Transcript primary disease processes resulting in heart failure

Dr Jafari
 coronary
arteries,
 myocardium,
 cardiac valves,
 pericardium,
 peripheral vessels, or
 lungs.
 Frequently
the cause is multifactorial
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almost 70% of patients
myocardial ischemia: ischemic cardiomyopathy
 fibrosis and scarring
 Aneurysmal dilation
 When approximately 40% of the LV muscle mass
is acutely infarcted, cardiogenic shock ensues.
 Diseases affecting the coronary microcirculation,
such as vaso-occlusive sickle cell anemia and
diabetes mellitus, result in similar pathology
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 Cardiomyopathy
is categorized as
primary if cause is unknown, or
secondary if some cause is identified.
 Clinically: dilated, hypertrophic, or
restrictive
 Dilated cardiomyopathy is much more
common than the other two and is the
second most common cause of HF.
 Cardiac
valvular disease is the third leading
cause of HF
 Mitral insufficiency and aortic stenosis are
most commonly associated with chronic HF
 Example: patients with decompensated aortic
stenosis should not receive vasodilator, as flow
cannot increase across a fixed obstruction.
These patients may become hypotensive
owing to reduced preload, with resultant
decreased perfusion. On the other hand,
patients with mitral regurgitation benefit
greatly from vasodilators.
 Pericardial
diseases may significantly
affect ventricular function, decreasing CO
and increasing intracardiac pressures
 Pulmonary
dysfunction reduces
myocardial oxygen supply while CO
must be increased
 Hypoxia: Chronic increases in pulmonary
arterial pressure lead to right ventricular
(RV) hypertrophy and dilation. When
compensatory mechanisms fail, the
patient develops right-sided HF (cor
pulmonale)
 Increase
in Stroke Volume: response to
increase in preload (Frank- Starling
mechanism): is limited response
 Increased Systemic Vascular Resistance:
redistribution, increases myocardial work
 Development of Cardiac Hypertrophy:
eventually becomes maladaptive,
accelerating myocyte death and reducing
pump function.
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Cardiac Neurohormonal Response: atrial, brain (BNP), and
C-type natriuretic peptide: promote water and sodium
excretion, increase peripheral vasodilation, and inhibit the
RAAS.
Central and Autonomic Nervous System Neurohormonal
Response: antidiuretic hormone, sympathetic activity
Renal Neurohormonal Response: RAAS, Renal adaptation to
hypoperfusion occurs mainly through production of
vasodilatory hormones such as prostacyclin, along with
prostaglandins PGI2 and PGE2. Except for aspirin, NSAIDs
optimally should be avoided in patients with chronic HF
Vascular Endothelial Neurohormonal Response:
ET-1, NO
 Many
different methods of classifying HF
exist, including:
acute versus chronic,
systolic versus diastolic,
right sided versus left sided,
and high output versus low output:
renal retention, AV fistulas, pregnancy,
cirrhosis, severe anemia, thyrotoxicosis,
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Careful consideration of the differential diagnosis of HF is
symptom based.
The most common manifestation of acute HF is respiratory distress
caused by pulmonary edema. Therefore the differential diagnosis
includes:
exacerbation of COPD or asthma,
pulmonary embolus,
pneumonia,
anaphylaxis,
other causes of acute respiratory distress.
Hypoperfusion may be caused by some of these as well as by:
sepsis syndrome,
hypovolemia,
hemorrhage,
cardiac tamponade,
tension pneumothorax.
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Most HF patients are hypertensive
Clammy, vasoconstricted patients with a thready pulse and
delayed capillary refill may have systemic hypoperfusion
despite adequate BP, which is maintained by intense
vasoconstriction.
Patients with pulmonary congestion: diffuse moist rales
Peribronchial edema may cause wheezing or rhonchi,
which can mimic bronchospastic disease (“cardiac
asthma”).
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A positive response to bronchodilator therapy does not
exclude HF.
Jugular venous distention is present in approximately 50%
of cases,
one third of patients have peripheral edema.
An S3 gallop may be present in up to 25% but is often
difficult to hear.
The presence of a third heart sound significantly increases
the likelihood of HF, whereas absence of rales decreases the
likelihood.
