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316 Pharmacology > Exam 2: Heart failure > Flashcards

Exam 2: Heart failure Flashcards

1
Q

Heart Failure

A

term used to describe a chronic, progressive cardiac dysfunction and pump failure

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2
Q

Heart failure is characterized by

A

Reduced cardiac output
Inadequate perfusion of the tissues
Fluid retention and volume overload

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3
Q

CARDIACT OUTPUT =

A

(Heart rate)(Stroke volume)

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4
Q

Ejection fraction

A

Amount of blood ejected with each beat

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5
Q

Stroke volume I influenced by

A

Contractility
Preload
Afterload

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6
Q

Contractility

A

Force of contraction

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7
Q

Preload

A

Volume (EDV)

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8
Q

Afterload

A

Pressure

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9
Q

Neurohormonal compensatory mechanisms for heart failure

A

Increase sympathetic tone

RASS ACTIVATION

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10
Q

RAAS activation =

A

Role of aldosterone
Non-osmotic vasopressin (ADH) release
Renal fluid retention and expansion of blood volume

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11
Q

Most important predisposing factors of heart failure

A

Ischemic heart failure disease and hypertension

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12
Q

Other risk factors for heart failure

A 
Age 
obesity 
diabetes 
renal failure 
valvular heart disease 
cardiomyopathies 
myocarditis 
congenital heart disease 
excessive alcohol use
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13
Q

Compensatory mechanism eventually become

A

Maladaptive, not good for long term!

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14
Q

Management of heart failure is

A

directed at attenuating the harmful consequences of compensatory mechanisms

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15
Q

Cardiac remodeling =

A

In an attempt to maintain CO, a change in the
SIZE
SHAPE
FUNCTION of heart

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16
Q

Initiation of ventricle dilation, hypertrophy, remodeling (increase collagen formation, fibrosis, changes in myocytes) from cardiac disease processes such as

A
  • unmanaged HTN
  • CAD (Coronary artery disease)
  • Myocardial Infarction
  • Valvular disease
  • Excessive RAAS activation
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17
Q

Changes in myocardium decrease contractility leads to

A

Pump failure

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18
Q

Most causes of heart failure result from dysfunction of

A

Left ventricle

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19
Q

The right ventricle may also be dysfunctional especially in

A

Pulmonary disease

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20
Q

Some conditions cause inadequate perfusion despite

A

Normal or even elevated in cardiac output

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21
Q

Left ventricular heart failure =

A

Inability of the left ventricle to provide adequate blood flow OUT the body

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22
Q

Decrease ability of left ventricle to pump leads to the following clinical manifestations

A

Forwards affects

Backward affects

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23
Q

Forward affects signs and symptoms will reflect

A

Inadequate peripheral perfusion

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24
Q

Backward effects signs and symptoms will reflect

A

Pulmonary congestion

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25
Q

LVHF: Manifestations of inadequate blood flow to the body and increased pressure in the pulmonary circulation :

A 
Dyspnea (cranial symptom and on exertion/exercis intolerance) 
Cough 
Orthopnea 
Paroxysmal nocturnal dyspnea 
Pulmonary crackles 
Weakness, fatigue 
Hypoxia, cyanosis
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26
Q

Right ventricular heart failure

A

Inability of the right ventricle to provide adequate blood flow to the pulmonary circulation

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27
Q

As the pressure in the pulmonary rises, the resistance to right ventricular emptying increases:

A

Increase pressure in pulmonary circulation
Increase resistance to right ventricular emptying
Right ventricular dilation and failure
-Back up in the systemic venous circulation
—- JVD
— Edema
— Hepatosplenomegaly
Fatigue

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28
Q

Drugs used in the treatment of heart failure:

A
  • Cardiac glycoside (digoxin)
  • Phosphodiesterase inhibitors (milrinone)
  • Angiotensin receptor-neprilysin inhibitors (ARNIs)
  • Agents that inhibit RAAS (ace inhibitors- stop the production of A2; ARBS - leads to inhibition of aldosterone release; aldosterone inhibitor)
  • Beat blockers (used in contraindication in HF; currently use B Blockers)
  • Diuretics
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29
Q

