2. Definition
Heart failure is a complex pathophysiologic state described by the
inability of the heart to fill with or eject blood at a rate
appropriate to meet tissue requirements.
The clinical syndrome is characterized by symptoms of dyspnea
and fatigue and signs of circulatory congestion or hypoperfusion.
3. Etiology
The principal pathophysiology of heart failure is the inability
of the heart to fill or empty the ventricle.
The most common cause of right ventricular failure is left
ventricular (LV) failure.
4. Etiology
Heart failure is most often due to
(1) impaired myocardial contractility secondary to ischemic heart disease or
cardiomyopathy;
(2) cardiac valve abnormalities;
(3) systemic hypertension;
(4) diseases of the pericardium; or
(5) pulmonary hypertension (cor pulmonale).
5. FORMS OF VENTRICULAR
DYSFUNCTION
Heart failure may be described in various ways:
systolic or diastolic,
acute or chronic,
left sided or right sided,
high output or low output.
6. Left ventricular dysfunction regardless of
cause, results in progressive remodeling of
the ventricular chamber leading to dilation
and a low ejection fraction.
7. Systolic Heart Failure
Causes of SHF
CAD,
Dilated cardiomyopathy (DCM),
Chronic pressure overload (aortic stenosis and chronic
hypertension),
Chronic volume overload (regurgitant valvular lesions and high
output cardiac failure).
8. Systolic Heart Failure
CAD typically results in regional defects in ventricular
contraction, which may become global over time
All other causes of SHF produce global ventricular dysfunction
Ventricular dysrhythmias are common in patients with LV
dysfunction.
Patients with left bundle branch block and SHF are at high risk of
sudden death.
9. Diastolic Heart Failure
DHF can be classified into four stages.
Class I DHF is characterized by an abnormal LV relaxation pattern
with normal left atrial pressure.
Classes II, III, and IV are characterized by abnormal relaxation as
well as reduced LV compliance resulting in an increase in LV end-
diastolic pressure (LVEDP)
As a compensatory mechanism, the pressure in the left atrium
increases so that LV filling can occur despite the increase in
LVEDP.
10. Diastolic Heart Failure
Ischemic heart disease, long-standing essential hypertension, and
progressive aortic stenosis are the most common causes of DHF.
In contrast to SHF, DHF affects women more than men.
Hospitalization and mortality rates are similar in patients with
SHF and DHF.
11.
12. ACUTE AND CHRONIC HEART FAILURE
Acute heart failure is defined as
a change in the signs and symptoms of heart failure requiring
emergency therapy.
In acute heart failure due to a sudden decrease in cardiac output,
systemic hypotension is typically present without signs of
peripheral edema.
13. ACUTE AND CHRONIC HEART FAILURE
Acute heart failure encompasses three clinical entities:
(1) worsening chronic heart failure;
(2) new-onset heart failure such as with cardiac valve rupture,
large myocardial infarction, or severe hypertensive crisis; and
(3) terminal heart failure, which is refractory to therapy.
14. ACUTE AND CHRONIC HEART FAILURE
Chronic heart failure is present in patients with long-standing
cardiac disease.
Typically, chronic heart failure is accompanied by venous
congestion, but blood pressure is maintained.
15. LEFT-SIDED AND RIGHT-SIDED HEART
FAILURE
In left-sided heart failure high LVEDP promotes
pulmonary venous congestion.
The patient complains of
dyspnea
orthopnea
and paroxysmal nocturnal dyspnea
which can evolve to pulmonary edema.
16. LEFT-SIDED AND RIGHT-SIDED HEART
FAILURE
Right-sided heart failure systemic venous congestion.
Peripheral edema and congestive hepatomegaly are the most
prominent clinical manifestations.
Right-sided heart failure may be caused by pulmonary
hypertension or right ventricular myocardial infarction,
but the most common cause is left-sided heart failure.
17. LOW-OUTPUT AND HIGH-OUTPUT
HEART FAILURE
The normal cardiac index varies between 2.2 and 3.5 L/min/m2.
The most common causes of low-output heart failure are CAD,
cardiomyopathy,
hypertension,
valvular disease,
pericardial disease.
