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adn semester 2 > ch 34 HF > Flashcards

ch 34 HF Flashcards

1
Q

is a complex clinical syndrome that develops in response to myocardial insult

A

Heart failure (HF)

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2
Q

results in the inability of the heart to provide sufficient blood to meet the oxygen (O2) needs of tissues and organs. The decreased cardiac output leads to decreased tissue perfusion, impaired gas exchange, fluid volume imbalance, and decreased functional ability.

A

Heart failure (HF)

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3
Q

percentage of the total blood volume in the left ventricle (LV) at the end of diastole that is pumped out of the LV with the next systole is called the l

A

left ventricular ejection fraction (LVEF)

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4
Q

a defect in either ventricular systolic function/LV contraction (heart failure with reduced ejection fraction [HFrEF]) and/or a defect in ventricular diastolic function/filling (heart failure with preserved ejection fraction [HFpEF]).1

A

HF manifestations occur due to

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5
Q

HTN and CAD are the

A

primary risk factors for HF.

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6
Q

congenital abnormalities (e.g., septal defects), infiltrative cardiomyopathies (e.g., sarcoidosis), infections and inflammatory processes (e.g., viral myocarditis), persistent dysrhythmias, and toxins (e.g., alcohol, drug use, chemotherapy).3

A

other causes of HF

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7
Q

(1) preload, (2) afterload, (3) myocardial contractility, and (4) HR

A

CO depends on

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8
Q

(1) primary causes

(2) precipitating causes

A

major causes of HF are divided into 2 subgroups:

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9
Q

often increase the workload of the heart, resulting in an acute condition and decreased heart function.

A

Precipitating causes

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10
Q

(heart muscle cell)

A

cardiomyocyte

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11
Q

responds to such a mutated gene.

A

body’s largest known protein, titin,

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12
Q

impair sarcomere function and disrupt chemical signaling, which negatively affects ventricular structure and stability.

A

Titin mutations

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13
Q

activated in response to myocardial dysfunction, leading to remodeling of myocardial structure and function (Fig. 34.1).

A

Manifestations of HF are the result of neurohormonal compensatory mechanisms

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14
Q
  • Cardiomyopathy (e.g., viral, postpartum, substance use)
  • Congenital heart defects (e.g., ventricular septal defect)
  • CAD, including MI
  • HTN, including hypertensive crisis
  • Hyperthyroidism
  • Myocarditis
  • Pulmonary HTN
  • Rheumatic heart disease
  • Valvular disorders (e.g., mitral stenosis)
A

Primary Causes of Heart Failure

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15
Q

Systolic HF

A

(heart failure with reduced ejection fraction [HFrEF])

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16
Q

diastolic HF

A

(heart failure with preserved ejection fraction [HFpEF]).1

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17
Q

, results either from the inability of the LV to (1) empty adequately during systole or (2) fill adequately during diastole. We can further classify left-sided HF as HFrEF (systolic HF), HFpEF (diastolic HF), or a combination of the two.

A

most common form of HF, left-sided HF

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18
Q

an inability of the heart to pump blood effectively.

A

HFrEF results from

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19
Q

is 55% to 65%

A

Normal LVEF

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20
Q

< 40%

-can be as low as 5% to 10%.

A

Patients with HFrEF generally have an LVEF

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21
Q

impaired contractile function (e.g., MI), increased afterload (e.g., HTN), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disorders).3

A

HFrEF is caused by

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22
Q

Over time, the LV becomes dilated and hypertrophied.

A

LV in HFrEF loses the ability to generate enough pressure to eject blood forward through the aorta.

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23
Q

the inability of the ventricles to relax and fill during diastole.

A

HFpEF results from

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24
Q

(1) signs and symptoms of HF, (2) normal LVEF, and (3) evidence of LV diastolic dysfunction by echocardiography or cardiac catheterization

A

diagnosis of HFpEF is based on (HTN is the primary cause of HFpEF.)

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25
Q

↓ O2-carrying capacity of the blood stimulating ↑ in CO to meet tissue demands, leading to increase in cardiac workload and increase in size of LV

A

anemia

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26
Q

Infection: ↑ metabolic demands and O2 requirements

Valvular dysfunction: causes stenosis or regurgitation

A

Bacterial endocarditis

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27
Q

May ↓ CO and ↑ workload and O2 requirements of myocardial tissue

A

Dysrhythmias

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28
Q

Hypervolemia

A

↑ Preload causing volume overload on the RV

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29
Q

Indirectly predisposes to ↑ atherosclerosis. Severe hypothyroidism decreases myocardial contractility.

A

Hypothyroidism

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30
Q

Have HFpEF more often than men.
• HTN is the most common cause of HF in women.
-Higher risk of ACE inhibitor–related cough than men.

