ACUTE HEART FAILURE, CAUSES, AND CLINICAL FEATURES

ACUTE HEART FAILURE

Heart failure mostly developing suddenly in hours or days in previously asymptomatic patients are called acute heart failure. The patient presents with the shortness of his breath due to acute pulmonary edema or with any cardiogenic shock.

It occurs in the following

Extensive loss of ventricular muscle happens in Myocardial infarction.
Other complications of MI such as mitral regurgitation due to rupture of chorda tendenae or papillary muscle and rupture of interventricular septum causing ventricular septal defect (VSD).

Acute valvular regurgitation such as aortic regurgitation in infective endocarditis and cr valvoplasty.

Myocarditis.

Acute pulmonary embolus causing obstruction of the circulation.
Cardiac tamponade: it is also a common condition usually as a complication of viral or tuberculous infection.

CAUSES OF ACUTE VALVE FAILURE

Aortic regurgitation
⦁ Aortic dissection
⦁ Infective endocarditis
⦁ Ruptured sinus of Valsalva

Mitral regurgitation

i. Papillary muscle rupture due to acute myocardial infarction
ii. Infective endocarditis
iii. Rupture of chordae due to myxomatous degeneration, or blunt chest wall trauma.
iv. Prosthetic valve failure

CLINICAL FEATURES

Acute cardiac failure may present in three ways:

1- Acute cardiogenic pulmonary edema
2- Cardiogenic shock
3- Acute decompensation of chronic heart failure

ACUTE CARDIOGENIC PULMONARY

EDEMA
An increase in the fluid content of the extravascular tissues of the lung is known as pulmonary edema. It is a life-threatening emergency characterized by extreme breathlessness.

Etiology

a. Left-sided heart failure is the cause of pulmonary edema that may result from:
b. Left ventricular systolic diastolic dysfunction as in myocardial infarction.
c. Left atrial outflow obstruction as in mitral stenosis.
d. Left ventricular outflow obstruction as in aortic stenosis, hypertrophic cardiomyopathy.
e. Left ventricular volume overload as in mitral and aortic regurgitation.

Pathogenesis

Pulmonary capillary pressure increase if left-sided failure.
. The high pulmonary capillary pressure causes increased filtration of fluid out of the capillaries into the interstitial space (interstitial edema). Further accumulation of fluid disrupts the intercellular membrane leading to the collection of fluid in the alveolar spaces (alveolar edema) resulting in hypoxemia and shortness of breath. decreased diffusing capacity,

Clinical features

Severe acute breathlessness
Wheezing

i. Productive cough with blood-tinged – (pink), copious frothy sputum (“cough, cough, cough spit, spit, spit”).
ii. Rapid breathing with the use of accessory muscles.
iii. Crepitations and rhonchi are heard throughout the chest.
iv. The patient sits upright or stand exhibiting air hunger.
v. Sweating is profuse, the skin is cold and cyanotic reflecting low cardiac output and increased sympathetic activity.
vi. The patient is extremely anxious and there is a feeling of drowning.

Cardiovascular features

⦁ Tachycardia
⦁ Raised JVP (in biventricular failure)
⦁ Cardiac auscultation is difficult due to respiratory sounds, however, gallop rhythm and may be audible.
⦁ Blood pressure is elevated above the patient’s baseline (unless cardiogenic shock is present) due to vasoconstriction due to increased sympathetic activity.

Investigation

ECG may be abnormal according to the cause:
⦁ Ischemia or MI
⦁ Left ventricular hypertrophy with strain pattern in hypertension.

X-ray chest;
⦁ Diffuse haziness due to alveolar fluid and
⦁ Kerley’s B lines of interstitial edema

Arterial blood gases:
⦁ Initially Pa02 and PaCO2 fall, later PaCO2 increases.
Elevated pulmonary capillary wedge pressure
Usually above 20 mmHg.

MANAGEMENT

1. Legs must be dangling sitting position over the side of the bed and this facilitates respiration and reduces venous return. For looking oxygen saturation oximeter should be connected.
2- Keep Po2 greater than 60 mmHg in high concentration oxygen by mask. Noninvasive pressure support ventilation may improve oxygenation and prevents CO2 retention. Mechanical ventilation and Endotracheal intubation may be necessary. If respiratory distress remains severe
Morphine
(4-8 mg 1/V) plus antiemetic metoclopramide (Maxolon 10 mg 1/V) because morphine induces vomiting. Morphine may be repeated after 2-4 hours decreases anxiety and increases venous capacitance leading to lowering of left atrial pressure that results in alleviation of breathlessness.
N.B. Morphine must be avoided if the systolic
B.P. is less than 90 mm Hg.
Diuretics: Inj. Lasix 40-80 mg I/V produces immediate vasodilatation (due to its direct

PERIPARTUM CARDIOMYOPATHY

Cardiac failure that develops during pregnancy (usually in last month) or during the first 6 months after delivery in a woman without a history of heart disease and with no other cause is termed peripartum cardiomyopathy.
Incidence: 1:4000 to 1:1000, highest in Africa, more often in older women, those with twins, and in patients with pregnancy-induced hypertension.
Etiology: unknown, maybe immune or viral.

Symptoms: features of CCF

Course: course of the disease is variable; many cases improve or resolve completely over several months, but others progress to refractory heart failure.

In patients’ symptoms and signs of the disease for more than 6 months who continue to have after delivery, In such cases the mortality rate is high and the subsequent pregnancy is especially dangerous.

ECG: Atrial, ventricular arrhythmia or tachycardia, may be present.
Echo: Mural thrombi and dilated heart chambers may be present (source of pulmonary and systemic emboli).

Management
⦁ Treatment of heart failure.
⦁ Anticoagulation, if echo shows mural thrombi.

Prognosis

1. If the cardiomegaly does not resolve in 6 months after the onset of symptoms, the 5-year mortality rate is 35%. If it is resolved tren mortality rate is still about 15%.
2. If cardiomegaly does not resolve and another pregnancy intervenes, cardiomyopathy recurs 50% of cases with an almost 100% mortality rate.

About the author: Soflay iNC
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