Exam 2: Heart failure Flashcards
1
Q
Heart Failure
A
term used to describe a chronic, progressive cardiac dysfunction and pump failure
2
Q
Heart failure is characterized by
A
Reduced cardiac output
Inadequate perfusion of the tissues
Fluid retention and volume overload
3
Q
CARDIACT OUTPUT =
A
(Heart rate)(Stroke volume)
4
Q
Ejection fraction
A
Amount of blood ejected with each beat
5
Q
Stroke volume I influenced by
A
Contractility
Preload
Afterload
6
Q
Contractility
A
Force of contraction
7
Q
Preload
A
Volume (EDV)
8
Q
Afterload
A
Pressure
9
Q
Neurohormonal compensatory mechanisms for heart failure
A
Increase sympathetic tone
RASS ACTIVATION
10
Q
RAAS activation =
A
Role of aldosterone
Non-osmotic vasopressin (ADH) release
Renal fluid retention and expansion of blood volume
11
Q
Most important predisposing factors of heart failure
A
Ischemic heart failure disease and hypertension
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
13
Q
Compensatory mechanism eventually become
A
Maladaptive, not good for long term!
14
Q
Management of heart failure is
A
directed at attenuating the harmful consequences of compensatory mechanisms
15
Q
Cardiac remodeling =
A
In an attempt to maintain CO, a change in the
SIZE
SHAPE
FUNCTION of heart
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
17
Q
Changes in myocardium decrease contractility leads to
A
Pump failure
18
Q
Most causes of heart failure result from dysfunction of
A
Left ventricle
19
Q
The right ventricle may also be dysfunctional especially in
A
Pulmonary disease
20
Q
Some conditions cause inadequate perfusion despite
A
Normal or even elevated in cardiac output
21
Q
Left ventricular heart failure =
A
Inability of the left ventricle to provide adequate blood flow OUT the body
22
Q
Decrease ability of left ventricle to pump leads to the following clinical manifestations
A
Forwards affects
Backward affects
23
Q
Forward affects signs and symptoms will reflect
A
Inadequate peripheral perfusion
24
Q
Backward effects signs and symptoms will reflect
A
Pulmonary congestion
25
LVHF: Manifestations of inadequate blood flow to the body and increased pressure in the pulmonary circulation :
```
Dyspnea (cranial symptom and on exertion/exercis intolerance)
Cough
Orthopnea
Paroxysmal nocturnal dyspnea
Pulmonary crackles
Weakness, fatigue
Hypoxia, cyanosis
```
26
Right ventricular heart failure
Inability of the right ventricle to provide adequate blood flow to the pulmonary circulation
27
As the pressure in the pulmonary rises, the resistance to right ventricular emptying increases:
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
28
Drugs used in the treatment of heart failure:
- 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
29
Cardiac glycoside:
Positive inotropic effects; negative chronotropic and dromotrophic effects
- Decrease neurohormonal effects
30
Phosphodiesterase inhibitors
Cardiotonic - inotropic agents; + inotropic effects and vasodilation
-Decrease preload and after load
31
Angiotensin receptor-neprilysin inhibitors (ARNIs)
Combination of drugs that increase levels of natriuretic peptides and block the effects of angiotensin II
32
Diuretics
Decreased preload!
