfusion increases in the short term

but now the heart has to push more volume against a higher pressure;

=> dec. EF => dec. renal perfusion => + fb on RAS

Front 24

negative effect of B-blockers on HF:

Back 24

they decrease contractility

Front 25

positive effects of B-blockers in HF:

(4)

Back 25

1. augment CO by decreasing HR
- make every beat count for more

2. block NOR-mediated arrhythmias

3. save lives

4. reverse downregulation of B-r's

Front 26

too much aldosterone causes:

(2)

Back 26

1. cardiac fibrosis

2. adverse ventricular remodeling

Front 27

what do Aldosterone Antagonists do?

(2)

Back 27

1. dec. retention of Na+/water

2. dec. hypertrophy/fibrosis

Front 28

2 Aldosterone Antagonists:

Back 28

1. Spironalactone

2. Eplerenone

Front 29

cardiac glycosides like Digoxin are:

Back 29

positive inotropes

Front 30

inotropes and B-blockers both ________________, such that __________________________________

Back 30

raise the curve,

such that at the same EDV, you get a higher SV => higher CO

Front 31

how does Digoxin work?

Back 31

inhibits Na+/Ca2+ pump of myocytes

=> more Ca2+ inside for heart to use

Front 32

what does Digoxin result in?

(3)

Back 32

1. inc. contractility

2. inc. CO

3. dec. LV size

Front 33

**who gets Digoxin?**

Back 33

**only pts with systolic dysfunction**

Front 34

why is Digoxin so rarely used?

(3)

Back 34

1. VERY toxic

2. causes arrhythmias due to hypokalemia

3. narrow therapeutic index

Front 35

hypokalemia refers to little K+ in:

Back 35

the blood

- b/c there's lots of Na+ coming out of myocytes in exchange for K+ coming in

Front 36

which drug is no good?

Back 36

nesiritide

- a recombinant natriuretic factor

Front 37

to treat *acute* HFwrEF:

(2)

Back 37

1. ***B-AGONISTS***

- b/c it's so life-threatening, you need an immediate short-term solution

2. PDE-3 inhibitors

Front 38

3 B-agonists used for acute HFwrEF:

Back 38

1. Dobutamine

2. Dopamine

3. Isoproterol

Front 39

what kind of acute HF is Dobutamine used for?

Back 39

acute HF WITHOUT hypotension

Front 40

what kind of acute HF is Dopamine used for?

Back 40

acute HF WITH hypotension and poor renal perfusion

Front 41

what kind of acute HF is Isoproterol used for?

Back 41

acute HF with slow HR, high BP

Front 42

of the 3 B-agonists, Dopamine is the only one that can increase:

Back 42

renal perfusion

Front 43

PDE-3 inhibitors increase:

Back 43

Contractility

Front 44

PDE-3 inhibitors are called:

Back 44

" - rinones"

Front 45

***when are PDE-3 inhibitors used?***

Back 45

when vasodilators, inotropic agents, and diuretics **have failed**

Front 46

****to treat HFpEF:****

(3)

Back 46

1. dec. pulmonary and systemic congestion

2. correct the UC of HF (HTN, ACS, etc)

3. NO role for ACEI's/, B-blockers, Inotropes

Front 47

cardiomyopathy =

Back 47

primary myocardial muscle disease

- excludes HF secondary to other causes, e.g. HTN, valvular disease, etc.

Front 48

"ischemic cardiomyopathy" is a misnomer; it actually means:

Back 48

CHF secondary to severe CAD

Front 49

2 major/general effects of cardiomyopathy:

Back 49

1. HF

2. arrhythmias

Front 50

3 major types of cardiomyopathy:

Back 50

1. Dilated CM

2. Hypertrophic CM

3. Restricted CM

Front 51

DCM can be caused by:

(2 general)

Back 51

insult or inheritance

(e.g. alcohol abuse)

Front 52

top 3 causes of DCM =

Back 52

1. idiopathic

2. genetic

3. viral

Front 53

DCM is most commonly inherited in:

Back 53

AD fashion

Front 54

DCM ~~ disease of:

Back 54

sarcomeric proteins

Front 55

DCM is characterized by:

(3)

Back 55

1. progressive dilation of ALL 4 chambers

2. => *systolic dysfunction*

3. progressive CHF

Front 56

appearance of DCM heart:

(3)

Back 56

1. severe cardiomegaly but *normal wall thickness*

2. dilation of ALL chambers

3. **intracardiac thrombi**

Front 57

histology of DCM:

Back 57

boxcar nuclei

Front 58

in DCM, the heart goes **straight to dilation (eccentric hypertrohy)**; dilation of chambers =>

Back 58

progressive failure of leaflet adjustment

=> mitral rugurg

=> worse HF

=> volume-overload of LV

=> exacerbation of remodeling

=> CHF

Front 59

DCM often manifests as:

Back 59

progressive CHF

Front 60

clinical manifestations of DCM:

(4)

Back 60

1. often asymp

2. symp's of HF

3. MV, TV regurg

4. arrhythmias

Front 61

diagnosis of DCM:

(2)

Back 61

1. EF <40%

2. no significant CAD

(both via echo)

Front 62

CXR of DCM: heart will be

Back 62

>50% of thoracic chamber

- not diagnostic, but helps

Front 63

death in DCM occurs from:

(3)

Back 63

1. intractable HF

2. embolism/complications

3. arrthymias/SCD

Front 64

treatment for DCM =

(4)

Back 64

1. transplant (definitive treatment)

2. ICD to dec. arrhythmias

3. mechanical pump, ACEI's/, B-blockers, and Aldo Antagonists for HF

4. screen first-degree relatives

Front 65

other features of DCM:

(4)

Back 65

1. most common reason for heart transplant

2. variable rates of progression

3. idiopathic cases most fatal

4. prophylaxis is NOT indicated for thromboembolic events

Front 66

HCM is also called:

(2)

Back 66

1. asymmetric septal hypertrophy

2. idiopathic hypertrophic subaortic stenosis

Front 67

3 main features of HCM:

Back 67

1. MASSIVE hypertrophy

2. stiff ventricle => abnormal filling (diastolic dysfunction)

3. intermittent outflow obstruction in 1/3

Front 68

appearance of heart in HCM:

(5)

Back 68

1. marked hypertrophy, esp. of IVS and LV
(more often IVS > LV)

2. myocyte disarray

3. LV outflow tract plaque

4. abnormal thickening/scarring of both the subaortic septum and the anterior leafet
(due to continuous abnormal contact b/w the two)

5. banana-shaped chamber-to-aorta

Front 69

***about 1/3 of pts with HCM have a:***

Back 69

dynamic outflow obstruction

Front 70

dynamic outflow obstruction is caused by:

Back 70

SAM

- systolic anterior motion

of the anterior leaflet when flow takes it

Front 71

what does SAM do?

Back 71

sucks in the anterior leaflet toward the aorta

=> obstruction

=> regurgitation

=> dec SV => dec. CO

Front 72

Venturi is exacerbated by a/t that:

Back 72

reduces ventricular volume

(dehydration, dec. venous return)

Front 73

**WITHOUT outflow obstruction, HCM looks like:

Back 73

exaggerated HFpEF

- SV and Contractility are normal, but Compliance is decreased

Front 74

HCM is 100% _______________

Back 74

genetic

- 50% of cases in AD fashion

Front 75

HCM ~~ powerful,

Back 75

hyperkinetic heart contractions

Front 76

clinical presentation of HCM:

(6)

Back 76

1. DOE (most common)

2. often asymp

3. MI and angina, even without athero

4. palpitations

5. syncope

6. SCD

Front 77

PhysEx/test findings of HCM:

(5)

Back 77

1. dec. SV

2. dynamic outflow murmur - crescendo-decresendo

3. S4

4. A-fib

5. mural thromboses

Front 78

angina in HCM results from:

Back 78

supply-demand imbalance

- HCM => inc. muscle mass (demand) without inc. in vasculature to supply it

- meanwhile, coronary arteries are compromised => further decrease in supply

Front 79

syncope is caused by:

Back 79

insufficient CO to the brain

- esp. in SAM

~ exercise, dehydration

Front 80

to prevent SCD:

Back 80

ICD's

(SCD ~~ disarray, fibrosis)

Front 81

criteria to qualify for an ICD in HCM:

(5)

Back 81

1. family history of SCD

2. history of syncope

3. non-sustained ventricular tachy

4. wall thickness >30 mm

5. abnormal BP response to exercise

Front 82

to diagnose HCM, it must meet these 3 criteria:

Back 82

1. LV wall thickness >15 mm (normal <10)

2. FH/ i.d. of genetic mutation

3. exclusion of other causes of hypertrophy (e.g. HTN)

Front 83

***an HCM murmur is decreased while:***

Back 83

***squatting***

- an AS murmur is decreased in valvsalva and standing

Front 84

gold-standard for HCM =

Back 84

echo

Front 85

EKG of HCM shows:

(2)

Back 85

1. LVH

2. T-wave inversions in v5, v6

Front 86

in HCM, the degree of fibrosis predicts:

Back 86

severity of disease and risk of arrhythmia

- fibrosis usually occurs in subaortic IVS, late

Front 87

HCM and genetic testing:

(4)

Back 87

1. NOT required for diagnosing it

2. negative tests don't exclude HCM

3. mutations do not change management

4. positive result => test first-degree family

Front 88

treatment of HCM:

(4)

Back 88

1. B-blockers for angina

2. surgical myectomy (gold standard)

3. alcohol septal ablation (if 2. no-go)

