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Cardiovascular System > Heart Failure Treatment > Flashcards

Heart Failure Treatment Flashcards

(65 cards)

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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
Blocking RAAS activation
``` ACEI (Ramipril) Angiotensin antagonist (Valsartan, Losartan) ```
26
Blocking effects of aldosterone
Spironolactone
27
Enhancing Beneficial Hormonal Change
Neprolysin
28
Action of Neprolysin (2)
Prevents metabolism | Enhances ANP/BNP actions
29
Atrial natriuretic and Brain Natriuretic peptides action (2)
Potent natriuretic agents and vasodilators
30
Enhancement of cardiac function (2)
Digoxin | Vasodilators
31
Action of Digoxin
Improves the ability of the heart to pump and so improves cardiac status
32
Action of Vasodilator
Hydralazine | Reduces preload and afterload to improve cardiac function (Isosorbide, mono or dinitrate)
33
Furosemide + Aminoglycosides
Aural and renal toxicity
34
Furosemide + Lithium
Renal toxicity
35
Furosemide + NSAIDs
Renal toxicity
36
Furosemide + Antihypertensives
Profound hypotension
37
Furosemide + Vancomycin
Renal toxicity
38
ACEI examples
Ramipril, Enalpril, Lisonopril
39
Action od ACEI (3)
* Completely block angiotensin converting enzyme * Prevent the conversion of angiotensin I to II * Reduce preload and afterload on the heart
40
Main studies of ACEI (5)
CONCENSUS, SOLVD, SAVE, AIRE, ISSIS-4
41
Adverse Drug reactions (6)
* First dose hypotension * Cough * Angioedema * Renal impairment * Renal failure * Hyperkalaemia
42
ACEI + NSAID
Acute renal failure
43
ACEI + Potassium supplements
Hyperkalaemia
44
ACEI + Potassium sparing diuretucs
Hyperkalaemia
45
When are Angiotensin Receptor Blockers used
When the patient is intolerant to AcEI
46
Action of ARB
Block the angiotensin II AT1 receptor
47
Major outcome studies involving ARB (3)
Elite II, Charm, ValHeft Valiant
48
AT1 receptor is responsible for the activation of (5)
``` Vasoconstriction Vascular proliferation Aldosterone secretion Cardiac myocyte proliferation Increased sympathetic tone ```
49
AT2 receptor is responsible for the activation of (3)
Vasodilation Antiproliferation Apoptosis
50
Valsartan and Sacubitril are
Angiotensin Receptor Neprilysin Inhibitors
51
Action is ARNI
stops the breakdown of ANP and BNP by neutral endopeptidases
52
Aldosterone antagonist
Spironolactone
53
Action of Spironolactone
Potassium sparing diuretic | Inhibits the actions of aldosterone
54
Where does Spironolactone act on
Distal Tube
55
What can Aldosterone antagonists be used with (2)
Loop diuretics | ACEI
56
Study associated with Aldosterone antagonists and ACEI
RALES
57
Beta Blockers
Carvedilol Bisprolol Metroprolol
58
Action of Beta blockers (4)
* 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
Ivabradine mode of action (3)
* 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
What kind of patients would Ivabradine be useful in? (3)
Symptomatic stable chronic HF Receiving standard therapy including beta blocker Have HR greater than 70 bpm at rest
61
Positive inotropes
Digoxin
62
Action of Digoxin
 Increases availability of calcium in the myocyte
63
Side effects of Digoxin (4)
 Narrow therapeutic index  Arrhythmias  Nausea  Confusion
64
Anticoagulants
Warfarin
65
What leads to thrombus formation and thromboembolic events
Dilated ventricle

Cardiovascular System (42 decks)

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