It may be difficult to diagnose low-output heart failure because a
patient may have a cardiac index that is nearly normal in the
resting state but does not respond adequately to stress or exercise.
18. LOW-OUTPUT AND HIGH-OUTPUT
HEART FAILURE
Causes of high cardiac output include
anemia,
pregnancy,
arteriovenous fistulas,
severe hyperthyroidism,
beriberi,
Paget's disease.
19. LOW-OUTPUT AND HIGH-OUTPUT
HEART FAILURE
The ventricle fails not only because of the increased
hemodynamic burden placed on it but also because of direct
myocardial toxicity as caused by thyrotoxicosis and beriberi
and myocardial anoxia caused by severe and prolonged
anemia.
20. PATHOPHYSIOLOGY OF HEART FAILURE
The initiating mechanisms of heart failure are
pressure overload (aortic stenosis, essential hypertension),
volume overload (mitral or aortic regurgitation),
myocardial ischemia/infarction,
myocardial inflammatory disease,
restricted diastolic filling (constrictive pericarditis, restrictive
myocarditis).
21. PATHOPHYSIOLOGY OF HEART FAILURE
In the failing ventricle, various adaptive mechanisms
These include
(1) the Frank-Starling relationship;
(2) activation of the sympathetic nervous system (SNS);
(3) alterations in the inotropic state, heart rate, and afterload; and
(4) humoral-mediated responses.
In advanced stages of heart failure mechanisms become
maladaptive myocardial remodeling,
the key pathophysiologic change responsible for the development
and progression of heart failure.
22. Frank-Starling Relationship
The Frank-Starling relationship
The increase in stroke volume that accompanies an increase
in LV end-diastolic volume and pressure
Stroke volume increases because the tension developed by
contracting muscle is greater when the resting length of that
muscle is increased.
The magnitude of the increase in stroke volume produced by
changing the tension of ventricular muscle fibers depends on
myocardial contractility.
23.
24. Frank-Starling Relationship
For example, when myocardial contractility is decreased, as in the
presence of heart failure, a lesser increase in stroke volume is
achieved relative to any given increase in LV end-diastolic
pressure.
Constriction of venous capacitance vessel shifts blood centrally,
increases preload, and helps maintain cardiac output by the Frank-
Starling relationship.
25. Activation of Sympathetic Nervous
System
Activation of the SNS promotes arteriolar and venous
constriction.
Arteriolar constriction serves to maintain systemic blood pressure
despite a decrease in cardiac output.
Increased venous tone shifts blood from peripheral sites to the
central circulation, thereby enhancing venous return and
maintaining cardiac output by the Frank-Starling relationship.
26. Activation of Sympathetic Nervous
System
Arteriolar constriction
redistribution of blood from the kidneys, splanchnic organs,
skeletal muscles, and skin
to maintain coronary and cerebral blood flow despite overall
decreases in cardiac output.
The decrease in renal blood flow
activates the renin-angiotensin-aldosterone system (RAAS)
which increases renal tubular reabsorption of sodium and
water,
increase in blood volume and ultimately cardiac output
27. Alterations in the Inotropic State, Heart
Rate, and Afterload
The inotropic state describes myocardial contractility as reflected
by the velocity of contraction developed by cardiac muscle.
The maximum velocity of contraction is referred to asVmax.
When the inotropic state of the heart is increased, as in the
presence of catecholamines,Vmax is increased.
Conversely,Vmax is decreased when myocardial contractility is
impaired as in heart failure.
28. Alterations in the Inotropic State, Heart
Rate, and Afterload
Afterload is the tension the ventricular muscle must develop to
open the aortic or pulmonic valve.
The afterload presented to the left ventricle is increased in the
presence of systemic arteriolar constriction and hypertension.
can be decreased by administering vasodilating drugs.
29. Alterations in the Inotropic State, Heart
Rate, and Afterload
In the presence of SHF and low cardiac output,
The stroke volume is relatively fixed with any increase in CO being
dependent on an increase in heart rate.
Tachycardia is an expected finding in the presence of SHF with a low
ejection fraction and reflects activation of the sympathetic nervous
system.
However, in the presence of DHF, tachycardia can produce a decrease in
CO due to inadequate ventricular filling time.