33
Decrease in cardiac preload also mean
Decrease in volume overload, pulmonary edema, and peripheral edema
34
Digoxin drug class
Cardiac glycoside
35
Digoxin is a
naturally occurring compound that has profound effects on mechanical & electrical properties of the heart
36
ISMP high alert medication
A dangerous drug because its NARROW therapeutic index
37
Digoxin administration
PO, IV
38
Initial dose often given as a loading dose
Digitalization
39
Digoxin indications
Hypertension
| dome dysrhythmias
40
MoA digoxin
Positive inotropic effect
Negative dromotropic effects
Negative chronotropic effects
Suppresses sympathetic outflow
41
Positive inotropic effect
Increase myocardial contractility by promoting calcium accumulation within myocytes
42
Digoxin increases
myocardial contractility by inhibiting an enzyme known as sodium, potassium-ATPase
43
Inhibition of Na/KATPase promotes
Calcium accumulation within myocytes
44
What happens after calcium is accumulated within the myocytes
Calcium augments contractile force by facilitating the interaction of myocardial contractile proteins: ACTIN & MYOSIN
45
Negative dromotropic effect
Slows conduction [alters electrical activity of non-contractile tissues (nodal tissues)}
46
Negative chronotropic effect
Decrease heart
47
Negative chronotropic effect decrease in heart rate is due to
Stimulation of the vagus nerve, which innervates SA node and AV nodes
48
Digoxin therapeutic hemodynamic effects
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
Adverse effects of digoxin
Cardiac dysrhythmias
Bradycardia
NORMAL K+ levels
50
Keep digoxin levels within therapeutic range
.5 - 2 ng/ml
| -- Lower range of .5-.8 ng/ml has been suggested
51
cardiac dysrhythmias for digoxin is common in patients with
HYPOkalemia
52
cardiac dysrhythmias for digoxin happens often as a consequence of concurrent use of
Diuretics!! may be also caused by vomitting and diarrhea
53
Non-cardiac adverse effects that often indicate digoxin toxicity and development of dysrhythmias
- Nausea, anorexia, vomiting
- Fatigue
- Visual disturbances: Blurred vision and color disturbances; yellow tinge to vision or yellow-green halos around dark objects
54
Nursing considerations for digoxin
- 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
Hold digoxin and notify HCP if
HR < 60 (or if rhythm change is detected)
56
Patient teaching that is vital to success of digoxin
- 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
Antidote to digoxin toxicity
Digoxin immune Fab
58
Administration for digoxin immune fab
Continuous IV infusion
59
Digoxin immune fab MoA
Digoxin immune-binding fragments bind with molecules of digoxin, leading to RENAL EXCRETION
60
Digoxin immune fab nursing considerations
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
Milrinone lactate drug class
Phosphodiesterase inhibitors
62
Milrinone lactate agent type
Cardiotonic-inotropic agent
63
Milrinone lactate MoA
- 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
Milrinone lactate indications
Heart failure with those whose symptoms are not controlled with digoxin and other pharmacotherapy
65
Milrinone lactate administation
IV
66
Milrinone lactate adverse effects
```
Most dangerous--> ventricular dysrhythmias
Hypotension
Supraventricular dysrhythmias
Chest pain
Angina
Headache
Thrombocytopenia
Hypokalemia
```
67
Milrinone lactate nursing care
- Asses patient for potential renal impairment prior to administer
- Vital signs, ECG, intake and output, and serum electrolytes throughout administration
68
Sacubitril/valsartan drug class
Angiotensin receptor - neprilysin inhibitors (ARNIs_
69
Sacubitril MoA
Increases levels of natriuretic peptides through inhibition of enzyme, neprilysin
-Vasodilation and Diuresis
70
Valsartan MoA
Vasodilation and reduced production of both aldosterone and vasopressin by blocking angiotensin II receptors
71
Sacubitril/valsartan indication
management of Heart failure
72
Sacubitril/valsartan administration
IV
73
Sacubitril/valsartan adverse effects
```
Hypotension
Hyperkalemia
Cough (less common than the ACEIs)
Dizziness
Renal impairment
Angioedema associated with laryngeal edema can also occur
```
74
Adjuvant medications used to treat heart failure
Diuretics
Beta blockers
ACE inhibitors
ARBs
75
First line medication for symptom improvement/manage fluid overload associated with heart failure
diuretics
76
What do beta blockers do
Suppress SNS and over time ventricular remodeling regresses, the heart returns toward a normal shape and function and cardiac output increase
77
ARBs promote
Vasodilation and decreases aldosterone secretion
78
Different ways to diagnosis heart failure
```
Blood tests
CT
Chest x-ray
Coronary angiogram
Echocardiogram
Electrocardiogram
MRI
Myocardial biopsy
Stress tess
```
79
Blood tests detect
Arterial natriuretic peptides
| Beta natriuretic peptides
80
Blood levels when heart failure
High levels of ANP & BNP
81
Class 1 heart failure
Asymptomatic
82
Class 2 heart heart failure
Symptomatic with moderate exerction
83
Class 3 heart failure
Symptomatic with minimal exertion
84
Class IV heart failure
Symptomatic at rest
85
Stage A heart failure
High risk for heart failure without structural heart disease or symptoms
86
Stage B heart failure
Structural heart disease but without symptoms of heart failure
87
Stage C heart failure
Structural heart disease with prior or current symptoms of HF
88
Stage D heart failure
Advanced structural heart disease with market symptoms of HF at rest despite maximal medical therapy.
--- Specialized interventions required
