Cardio L28 Drug theraoy 4 Heart Failure Flashcards Preview

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Flashcards in Cardio L28 Drug theraoy 4 Heart Failure Deck (53)
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1
Q

→ Chronic heart failure is a syndrome characterised:

A
  • By progressive cardiac dysfunction
  • Breathlessness
  • Tiredness
  • Neuro-hormonal disturbances
  • Oedema
  • Sudden death
2
Q

Chronic Heart Failure

A
  • 2-5% of population affected
  • Increases with age
  • Commonly due to coronary artery disease but can also reflect infection, physical injury and genetics.
  • Has a poor prognosis with a 5 year mortality of 50% rising to 80% in a year for some patients.
3
Q

HF Causes

A

Volume overload
Pressure overload
Loss of muscle
Restricted filling

4
Q

Volume overload

A

Valve regurgitation

5
Q

Pressure overload

A

Systemic hypertension

Outflow obstruction

6
Q

Loss of muscle

A

Post MI: Chronic ischemia
Connective tissue disease
Infection, Poisons (drugs?)

7
Q

Restricted filling

A

Pericardial diseases
Restrictive cardiomyopathy
Tachyarrhythmia

8
Q

Increased Sympathetic activity

Favourable effect
Undesired effect

A

Increased Heart rate and Increased contractility.

Vasoconstriction leads to increased venous return and increased filling,

Arteriolar constriction leads to
After load and increased workload
Therefore increased oxygen consumption

9
Q

Increased RAA
Favourable effect
Undesired effect

A

Salt and water retention and increased VR

Vasoconstriction and increased after load

10
Q

Increased Vasopressin (ADH)
Favourable effect
Undesired effect

A

Salt and water retention and increased VR

Vasoconstriction and increased after load

11
Q

Increased interleukins and TNFalpha
Favourable effect
Undesired effect

A

May have roles in myocyte hypertrophy

Apoptosis

12
Q

Increased endothlin
Favourable effect
Undesired effect

A

Vasoconstriction and increase VR Increased

Afterload

13
Q

Heart Failure:

A
  1. Heart failure is the condition where the heart fails to provide sufficient CO.
  2. Can be the result of genetic predisposition, infection, infarction, valve problems or physical injury
  3. With decreasing contractility the heart will dilate as atrial (R and/ or L) pressures increase…
14
Q

Physiological adaptation: description and achieved by

A
  1. With reduced CO arterial pressure is maintained by increasing TPR (BP = CO x TPR).
    a. Achieved by: increasing sympathetic tone (further increasing cardiac work).
  2. R-A-A vasopressin systems is activated to raise blood volume and filling pressure.
    a. Peripheral and pulmonary oedema will appear.
15
Q

Heart Failure:

A
  1. The rise in RAP serves to dilate the heart which via Frank-Starling should increase CO.
  2. The failing heart does not respond well to stretch so dilates (increasing wall stress) and the patient develops oedema.
  3. Further demands may increase RAP further which can decrease CO
  4. Vicious CYCLE → increasing dilation → decreasing contraction strength.
16
Q

Problems

A

Inadequate tissue perfusion

Volume overload

17
Q

Cardiac remodelling

A

Enlarged ventricles
Spherical shape
Reduced efficiency

18
Q

To improve symptoms

A
  1. Diuretics
  2. Digoxin
  3. ACE inhibitors
19
Q

To improve survival

A
  1. ACE inhibitors
  2. Beta blockers
  3. Spironolacetone
20
Q

Drugs for Heart failure:

A
  1. Diuretics
  2. Vasodilators
    a. Nitrates mono/dinitrate
  3. ACE inhibitors
    a. Catopril, enalopril
  4. Angiotensin II receptors antagonists
    a. Iosartan
  5. Positive inotropic drugs
    a. Cardiac glycosides such as Digoxin
    b. Sympathomimetics such as Dobutamine
    c. (Phosphodisterase inhibitors)
21
Q

Structure and profile of most important digoxins:

slow

A
  • Digitoxin long duration and slow onset (half-life 5-7 days)
  • Lipophilic, good absorption, strong binding and serum proteins.
22
Q

Structure and profile of most important digoxins:

A
  • Digoxin, rapid onset of action and low oral activity (half-life 1-2 dyas)
  • Hydrophilic, low affinity for serum proteins.
23
Q

Site of action and action

A

Na/K ATPase

• Act by inhibiting the action of the Na+/k+ pump

24
Q

Mechanism of action

A

Na/K pump inhibition leads to:

  1. [Na[I and some depolarization
  2. [Na]I and [Ca]I via Na/ca exchngae
  3. [Ca]I SR Ca content via SR pump
  4. SR Ca content SR release via CLCR
  5. Contraction strength
25
Q

Actions

A

Increase force
Increase excitability
Increase AV conduction
Reduced rate

26
Q

Side effects

A
Effective range =1.0-2.5 ng/ml
Toxic range >1.5 ng/ml
GI: related to vagal effects
1.	Anorexia
2.	Abdominal pain
3.	Vomiting
4.	Diarrhoea
Arrhythmias
1.	PVCs
2.	Atrial tachycardias
AV dissociations
27
Q

Transduction Sympathomimetics:
examples
action

A
  1. Milrinone and Amrinone
  2. Increase activity of CAMP by inhibiting cAMP phosphodiesterase. This increases protein kinase A activity – hence ‘transduction sympathomimetic.
  3. Used when other therapies fail.
28
Q

Nirtates: examples

A

GTN (Glycerol trinitrate) see Angina notes

29
Q

Nirtates: action

A

Rapidly metabolized to release NO

30
Q

Nirtates: function

A

Causes relaxation of vascular smooth muscle – arteriolar and venous.
Decrease pre- and after-load.

31
Q

Nirtates:allows

A

VR curve to move down to increase CO when decompensated. Also ease angina.

32
Q

Nirtates: administration

A

Sub-lingual or injection. Only useful in acute cases as adaptation.

33
Q

Nirtates: side effects

A

Headache

Dizzyness

34
Q

Loop agents

A

Furosemide (powerful removal of NA)

35
Q

Thiazide

A

Hydroclorothiazide (mild diuretic)

36
Q

K sparing

A

Amiloride, Spironolacetone (weak)

37
Q

Osmotic

A

Not useful in heart failure due to pulmonary oedema

38
Q

Thiazide effect

A

Mild diuretic effect (<10% filtered Na)

39
Q

Thiazide action site

A

Mainly acts at distal tubule

40
Q

Thiazide action

A

Direct vasodilator action on smooth muscle

41
Q

Thiazide limited because

A

Limited diuresis indicates limited use but potentially good for hypertensives

42
Q

Thiazide side effect

A

K loss

Hypotension

43
Q

loop agents: effect

A

Powerful up to 30% filtered Na

44
Q

Loop agents: useful for

A

Pulmonary and refractory oedema

Kidney failure

45
Q

Loop agents: side effects

A

Ototoxicity
Hypovoleamia
Hypokalemia
Hypomagnesia

46
Q

K sparing agents:

Effect

A

Weak diuresis (<5% filtered Na)

47
Q

K sparing agents:

Useful for

A

Controlling K loss

48
Q

K sparing agents:

Side effects

A

Hyperkalemia

Spironolactone has oestrogen-like effects

49
Q

ACE inhibitors: Example

A

Captopril

Analpril

50
Q

ACE inhibitors: Function

A

Inhibit production of AII:

  1. Inhibit aldosterone production
  2. Vasodilate (inhibits bradykinin breakdown)
51
Q

ACE inhibitors: Useful for

A

Controlling K loss

Hypertension

52
Q

ACE inhibitors: side effects

A

Cough
Hypotension
Hyperkalemia

53
Q

Receptor blockers:

A
Losartan blocks -> the AT1 receptor
•	Does not affect bradykinin (no cough)
•	Reduces BP
•	Better tolerated than ACE inhibitors
•	Side effects:
o	Less vasodilation than ACE inhibitors
o	Birth defects

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