Cardio Lecture 17--Pathophysiology Of Heart Failure

Front 1

What two big picture events lead to cardiac failure?

Back 1

Acute load followed by a compensatory mechanism(like dilation)

Front 2

What is systolic HF?

Back 2

inability of heart to contract that results in a decreased EF from the weak ventricle and may lead to diastolic dysfunction

Front 3

What is diastolic HF?

Back 3

Inability of heart to relax--EF is still normal even though the ventricle is stiff and unable to relax properly

Front 4

On what level does hypertrophy of the heart occur?

Back 4

cellular level, extracellular matrix level, and chamber as a whole

Front 5

What causes eccentric hypertrophy vs. concentric hypertrophy?

Back 5

Volume overload(systolic HF)--pressure overload(hypertension and aortic stenosis)

Front 6

What does it look like on the cellular level when Systolic HF or Eccentric LVH occurs?

Back 6

Cell is longer and thinner than usual and collagen weave is lost--the transmission of force between cells is impaired

Front 7

What does it look like on the cellular level when systolic HF or Eccentric LVH occurs?

Back 7

muscle is big, cells are big, and there is a lot of collagen

Front 8

What mediates the changes in heart tissue in eccentric and concentric LVH? What activates these things?

Back 8

Metalloproteinases--Endothelins, Angiotensin, cytokines likee TNF-Alpha, oxidative stress, and catecholamines

Front 9

What hemodynamic alterations are made in the case of LV dystfunction?

Back 9

Increased skeletal and renal blood flow, Na retention, edema, congestion, and exercise intolerance

Front 10

A problem with systolic function will alter ______. A problem with diastolic function will alter _____. (PV curve)

Back 10

ESPVR = systolic function problem
EDPVR = diastolic function problem

Front 11

What are the compensatory long term and short term mechanisms for HF?

Back 11

Short term = volume expansion, vasoconstriction, and vascular redistribution
Long term = remodeling

Front 12

See slide--The Road to Failure

Back 12

do it

Front 13

Injury to the heart activates what neurohormonal systems?

Back 13

Renin/Angiotensin, SNS--leads to peripheral vascular constriction and hemodynamic interactions as well as progressive dilatation--then more Renin/Angiotensin is activated

Front 14

Blocking what two major neurohormonal responses to HF leads to a benefit?

Back 14

Norepinephrine and Angiotensin II

Front 15

Which receptor is causing all the bad effects of the Renin/A System?

Back 15

AT1 receptor--use an ACE inhibitor

Front 16

A failing heart shows what Alpha Beta ratio?

Back 16

50B1:25B2:25A1--there should be way more B1

Front 17

What are the effects of ANP in the system?

Back 17

Decreased aldosterone and renal function, decreased effects of Angiotensin II and endothelin; Increased renal blood flow and natiuresis

Front 18

Does blocking endothelin do anything for HF patients?

Back 18

NO

Front 19

What can take a patient from compensated to decompensated?

Back 19

Increased metabolic demands, increased volume, increased afterload, impaired contractility, withdrawal of meds, slow heart rate

Front 20

How are heart failure patients treated today?

Back 20

Block neurohormonal stimulation with beta blockers, use ANP or vasodilators to help the heart, diuretics for sodium retention, anti-arrhythmics and pacemakers for rhythms--all of this has nothing to do with the pathophys...just treats the symptoms

Front 21

Look at the scenarios

Back 21

Do it