4. exclude most competitive sports

Front 89

Restrictive CM =

Back 89

HFpEF taken to the extreme

Front 90

3 features of Restrictive CM:

Back 90

1. diastolic problem => can't fill

2. amyloid, sarcoid, iron, etc get into wall, heart can't expand

3. => stiff, inelastic ventricle w/ diastolic dysfunction

Front 91

stiff, inelastic ventricle w/ diastolic dysfunction =>

Back 91

dec. contractility => CHF, eventually

RCM presents as CHF

- low-voltage EKG, diminished QRS amplitude

Front 92

amyloid RCM ~~

(2)

Back 92

1. Congo red => bright green

2. poor compliance

Front 93

sarcoid RCM ~~

(4)

Back 93

1. granulomas

2. also in hilar LN's, lungs

3. treat with glucocorticoids

4. better prognosis than amyloid RCM

Front 94

hemochromatic RCM ~~

(1)

Back 94

hemosiderin (iron) accumulates in heart

Front 95

fibroelastic RCM ~~

(1)

Back 95

children <2 y.o.

Front 96

arrhythrogenic RV CM (aka ARVD) =

Back 96

fibrofatty infiltration of RV,

which causes arrhythmias

Front 97

3 pitfalls of the ">50% of thoracic cavity" rule:

Back 97

1. elevated hemidiaphragm

2. narrow ant-post diameter

3. pericardial effusion

Front 98

inc. pulmonary venous pressure on CXR shows:

Back 98

redistribution of flow from the bases of the lung to the apices

Front 99

***CXR should be ordered for a/o presenting with:

(2)

Back 99

chest pain or dyspnea

- can sense PE, pleural effusion

Front 100

the doppler is great for assessing:

Back 100

flow through the valves

Front 101

the trans-esophageal echo is the gold standard for:

Back 101

excluding intrathoracic thrombus

Front 102

2 features of Echo:

Back 102

1. NO risk

2. gold standard for evaluating *valvular* structure and function

Front 103

***echo should be ordered for all pts who present with:

(2)

Back 103

1. HF

2. dyspena of unclear etiology

Front 104

nuclear imaging:

(3)

Back 104

1. uses Thallium or Technetium

2. tracks markers to find *hypo*perfusion

3. *enhances ischemic stress test*

Front 105

cardiac cathetirezation:

(3)

Back 105

1. measures pressure in the cardiac chambers

2. m's blood flow to calculate CO, vascular R

3. ~angiography

Front 106

pulmonary artery wedge pressure:

Back 106

***closely matches LA pressure***

=> *estimates LV EDV/preload*

Front 107

***elevated PWP ~~ ***

Back 107

**LHF** of any sort

Front 108

summary of cath:

(4)

Back 108

1. invasive

2. exposure to Rx and dye

3. expensive

4. gold stand. for assessing filling pressure and CO, finding stenoses

Front 109

MRI should be ordered to characterize:

Back 109

structure/function that's still unclear after echo

Front 110

MRI is the gold stand. for assessing:

Back 110

*cardiac* structure/function

- esp. in congenital heart disease

Front 111

what is used to image a suspected aortic dissection?

Back 111

CT

Front 112

MRI cannot be used in:

Back 112

pts with ICD, pacemaker

Front 113

Ca2+ blockers are contraindicated in:

Back 113

LV (systolic) dysfunction - whenever EF is reduced

Front 114

a cardiac index of 2.2 is:

Back 114

very low and suggests hypoperfusion

Front 115

ADHF is a sudden HF that can:

Back 115

fall under EITHER heart failure,

HFwrEF *or* HFpEF,

Front 116

the same device can serve as both:

Back 116

ICD and CRT => called a biventricular ICD

- but the problems each addresses (a-fib vs. dyssynchrony) are different

Front 117

PV loop: an increase in preload causes:

(3)

Back 117

1. inc. EDV

2. => inc. SV

3. dec. iso-contraction (due to higher volume, pressure nec. to open A3 is reached faster)

Front 118

PV loop: increase in AF causes:

(3)

Back 118

1. LARGE inc. in iso-contraction (due to inc. in Pressure necessary to overcome and push blood out)

2. inc. ESV

3. dec. SV

Front 119

PV loop: increase in Contractility causes:

(4)

Back 119

1. inc. iso-contraction

2. "longer" systole

3. dec. ESV

4. inc. SV

Front 120

how does HTN lead to LHF?

Back 120

if the resulting, necessary hypertrophy becomes too much

Front 121

paroxysmal nocturnal dyspnea ~~

Back 121

hours

- vs. orthopnea, which ~~ minutes

Front 122

HF cells =

Back 122

hemosiderin-laden cells in the *lungs*

Front 123

RAS is activated when:

Back 123

CO is decreased

Front 124

cor pulmonale =

Back 124

RHF due to PHTN

Front 125

Rheumatic fever most commonly affects:

Back 125

the Mitral Valve