Introduction
Acute heart failure occurs suddenly, often within hours or days, in individuals who previously showed no symptoms. It manifests as severe shortness of breath due to pulmonary edema or as cardiogenic shock. Various conditions can trigger acute heart failure, including extensive damage to the ventricular muscle from myocardial infarction or complications such as mitral regurgitation due to ruptured chordae tendineae. Additionally, acute valvular regurgitation, myocarditis, and pulmonary embolism may contribute to this life-threatening condition.
Heart failure can also result from acute valve dysfunction. Aortic regurgitation may stem from aortic dissection or infective endocarditis, while mitral regurgitation can be caused by papillary muscle rupture, endocarditis, or valve degeneration. Clinically, acute heart failure presents in different forms, including pulmonary edema, cardiogenic shock, and decompensation of chronic heart failure.
Pulmonary edema, a critical complication, leads to severe breathlessness and hypoxemia as fluid accumulates in lung tissues. Management focuses on immediate intervention, including oxygen support, medication such as diuretics and morphine, and, in severe cases, mechanical ventilation. Additionally, conditions like peripartum cardiomyopathy may lead to heart failure in pregnant women, requiring careful monitoring and intervention. Understanding acute heart failure is essential for prompt diagnosis and effective treatment, improving patient outcomes.
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.
Myocarditis is an inflammatory condition affecting the heart muscle, often triggered by infections, autoimmune diseases, or toxic exposures. It disrupts normal cardiac function, leading to symptoms such as chest pain, fatigue, and arrhythmias. In severe cases, myocarditis can cause heart failure, requiring urgent medical intervention. Early diagnosis and appropriate treatment play a crucial role in managing this condition and preventing long-term complications.
Similarly, acute pulmonary embolism poses a serious threat by obstructing blood flow in the lungs. This condition occurs when a blood clot travels to the pulmonary arteries, blocking circulation and impairing oxygen exchange. Patients often experience sudden shortness of breath, chest pain, and an increased heart rate. If untreated, pulmonary embolism can lead to life-threatening complications, making prompt medical attention essential.
Another critical cardiac emergency is cardiac tamponade, a condition where excess fluid accumulates in the pericardial sac, compressing the heart and restricting its ability to pump effectively. This condition frequently arises due to viral or tuberculous infections, leading to symptoms such as hypotension, distended neck veins, and muffled heart sounds. Immediate intervention, often through pericardiocentesis, is necessary to relieve pressure and restore normal cardiac function. Understanding these life-threatening conditions helps ensure timely diagnosis and proper treatment, improving patient outcomes.
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
Acute valve failure occurs when the heart’s valves suddenly lose their ability to function properly, leading to severe complications. Aortic regurgitation is a major cause, often resulting from aortic dissection, infective endocarditis, or rupture of the sinus of Valsalva. These conditions impair the valve’s ability to close fully, causing blood to flow backward into the heart and increasing strain on the cardiovascular system.
Similarly, mitral regurgitation can develop due to various factors. One critical cause is papillary muscle rupture following an acute myocardial infarction, which disrupts normal valve function. Infective endocarditis can also weaken the valve, leading to improper closure. Additionally, chordae tendineae rupture due to myxomatous degeneration or blunt chest trauma further contributes to mitral valve insufficiency. In some cases, prosthetic valve failure exacerbates the condition, requiring urgent medical intervention.
When acute valve failure occurs, it can rapidly lead to heart failure, pulmonary congestion, and decreased cardiac output. Patients often experience severe symptoms such as breathlessness, fatigue, and circulatory collapse. Prompt diagnosis and appropriate treatment, including surgical repair or valve replacement, are essential to restoring heart function and preventing life-threatening complications. Understanding these causes enables early detection and effective management of acute 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 cardiac failure can manifest in several forms, each presenting unique challenges and requiring immediate medical attention. One common presentation is acute cardiogenic pulmonary edema, where excess fluid accumulates in the lungs, causing severe breathlessness and respiratory distress. Patients often struggle for air, experience wheezing, and produce frothy, blood-tinged sputum. This condition demands urgent intervention to stabilize oxygen levels and relieve fluid buildup.
Another critical manifestation is cardiogenic shock, which occurs when the heart fails to pump enough blood to meet the body’s needs. This leads to dangerously low blood pressure, cold and clammy skin, and altered mental status. Patients may exhibit signs of extreme anxiety, reflecting the body’s struggle to maintain circulation. Without immediate treatment, cardiogenic shock can quickly become life-threatening.
Additionally, acute decompensation of chronic heart failure presents when a previously stable patient experiences a sudden worsening of symptoms. Fluid overload, fatigue, and difficulty breathing become pronounced, often triggered by infections, medication issues, or excessive salt intake. Managing acute heart failure requires rapid assessment and appropriate medical intervention to stabilize the patient and prevent further complications. Recognizing these clinical features early can significantly improve outcomes and enhance patient survival rates.
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
Left Ventricular Dysfunction
Systolic and diastolic dysfunction, often resulting from myocardial infarction.