Therefore, heart rate control is a target for therapy of DHF.
30. Humoral-Mediated Responses and
Biochemical Pathways
As heart failure progresses, various neurohumoral pathways are
activated
to maintain adequate cardiac output during exercise and
ultimately even at rest.
Generalized vasoconstriction is initiated via several mechanisms
including increased activity of the SNS and RAAS,
parasympathetic withdrawal,
high levels of circulating vasopressin,
endothelial dysfunction,
and release of inflammatory mediators.
31. Humoral-Mediated Responses and
Biochemical Pathways
Heart as a “an endocrine organ.”
Atrial natriuretic peptide
is stored in atrial muscle and released in response to
increases in atrial pressures, such as produced by
tachycardia or hypervolemia.
32. Humoral-Mediated Responses and
Biochemical Pathways
B-type natriuretic peptide (BNP)
It is secreted by both the atrial and ventricular myocardium.
In the failing heart, the ventricle becomes the principal site for
BNP production.
The natriuretic peptides promote blood pressure control and
protect the cardiovascular system from the effects of volume and
pressure overload.
Physiologic effects of the natriuretic peptides include diuresis,
natriuresis, vasodilation, antihypertrophy, anti-inflammation, and
inhibition of the RAAS and SNS
33. Myocardial Remodeling
It is the process by which mechanical, neurohormonal, and
genetic factors change the LV size, shape, and function.
The process includes
myocardial hypertrophy,
myocardial dilation and wall thinning,
increased interstitial collagen deposition,
myocardial fibrosis, and scar formation due to myocyte
death.
34. Myocardial Remodeling
Myocardial hypertrophy compensatory mechanism to
chronic pressure overload.
Cardiac dilation to volume overload and increases
the CO.
also associated with increased myocardial oxygen
requirements and decreased cardiac efficiency.
most common cause of myocardial remodeling is ischemic
injury.
both hypertrophy and dilation of the left ventricle.
35. SIGNS AND SYMPTOMS OF HEART
FAILURE
LV failure results in signs and symptoms of pulmonary
edema,
right ventricular failure results in systemic venous
hypertension and peripheral edema.
Patient fatigue and organ system dysfunction are related to
inadequate CO.
36. Symptoms of Heart Failure
Dyspnea reflects increased work of breathing due to stiffness of the
lungs produced by interstitial pulmonary edema.
Patients experiencing angina pectoris may interpret substernal
discomfort as breathlessness.
Dyspnea related to heart failure will be linked to other supporting
evidence
history of orthopnea,
paroxysmal nocturnal dyspnea,
third heart sound,
rales on physical examination,
elevated BNP levels.
37. Symptoms of Heart Failure
Orthopnea reflects the inability of the failing left ventricle to
handle the increased venous return associated with the recumbent
position.
manifested as a dry, nonproductive cough that develops when in
the supine position and that is relieved by sitting up.
Paroxysmal nocturnal dyspnea is shortness of breath that awakens
a patient from sleep.
Paroxysmal nocturnal dyspnea and wheezing caused by pulmonary
congestion (“cardiac asthma”) are accompanied by radiographic
evidence of pulmonary congestion.
38. Symptoms of Heart Failure
Fatigue and weakness at rest or with minimal exertion.
Anorexia, nausea, or abdominal pain related to increased liver
congestion and prerenal azotemia.
Decreases in cerebral blood flow may produce confusion,
difficulty concentrating, insomnia, anxiety, or memory deficits.
Nocturia may contribute to insomnia.
39. Physical Examination
tachypnea and the presence of moist rales.
resting tachycardia and a third heart sound (S3 gallop or
ventricular diastolic gallop).
This heart sound is produced by blood entering and
distending a relatively noncompliant left ventricle.
40. Physical Examination
Systemic hypotension with cool and pale extremities.
Lip and nail bed cyanosis
A narrow pulse pressure with a high diastolic pressure
Marked weight loss
Increase in the metabolic rate, anorexia and nausea, decreased
intestinal absorption of food caused by splanchnic venous
congestion.
41. Physical Examination
In the presence of right heart or biventricular failure,
jugular venous distention
may be present or inducible by pressing on the liver
(hepatojugular reflux).