A

women HFpEF

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31
Q
  • Have HFrEF more often than women.
  • Ischemic heart disease (MI, CAD) is the most common cause of HF in men.
  • ACE inhibitor therapy reduces mortality more in asymptomatic.
A

men HFrEF

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32
Q

of any type may have low BP, low CO, and poor renal perfusion

A

ventricular failure vitals

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33
Q

occurs when the right ventricle (RV) does not pump effectively.

A

Right-sided HF

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34
Q

movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention[JVD]).

A

When the RV fails, fluid backs up into the venous system. This causes

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35
Q

is left-sided HF.

A

most common cause of right-sided HF

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36
Q

LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. The RV must work harder to push blood to the pulmonary system. Over time, this increased workload weakens the RV and gradually it fails

A

most common cause of right-sided HF reasoning

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37
Q

(independent of the function of the LV) include RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease)

A

Other causes of right-sided HF

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38
Q

includes both LV and RV dysfunction, the inability of both ventricles to pump effectively. Because of decreased contractility, fluid build-up and systemic venous engorgement occur.

A

Biventricular failure

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39
Q

include (1) neurohormonal responses: renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS); (2) ventricular dilation; and (3) ventricular hypertrophy.

A

2 main main compensatory mechanisms for HF

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40
Q

is augmentation of preload and ventricular contractility to maintain CO.

A

goal of RAAS activation

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41
Q

retention of fluid and sodium

A

RAAS activation promotes

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42
Q

juxtaglomerular apparatus in the kidneys senses decreased renal perfusion from a falling CO. In response, the kidneys release renin, which converts angiotensinogen to angiotensin I. Angiotensin I is next converted to angiotensin II by a converting enzyme made in the lungs. Angiotensin II is a potent vasoconstrictor that stimulates renal water and sodium retention and the release of aldosterone from the adrenal gland. Aldosterone acts in the nephron to stimulate sodium retention and potassium excretion and promoting myocardial fibrosis in the failing heart.

A

pathophysiology of RAAS

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43
Q

stimulated by response to arterial low pressure/under filling via baroreceptor signals

A

ADH regulates water retention by stimulating renal tubular reabsorption.

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44
Q

stiff hard muscles

A

fibrosis

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45
Q

(programmed cell death)

A

myocyte apoptosis

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46
Q

such as cardiac myocyte apoptosis (programmed cell death), hypertrophy, and fibrosis

A

Chronic activation of the RAAS can cause harmful effects

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47
Q

stimulating the SNS to try to maintain

A

Baroreceptors sense low arterial pressure

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48
Q

(epinephrine and norepinephrine)

A

Catecholamines (SNS)

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49
Q

Baroreceptors sense low arterial pressure, stimulating the SNS to try to maintain CO. Catecholamines (epinephrine and norepinephrine) are released. Stimulation of β-adrenergic receptors increases HR (chronotropy) and ventricular contractility (inotropy). Ultimately, chronic SNS stimulation increases myocardial O2 demand on the already weakened heart.

A

SNS compensation process

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50
Q

(RAAS and SNS)

A

neurohormonal responses

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51
Q

high levels of ADH, endothelin, and proinflammatory cytokines. Together, these factors further increase in the heart’s workload, intensify ventricular dysfunction, and force ventricular remodeling.

A

Continuous activation of the neurohormonal responses (RAAS and SNS) in HF leads to

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52
Q

, a vasoconstrictor peptide made by the vascular endothelial cells, is stimulated by hypoxia, ischemia, neurohormones, and inflammatory cytokines.

A

Endothelin

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53
Q

, acting as a negative inotrope. This serves to decrease ventricular contractility in the failing heart.

A

endothelin stimulates contraction in most smooth muscles, it has the opposite effect on the heart

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54
Q

are released by myocytes in response to heart injury (e.g., MI, HF)

A

Proinflammatory cytokines

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55
Q

exerting a negative inotropic effect, causing myocyte hypertrophy and apoptosis.

A

Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress heart function by

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56
Q

in an increase in the heart’s workload, progressive LV dysfunction, myocyte hypertrophy, and ventricular remodeling.

A

High levels of endothelin and proinflammatory cytokines result

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57
Q

is an enlargement of the heart chambers

A

Dilation

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58
Q

occurs when pressure in the heart chambers (usually the LV) is elevated over time.

A

Dilation

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59
Q

, the strength of the heart’s contraction is directly proportional to its diastolic expansion. The implication is that increased preload (a greater influx of blood into the ventricle during diastole) will cause a more forceful contraction

A

Frank-Starling Law

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60
Q

cardiac muscle fibers are overstretched, and further increases in preload no longer increase CO.

A

excessive preload exhausts the Frank-Starling mechanism,

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61
Q

is an adaptive increase in the muscle mass and heart wall thickness as a slow response to overwork and strain

A

Hypertrophy

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62
Q

Initially, the increased contractile power of the muscle fibers leads to an increase in CO and maintains tissue perfusion. Over time, hypertrophic heart muscle has poor contractility, needs more O2 to perform work, has poor coronary artery circulation (tissue becomes ischemic more easily), and is prone to dysrhythmias.