Cardiac glycoside:

A

Positive inotropic effects; negative chronotropic and dromotrophic effects
- Decrease neurohormonal effects

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30
Q

Phosphodiesterase inhibitors

A

Cardiotonic - inotropic agents; + inotropic effects and vasodilation
-Decrease preload and after load

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31
Q

Angiotensin receptor-neprilysin inhibitors (ARNIs)

A

Combination of drugs that increase levels of natriuretic peptides and block the effects of angiotensin II

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32
Q

Diuretics

A

Decreased preload!

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33
Q

Decrease in cardiac preload also mean

A

Decrease in volume overload, pulmonary edema, and peripheral edema

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34
Q

Digoxin drug class

A

Cardiac glycoside

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35
Q

Digoxin is a

A

naturally occurring compound that has profound effects on mechanical & electrical properties of the heart

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36
Q

ISMP high alert medication

A

A dangerous drug because its NARROW therapeutic index

37
Q

Digoxin administration

A

PO, IV

38
Q

Initial dose often given as a loading dose

A

Digitalization

39
Q

Digoxin indications

A

Hypertension

dome dysrhythmias

40
Q

MoA digoxin

A

Positive inotropic effect
Negative dromotropic effects
Negative chronotropic effects
Suppresses sympathetic outflow

41
Q

Positive inotropic effect

A

Increase myocardial contractility by promoting calcium accumulation within myocytes

42
Q

Digoxin increases

A

myocardial contractility by inhibiting an enzyme known as sodium, potassium-ATPase

43
Q

Inhibition of Na/KATPase promotes

A

Calcium accumulation within myocytes

44
Q

What happens after calcium is accumulated within the myocytes

A

Calcium augments contractile force by facilitating the interaction of myocardial contractile proteins: ACTIN & MYOSIN

45
Q

Negative dromotropic effect

A

Slows conduction [alters electrical activity of non-contractile tissues (nodal tissues)}

46
Q

Negative chronotropic effect

A

Decrease heart

47
Q

Negative chronotropic effect decrease in heart rate is due to

A

Stimulation of the vagus nerve, which innervates SA node and AV nodes

48
Q

Digoxin therapeutic hemodynamic effects

A

DECREASE IN

  • heart rate
  • fluid retention
  • constriction of arteries and veins
  • peripheral and pulmonary edema
  • blood volume
  • weight
  • preload/afterload
  • size of heart

INCREASE IN

  • Cardiac output
  • Exercise tolerance
49
Q

Adverse effects of digoxin

A

Cardiac dysrhythmias
Bradycardia
NORMAL K+ levels

50
Q

Keep digoxin levels within therapeutic range

A

.5 - 2 ng/ml

– Lower range of .5-.8 ng/ml has been suggested

51
Q

cardiac dysrhythmias for digoxin is common in patients with

A

HYPOkalemia

52
Q

cardiac dysrhythmias for digoxin happens often as a consequence of concurrent use of

A

Diuretics!! may be also caused by vomitting and diarrhea

53
Q

Non-cardiac adverse effects that often indicate digoxin toxicity and development of dysrhythmias

A
  • Nausea, anorexia, vomiting
  • Fatigue
  • Visual disturbances: Blurred vision and color disturbances; yellow tinge to vision or yellow-green halos around dark objects
54
Q

Nursing considerations for digoxin

A
  • Apical pulse for full minute before administration
    -Toxicity may be treated with drugs that counteracts its effects and/or by administering
    digoxin immune Fab
55
Q

Hold digoxin and notify HCP if

A

HR < 60 (or if rhythm change is detected)

56
Q

Patient teaching that is vital to success of digoxin

A
  • Teach patient how to take pulse
  • Inform patient about S/S of developing toxicity and to cal HCP if they occur
  • If K+ supplement, K+ sparing diuretic or ACE inhibitor is part of regimen, take drugs exactly as prescribed
57
Q

