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
What degrades cAMP?
PDEs
26
What happens when cAMP microdomain is disrupted?
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
How does the downregulation of beta1 signalling be protective?
Failing heart prevented from increasing workload
28
What are the main therapeutic goals in HF?
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
What are 4 drugs used to treat HF?
ACE inhibitors (captopril) & angiotensin blockers (Iosartan) -> reduce RAAS diuretics (flurosemide) beta1-adrenoreceptor blockers beta1 adrenoreceptor agonists (dopamine) -> only short term emergencies