The liver is typically the first organ to become engorged with
blood in the presence of right or biventricular failure.
42. Physical Examination
Right upper quadrant pain and tenderness or even jaundice in
severe cases.
Pleural effusions (usually right sided) may be present.
Bilateral pitting pretibial leg edema is typically present with
right ventricular failure and reflects both venous congestion
and sodium and water retention.
43. DIAGNOSIS OF HEART FAILURE
The diagnosis of heart failure is based on the
History,
Physical examination,
Interpretation of laboratory and diagnostic tests.
44. Laboratory Diagnosis
Plasma BNP levels
Below 100 pg/mL indicate that heart failure is unlikely (90% negative
predictive value);
BNP in the range of 100 to 500 pg/mL suggests an intermediate
probability for heart failure;
Levels above 500 pg/mL are consistent with the diagnosis of heart
failure (90% positive predictive value).
Plasma levels of BNP may be affected by other factors such as sex, advanced age, renal
clearance, obesity, pulmonary embolism, atrial fibrillation, and/or other cardiac
tachydysrhythmias.
45. Laboratory Diagnosis
Decreases in renal blood flow may lead to prerenal azotemia
characterized by a disproportionate increase in blood urea
nitrogen concentration relative to the serum creatinine
concentration.
When moderate liver congestion is present, LFT may be mildly
elevated, and when liver engorgement is severe, the prothrombin
time may be prolonged.
Hyponatremia, hypomagnesemia, and hypokalemia may be
present.
46. Electrocardiography
Patients with heart failure usually have an abnormal 12-lead
electrocardiogram (ECG).
Low predictive value for the diagnosis of heart failure.
The ECG may show evidence of
A previous myocardial infarction,
LV hypertrophy,
Conduction abnormalities (left bundle branch block,
widened QRS), or various cardiac dysrhythmias, especially
atrial fibrillation and ventricular dysrhythmias.
47. Chest Radiography
Detecting the presence of pulmonary disease, cardiomegaly,
pulmonary venous congestion, and interstitial or alveolar
pulmonary edema.
Distention of the pulmonary veins in the upper lobes of the
lungs.
Perivascular edema appears as hilar or perihilar haze.
The hilus appears large with ill-defined margins.
48. Chest Radiography
Kerley lines, reflecting edematous interlobular septae in the
upper lung fields (KerleyA lines),
lower lung fields (Kerley B lines),
or basilar regions of the lungs producing a honeycomb
pattern (Kerley C lines) may also be present.
49. Chest Radiography
Alveolar edema produces homogeneous densities in the lung
fields, typically in a butterfly pattern.
Pleural effusion and pericardial effusion may be observed.
Radiographic evidence of pulmonary edema may lag behind the clinical
evidence of pulmonary edema by up to 12 hours.
Likewise, radiographic patterns of pulmonary congestion may persist for several
days after normalization of cardiac filling pressures and resolution of symptoms.
50. Echocardiography
The most useful test.
assess whether any abnormalities of the myocardium, cardiac
valves, or pericardium are present.
This examination addresses the following topics:
ejection fraction, LV structure and functionality,
the presence of other structural abnormalities such as
valvular and pericardial disease
and the presence of diastolic dysfunction and right
ventricular function.
A preoperative echocardiographic evaluation can serve as a baseline for comparison
with perioperative echocardiography if a patient's condition deteriorates.
51. CLASSIFICATION OF HEART FAILURE
There are four functional classes:
Class I: Ordinary physical activity does not cause symptoms
Class II: Symptoms occur with ordinary exertion
Class III: Symptoms occur with less than ordinary exertion
Class IV: Symptoms occur at rest
52. CLASSIFICATION OF HEART FAILURE
American HeartAssociation published the 2005 Guideline
Update
Stage A: Patients at high risk of heart failure but without structural
heart disease or symptoms of heart failure
Stage B: Patients with structural heart disease but without
symptoms of heart failure
Stage C: Patients with structural heart disease with previous or
current symptoms of heart failure
Stage D: Patients with refractory heart failure requiring
specialized interventions
53. Management of Chronic Heart Failure
lifestyle modification,
patient and family education,
medical therapy,
corrective surgery,
implantable devices,
and cardiac transplantation
54. Lifestyle Modifications
Lifestyle modifications are aimed at decreasing the risk of
heart disease and include
smoking cessation,
a healthy diet with moderate sodium restriction,
weight control,
exercise,
moderate alcohol consumption,
and adequate glycemic control.