Antidote to digoxin toxicity

A

Digoxin immune Fab

58
Q

Administration for digoxin immune fab

A

Continuous IV infusion

59
Q

Digoxin immune fab MoA

A

Digoxin immune-binding fragments bind with molecules of digoxin, leading to RENAL EXCRETION

60
Q

Digoxin immune fab nursing considerations

A

If digoxin was used to treat HF, assess cardiac status, vital signs before, during, and following infusion

  • Monitor K+ as digoxin lowers it
  • If possible suicidal attempt, consider other drug toxicities
61
Q

Milrinone lactate drug class

A

Phosphodiesterase inhibitors

62
Q

Milrinone lactate agent type

A

Cardiotonic-inotropic agent

63
Q

Milrinone lactate MoA

A
  • Increase cAMP in myocardial cells by inhibiting action of phosphodiesterase
  • Increase ventricular force of contraction
  • Vasodilation by exerting a direct relaxant effect on the vascular smooth muscle
64
Q

Milrinone lactate indications

A

Heart failure with those whose symptoms are not controlled with digoxin and other pharmacotherapy

65
Q

Milrinone lactate administation

A

IV

66
Q

Milrinone lactate adverse effects

A 
Most dangerous--> ventricular dysrhythmias 
Hypotension 
Supraventricular dysrhythmias 
Chest pain 
Angina 
Headache 
Thrombocytopenia 
Hypokalemia
67
Q

Milrinone lactate nursing care

A
  • Asses patient for potential renal impairment prior to administer
  • Vital signs, ECG, intake and output, and serum electrolytes throughout administration
68
Q

Sacubitril/valsartan drug class

A

Angiotensin receptor - neprilysin inhibitors (ARNIs_

69
Q

Sacubitril MoA

A

Increases levels of natriuretic peptides through inhibition of enzyme, neprilysin
-Vasodilation and Diuresis

70
Q

Valsartan MoA

A

Vasodilation and reduced production of both aldosterone and vasopressin by blocking angiotensin II receptors

71
Q

Sacubitril/valsartan indication

A

management of Heart failure

72
Q

Sacubitril/valsartan administration

A

IV

73
Q

Sacubitril/valsartan adverse effects

A 
Hypotension 
Hyperkalemia 
Cough (less common than the ACEIs)
Dizziness 
Renal impairment 
Angioedema associated with laryngeal edema can also occur
74
Q

Adjuvant medications used to treat heart failure

A

Diuretics
Beta blockers
ACE inhibitors
ARBs

75
Q

First line medication for symptom improvement/manage fluid overload associated with heart failure

A

diuretics

76
Q

What do beta blockers do

A

Suppress SNS and over time ventricular remodeling regresses, the heart returns toward a normal shape and function and cardiac output increase

77
Q

ARBs promote

A

Vasodilation and decreases aldosterone secretion

78
Q

Different ways to diagnosis heart failure

A 
Blood tests 
CT
Chest x-ray 
Coronary angiogram 
Echocardiogram 
Electrocardiogram 
MRI 
Myocardial biopsy 
Stress tess
79
Q

Blood tests detect

A

Arterial natriuretic peptides

Beta natriuretic peptides

80
Q

Blood levels when heart failure

A

High levels of ANP & BNP

81
Q

Class 1 heart failure

A

Asymptomatic

82
Q

Class 2 heart heart failure

A

Symptomatic with moderate exerction

83
Q

Class 3 heart failure

A

Symptomatic with minimal exertion

84
Q

Class IV heart failure

A

Symptomatic at rest

85
Q

Stage A heart failure

A

High risk for heart failure without structural heart disease or symptoms

86
Q

Stage B heart failure

A

Structural heart disease but without symptoms of heart failure

87
Q

Stage C heart failure

A

Structural heart disease with prior or current symptoms of HF

88
Q

Stage D heart failure

A

Advanced structural heart disease with market symptoms of HF at rest despite maximal medical therapy.
— Specialized interventions required

316 Pharmacology (19 decks)

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