A

Hypertrophy compensation process

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63
Q

occurs over time in response to pressure or volume overload and/or cardiac injury and the subsequent compensatory mechanisms.

A

Ventricular remodeling in HF

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64
Q

is an actual change in the structure (dimensions, mass, shape) of the heart

A

Pathologic ventricular remodeling

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65
Q

neurohormonal (RAAS& SNS), ET (endothelin), and cytokine (pro inflammatory) activation and ventricular adaptations, including dilatation and hypertrophy.

A

ventricular remodelling compensating mechanism include

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66
Q

increased ventricular mass, increased wall tension, increased O2 consumption, and impaired contractility.

A

altered shape of the ventricles eventually leads to

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67
Q
  • become less effective pumps.

- The LVEF further declines due to loss of mechanical advantage from altered ventricular geometry.

A

ventricular remodelling outcome

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68
Q

Increases in angiotensin II, aldosterone (increase bp/preload), and cytokines stimulate collagen (inflammation) synthesis leading to fibrosis (stiff muscle) and further impaired pumping ability.

A

ventricular remodelling declining results

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69
Q

dysrhythmias and sudden cardiac death (SCD).

A

Ventricular remodeling is a risk factor for life-threatening

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70
Q

ACE inhibitors (stop RAAS), β-adrenergic blockers (β-blockers), and aldosterone antagonists.

A

Drugs to prevent or reverse Ventricular remodeling

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71
Q

Natriuretic peptides (atrial natriuretic peptide [ANP] and brain [b-type] natriuretic peptide [BNP]) are

A

hormones made by the heart muscle.

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72
Q

the atria in response to increased blood volume and ventricular wall stretching.

A

ANP is released from

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73
Q

from the ventricles in response to increased blood volume and ventricular wall stretching.

A

BNP is released

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74
Q

have beneficial renal, cardiovascular, and hormonal effects.

A

natriuretic peptides

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75
Q

-Renal effects include: (1) increased glomerular filtration rate and diuresis and (2) excretion of sodium (natriuresis). -Cardiovascular effects include vasodilation and decreased BP. -Hormonal effects include (1) inhibition of aldosterone and renin secretion and (2) interference with ADH release.

A

combined effects of ANP and BNP help to counter the adverse effects of the SNS and RAAS

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76
Q

mortality in HF.

A

. High serum BNP corresponds proportionately with fluid retention and is a predictor of

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77
Q

are counterregulatory substances released from the vascular endothelium in response to the compensatory mechanisms activated in HF.

A

Nitric oxide (NO) and prostaglandin (compensating)

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78
Q

to relax the arterial smooth muscle, resulting in vasodilation and decreased afterload.10

A

NO and prostaglandin work

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79
Q

occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion.

A

Compensated HF

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80
Q

occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.

A

Decompensated HF

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81
Q

that emphasizes the evolution and progression of HF as well as treatment strategies

A

American College of Cardiology Foundation and the American Heart Association (ACCF/AHA) more recently developed a staging system (A–D)

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82
Q

people at risk for developing HF who do not currently

A

have heart disease (stage A)

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83
Q

is an increase (usually sudden) in symptoms of HF with a decrease in functional status, often requiring rapid escalation of therapy and hospital admission

A

Acute decompensated heart failure (ADHF)

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84
Q

pulmonary congestion and volume overload.

A

presentation of ADHF typically includes symptoms and signs related to

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85
Q

through the kidneys that results in sodium and fluid accumulation

A

Neurohormonal activation in Acute decompensated HF leads to impaired regulation of sodium excretion

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86
Q

If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove resulting in interstitial edema

  • Tachypnea develops, and short of breath
  • alveoli edema
  • respiratory acidosis cuz no O2
A

Acute decompensated heart failure (ADHF)

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87
Q

This is an acute, life-threatening situation, in which the lung alveoli become filled with serosanguineous (blood & liquid part of serum) fluid

A

ADHF can manifest as pulmonary edema.

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88
Q

pulmonary edema include acute manifestations of left HF, such as dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. JVD is often present and is the most sensitive and specific sign for elevated LV filling pressures. Coughing, crackles and wheezes, alveolar edema, s3,s4 heard, BP can be high or low depends on severity.

A

ADHF (cause Left HF)

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89
Q

Hypotension indicates severe LV systolic dysfunction and the chance of cardiogenic shock

A

low bp in ADHF (cause left HF) indication

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90
Q

hoarseness may be present because of compression of the recurrent laryngeal nerve from an enlarged LA (Ortner sign).

A

ADHF (cause left HF) indication

91
Q

reduced CO and increased venous pressure, associated with underlying molecular changes that result in the death of cardiac muscle cells

A

Chronic HF is a progressive syndrome characterized by

92
Q

(alternating pulses: strong, weak)

A

Pulsus alternans

93
Q

found if pt has disease with ADHF

A

Frothy, pink-tinged sputum (advanced pulmonary edema) in ADHF

94
Q

manifestation of chronic HF

-caused by increased pulmonary pressures from interstitial and alveolar edema

A

Dyspnea is the most common

95
Q

occurs due to redistribution of fluid from the lower extremities into the lungs while in a supine position

A

Orthopnea

96
Q

is episodic, sudden dyspnea that wakes a patient at night. PND is caused by fluid accumulation in the lungs entering the alveoli while the patient is supine.

A

Paroxysmal nocturnal dyspnea (PND)

97
Q

that is worse in the recumbent position is often associated with pulmonary congestion and can be a sign of HF.
-Other potential causes of cough include gastric conditions, medications (e.g., ACE inhibitors due to increased bradykinin levels), and pulmonary conditions.

A

chronic, nonproductive cough

98
Q

causes chronic, nonproductive cough

A

ACE inhibitors due to increased bradykinin levels (produce vasodilators like endothilem, prostaglandin

99
Q

Tachycardia is an

A

early sign of HF.

100
Q

, or an irregular heartbeat

A

Palpitations aka (occur inHF esp A.fib)

101
Q

, or “skipped beats”

A

fluttering sensation aka

102
Q

dyspnea, lightheadedness, or near syncope if the dysrhythmia further decreases CO.

A

Palpitations may be accompanied by

103
Q

It may occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion).

A

Edema is a common sign of HF.

104
Q

Hypoproteinemia, renal insufficiency, cellulitis, venous stasis, cirrhosis, and certain drugs can cause peripheral edema.

A

not all lower extremity edema is a result of HF. Other include

105
Q

of decreased renal perfusion.

A

Urine output may be decreased because

106
Q

is the tendency to urinate excessively during the night due to increased renal perfusion in the supine position.

A

Nocturia

107
Q

a blue or gray coloring.

A

low CO can result in decreased perfusion to the skin of the extremities resulting in mottling

108
Q

A coolness or clammy feeling to touch can occur with poor perfusion. Because tissue capillary O2 extraction is increased with chronic HF,

A

the skin may appear dusky.

109
Q

The skin can become dry from overdiuresis. It is important to recognize integumentary signs of other conditions, such as venous stasis, peripheral arterial disease, and cellulitis.

A

Chronic edema can result in pigment changes.

110
Q

Hypotension secondary to HF medications and hypovolemia are

A

common causes of neurologic symptoms in chronic HF.

111
Q

occur because of hypoxia to the brain from decreased CO.

A

Cerebral hypoperfusion may

112
Q

, a common confounding condition with chronic HF.

A

Snoring and daytime sleepiness can indicate sleep apnea

113
Q

could be due to psychologic issues, including anxiety or depression, or due to excessive daytime napping. The need to void often with nocturia may disturb the patient’s rest.

A

insomnia

114
Q

associated with HF compounded with CAD

A

Chest pain or angina can be the result of the reduced CO

115
Q

from volume overload

A

Chest pain in HF can also occur due to myocardial stretch

116
Q

with muscle wasting and fat loss.

A

HF advances, the patient may have cardiac cachexia

117
Q

anorexia and nausea

A

Abdominal fullness from ascites and hepatomegaly often causes

118
Q

, fluid between the 2 tissue layers (pleura) that cover the lung and line the chest wall, is a common complication in HF.

A

Pleural effusion

119
Q

Increased capillary hydrostatic pressure in the systemic or pulmonary circulation from HF causes fluid leakage into the pleural space

A

Pleural effusion pathophysiology

120
Q

dyspnea, cough, and chest pain

A

Pleural effusions may result in symptoms of

121
Q

Loss of “atrial kick” during systole may contribute to decreased CO and worsening HF symptoms.

A

AF occurs when numerous sites in the atria fire spontaneously and rapidly, and organized atrial depolarization (contraction) no longer occurs.

122
Q

Thrombi can break loose and form emboli, placing patients at significant risk for stroke.

A

AF promotes thrombus formation within the atria.

123
Q

in the LV.

A

enlarged LV and very low LVEF also increase the risk for thrombus formation

124
Q

(e.g., ventricular tachycardia [VT], ventricular fibrillation [VF]). SCD (sudden loss of cardiac function due to a fatal ventricular tachyarrhythmia), is a major cause of death in the HF population.

A

HF are at risk for dangerous ventricular dysrhythmias

125
Q

Patients with HFrEF

A

are at greatest risk for SCD.

126
Q

who are NYHA Class II or III.

A

implantation of a prophylactic implantable cardioverter-defibrillator (ICD) for patients with an LVEF < 35%,

127
Q

One ventricle may contract prior to the other ventricle, leading to suboptimal ventricular filling (preload), reduced force of ventricular contraction (systole), and severe mitral regurgitation (MR)

A

Ventricular remodeling can lead to dyssynchrony in ventricular contractions.

128
Q

liver becomes congested with venous blood from right HF or ADHF.

A

severe hepatomegaly.

129
Q

hepatic congestion can lead to impaired liver function. Eventually liver cells die, fibrosis occurs, and

A

cirrhosis can develop

130
Q

Neurohormonal activation causes sodium and water retention, worsening HF symptoms and renal function

(kidney dysfunction alone can be risk HF)

A

Reduction in CO results in decreased renal perfusion, decreased glomerular filtration rate, and increased serum creatinine.

131
Q

is chronic kidney insufficiency due to the renal vasoconstriction that often occurs with HF.

A

primary cause of anemia in chronic HF

132
Q

production in the kidney, leading to anemia.

A

vasoconstriction results in reduced erythropoietin

133
Q

information about chamber size and function, LVEF, heart valve function, wall thickness and motion, presence of effusion or thrombus, and intracardiac and pulmonary pressures. This test helps to distinguish between HFrEF and HFpEF.

A

echocardiogram gives

134
Q

of LV failure

A

BNP and N-terminal prohormone of BNP (NT-proBNP) levels correlate positively with the degree

135
Q

including pulmonary embolism, renal failure, and acute coronary syndrome.

A

Increases in BNP or NT-proBNP levels can be caused by conditions other than HF,

136
Q

(1) symptom relief; (2) optimizing volume status; (3) supporting oxygenation, ventilation, CO, and end organ perfusion; (4) identifying and addressing the cause of the ADHF; (5) avoiding complications; (6) providing patient teaching addressing factors that precipitated HF exacerbation; and (7) discharge planning.

A

Goals of therapy for the patient hospitalized with ADHF include

137
Q

CO and pulmonary artery wedge pressure (PAWP) are routinely monitored.

A

pulmonary artery (PA) catheter is placed,

138
Q

is an indirect measurement of LA filling pressure measured from the tip of the PA catheter when inflated in a capillary artery.
-A normal PAWP is 6 to 15 mm Hg.

A

PAWP

139
Q

30 mm Hg

-Therapies are adjusted to maximize CO and reduce PAWP

A

Patients with ADHF may have a PAWP as high as

140
Q

also decreases preload

-used for pulmonary oedema

A

BiPAP

141
Q

noninvasive positive pressure ventilation (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation

A

severe pulmonary edema, the patient may need

142
Q

is an option for the patient with volume overload when diuretics have not been effective

A

Ultrafiltration, or aquapheresis,

143
Q

is a device that increases coronary blood flow to the heart muscle and decreases the heart’s workload through a process called counterpulsation

A

intraaortic balloon pump (IABP)

144
Q

, a biventricular pacemaker, may be considered for patients with ADHF

A

Implantation of CRT

145
Q

because it can decrease pulmonary artery pressures and systemic vascular resistance (SVR), leading to improved CO

A

IABP(intraaortic balloon pump) is useful in hemodynamically unstable patients

146
Q

can help maintain the pumping action of a weakened heart. A VAD is a surgically implanted mechanical pum

A

Ventricular assist devices (VADs)

147
Q

are the first line for treating patients with volume overload

A

Diuretics

148
Q

Decreasing intravascular volume with diuretics reduces volume returning to the LV (preload). This allows for more efficient LV pumping, decreased pulmonary vascular pressures, and improved alveolar gas exchange.

A

Diuretics function

149
Q

IV administration of loop diuretics (e.g., furosemide) by bolus or infusion is preferred.

A

preferred Diuretics

150
Q

ADHF

A

Vasodilators are used to treat

151
Q

that reduces circulating blood volume.

  • NTG reduces preload, slightly reduces afterload (in high doses), and increases myocardial O2 supply. Tolerance often develops with continued IV use, requiring higher doses.
  • monitor BP every 5-10 mins
A

IV nitroglycerin (NTG) is a primary venodilator

152
Q

is a potent IV arterial vasodilator that reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. Complications of therapy include hypotension and, at high doses, thiocyanate (cyanide) toxicity. It is given in an ICU.

A

Sodium nitroprusside (Nitropress)

153
Q

used for short-term treatment of ADHF after a failed response to IV diuretics.1 As a venous and arterial vasodilator, its main effects include a reduction in PAWP and decrease in dyspnea. Because the primary adverse effect is symptomatic hypotension, BP is carefully monitored.

A

IV nesiritide is a recombinant form of BNP

154
Q

, reducing preload and afterload. It is often given in small IV boluses for the dyspnea associated with ADHF

A

Morphine dilates pulmonary and systemic blood vessels

155
Q

or with low CO. Drugs include β-agonists (e.g., dopamine, dobutamine, norepinephrine [Levophed]) and phosphodiesterase inhibitors (milrinone)

A

Inotropic drugs increase myocardial contractility and are used for patients with evidence of cardiogenic shock

156
Q

are used as a short-term treatment of ADHF

A

β-Agonists (inotropic drugs)

157
Q

dilates the renal blood vessels and enhances urine output.

A

dopamine (inotropic)/ last resort

158
Q

that works mainly on the β1-receptors in the heart and does not increase SVR. Effectiveness of inotropes is evaluated by assessing for improved CO, BP, urine output, and reduced filling pressures.

A

Unlike dopamine, dobutamine is a selective β-agonist

159
Q
  • Monitor IV site. Tissue necrosis and sloughing can occur with drug extravasation.
  • High doses may produce ventricular dysrhythmias.
A

Dopamine drug alert

160
Q

has both inotropic and vasodilator properties

A

Milrinone (inotropine-last resort)

161
Q

. Like dopamine and dobutamine, this drug is available only for IV use.
-Adverse effects include dysrhythmias, thrombocytopenia, and hepatotoxicity.

A

Milrinone improves myocardial contractility, increases CO, and reduces BP (decreases afterload)

162
Q

. Digoxin can mildly increase contractility but also increases myocardial O2 consumption. It can optimize heart rate, especially in those with atrial fibrillation.

-Monitor potassium and Mg

A

Digitalis (intro pine) is a weaker positive inotrope that can be added if symptoms persist after other medications have been started

163
Q

(e.g., diuretics, vasodilators, morphine).1

A

last resort drug– use of inotropic therapy only for the short-term management of patients with ADHF who have not responded to conventional drug therapy

164
Q

vasodilators and inotropes.

A

use an infusion pump whenever you are giving IV

165
Q

(1) optimal symptom management, (2) mortality and morbidity benefit, (3) minimizing side effects, and (4) monitoring responses to therapies. Specifically, these therapies treat the underlying cause and contributing factors, maximize CO, improve ventricular function, improve quality of life (QOL), and preserve target organ function.

A

goals of chronic HF therapies include

166
Q

The result of neurohormonal blockade is decreased plasma aldosterone levels, decreased SNS activity, vasodilation, and sodium and water excretion.

A

cornerstone of drug therapy in chronic HF is neurohormonal blockade.

167
Q

for chronic HFrEF.

- reduce afterload and SVR and inhibit the development of ventricular remodeling by inhibiting ventricular hypertrophy.

A

ACE inhibitors are first-line drugs

168
Q

include symptomatic hypotension, intractable cough, hyperkalemia, angioedema (allergic reaction involving edema of the face and airways), and renal insufficiency (when used in high doses). Aging and renal insufficiency slow the metabolism of ACE inhibitors and may lead to increased serum drug level

A

ACE inhibitiors Major side effects

169
Q

Monitor patient for first-dose hypotension (first-dose syncope).
• Skipping doses or discontinuing the drug can result in rebound HTN.

A

Captopril drug alert (ACE)

170
Q

, angiotensin II receptor blockers (ARBs)

A

patients who are unable to tolerate ACE inhibitors take

171
Q
  • prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites.
  • ARBs promote afterload reduction and vasodilation.
  • side effects are similar to those of ACE inhibitors except that ARBs do not typically cause a cough. Angioedema is less common. Monitoring is similar to that for ACE inhibitors.
A

ARBs

172
Q

, an enzyme that degrades natriuretic peptides (destroys BNP- B receptor to contract)

A

neprilysin

173
Q

is a combination of a neprilysin inhibitor (sacubitril) and an ARB (valsartan)

A

Sacubitril/valsartan (Entresto)

174
Q

drug provides dual blockade of the RAAS and the natriuretic peptide system (remodelling of ventricle)

A

Sacubitril/valsartan (Entresto)

175
Q

, inhibits neprilysin, an enzyme that degrades natriuretic peptides.

A

Sacubitril, a recombinant form of BNP (imitation of BNP)

176
Q

allows for more available circulating BNP. This results in decreased SVR, afterload, and CVP and increased natriuresis(excretion of Na in urine)=low BP and diuresis.

A

Sacubitril inhibition

177
Q

in patients meeting criteria with symptomatic HFrEF and reduces death and hospitalization.
- monitored for hypotension, renal insufficiency, and angioedema

A

Sacubitril inhibition is alternative to ACE inhibitors and ARBs

178
Q

are potassium-sparing diuretics that inhibit aldosterone activation

  • prolong survival in patients with HFrEF
  • Use with caution in patients taking digoxin, since hyperkalemia may reduce the effects of digoxin
  • ssess male patients for gynecomastia,
A

Spironolactone (Aldactone) and eplerenone (Inspra)

179
Q

directly block the negative effects of the SNS (e.g., increased HR) on the failing heart

A

β-Blockers

180
Q

These β-blockers may also increase LVEF.

A

Three β-blockers decrease mortality in patients with HFrEF: metoprolol succinate (Toprol XL), bisoprolol (Zebeta), and carvedilol (Coreg).

181
Q

, care must be taken in patients with volume overload

-Major side effects include worsening of HF symptoms, hypotension, fatigue, and bradycardia..

A

because β-blockers can reduce myocardial contractility

182
Q

Overdose can cause profound bradycardia, hypotension, bronchospasm, and cardiogenic shock.
-Abrupt withdrawal may result in sweating, palpitations, and headaches.

A

carvedilol

183
Q

, resulting in a decreased HR. It can decrease hospitalizations in patients with HFrEF who are in sinus rhythm with an HR greater than 70 bpm and have symptoms despite optimal doses of other medications. Monitor patients for bradycardia and lightheadednes

A

Ivabradine selectively inhibits a particular sodium/potassium current in the SA node

184
Q

drug is a fixed combination of the vasodilator hydralazine and isosorbide dinitrate.
-reduce mortality and improve LVEF and exercise tolerance by reducing afterload through blood vessel vasodilation. The drug is specifically effective in blacks with HFrEF already receiving optimal doses of other evidence-based medications

A

Hydralazine/isosorbide dinitrate combination (Bidil)

185
Q

Major side effects include hypotension and headache. Like other nitrates, it should not be used with phosphodiesterase inhibitors, such as sildenafil (Viagra).

A

Hydralazine/isosorbide dinitrate combination (Bidil) drug alert

186
Q

a weak positive inotrope, acts primarily as a neurohormonal modulator that reduces the effects of the SNS and suppresses renin secretion from the kidneys. Low-dose digitalis decreases HF hospitalizations and symptoms in patients who are still symptomatic despite standard HF therapies
- Better outcomes occur with digoxin serum levels of <0.9 ng/ml

A

Digitalis (digoxin),

187
Q

HFrEF and HFpEF.

A

Diuretics reduce symptoms of fluid overload and congestion in both

188
Q

edema, pulmonary venous pressure, and preload

A

Diuretics reduce

189
Q

act on the ascending loop of Henle to promote sodium, chloride, and water excretion

A

Loop diuretics (e.g., furosemide (Lasix) and bumetanide [Bumex])

190
Q

include low serum potassium levels, ototoxicity, and possible allergic reaction in patients sensitive to sulfa-type drugs.

A

Problems in using loop diuretics

191
Q

inhibit sodium reabsorption in the distal tubule, promoting excretion of sodium and water. They also can severely lower potassium levels.

A

Thiazide diuretics (more mild)

192
Q

dehydration, hypotension, orthostasis, renal dysfunction, and electrolyte abnormalities. Diuretic resistance can occur in HF patients, necessitating dosing augmentation (longer) and the addition of different diuretic classes.

A

chronic HF, the lowest effective dose of diuretic should be used. Side effects of diuretics include

193
Q

for primary prevention of SCD in these patients

A

ICD is recommended ( implantable cardiac devices.)

194
Q

implantable cardiac devices. H

A

Patients with HFrEF may benefit from

195
Q

neurohormonal effects and cardiac remodeling can result in dyssynchronous contraction of the LV and RV, contributing to poor ventricular filling and reduced CO

A

In patients with a LVEF <35%,= recommend CRT

196
Q

, an extra pacing lead is placed through the coronary sinus to a coronary vein of the LV. This lead coordinates right and left ventricular contractions

A

With CRT

197
Q

pt symptomatic HFrEF

A

often need both CRT and an ICD

198
Q

remotely monitoring HF patients.

A

mplanted ICD and CRT devices can be used for

199
Q

can be implanted in the pulmonary artery during a right heart catheterization. It can provide information about HR, systolic, diastolic, and mean pulmonary artery pressure. Detection of early hemodynamic and fluid status changes can allow for proactive management to reduce fluid overload, which decreases hospitalizations in patients withHFrEF. 17

A

pulmonary artery sensor

200
Q

2 grams per day

A

sodium intake is restricted to

201
Q

Tell patients to call the HCP about a weight gain of 3 lb (1.4 kg) over 2 days or a 3- to 5-lb (2.3-kg) gain over a week.12

A

weight gain of 3 lb (1.4 kg) over 2 days

202
Q

(1) decrease in symptoms (e.g., shortness of breath, fatigue); (2) decrease in peripheral edema; (3) increase in exercise tolerance; (4) adherence with the treatment plan, including appropriate evidence-based medication and device therapies; and (5) no complications related to HF.

A

overall goals for the patient with HF include

203
Q

with CAD.

A

Coronary revascularization procedures should be considered in patients

204
Q

patients with serious dysrhythmias or conduction disturbances.

A

Antidysrhythmic drugs or pacing therapy may be indicated for

205
Q

(1) HF is a progressive disease; (2) treatment plans are established with QOL goals; (3) symptom management depends to a significant degree on adherence to self-management protocols (e.g., daily weights, diet, exercise, recognizing signs and symptoms of decompensation); and drug and device therapies; (4) precipitating factors, etiologies, and contributing comorbid conditions must be addressed; (5) complex care needs often require care in multiple settings, increasing risk for fragmented care; and (6) support systems are essential to the success of the entire treatment plan.

A

Successful HF care depends on several important principles:

206
Q

(1) chronic inotropic therapy, (2) mechanical circulatory support (MCS) devices, (3) palliative care and hospice that may or may not include ICD deactivation, and (4) heart transplant.

A

Therapeutic options for stage D HF patients include:

207
Q

can be beneficial to carefully selected patients for short-term management, long-term and bridge-to-transplant management, or as destination therapy

A

MCS devices

208
Q

MCS. Short-term MCS include IABP, extracorporeal membrane oxygenation (ECMO), and various continual flow pumps. The limitations of bed rest and the risk for infection and vascular complications prevent long-term use of these devices.

A

Patients who are ineligible for heart transplant may be candidates for lifelong

209
Q

include IABP, extracorporeal membrane oxygenation (ECMO), and various continual flow pumps. The limitations of bed rest and the risk for infection and vascular complications prevent long-term use of these devices.

A

Short-term MCS

210
Q

include LV assist devices (VADs), including percutaneous devices (PVAD) and transplanted devices (LAVDs, BiVADs)

A

Long-term MCS devices

211
Q

long-term support and have become standard care in many heart transplant centers.

  • e heart pump runs via a driveline that exits the abdominal wall and attaches to a system controller with patient specific settings.
  • operate on AC current or batteries
A

VADs provide highly effective

212
Q

(1) unifying the patient, family, and health care team in formulating a plan of care;
(2) aggressive symptom management;
(3) avoiding therapies that are no longer appropriate or effective and may prolong suffering;
(4) integrating emotional and spiritual support for patient and family; and (5) determining when a patient may be ready to consider hospice care.

A

Palliative nursing care of the HF patient emphasizes

213
Q

(1) an HCP certifies that a life expectancy of 6 months or less is expected assuming the disease takes its normal course, (2) the patient has received optimal medical treatment and is not a candidate for further invasive procedures, and (3) the patient is assessed at NYHA Class IV. End-stage HF patients who meet hospice criteria are often referred late or not at all.

A

Patients with advanced CVD are eligible for hospice when

214
Q

(1) difficulties with accurate life expectancy prediction, (2) reluctance to accept a DNR order due to multiple resuscitation survivals and implantable devices, and (3) a lack of patient and family understanding as to the chronic and terminal nature of HF.20,21

A

Challenges in referring these patients to hospice include

215
Q
  • End-stage HF refractory to medical care
  • Severe, decompensated, inoperable, valvular heart disease
  • Recurrent life-threatening dysrhythmias not responsive to maximal interventions, including defibrillators
  • Any other heart abnormalities that severely limit normal function and/or have a mortality risk of more than 50% within 2 years
A

Common Indications for Heart Transplantation

216
Q

Chronologic age over 70 years or physiologic age over 65 years
• Life-threatening illness (e.g., cancer) that will limit survival to <5 years despite therapy
• Advanced cerebral or peripheral vascular disease not amenable to correction
• Active infection, including HIV infection
• Severe pulmonary disease that will likely result in the patient being ventilator-dependent after transplant

A

Absolute Contraindications for Heart Transplantation

217
Q
  • Severe obesity
  • Psychologic impairment
  • Active substance use (e.g., alcohol, drugs, tobacco)
  • Uncontrolled diabetes with vascular and neurologic complications
  • Irreversible liver or kidney dysfunction not explained by HF
  • Evidence of noncompliance with accepted medical practices
  • Lack of social support network that can make long-term commitment for patient’s welfare
  • Unrealistic expectations by the patient or caregiver about transplant, its risks, and its benefits
A

relative Contraindications for Heart Transplantation

218
Q

is the transfer of a healthy donor heart to a patient with a diseased heart.
-The 1-year transplant survival rate is 85% to 90%, while the 3-year survival rate is about 75%

A

Heart transplantation

219
Q

body and heart size and an immunologic assessment. That assessment includes ABO blood type, antibody screen, panel of reactive antibody (PRA) level, and human leukocyte antigen typing.

A

Donor and recipient matching is based on

220
Q

In the biatrial approach, the recipient’s damaged heart is removed at the midatrial level and the donor heart connected at the LA, pulmonary artery, aorta, and RA

A

donor heart is then implanted into the recipient using 1 of 2 approaches.

221
Q

.In the bicaval approach the RA of the recipient’s heart (with the SA node and atrial conduction intact) is preserved and then the donor heart is connected. Cardiopulmonary bypass is needed during the surgical procedure to maintain oxygenation and perfusion to vital organs.

A

2nd approach for heart transplant (. In the bicaval approach)

222
Q

In the first year after transplantation, the major causes of death are infection and acute rejection.

A

post heart transplantation

223
Q

On a long-term basis, immunosuppressive therapy increases the risk for cancers, especially lymphomas, and cardiac vasculopathy (accelerated CAD)

A

Because of the use of immunosuppressive therapy, infection is a primary concern after transplant surgery.

224
Q

on a weekly basis for the first month, monthly for the next 6 months, and yearly thereafter. In this procedure, the HCP inserts a catheter into the jugular vein and moves it into the RV.

A

To detect rejection, an endomyocardial biopsy is done

adn semester 2 (19 decks)

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