55.
56. Management of Systolic Heart Failure
Angiotensin-Converting Enzyme Inhibitors
Beneficial effects include promoting vasodilation, reducing water
and sodium reabsorption, and supporting potassium conservation.
decrease ventricular remodeling and even to potentiate the
“reverse-remodeling” phenomenon.
For this reason, they are considered the first line of treatment
in heart failure.
Side effects ofACEIs include hypotension, syncope, renal
dysfunction, hyperkalemia, and development of a nonproductive
cough and angioedema.
57. Management of Systolic Heart Failure
Angiotensin II Receptor Blockers
These drugs have similar but not superior efficacy compared to
ACEIs.
only recommended for patients who cannot tolerateACEIs.
In some patients treated with ACEIs, angiotensin levels may return
to normal due to alternative pathways of angiotensin production.
Such patients may benefit from the addition of an angiotensin
receptor blocker to the medical therapy.
58. Management of Systolic Heart Failure
AldosteroneAntagonists
In advanced stages of heart failure, there are high circulating levels
of aldosterone.
Aldosterone stimulates sodium and water retention, hypokalemia,
and ventricular remodeling.
Spironolactone, an aldosterone antagonist, may reverse all these
effects.
During therapy with spironolactone, patients should have renal
function and potassium levels monitored and the dose of
spironolactone adjusted accordingly.
59. Management of Systolic Heart Failure
β-Blockers
β-Blockers are used to reverse the harmful effects of SNS activation in
heart failure.
reduce morbidity and the number of hospitalizations and improve both
quality of life and survival.
β-Blockers improve the ejection fraction and decrease ventricular
remodeling.
Caution should be used when administering β-blockers to patients with
reactive airway disease,
diabetics with frequent hypoglycemic episodes,
and patients with bradydysrhythmias or heart block.
60. Management of Systolic Heart Failure
Diuretics
Diuretics can relieve circulatory congestion and the accompanying
pulmonary and peripheral edema more rapidly than any other drugs.
Diuretic-induced decreases in ventricular diastolic pressure will
decrease diastolic ventricular wall stress and prevent the persistent
cardiac distention
Thiazide and/or loop diuretics are recommended as an essential part of
the therapy of heart failure.
Potassium and magnesium supplementation may be needed
Excessive doses of diuretics may cause hypovolemia, prerenal azotemia,
or an undesirably low cardiac output and are associated with worse
clinical outcomes.
61. Management of Systolic Heart Failure
Digitalis
Digitalis enhances the inotropy of cardiac muscle and decreases
activation of the SNS and the RAAS.
may impede the worsening of heart failure and result in fewer
hospitalizations.
Digitalis can be added to standard therapy when patients are still
symptomatic despite treatments with diuretics,ACEIs, and β-blockers.
Patients with the combination of atrial fibrillation and heart failure
present another subgroup that may benefit from digoxin therapy.
62. Management of Systolic Heart Failure
Caution in elderly patients or to those with impaired renal
function
Manifestations of digitalis toxicity include anorexia, nausea,
blurred vision, and cardiac dysrhythmias.
Treatment of toxicity may include reversing hypokalemia, treating
cardiac dysrhythmias, administering antidigoxin antibodies,
and/or placing a temporary cardiac pacemaker.
63. Management of Systolic Heart Failure
Vasodilators
Vasodilator therapy relaxes vascular smooth muscle,
decreases resistance to LV ejection, and increases venous
capacitance.
In patients with dilated left ventricles, administration of
vasodilators results in increased stroke volume and decreased
ventricular filling pressures.
64. Management of Systolic Heart Failure
Statins
By their anti-inflammatory and lipid-lowering effects
decrease morbidity and mortality in patients with SHF.
Promising studies suggest that DHF patients could derive similar
benefits from statin therapy.
