Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Med Surg > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Major cause of mortality and morbidity in the US
Over 5 million Americans currently
African Americans are twice as likely to develop
550,000 cases each year

A

heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

broadly describe heart failure

A

Heart pump actually fails
The heart is unable to pump blood in sufficient amounts from the ventricles to meet the body’s metabolic needs
Results in decreased CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

causes of HF

A 
Cardiac defect:
Myocardial infarction
Valve deficiency
Defect outside the heart:
Coronary artery disease
Pulmonary hypertension
Diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

decrease C.O., increased pressure in lungs, DOE, cough, inc. PCWP
Most heart failure begins with failure of this ventricle and progresses to failure of both

A

left sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

backs up from Left, to body, edema, organ congestion, inc. CVP
High output heart failure – caused by increased metabolic needs, septicemia, anemia and hyperthyroidism

A

right sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

treatments for HF

A

O2, meds: diuretics, vasodilators, ACE & Beta blocker, digoxin
Monitor wt gain & activity level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HF can result from:

A 
Ischemic heart disease, MI
1/3 of all MI patients
Chronic HTN
75% of cases
Valve disease
Third most common cause
Cardiomyopathy
Myocarditis
Rheumatoid arthritis, Lupus erythematosis
Substance abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathophysiology of HF

A

Decreased tissue perfusion from poor cardiac output and pulmonary congestion occurs r/t increased pressure in the pulmonary vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

two types of left HF

A

Systolic heart failure

Diastolic Heart Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cardiac output is decreased, fluid backs up into the pulmonary system

A

forward failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Heart can’t contract forcefully to eject enough blood (decreased ejection fraction to <40%), What can cause this??
Preload increases and afterload increases because of peripheral resistance from compensatory mechanisms
Tissue perfusion diminishes and blood accumulates
Forward failure-

A

systolic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Preserved LV function
Left ventricle can’t relax during diastole becomes stiff
Prevents the ventricle from filling with enough blood to maintain the cardiac output
Ejection fraction is >40%, becomes stiffer with time
Usually the result of chronic HTN

A

diastolic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Caused by left ventricular failure, right ventricular MI or pulmonary hypertension
RV can not empty, increased volume and pressure develops in the venous system, peripheral edema results

A

right sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

AHA Stages of Heart Failure

A

Class 1 NYHA- high risk for developing heart failure
Class II NYHA- cardiac structural abnormalities or remodeling who have not developed HF symptoms
Class III NYHA- current or prior symptoms of heart failure
Class IV NYHA- refractory end-stage heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe stimulation of sympathetic NS as a compensatory mechanism

A

Catecholamines, epinephrine and norepinephrine to increase HR and BP- immediate response
Increasing HR causes a decrease in fill time increase preload
Increased SV  increased stretch and Hypertrophy
Arterial vasoconstriction occurs to maintain BP and low C.O. increased afterloadLV overworks and SV may decline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Reduced blood flow to the kidneys causes the RAAS system to activate vasoconstriction and water and sodium retention
Preload and afterload increase
Angiotensin II ventricular remodeling myocyte contractile dysfunction (can’t contract)

A

RAAS system (compensatory mechanism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q 
Immune response r/t heart cell injury
Cytokines, TNF and interleukins IL-1 and 6, these contribute to ventricular remodeling
Natriuretic Peptides (neurohormones) promote vasodilation and diuresis through Na loss in the kidneys
BNP B-type natriuretic peptide released by the ventricles when fluid overload, levels raise dramatically
ADH (vasopressin) levels and Endothelin levels also rise in response to low fluid output and stretch of myocardial fibers worsening HF
A

chemical response (compensatory mechanism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

specific questions to ask regarding signs/symptoms of heart failure

A 
FACES:
Fatigue
Activity intolerance
Chest congestion 
Edema 
Shortness of breath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

visual inspection of assessment

A 
Altered LOC
Respiratory distress
JVD, how do you measure this?? 
Cyanosis
Peripheral edema
Tachypnea with minimal exertion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

palpation during assessment

A

Enlarged, laterally displaced PMI
Thrill may be felt along left sternal border
Palpate abdomen
Ascites
Hepatomegaly
Check for presence of edema in lower extremities
Check peripheral pulses
Check for lower extremity cyanosis
Note ADL’s, can they climb stairs, how far can they walk?
Exertional Dyspnea, Orthopnea and PND (paroxysmal nocturnal dyspnea),

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

auscultation during assessment

A 
S3, why would they have this? 
Mitral murmur
Holosystolic
Heard best at apex
Radiating to axilla
Cardiac rhythm irregularities
A fib / PVC / ventricular tachycardia / v fib
Crackles, wheezes, decreased breath sounds
Cough may be present
Indicative of pulmonary edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

clinical manifestations of left sided failure

A 
Decreased Cardiac Output:
Fatigue
Weakness
Oliguria in day and nocturia at night
Angina
Confusion
Dizziness/tachycardia
Weak pulses and cool extremities
Pulmonary Congestion:
Hacking cough, worse at night
Dyspnea/breathlessness/tachypnea
Crackles/wheezes
Frothy pink sputum
S3 and S4 gallop
23
Q

clinical manifestations in right sided failure

A 
Systemic Congestion
JVD
Enlarged liver and spleen
Anorexia and nausea, why??
Dependent edema
Distended abdomen
Swollen hands and fingers
Polyuria at night
Weight gain
Increased BP at first from volume, then decreased BP from output
24
Q

diagnostic testing for HF

A

ECG, CXR, CBC, UA, serum creatine, albumin, electrolytes

25
Q

Secreted by the ventricular tissue in the heart when ventricular volume and pressure is increased
Sensitive indicator
Can be positive for heart failure when CXR does not indicate a problem