Atrial Outflow Obstruction (Left)
Mitral stenosis restricting blood flow.
Ventricular Outflow Obstruction (Left)
Conditions like aortic stenosis and hypertrophic cardiomyopathy limiting circulation.
Ventricular Volume Overload (Left)
Excessive blood flow due to mitral and aortic regurgitation.
These factors contribute to increased pulmonary capillary pressure, leading to fluid accumulation in the lungs and respiratory distress.
Acute cardiogenic pulmonary edema occurs when excess fluid accumulates in the lungs, leading to severe breathlessness and impaired oxygen exchange. This life-threatening condition develops suddenly and requires immediate medical intervention to prevent complications. The underlying cause is left-sided heart failure, which disrupts normal blood flow and increases pressure within the pulmonary capillaries.
Several factors contribute to pulmonary edema. One major cause is left ventricular systolic or diastolic dysfunction, often seen in myocardial infarction. When the heart muscle weakens, it struggles to pump blood effectively, causing fluid buildup. Additionally, left atrial outflow obstruction, such as mitral stenosis, prevents smooth blood circulation, leading to congestion in the lungs. Left ventricular outflow obstruction, as seen in aortic stenosis and hypertrophic cardiomyopathy, further exacerbates the problem by restricting proper blood flow.
Moreover, left ventricular volume overload plays a critical role in pulmonary edema development. Conditions like mitral and aortic regurgitation allow excess blood to flow back into the heart, creating additional strain on the pulmonary system. As fluid accumulates, breathing becomes increasingly difficult, and oxygen levels drop. Recognizing the causes of acute cardiogenic pulmonary edema is crucial for timely diagnosis and effective treatment, ultimately improving patient outcomes.
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.
What are the main causes of acute heart failure?
What are the early symptoms of acute heart failure?
How is acute heart failure diagnosed?
What are the risk factors for developing acute heart failure?
Can acute heart failure be prevented?
What complications can arise from acute heart failure?
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.
Pulmonary edema develops when left-sided heart failure leads to increased pulmonary capillary pressure. As pressure rises, fluid filters out of the capillaries and accumulates in the interstitial space, causing interstitial edema. As more fluid builds up, it disrupts the intercellular membrane, allowing fluid to enter the alveolar spaces. This results in alveolar edema, severely impairing gas exchange and leading to hypoxemia and shortness of breath. The reduced ability of the lungs to diffuse oxygen further worsens respiratory distress.
Clinically, patients experience severe acute breathlessness and wheezing, making breathing increasingly difficult. They often present with a productive cough, producing pink, frothy sputum. Rapid breathing with the use of accessory muscles is common, as the body struggles to compensate for the loss of oxygen. Crepitations and rhonchi can be heard throughout the chest, indicating fluid accumulation in the lungs.
Additionally, patients show signs of extreme distress. They prefer sitting upright or standing, desperately trying to improve airflow. Profuse sweating, cold and cyanotic skin reflect low cardiac output and heightened sympathetic activity. Anxiety is overwhelming, with patients often describing a sensation of drowning. Recognizing these symptoms is crucial for timely intervention, reducing complications, and improving survival rates.
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.
Acute heart failure often presents with distinct cardiovascular features that indicate severe cardiac distress. One common symptom is tachycardia, where the heart beats faster than normal in an attempt to compensate for reduced cardiac output. This excessive heart rate places further strain on an already weakened heart, potentially worsening the condition.
Additionally, patients may exhibit raised jugular venous pressure (JVP), particularly in cases of biventricular failure. This occurs when increased pressure in the venous system signals worsening heart function. Observing JVP levels provides valuable insight into the severity of heart failure and fluid overload in the body.
Cardiac auscultation becomes challenging due to respiratory sounds. However, physicians may still detect a gallop rhythm, which indicates abnormal heart activity. The presence of an additional heart sound suggests the heart is struggling to maintain normal function.
Moreover, blood pressure often rises above the patient’s baseline unless cardiogenic shock is present. In most cases, vasoconstriction due to heightened sympathetic activity leads to increased blood pressure. However, if the patient is experiencing cardiogenic shock, blood pressure may drop significantly, exacerbating the crisis. Recognizing these cardiovascular features allows for rapid diagnosis and timely intervention, improving the chances of stabilizing the patient and preventing further complications.
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.
Investigating acute heart failure requires various diagnostic tests to assess the severity and underlying cause. An electrocardiogram (ECG) plays a vital role in detecting abnormalities. Depending on the condition, the ECG may reveal signs of ischemia or myocardial infarction (MI) or indicate left ventricular hypertrophy with a strain pattern, commonly seen in hypertension. Identifying these irregularities allows for early intervention and targeted treatment.
In addition, a chest X-ray provides crucial insights into pulmonary involvement. In cases of fluid accumulation, the X-ray often displays diffuse haziness, a clear sign of alveolar edema. Furthermore, the presence of Kerley B lines suggests interstitial edema, indicating increased pressure within the lungs. This imaging technique helps clinicians determine the extent of pulmonary congestion and assess disease progression.