65.
66. Surgical Management of Heart Failure
LV ischemia may be treated with
Percutaneous coronary interventions
or coronary artery bypass surgery.
Correctable cardiac valve lesions may be alleviated surgically.
Ventricular aneurysmectomy may be useful in patients with large
ventricular scars after myocardial infarction.
The definitive treatment for heart failure is heart transplantation.
67. Surgical Management of Heart Failure
Cardiac resynchronization therapy (CRT) is aimed at
patients
with advanced stages of heart failure who have a ventricular
conduction delay (QRS prolongation on the ECG).
CRT, also known as biventricular pacing, consists of
the placement of a dual-chamber cardiac pacemaker but with
an additional lead introduced into the coronary
sinus/coronary vein until it reaches the dyssynchronous LV
wall.
68. Surgical Management of Heart Failure
CRT is recommended for
NYHA Class II/IV patients with an LV ejection fraction less
than 35% and a QRS duration between 120 and 150
milliseconds.
Patients undergoing CRT may have
fewer symptoms,
better exercise tolerance,
and improved ventricular function
The reverse remodeling induced by CRT may also improve
survival in these patients.
69.
70. Management of Acute Heart Failure
Acute heart failure therapy has three phases:
the emergency phase,
the in-hospital management phase,
and the predischarge phase.
For the anesthesiologist, the emergency phase is of most
interest
71. Management of Acute Heart Failure
Diuretics andVasodilators
Loop diuretics can improve symptoms rapidly, but in high
doses, they may have deleterious effects
Use a combination of a low dose of loop diuretic with an
intravenous vasodilator.
Nitroglycerin and nitroprusside reduce LV filling pressure
and SVR and increase stroke volume.
However, nitroprusside may have a negative impact in
patients with acute myocardial infarction.
72. Management of Acute Heart Failure
Inotropic Support
Positive inotropic drugs have been the mainstay of treatment
for patients in cardiogenic shock.
via an increase in cyclic adenosine monophosphate, which
promotes an increase in intracellular calcium levels
Catecholamines (epinephrine, norepinephrine, dopamine,
and dobutamine) do so by direct β-receptor stimulation,
whereas phosphodiesterase inhibitors (amrinone, milrinone)
block the degradation of cyclic adenosine monophosphate.
73. Management of Acute Heart Failure
Side effects of inotropic drugs include
tachycardia,
increased myocardial energy demand and oxygen
consumption,
dysrhythmias,
worsening of DHF,
and down-regulation of β-receptors.
Long-term use of these drugs may result in cardiotoxicity
and accelerate myocardial cell death.
74. Management of Acute Heart Failure
Calcium Sensitizers
increase contractility without increasing intracellular levels of
calcium.
Therefore, there is no significant increase in myocardial oxygen
consumption or heart rate and no propensity for dysrhythmias.
The most widely used medication in this class is levosemindan.
It is an inodilator increasing myocardial contractile strength and
promoting dilation of systemic, pulmonary, and coronary arteries.
It does not worsen diastolic function.
75. Management of Acute Heart Failure
Exogenous B-Type Natriuretic Peptide
Nesiritide (Natrecor) is recombinant BNP that binds to both the
A- and B-type natriuretic receptors.
It promotes arterial, venous, and coronary vasodilation, thereby
decreasing LVEDP and improving dyspnea.
Nesiritide induces diuresis and natriuresis.
It has many effects similar to nitroglycerin but generally produces
less hypotension
and more diuresis than nitroglycerin.
76. Management of Acute Heart Failure
Nitric Oxide Synthase Inhibitors
The inflammatory cascade results in production of a large
amount of nitric oxide in the heart and vascular endothelium.
These high levels of nitric oxide have a negative inotropic and
profound vasodilatory effect leading to cardiogenic shock and
vascular collapse.
Inhibition of nitric oxide synthase should decrease these
harmful effects.
L-NAME (N-nitro-L-arginine methyl ester) is the principal
drug in this class under investigation.
77. Management of Acute Heart Failure
Mechanical Devices
If the etiology of acute heart failure is a large myocardial
infarction,
the insertion of an intra-aortic balloon pump should be
considered.
