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Cardiovascular System > Heart Failure Treatment > Flashcards

Heart Failure Treatment Flashcards

1
Q

Chronic Heart Failure is a syndrome characterized by (5)

A
  • Progressive cardiac dysfunction
  • Breathlessness
  • Tiredness
  • Neurohormonal disturbances
  • Sudden death
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2
Q

CHF is a state in which___

A

the heart is unable to pump blood at a rate commensurate with the requirements of the tissues or can do so only from high pressures

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3
Q

Types of Heart Failure (2)

A

Systolic

Diastolic

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4
Q

Systolic heart failure

A

Decreased pumping function of the heart which results in fluid back up in the lungs and heart failure

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5
Q

Diastolic Heart Failure

A

Involves a thickened or stuff heart muscle.Heart does not fill with blood properly and results in fluid backup in the lungs and heart failure

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6
Q

Risk Factors for Heart failure (7)

A
  • Coronary artery disease
  • Hypertension- no.1 link
  • Valvular heart disease
  • Alcoholism
  • Infection (viral)
  • Diabetes
  • Congenital heart defects
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7
Q

Number 1 link to heart failure

A

Hypertension

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8
Q

Other factors that increase the risk of heart failure (5)

A 
	Obesity
	Age
	Smoking
	High or low haematocrit level
	Obstructive sleep apnoea
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9
Q

What is the pathological progression of CV Disease

A

Diseases leads to myocardial injury
Myocardial injury triggers neurohormonal stimulation and myocardial toxicity and pathological remodelling
Low ejection fraction produced symptoms such as dyspnoea, fatigue and oedema
Leads to death if not treated

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10
Q

Frank-Starling Law

A

if the muscle of a healthy heart is stretched it will contract with greater force and pump out more blood

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11
Q

How is the Frank-Starling Law lost in a damaged heart (2)

A
  • As circulatory volume increases the heart dilates, the force of contraction weakens and cardiac output drops further
  • Decrease in CO activates the RAAS further
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12
Q

As the damaged heart starts to dilate what happens to the myocytes

A

They undergo hypertrophy and then fibrosis and thus the heart is further weakened

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13
Q

Salt and water excretion and vasodilation and controlled by (3)

A
  • Natriuretic peptide system ANP/BNP
  • EDRF
  • Atrial and Brain Natriuretic peptides
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14
Q

What are the 2 aimes of usual treatment

A

Improve symptoms and survival

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15
Q

What improves symptoms (2)

A

 Diuretics

 Digoxin

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16
Q

What improves symptoms and survival (3)

A

 ACEI/ARB
 Spironolactone
 Valsartan-sacubitril

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17
Q

What treatment improves survival (2)

A

 Beta blockers

 Ivabradine

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18
Q

Symptomatic Treatment (3)

A
  • Inhibition of detrimental neurohormonal adaptions
  • Enhancement of beneficial neurohormonal adaptions
  • Enhancement of cardiac function
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19
Q

Symptomatic treatment examples

A

Loop diuretics

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20
Q

Examples of loop diuretics

A

Furosemide or Bumetanide

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21
Q

Action of Furosemide (4)

A

Remove excess salt and water
Induce diuresis
Inhibit the Na-K-cl transporter in the loop of henle
Works at a low GFR

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22
Q

If someone is resistant to diuretics what do you give them

A

Thiazide diuretics

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23
Q

Adverse drug reaction of thiazide (6)

A 
Dehydration
Hypotension
Hyperkalaemia 
Hyponatraemia
Impaired glucose tolerance
Diabetes
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24
Q

Blocking sympathetic action (4)

A

Carvedilol
Bisoprolol
Metroprolol
Beta blockers

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25
Q

Blocking RAAS activation

A 
ACEI (Ramipril)
Angiotensin antagonist (Valsartan, Losartan)
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26
Q

Blocking effects of aldosterone

A

Spironolactone

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27
Q

Enhancing Beneficial Hormonal Change

A

Neprolysin

28
Q

Action of Neprolysin (2)

