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Physiology of Disease > Heart Failure with Reduced Ejection Fraction > Flashcards

Heart Failure with Reduced Ejection Fraction Flashcards

1
Q

what does preload improve?

A

Cardiac contractions

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2
Q

What is the main determiner of filling volumne?

A

How much pressure is on venous side of the heart

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3
Q

What is the cardiac function curve?

A

CO dependent on CVP

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4
Q

What is the vascular function curve?

A

CVP dependent on CO

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5
Q

What are 4 common causes of LVF?

A

chronic ischemic heart disease
arterial hypertension
cardiomyopathy
valve dysfunctions

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6
Q

What are 2 common causes of RVF?

A

pulmonary hypertension
left ventricular failure

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7
Q

What are symptoms of LVF?

A

dyspnoea
pulmonary fluid retention

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8
Q

What causes pulmonary fluid retention in LVF?

A

oedema, increase pulmonary venous & capillary pressure due to increased transcapillary filtration of fluid into interstitial tissue of lung

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9
Q

What are symptoms of RVF?

A

Swelling of feet, ankles & legs
fluid in abdominal cavity

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10
Q

Why does subcutaenous oedema worsen in the day?

A

increased CVP & salt & water retention lead to increased transcapillary filtration of fluid & retention of fluid

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11
Q

What is HFREF characterized by?

A

Reduction in myocardial contractility

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12
Q

How do you calculate ejection fraction?

A

stroke volume/EDV x 100

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13
Q

What is the reduction in myocardial contractility compensated by?

A

Increased preload

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14
Q

What 3 things increase preload?

A

Reduced ejection fraction
increased sympathetic activity -> increase venous tone
increased salt & water retention (RASS)

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15
Q

What does chronically increased preload lead to?

A

distension of heart resulting in further reduced cardiac function

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16
Q

What happens to CO in decompensated HF?

A

CO is permanently reduced

17
Q

What does CO fail to increase normally during HF during exercise?

A

reduced SV due to reduced contractility
impaired response to sympathetic stimulation

18
Q

What is Ca2+ cycling?

A

plasma membrane of cardiac myocytes is invaginated into T-tubules which contact SR (main store of Ca2+)

19
Q

What happens in contraction coupling in failing cardiac myocytes?

A

Reduced Ca2+ pumping into DR by SERCA
impaired/leaky SR Ca2+ release channels
fall in sensitivity of troponin
upregulation of Na+Ca2+ exchangers
downregulation of K= channels
impaired ATP supply
switch from FA to glucose as chief energy substrate

20
Q

What does impaired conduction & excitation issues cause?

A

Arrhythmias

21
Q

How does the sympathetic system enhance cardiac muscle contractility?

A

Through cAMP signaling pathways -> stimulate VG Ca2+ channels through phosphorylation of channel inhibitor protein Rad

22
Q

Which NT affects cAMP?

A

Noradrenaline

23
Q

What facilitates communication between receptor and specific targets like PLN/SERCA?

A

B1 adrenoreceptor-cAMP microdomain in subcellular compartments

24
Q

What part of cAMP signaling gets disrupted in HF?

A

Subcellular compartment -> loss of PDE type 4

25
Q

What degrades cAMP?

A

PDEs

26
Q

What happens when cAMP microdomain is disrupted?

A

Reduced responsiveness to receptor activation
reduced PKA activation
loss of regulation of downstream targets like PLN & SERCA
expression of cardiac beta1 adrenoreceptors is downregulated

27
Q

How does the downregulation of beta1 signalling be protective?

A

Failing heart prevented from increasing workload

28
Q

What are the main therapeutic goals in HF?

A

reduce cardiac work & O2 demand
improve SV by reducing arterial BP -> reduce after load
improved mechanical efficiency -> reduce dilatation
reduce cardiac congestion/oedema
prevent arrythmias
improve cardiac contractility

29
Q

What are 4 drugs used to treat HF?

A

ACE inhibitors (captopril) & angiotensin blockers (Iosartan) -> reduce RAAS
diuretics (flurosemide)
beta1-adrenoreceptor blockers
beta1 adrenoreceptor agonists (dopamine) -> only short term emergencies

Physiology of Disease (15 decks)

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