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An upright chest radiograph: enlarged cardiac silhouette
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ECG for arrhythmia, as well as for ACS
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Absence of cardiomegaly on CXR and a normal ECG greatly decrease
the likelihood that HF is causing the presentation
CBC to evaluate for anemia
basic metabolic panel to determine electrolyte status as well as renal
function is generally useful.
Cardiac biomarkers help evaluate for ongoing myocyte injury, which
may be clinically silent.
NT-proBNP and BNP (100,500 pg/ml) levels help identify patients with
HF.
 Echocardiography
and Bedside
ultrasoundan: important ED screening tool
 CT
coronary angiography(not in acute)
 Radionuclide
in acute)
imaging and cardiac MRI (not
 The
approach focuses on
(1) determining underlying cardiac pathology,
(2) identifying the acute precipitant,
(3) mitigating the acute decompensation.
 The
acute congestive state can be controlled by
(1) reducing cardiac workload through decreased
preload and afterload,
(2) controlling excessive retention of salt and
water
(3) improving cardiac contractility
 alteration
in the permeability of the
pulmonary capillary membrane:
 septic shock,
 inhalation injuries,
 drugs or toxins,
 aspiration syndromes,
 fat emboli syndrome,
 neurogenic causes,
 high altitude.
 Hypertensive
PE is easier to manage
because afterload reduction with
vasodilators is extremely effective.
 Therapy
for APE with adequate perfusion
should begin with upright positioning,
supplemental oxygen, nitrates, morphine
sulfate, and loop diuretics
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Excessive oxygen therapy, may significantly increase afterload
Fulminant APE may have lactic acidosis, and many also have
concomitant respiratory alkalosis resulting from the tachypnea
In more severe cases, respiratory acidosis ensues as the patient
fatigues and respirations fail
O2: nasal, face mask, NIV(CPAP, BiPAP)
Intubation is indicated for apneic patients and those with
respiratory distress, agitation, or hypoxemia not responsive to
high-flow oxygen or NIV.
 Nitrates
and Nitroprusside
 Morphine Sulfate
 Nesiritide
 Loop Diuretics
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relaxes vascular smooth muscle
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At lower doses, nitrates are primarily venodilators.
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At higher doses, causes arteriolar dilation that decreases BP and
afterload.
may reduce myocardial ischemia by its direct coronary
vasodilator effect
Prolonged therapy over hours to days leads to tachyphylaxis
secondary to depletion of intracellular sulfhydryl groups.
Intravenous nitroglycerin has rapid onset and offset of action.
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should be avoided in impotence medications (PDE type 5 inhibitors) previous
24 h (up to 48 h for tadalafil), as the combination may precipitate refractory
hypotension.
Transcutaneous?: diaphoresis and poor skin perfusion, ignite during
defibrillation
Sodium nitroprusside: intra-arterial pressure monitoring, useful for PE and
systemic HTN.
In the presence of acute myocardial ischemia or infarction, nitroglycerin is
preferable because it avoids the coronary steal syndrome
Patients with renal failure may experience thiocyanate toxicity from high-dose
nitroprusside infusions.
Nitroglycerin is thus preferred over nitroprusside in HF.
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reduces pulmonary congestion through a central sympatholytic effect
and release of vasoactive histamine, causing peripheral vasodilation
and reduced preload.
through reduced systemic catecholamines, decreases HR, BP, cardiac
contractility, and myocardial oxygen consumption
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The calming effect of morphine is advantageous for agitation
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is administered in repetitive 2- to 5-mg IV doses
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In APE, mild CO2 retention does not contraindicate morphine use
because it results from acute alveolar flooding
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a recombinant human BNP, is a balanced vasodilator
that reduces aldosterone and ET levels while
increasing sodium and water excretion
Meta-analyses of studies using nesiritide in acute HF
suggest the possibility of increased drug-related
mortality
Nesiritide is not indicated in the emergency
department treatment of episodes of acute HF.
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Although the renal effects of IV administered loop
diuretics begin within 10 minutes, symptom relief in
patients with APE often occurs much faster, probably
the result of diuretic-induced neurohumoral changes.
Furosemide acts as a vasodilator, promoting both renal
PGE2 and natriuretic peptide secretion, and as a
vasoconstrictor, stimulating renin release
Continuous infusion of furosemide is not superior to
bolus therapy.
Diuretic therapy causes depletion of the important
cations K+ and Mg2+