A

Prevents metabolism

Enhances ANP/BNP actions

29
Q

Atrial natriuretic and Brain Natriuretic peptides action (2)

A

Potent natriuretic agents and vasodilators

30
Q

Enhancement of cardiac function (2)

A

Digoxin

Vasodilators

31
Q

Action of Digoxin

A

Improves the ability of the heart to pump and so improves cardiac status

32
Q

Action of Vasodilator

A

Hydralazine

Reduces preload and afterload to improve cardiac function (Isosorbide, mono or dinitrate)

33
Q

Furosemide + Aminoglycosides

A

Aural and renal toxicity

34
Q

Furosemide + Lithium

A

Renal toxicity

35
Q

Furosemide + NSAIDs

A

Renal toxicity

36
Q

Furosemide + Antihypertensives

A

Profound hypotension

37
Q

Furosemide + Vancomycin

A

Renal toxicity

38
Q

ACEI examples

A

Ramipril, Enalpril, Lisonopril

39
Q

Action od ACEI (3)

A
  • Completely block angiotensin converting enzyme
  • Prevent the conversion of angiotensin I to II
  • Reduce preload and afterload on the heart
40
Q

Main studies of ACEI (5)

A

CONCENSUS, SOLVD, SAVE, AIRE, ISSIS-4

41
Q

Adverse Drug reactions (6)

A
  • First dose hypotension
  • Cough
  • Angioedema
  • Renal impairment
  • Renal failure
  • Hyperkalaemia
42
Q

ACEI + NSAID

A

Acute renal failure

43
Q

ACEI + Potassium supplements

A

Hyperkalaemia

44
Q

ACEI + Potassium sparing diuretucs

A

Hyperkalaemia

45
Q

When are Angiotensin Receptor Blockers used

A

When the patient is intolerant to AcEI

46
Q

Action of ARB

A

Block the angiotensin II AT1 receptor

47
Q

Major outcome studies involving ARB (3)

A

Elite II, Charm, ValHeft Valiant

48
Q

AT1 receptor is responsible for the activation of (5)

A 
Vasoconstriction
Vascular proliferation
Aldosterone secretion
Cardiac myocyte proliferation
Increased sympathetic tone
49
Q

AT2 receptor is responsible for the activation of (3)

A

Vasodilation
Antiproliferation
Apoptosis

50
Q

Valsartan and Sacubitril are

A

Angiotensin Receptor Neprilysin Inhibitors

51
Q

Action is ARNI

A

stops the breakdown of ANP and BNP by neutral endopeptidases

52
Q

Aldosterone antagonist

A

Spironolactone

53
Q

Action of Spironolactone

A

Potassium sparing diuretic

Inhibits the actions of aldosterone

54
Q

Where does Spironolactone act on

A

Distal Tube

55
Q

What can Aldosterone antagonists be used with (2)

A

Loop diuretics

ACEI

56
Q

Study associated with Aldosterone antagonists and ACEI

A

RALES

57
Q

Beta Blockers

A

Carvedilol
Bisprolol
Metroprolol

58
Q

Action of Beta blockers (4)

A
  • Potentially hazardous method of treating CHF
  • Block the actions of the sympathetic system
  • My precipitate severe deterioration
  • Should be used only when a patient has been stabilised and not during an acute presentation
59
Q

Ivabradine mode of action (3)

A
  • Ivabradine is a specific inhibitor of the of current in the SA node
  • No action on other channels in the heart or vascular system
  • Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function
60
Q

What kind of patients would Ivabradine be useful in? (3)

A

Symptomatic stable chronic HF
Receiving standard therapy including beta blocker
Have HR greater than 70 bpm at rest

61
Q

Positive inotropes

A

Digoxin

62
Q

Action of Digoxin

A

 Increases availability of calcium in the myocyte

63
Q

Side effects of Digoxin (4)

A

 Narrow therapeutic index
 Arrhythmias
 Nausea
 Confusion

64
Q

Anticoagulants

A

Warfarin

65
Q

What leads to thrombus formation and thromboembolic events

A

Dilated ventricle

Cardiovascular System (42 decks)

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