The intra-aortic balloon pump is a mechanical device
inserted via the femoral artery and positioned just below the
left subclavian artery.
78. Management of Acute Heart Failure
Its balloon inflates in diastole increasing aortic diastolic
blood pressure and coronary perfusion pressure.
The balloon deflates in systole creating a “suction” effect that
enhances LV ejection.
Complications of intra-aortic balloon pump placement
include femoral artery or aortic dissection, bleeding,
thrombosis, and infection.
79. Prognosis
The mortality rate during the first 4 years following the diagnosis
of heart failure approaches 40%.
Certain factors have been associated with a poor prognosis and
include
increased urea and creatinine levels,
hyponatremia, hypokalemia,
severely depressed ejection fraction,
high levels of endogenous BNP,
very limited exercise tolerance,
and the presence of multifocal premature ventricular
contractions.
80. MANAGEMENT OF ANESTHESIA
Preoperative Evaluation and
Management
Patients treated for heart failure are usually on several medications
that may affect anesthetic management.
It is generally accepted that diuretics may be discontinued on the
day of surgery.
Maintaining β-blocker therapy is essential since many studies have
shown that β-blockers reduce perioperative morbidity and
mortality.
81. Preoperative Evaluation and
Management
Due to inhibition of the RAAS,ACEIs may put patients at
increased risk of intraoperative hypotension.
This hypotension can be treated with a sympathomimetic drug
such as ephedrine, an α-agonist such as phenylephrine, or
vasopressin or one of its analogues.
82. Preoperative Evaluation and
Management
If ACEIs are being used to prevent ventricular remodeling in heart
failure patients and kidney dysfunction in diabetic patients, then
stopping the medication for 1 day will not significantly alter these
effects.
However, ifACEIs are used to treat hypertension, then
discontinuing therapy the day of or the day before surgery may
result in significant hypertension.
83. Preoperative Evaluation and
Management
Angiotensin receptor blockers produce profound RAAS
blockade and should be discontinued the day before surgery.
Digoxin therapy can be continued until the day of surgery.
Results of recent electrolyte, renal function, and liver
function tests and the most recent ECG and echocardiogram
should be evaluated
84. Intraoperative Management
All types of general anesthetics have been successfully used in
patients with heart failure.
However, drug doses may need to be adjusted.
Opioids seem to have a particularly beneficial effect in heart
failure patients because of their effect on the δ-receptor,
which inhibits adrenergic activation.
PPV and PEEP may be beneficial in decreasing pulmonary
congestion and improving arterial oxygenation.
85. Intraoperative Management
Intra-arterial pressure monitoring in a major operation is
required
Fluid overload is avoided.
Intraoperative use of a pulmonary artery catheter
Transesophageal echocardiography may be a better
alternative, allowing not only monitoring of ventricular
filling but also ventricular wall motion and valvular function.
86. Regional anesthesia
Regional anesthesia is acceptable for suitable operations
In fact, the modest decrease in systemic vascular resistance
secondary to peripheral SNS blockade may increase cardiac
output.
However, the decreased systemic vascular resistance produced by
epidural or spinal anesthesia is not always predictable or easy to
control.
87. Intraoperative Management
Special consideration
cardiac transplanted pts requiring other surgeries.
These patients are on long-term immunosuppressive therapy
and are at high risk of infection.
Strict aseptic technique is necessary when performing any
invasive procedure such as central line placement or
neuraxial block.
88. Intraoperative Management
The transplanted heart is denervated.
An increase in heart rate can only be achieved by
administering direct acting β-adrenergic agonists such as
isoproterenol and epinephrine.
An increase in heart rate will not occur with administration
of atropine or pancuronium.
89. A blunted response to α-adrenergic agonists may also be
observed.
The transplanted heart increases cardiac output by increasing
stroke volume.
Therefore, these patients are preload dependent and require
adequate intravascular volume.
90. Postoperative Management
Patients who have evidence of acute heart failure during
surgery should be transferred to ICU where invasive
monitoring can be continued postoperatively.
Pain should be aggressively treated since its presence and
hemodynamic consequences may worsen heart failure.
Patients should have their usual medications restarted as soon
as possible.
