Lecture 7 - Cardiac Disorders Flashcards

(38 cards)

1
Q

HF definition

A

Inability of the heart to maintain enough CO to meet body needs

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2
Q

Pathogenesis of HF

A

Structural or functional abnormalities impair ability of heart to contract, relax, or both

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3
Q

Preload

A

Degree of stretch on heart muscle fibres just before contraction

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4
Q

After load

A

Pressure the heart must work against to eject blood during systole

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5
Q

Ejection fraction

A

% of blood teh heart pumps out each beat as a fraction of how much it filled iwth

Systolic vol/end diastolic vol = EF

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6
Q

Systolic dysfunction is most commonly due to

A

IHD and valve diseases

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7
Q

What is systolic dysfunction

A

Impaired contractility due to loss of cells, fibrosis, or reduced ATP production

Leads to a reduced ejection fraction

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8
Q

Diastolic dysfunction is

A

Impaired myocardial relaxation du ego altered calcium handling or collagen deposition

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9
Q

Ejection fraction in diastolic dysfunction

A

EF may be normal % wise, but the fill is less

If heart fills 50ml and ejects 35, EF = 70%

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10
Q

Causes of diastolic dysfunction

A

Pericardium effusion, IHD, hypertrophic cardiomyopathy

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11
Q

Compensatory mechanisms in HF

A

SNS
Increased preload
Myocardial hypertrophy

Help restore CO, harmful long term

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12
Q

SNS compensatory mechanism

A

NE release -> increase HR and contractility

Venoconstriction -> increase venous return -> increases preload

RAA pathway activation -> increase blood volume

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13
Q

Problems with SNS compensatory mechanism

A

Tachycardia increase o2 use

Cardiac remodeling

Increase after load due to higher SVR

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14
Q

Increased preload compensatory mechanism initiated by (3)

A

Reduced EF, RAA activation, venoconstriction

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15
Q

Frank starling curve

A

Graph that says increasing preload in HF is pointless because no matter how much you increase the preload, stroke volume caps out at about 50

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16
Q

Problems with chronic increase of end diastolic pressure

A

Pulmonary congestion

Stretching of heart muscle increases o2 consumption

17
Q

Myocardial hypertrophy

A

Ventricles undergo hypertrophy in response to increased work/loss of myocytes
- slowest compensatory mechanism

2 types

18
Q

2 types of myocardial hypertrophy

A

Concentric

Eccentric

19
Q

Concentric myocardial hypertrophy

A

Occurs in response to increased pressure work

Heart requires more force to generate pressure

Sarcomeres are added in parallel (thick ass walls)

20
Q

Eccentric myocardial hypertrophy

A

Occurs in response to increased volume work

Pathways are forced open, sarcomeres form in series (line)

Stretched out walls

21
Q

Key point in myocardial hypertrophy

A

Remodeling makes ventricles weaker and eventually leads to decreased function

22
Q

Important factor in driving myocardial hypertrophy

A

Angiotensin 2

Blocking it can slow hypertrophy

23
Q

Which HF is more common

A

Left

Left often leads to right as well

24
Q

When ventricles fail, it caused forward and backward failures

A

Forward
- insufficient pumping and poor CO

Backward
- congestion of blood behind the pumping chamber

25
Etiology of left sided HF
IHD, HTN, valve diseased, myocardial disease
26
Backwards effect of left sided HF
Accumulation of blood within pulmonary circulation, pulmonary edema Caused dyspnea, orthopaedic (lying SOB), nocturnal dyspnea, cough, crackles, etc
27
Forwards effect of left sided HF
Insufficient CO with low O2 and nutrient delivery to peripheral tissues and organs
28
Complications of left sided HF
Increase left atrial pressure leads to atrial dilation Can cause AFIB, stasis and thrombosis
29
Backward effects of left sided HF are all
Lung related
30
Etiology of right sided HF
Most caused by left sided HF Isolated right sided failure mostly due to cor pulmonale
31
Cor pulmonale + how to leads to right sided HF
It is a lung issue Pulmonary disorder = pulmonary HTN = high after load = RV hypertrophy = RV failure
32
Backwards effects of right sided HF
Congestion in systemic circuit System is edema
33
Forward effects of right sided HF
Low output to LV leading to low CO
34
Nutmeg liver
Blood spots due to backup of blood stretching the capillaries in right sided HF
35
HF s/s (acronym)
FACES (fatigue, activity limitation, congestion, edema, SOB)
36
Diagnosis of HF includes
S/S Echocardiography (Chamber size/volume, EF, valve problems) Natriuretic peptide level - synthesized by ventricles in response to fluid overload
37
B type natriuretic peptide levels indicate:
Released by ventricles when fluid vol is high
38
Treatment of HF (goal, methods)
Goal to improve CO and minimize congestive symptoms and cardiac workload Reduce preload (diuretics, ACE) Improve contractility Reduce AG2 effects (drugs like ACE/ARBS) Implantable defibrillators Surgery (Valve replacement)