A

B-type Natriuretic peptide

26
Q

Best tool for diagnosing HF

Looks at the pumping action or ejection fraction of the heart muscles

A

echocardiogram

27
Q

congestive heart failure treatment and interventions

A

UNLOAD FAST
Upright position, Nitrates, Lasix, Oxygen, ACE Inhibitors, Digoxin
Fluids (decreased), Afterload (decreased), Sodium restriction, Test (digoxin level, ABGs, K level)

28
Q

standard med therapy for heart failure

A

Standard medication therapy is ACE inhibitors and ARBS

29
Q

Block the effects of Angiotensin II receptors decrease in arterial resistance and decreased blood pressure

A

ARBS

30
Q

Suppress Renin Angiotensin System  prevents conversion of Angiotensin I to Angiotensin II arterial dilation and increased stroke volume

A

ACE Inhibitors

31
Q

Both ACEI s and ARBs block

A

aldosterone which causes patients to lose sodium which in turn will cause the client to lose sodium and water and retain potassium…MONITOR FOR Hyperkalemia!!

32
Q

drugs that Increase the force of myocardial contraction

A

Positive inotropic drugs

33
Q

drugs that increase heart rate

A

Positive chronotropic drugs

34
Q

drugs that Accelerate cardiac conduction

A

Positive dromotropic drugs

35
Q

all the potential drug therapy for HF

A 
ACE inhibitors
Angiotensin II receptor blockers
Beta blockers
Aldosterone antagonists
B-type natriuretic peptides
Phosphodiesterase inhibitors
Cardiac glycosides
36
Q

Prevent sodium and water resorption by inhibiting aldosterone secretion
Diuresis results, which decreases preload, or the left ventricular end-volume, and the work of the heart

A

ACE Inhibitors

37
Q

examples of ace inhibitors

A

lisinopril, enalapril, fosinopril, quinapril, captopril, ramipril, trandolapril, and perindopril

38
Q

Potent vasodilators; decrease systemic vascular resistance (afterload)

A

Angiotensin II Receptor Blockers (ARBs)

39
Q

examples of ARBs

A

valsartan (Diovan), candesartan (Atacand), eprosartan (Teveten), irbesartan (Avapro), telmisartan (Micardis), olmesartan (Benicar), and losartan (Cozaar)

40
Q

work by reducing or blocking sympathetic nervous system stimulation to the heart and the heart’s conduction system
Reduced heart rate, delayed AV node conduction, reduced myocardial contractility, and decreased myocardial automaticity result

A

beta blockers

41
Q

examples of beta blockers

A

metoprolol, carvedilol (Coreg)

42
Q

Potassium-sparing diuretic

Also acts as an aldosterone antagonist, which has been shown to reduce the symptoms of heart failure

A

spironolactone (Aldactone)

43
Q

Selective aldosterone blocker

treats HF

A

eplerenone (Inspra)

44
Q

First drug approved for a specific ethnic group, namely African Americans
treats HF

A

hydralazine/isosorbide dinitrate (BiDil)

45
Q

Beta1-selective vasoactive adrenergic drug

Structurally similar to dopamine

A

dobutamine

46
Q

Used in the intensive care setting as a final effort to treat severe, life-threatening heart failure, often in combination with several other cardiostimulatory medications

A

nesiritide (Natrecor)

47
Q

B-type Natriuretic Peptides:Mechanism of Action

A

Effects include diuresis (urinary fluid loss), natriuresis (urinary sodium loss), and vasodilation
Vasodilating effects on both arteries and veins
Indirectly increases cardiac output
Suppresses renin-angiotensin system

48
Q

B-type Natriuretic Peptides:Adverse Effects

A

Hypotension
Dysrhythmia
Headache
Abdominal pain

49
Q

Work by inhibiting the enzyme phosphodiesterase
Results in:
Positive inotropic response
Vasodilation

A

Phosphodiesterase Inhibitors

50
Q

indications of Phosphodiesterase Inhibitors

A

Short-term management of heart failure
Given when patient does not respond to treatment with digoxin, diuretics, and/or vasodilators
AHA and ACC advise against long-term infusions

51
Q

adverse effects of milrinone

A 
Dysrhythmia
Hypotension
Angina (chest pain)
Hypokalemia
Tremor
Thrombocytopenia
52
Q

No longer used as first-line treatment
Originally obtained from Digitalis plant, foxglove
Digoxin is the prototype
Used in heart failure and to control ventricular response to atrial fibrillation or flutter
Increase myocardial contractility

A

Cardiac Glycosides

53
Q

effects of cardiac glycosides

A

Increased force and velocity of myocardial contraction (without an increase in oxygen consumption)
Reduced heart rate
Decreased automaticity at SA node, decreased AV nodal conduction, and other effects

54
Q

Increased stroke volume
Reduction in heart size during diastole
Decrease in venous BP and vein engorgement
Increase in coronary circulation
Promotion of diuresis because of improved blood circulation
Palliation of exertional and paroxysmal nocturnal dyspnea, cough, and cyanosis

A

effects of cardiac glycosides

Med Surg (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions