ch 34 HF Flashcards
1
Q
is a complex clinical syndrome that develops in response to myocardial insult
A
Heart failure (HF)
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)
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)
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
5
Q
HTN and CAD are the
A
primary risk factors for HF.
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
7
Q
(1) preload, (2) afterload, (3) myocardial contractility, and (4) HR
A
CO depends on
8
Q
(1) primary causes
(2) precipitating causes
A
major causes of HF are divided into 2 subgroups:
9
Q
often increase the workload of the heart, resulting in an acute condition and decreased heart function.
A
Precipitating causes
10
Q
(heart muscle cell)
A
cardiomyocyte
11
Q
responds to such a mutated gene.
A
body’s largest known protein, titin,
12
Q
impair sarcomere function and disrupt chemical signaling, which negatively affects ventricular structure and stability.
A
Titin mutations
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
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
15
Q
Systolic HF
A
(heart failure with reduced ejection fraction [HFrEF])
16
Q
diastolic HF
A
(heart failure with preserved ejection fraction [HFpEF]).1
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
18
Q
an inability of the heart to pump blood effectively.
A
HFrEF results from
19
Q
is 55% to 65%
A
Normal LVEF
20
Q
< 40%
-can be as low as 5% to 10%.
A
Patients with HFrEF generally have an LVEF
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
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.
23
Q
the inability of the ventricles to relax and fill during diastole.
A
HFpEF results from
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.)
25
↓ 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
anemia
26
Infection: ↑ metabolic demands and O2 requirements
Valvular dysfunction: causes stenosis or regurgitation
Bacterial endocarditis
27
May ↓ CO and ↑ workload and O2 requirements of myocardial tissue
Dysrhythmias
28
Hypervolemia
↑ Preload causing volume overload on the RV
29
Indirectly predisposes to ↑ atherosclerosis. Severe hypothyroidism decreases myocardial contractility.
Hypothyroidism
30
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.
women HFpEF
31
* 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.
men HFrEF
32
of any type may have low BP, low CO, and poor renal perfusion
ventricular failure vitals
33
occurs when the right ventricle (RV) does not pump effectively.
Right-sided HF
34
movement of fluid into the tissues and organs (e.g., peripheral edema, abdominal ascites, hepatomegaly, jugular venous distention [JVD]).
When the RV fails, fluid backs up into the venous system. This causes
35
is left-sided HF.
most common cause of right-sided HF
36
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
most common cause of right-sided HF reasoning
37
(independent of the function of the LV) include RV infarction, pulmonary embolism, and cor pulmonale (RV dilation and hypertrophy caused by pulmonary disease)
Other causes of right-sided HF
38
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.
Biventricular failure
39
include (1) neurohormonal responses: renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system (SNS); (2) ventricular dilation; and (3) ventricular hypertrophy.
2 main main compensatory mechanisms for HF
40
is augmentation of preload and ventricular contractility to maintain CO.
goal of RAAS activation
41
retention of fluid and sodium
RAAS activation promotes
42
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.
pathophysiology of RAAS
43
stimulated by response to arterial low pressure/under filling via baroreceptor signals
ADH regulates water retention by stimulating renal tubular reabsorption.
44
stiff hard muscles
fibrosis
45
(programmed cell death)
myocyte apoptosis
46
such as cardiac myocyte apoptosis (programmed cell death), hypertrophy, and fibrosis
Chronic activation of the RAAS can cause harmful effects
47
stimulating the SNS to try to maintain
Baroreceptors sense low arterial pressure
48
(epinephrine and norepinephrine)
Catecholamines (SNS)
49
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.
SNS compensation process
50
(RAAS and SNS)
neurohormonal responses
51
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.
Continuous activation of the neurohormonal responses (RAAS and SNS) in HF leads to
52
, a vasoconstrictor peptide made by the vascular endothelial cells, is stimulated by hypoxia, ischemia, neurohormones, and inflammatory cytokines.
Endothelin
53
, acting as a negative inotrope. This serves to decrease ventricular contractility in the failing heart.
endothelin stimulates contraction in most smooth muscles, it has the opposite effect on the heart
54
are released by myocytes in response to heart injury (e.g., MI, HF)
Proinflammatory cytokines
55
exerting a negative inotropic effect, causing myocyte hypertrophy and apoptosis.
Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress heart function by
56
in an increase in the heart’s workload, progressive LV dysfunction, myocyte hypertrophy, and ventricular remodeling.
High levels of endothelin and proinflammatory cytokines result
57
is an enlargement of the heart chambers
Dilation
58
occurs when pressure in the heart chambers (usually the LV) is elevated over time.
Dilation
59
, 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
Frank-Starling Law
60
cardiac muscle fibers are overstretched, and further increases in preload no longer increase CO.
excessive preload exhausts the Frank-Starling mechanism,
61
is an adaptive increase in the muscle mass and heart wall thickness as a slow response to overwork and strain
Hypertrophy
62
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.
Hypertrophy compensation process
63
occurs over time in response to pressure or volume overload and/or cardiac injury and the subsequent compensatory mechanisms.
Ventricular remodeling in HF
64
is an actual change in the structure (dimensions, mass, shape) of the heart
Pathologic ventricular remodeling
65
neurohormonal (RAAS& SNS), ET (endothelin), and cytokine (pro inflammatory) activation and ventricular adaptations, including dilatation and hypertrophy.
ventricular remodelling compensating mechanism include
66
increased ventricular mass, increased wall tension, increased O2 consumption, and impaired contractility.
altered shape of the ventricles eventually leads to
67
- become less effective pumps.
| - The LVEF further declines due to loss of mechanical advantage from altered ventricular geometry.
ventricular remodelling outcome
68
Increases in angiotensin II, aldosterone (increase bp/preload), and cytokines stimulate collagen (inflammation) synthesis leading to fibrosis (stiff muscle) and further impaired pumping ability.
ventricular remodelling declining results
69
dysrhythmias and sudden cardiac death (SCD).
Ventricular remodeling is a risk factor for life-threatening
70
ACE inhibitors (stop RAAS), β-adrenergic blockers (β-blockers), and aldosterone antagonists.
Drugs to prevent or reverse Ventricular remodeling
71
Natriuretic peptides (atrial natriuretic peptide [ANP] and brain [b-type] natriuretic peptide [BNP]) are
hormones made by the heart muscle.
72
the atria in response to increased blood volume and ventricular wall stretching.
ANP is released from
73
from the ventricles in response to increased blood volume and ventricular wall stretching.
BNP is released
74
have beneficial renal, cardiovascular, and hormonal effects.
natriuretic peptides
75
-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.
combined effects of ANP and BNP help to counter the adverse effects of the SNS and RAAS
76
mortality in HF.
. High serum BNP corresponds proportionately with fluid retention and is a predictor of
77
are counterregulatory substances released from the vascular endothelium in response to the compensatory mechanisms activated in HF.
Nitric oxide (NO) and prostaglandin (compensating)
78
to relax the arterial smooth muscle, resulting in vasodilation and decreased afterload.10
NO and prostaglandin work
79
occurs when compensatory mechanisms succeed in maintaining an adequate CO that is needed for tissue perfusion.
Compensated HF
80
occurs when these mechanisms can no longer maintain adequate CO and inadequate tissue perfusion results.
Decompensated HF
81
that emphasizes the evolution and progression of HF as well as treatment strategies
American College of Cardiology Foundation and the American Heart Association (ACCF/AHA) more recently developed a staging system (A–D)
82
people at risk for developing HF who do not currently
have heart disease (stage A)
83
is an increase (usually sudden) in symptoms of HF with a decrease in functional status, often requiring rapid escalation of therapy and hospital admission
Acute decompensated heart failure (ADHF)
84
pulmonary congestion and volume overload.
presentation of ADHF typically includes symptoms and signs related to
85
through the kidneys that results in sodium and fluid accumulation
Neurohormonal activation in Acute decompensated HF leads to impaired regulation of sodium excretion
86
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
Acute decompensated heart failure (ADHF)
87
This is an acute, life-threatening situation, in which the lung alveoli become filled with serosanguineous (blood & liquid part of serum) fluid
ADHF can manifest as pulmonary edema.
88
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.
ADHF (cause Left HF)
89
Hypotension indicates severe LV systolic dysfunction and the chance of cardiogenic shock
low bp in ADHF (cause left HF) indication
90
hoarseness may be present because of compression of the recurrent laryngeal nerve from an enlarged LA (Ortner sign).
ADHF (cause left HF) indication
91
reduced CO and increased venous pressure, associated with underlying molecular changes that result in the death of cardiac muscle cells
Chronic HF is a progressive syndrome characterized by
92
(alternating pulses: strong, weak)
Pulsus alternans
93
found if pt has disease with ADHF
Frothy, pink-tinged sputum (advanced pulmonary edema) in ADHF
94
manifestation of chronic HF
| -caused by increased pulmonary pressures from interstitial and alveolar edema
Dyspnea is the most common
95
occurs due to redistribution of fluid from the lower extremities into the lungs while in a supine position
Orthopnea
96
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.
Paroxysmal nocturnal dyspnea (PND)
97
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.
chronic, nonproductive cough
98
causes chronic, nonproductive cough
ACE inhibitors due to increased bradykinin levels (produce vasodilators like endothilem, prostaglandin
99
Tachycardia is an
early sign of HF.
100
, or an irregular heartbeat
Palpitations aka (occur inHF esp A.fib)
101
, or “skipped beats”
fluttering sensation aka
102
dyspnea, lightheadedness, or near syncope if the dysrhythmia further decreases CO.
Palpitations may be accompanied by
103
It may occur in dependent body areas (peripheral edema), liver (hepatomegaly), abdominal cavity (ascites), and lungs (pulmonary edema and pleural effusion).
Edema is a common sign of HF.
104
Hypoproteinemia, renal insufficiency, cellulitis, venous stasis, cirrhosis, and certain drugs can cause peripheral edema.
not all lower extremity edema is a result of HF. Other include
105
of decreased renal perfusion.
Urine output may be decreased because
106
is the tendency to urinate excessively during the night due to increased renal perfusion in the supine position.
Nocturia
107
a blue or gray coloring.
low CO can result in decreased perfusion to the skin of the extremities resulting in mottling
108
A coolness or clammy feeling to touch can occur with poor perfusion. Because tissue capillary O2 extraction is increased with chronic HF,
the skin may appear dusky.
109
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.
Chronic edema can result in pigment changes.
110
Hypotension secondary to HF medications and hypovolemia are
common causes of neurologic symptoms in chronic HF.
111
occur because of hypoxia to the brain from decreased CO.
Cerebral hypoperfusion may
112
, a common confounding condition with chronic HF.
Snoring and daytime sleepiness can indicate sleep apnea
113
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.
insomnia
114
associated with HF compounded with CAD
Chest pain or angina can be the result of the reduced CO
115
from volume overload
Chest pain in HF can also occur due to myocardial stretch
116
with muscle wasting and fat loss.
HF advances, the patient may have cardiac cachexia
117
anorexia and nausea
Abdominal fullness from ascites and hepatomegaly often causes
118
, fluid between the 2 tissue layers (pleura) that cover the lung and line the chest wall, is a common complication in HF.
Pleural effusion
119
Increased capillary hydrostatic pressure in the systemic or pulmonary circulation from HF causes fluid leakage into the pleural space
Pleural effusion pathophysiology
120
dyspnea, cough, and chest pain
Pleural effusions may result in symptoms of
121
Loss of “atrial kick” during systole may contribute to decreased CO and worsening HF symptoms.
AF occurs when numerous sites in the atria fire spontaneously and rapidly, and organized atrial depolarization (contraction) no longer occurs.
122
Thrombi can break loose and form emboli, placing patients at significant risk for stroke.
AF promotes thrombus formation within the atria.
123
in the LV.
enlarged LV and very low LVEF also increase the risk for thrombus formation
124
(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.
HF are at risk for dangerous ventricular dysrhythmias
125
Patients with HFrEF
are at greatest risk for SCD.
126
who are NYHA Class II or III.
implantation of a prophylactic implantable cardioverter-defibrillator (ICD) for patients with an LVEF < 35%,
127
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)
Ventricular remodeling can lead to dyssynchrony in ventricular contractions.
128
liver becomes congested with venous blood from right HF or ADHF.
severe hepatomegaly.
129
hepatic congestion can lead to impaired liver function. Eventually liver cells die, fibrosis occurs, and
cirrhosis can develop
130
Neurohormonal activation causes sodium and water retention, worsening HF symptoms and renal function
(kidney dysfunction alone can be risk HF)
Reduction in CO results in decreased renal perfusion, decreased glomerular filtration rate, and increased serum creatinine.
131
is chronic kidney insufficiency due to the renal vasoconstriction that often occurs with HF.
primary cause of anemia in chronic HF
132
production in the kidney, leading to anemia.
vasoconstriction results in reduced erythropoietin
133
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.
echocardiogram gives
134
of LV failure
BNP and N-terminal prohormone of BNP (NT-proBNP) levels correlate positively with the degree
135
including pulmonary embolism, renal failure, and acute coronary syndrome.
Increases in BNP or NT-proBNP levels can be caused by conditions other than HF,
136
(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.
Goals of therapy for the patient hospitalized with ADHF include
137
CO and pulmonary artery wedge pressure (PAWP) are routinely monitored.
pulmonary artery (PA) catheter is placed,
138
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.
PAWP
139
30 mm Hg
| -Therapies are adjusted to maximize CO and reduce PAWP
Patients with ADHF may have a PAWP as high as
140
also decreases preload
| -used for pulmonary oedema
BiPAP
141
noninvasive positive pressure ventilation (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation
severe pulmonary edema, the patient may need
142
is an option for the patient with volume overload when diuretics have not been effective
Ultrafiltration, or aquapheresis,
143
is a device that increases coronary blood flow to the heart muscle and decreases the heart’s workload through a process called counterpulsation
intraaortic balloon pump (IABP)
144
, a biventricular pacemaker, may be considered for patients with ADHF
Implantation of CRT
145
because it can decrease pulmonary artery pressures and systemic vascular resistance (SVR), leading to improved CO
IABP(intraaortic balloon pump) is useful in hemodynamically unstable patients
146
can help maintain the pumping action of a weakened heart. A VAD is a surgically implanted mechanical pum
Ventricular assist devices (VADs)
147
are the first line for treating patients with volume overload
Diuretics
148
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.
Diuretics function
149
IV administration of loop diuretics (e.g., furosemide) by bolus or infusion is preferred.
preferred Diuretics
150
ADHF
Vasodilators are used to treat
151
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
IV nitroglycerin (NTG) is a primary venodilator
152
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.
Sodium nitroprusside (Nitropress)
153
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.
IV nesiritide is a recombinant form of BNP
154
, reducing preload and afterload. It is often given in small IV boluses for the dyspnea associated with ADHF
Morphine dilates pulmonary and systemic blood vessels
155
or with low CO. Drugs include β-agonists (e.g., dopamine, dobutamine, norepinephrine [Levophed]) and phosphodiesterase inhibitors (milrinone)
Inotropic drugs increase myocardial contractility and are used for patients with evidence of cardiogenic shock
156
are used as a short-term treatment of ADHF
β-Agonists (inotropic drugs)
157
dilates the renal blood vessels and enhances urine output.
dopamine (inotropic)/ last resort
158
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.
Unlike dopamine, dobutamine is a selective β-agonist
159
* Monitor IV site. Tissue necrosis and sloughing can occur with drug extravasation.
* High doses may produce ventricular dysrhythmias.
Dopamine drug alert
160
has both inotropic and vasodilator properties
Milrinone (inotropine-last resort)
161
. Like dopamine and dobutamine, this drug is available only for IV use.
-Adverse effects include dysrhythmias, thrombocytopenia, and hepatotoxicity.
Milrinone improves myocardial contractility, increases CO, and reduces BP (decreases afterload)
162
. 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
Digitalis (intro pine) is a weaker positive inotrope that can be added if symptoms persist after other medications have been started
163
(e.g., diuretics, vasodilators, morphine).1
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
vasodilators and inotropes.
use an infusion pump whenever you are giving IV
165
(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.
goals of chronic HF therapies include
166
The result of neurohormonal blockade is decreased plasma aldosterone levels, decreased SNS activity, vasodilation, and sodium and water excretion.
cornerstone of drug therapy in chronic HF is neurohormonal blockade.
167
for chronic HFrEF.
| - reduce afterload and SVR and inhibit the development of ventricular remodeling by inhibiting ventricular hypertrophy.
ACE inhibitors are first-line drugs
168
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
ACE inhibitiors Major side effects
169
Monitor patient for first-dose hypotension (first-dose syncope).
• Skipping doses or discontinuing the drug can result in rebound HTN.
Captopril drug alert (ACE)
170
, angiotensin II receptor blockers (ARBs)
patients who are unable to tolerate ACE inhibitors take
171
- 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.
ARBs
172
, an enzyme that degrades natriuretic peptides (destroys BNP- B receptor to contract)
neprilysin
173
is a combination of a neprilysin inhibitor (sacubitril) and an ARB (valsartan)
Sacubitril/valsartan (Entresto)
174
drug provides dual blockade of the RAAS and the natriuretic peptide system (remodelling of ventricle)
Sacubitril/valsartan (Entresto)
175
, inhibits neprilysin, an enzyme that degrades natriuretic peptides.
Sacubitril, a recombinant form of BNP (imitation of BNP)
176
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.
Sacubitril inhibition
177
in patients meeting criteria with symptomatic HFrEF and reduces death and hospitalization.
- monitored for hypotension, renal insufficiency, and angioedema
Sacubitril inhibition is alternative to ACE inhibitors and ARBs
178
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,
Spironolactone (Aldactone) and eplerenone (Inspra)
179
directly block the negative effects of the SNS (e.g., increased HR) on the failing heart
β-Blockers
180
These β-blockers may also increase LVEF.
Three β-blockers decrease mortality in patients with HFrEF: metoprolol succinate (Toprol XL), bisoprolol (Zebeta), and carvedilol (Coreg).
181
, care must be taken in patients with volume overload
| -Major side effects include worsening of HF symptoms, hypotension, fatigue, and bradycardia..
because β-blockers can reduce myocardial contractility
182
Overdose can cause profound bradycardia, hypotension, bronchospasm, and cardiogenic shock.
-Abrupt withdrawal may result in sweating, palpitations, and headaches.
carvedilol
183
, 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
Ivabradine selectively inhibits a particular sodium/potassium current in the SA node
184
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
Hydralazine/isosorbide dinitrate combination (Bidil)
185
Major side effects include hypotension and headache. Like other nitrates, it should not be used with phosphodiesterase inhibitors, such as sildenafil (Viagra).
Hydralazine/isosorbide dinitrate combination (Bidil) drug alert
186
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
Digitalis (digoxin),
187
HFrEF and HFpEF.
Diuretics reduce symptoms of fluid overload and congestion in both
188
edema, pulmonary venous pressure, and preload
Diuretics reduce
189
act on the ascending loop of Henle to promote sodium, chloride, and water excretion
Loop diuretics (e.g., furosemide (Lasix) and bumetanide [Bumex])
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include low serum potassium levels, ototoxicity, and possible allergic reaction in patients sensitive to sulfa-type drugs.
Problems in using loop diuretics
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inhibit sodium reabsorption in the distal tubule, promoting excretion of sodium and water. They also can severely lower potassium levels.
Thiazide diuretics (more mild)
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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.
chronic HF, the lowest effective dose of diuretic should be used. Side effects of diuretics include
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for primary prevention of SCD in these patients
ICD is recommended ( implantable cardiac devices.)
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implantable cardiac devices. H
Patients with HFrEF may benefit from
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neurohormonal effects and cardiac remodeling can result in dyssynchronous contraction of the LV and RV, contributing to poor ventricular filling and reduced CO
In patients with a LVEF <35%,= recommend CRT
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, 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
With CRT
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pt symptomatic HFrEF
often need both CRT and an ICD
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remotely monitoring HF patients.
mplanted ICD and CRT devices can be used for
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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 with HFrEF. 17
pulmonary artery sensor
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2 grams per day
sodium intake is restricted to
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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
weight gain of 3 lb (1.4 kg) over 2 days
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(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.
overall goals for the patient with HF include
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with CAD.
Coronary revascularization procedures should be considered in patients
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patients with serious dysrhythmias or conduction disturbances.
Antidysrhythmic drugs or pacing therapy may be indicated for
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(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.
Successful HF care depends on several important principles:
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(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.
Therapeutic options for stage D HF patients include:
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can be beneficial to carefully selected patients for short-term management, long-term and bridge-to-transplant management, or as destination therapy
MCS devices
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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.
Patients who are ineligible for heart transplant may be candidates for lifelong
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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.
Short-term MCS
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include LV assist devices (VADs), including percutaneous devices (PVAD) and transplanted devices (LAVDs, BiVADs)
Long-term MCS devices
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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
VADs provide highly effective
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(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.
Palliative nursing care of the HF patient emphasizes
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(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.
Patients with advanced CVD are eligible for hospice when
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(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
Challenges in referring these patients to hospice include
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* 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
Common Indications for Heart Transplantation
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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
Absolute Contraindications for Heart Transplantation
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* 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
relative Contraindications for Heart Transplantation
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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%
Heart transplantation
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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.
Donor and recipient matching is based on
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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
donor heart is then implanted into the recipient using 1 of 2 approaches.
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.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.
2nd approach for heart transplant (. In the bicaval approach)
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In the first year after transplantation, the major causes of death are infection and acute rejection.
post heart transplantation
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On a long-term basis, immunosuppressive therapy increases the risk for cancers, especially lymphomas, and cardiac vasculopathy (accelerated CAD)
Because of the use of immunosuppressive therapy, infection is a primary concern after transplant surgery.
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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.
To detect rejection, an endomyocardial biopsy is done