Arterial blood gas analysis is another essential tool in evaluating oxygen levels and respiratory function. Initially, PaO2 and PaCO2 levels drop, reflecting poor oxygen exchange. However, as the condition worsens, PaCO2 levels start to rise, signaling respiratory distress. Moreover, an elevated pulmonary capillary wedge pressure, typically above 20 mmHg, confirms excessive fluid retention and heightened cardiac strain. Timely diagnosis through these investigations enhances treatment strategies and improves patient outcomes.
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.
Management of Acute Cardiac Failure
Managing acute cardiac failure requires prompt intervention to stabilize breathing and circulation. First, the patient should sit with legs dangling over the side of the bed. This position helps facilitate respiration and reduces venous return, easing the workload on the heart. To monitor oxygen levels, an oximeter should be connected to ensure adequate saturation.
Maintaining PaO2 above 60 mmHg is crucial, and administering high-concentration oxygen via a mask improves oxygenation. Noninvasive pressure support ventilation can also help prevent CO2 retention, ensuring better respiratory function. In cases of severe distress, mechanical ventilation or endotracheal intubation may become necessary.
For symptom relief, morphine (4-8 mg IV) is administered, along with metoclopramide (Maxolon 10 mg IV) to counteract nausea. Morphine effectively reduces anxiety and increases venous capacitance, thereby lowering left atrial pressure and alleviating breathlessness. However, it must be avoided if systolic blood pressure falls below 90 mmHg, as it may further compromise circulation.
Additionally, intravenous diuretics like Lasix (40-80 mg IV) promote rapid vasodilation, easing cardiac strain and reducing fluid overload. Immediate action with these measures significantly improves symptoms, stabilizes the patient, and prevents further complications in acute cardiac failure. Close monitoring ensures effective treatment and recovery.
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.
Peripartum cardiomyopathy is a rare but serious condition that leads to heart failure during pregnancy or within six months after delivery. It occurs in women who have no prior history of heart disease, making it an unexpected and potentially life-threatening complication. The condition typically develops in the last month of pregnancy, causing symptoms such as extreme fatigue, shortness of breath, and swelling in the legs. If left untreated, it can progress rapidly, leading to severe cardiac dysfunction.
The incidence of peripartum cardiomyopathy varies, ranging from 1 in 4,000 to 1 in 1,000 pregnancies. The risk is highest in Africa and is more common in older women, those carrying twins, and patients with pregnancy-induced hypertension. Though the exact cause remains unknown, researchers suspect immune system involvement or viral infections may trigger the disease.
Early diagnosis and appropriate management are crucial for improving outcomes. Treatment focuses on stabilizing heart function and preventing complications. In many cases, heart function gradually improves over several months, but some patients may experience persistent heart failure. Women diagnosed with this condition should receive close medical monitoring, especially if they plan future pregnancies, as recurrence can be life-threatening.
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.
Peripartum cardiomyopathy presents with symptoms similar to congestive heart failure, including fatigue, breathlessness, and fluid retention. Some patients experience atrial or ventricular arrhythmias, leading to palpitations and an irregular heartbeat. Tachycardia may also be present, signaling increased strain on the heart. The severity of symptoms varies, with some cases resolving over months while others progress to refractory heart failure, requiring lifelong management.
The disease course is unpredictable. Many women recover completely, but those whose symptoms persist for more than six months face a higher mortality risk. A subsequent pregnancy poses significant danger, as it can worsen cardiac function, increasing the risk of heart failure and complications.
Diagnostic tests help assess the severity of the condition. An ECG may reveal arrhythmias or tachycardia, indicating abnormal electrical activity in the heart. An echocardiogram often detects mural thrombi and dilated heart chambers, which can lead to pulmonary or systemic embolism.
Management focuses on stabilizing heart function and preventing complications. Treating heart failure with medications such as diuretics and beta-blockers helps alleviate symptoms. If an echocardiogram shows mural thrombi, anticoagulation therapy is recommended to reduce the risk of blood clots. Early intervention improves prognosis and enhances recovery outcomes.
Prognosis
The prognosis for peripartum cardiomyopathy varies significantly based on recovery and future pregnancies. If cardiomegaly does not resolve within six months of symptom onset, the five-year mortality rate stands at approximately 35%. However, even if heart size returns to normal, the risk remains, with a 15% mortality rate over five years. This highlights the importance of early detection and ongoing medical care.
The risks are even higher for women who experience persistent cardiomegaly and become pregnant again. In these cases, cardiomyopathy recurs in 50% of pregnancies, often leading to worsening heart failure. Alarmingly, the mortality rate for these patients approaches 100%, making another pregnancy highly dangerous. Medical professionals strongly advise against subsequent pregnancies for those whose heart function has not fully recovered.
Careful monitoring and appropriate treatment can improve outcomes, but the long-term prognosis depends on the severity of heart dysfunction and individual response to therapy. Patients who recover within six months have a better chance of leading a stable life, though they still require ongoing cardiac assessment. Understanding these risks allows for informed decisions, ensuring the best possible care and reducing the likelihood of complications in the future.
