| disease | Acute Cardiac Insufficiency |
| alias | Acutecardiacinsufficiency, Acutecardiac Insufficiency |
With the deepening of basic and clinical research on cardiac insufficiency, new insights into its pathophysiology and clinical treatment have altered traditional concepts. Cardiac insufficiency is now defined as a cardiac systolic and diastolic dysfunction caused by various disease etiologies, progressing to a state where cardiac output cannot meet the metabolic demands of blood flow under normal circulatory volume and vasomotor function. This results in a clinical syndrome characterized by hemodynamic abnormalities and neurohormonal system activation, also referred to as cardiac insufficiency syndrome or heart failure syndrome. The term "pump failure" originally referred to left heart failure in acute myocardial infarction, but it is now sometimes used broadly to describe impaired cardiac pumping function due to various disease causes. Traditionally, it was believed that all patients with cardiac insufficiency exhibited symptoms of organ congestion, hence the term "congestive heart failure." However, the modern concept recognizes that cardiac insufficiency can be divided into asymptomatic and symptomatic stages. The asymptomatic stage involves objective evidence of ventricular dysfunction (e.g., reduced left ventricular ejection fraction) without typical congestive heart failure symptoms, corresponding to NYHA (New York Heart Association) Class I. This stage is considered the precursor to symptomatic heart failure, and without effective treatment, it will eventually progress to symptomatic cardiac insufficiency. Depending on the speed of onset and the degree of circulatory system compensation, clinical manifestations can vary, including acute cardiac insufficiency, chronic cardiac insufficiency, and compensated cardiac insufficiency.
bubble_chart EtiologyThe following various causes lead to a sharp decline in cardiac output within a short period, or even the loss of blood-pumping function, resulting in acute cardiac insufficiency.
1. Acute diffuse myocardial damage causes weakened myocardial contraction, such as acute myocarditis, extensive myocardial infarction, etc.
2. Sudden mechanical obstruction increases the cardiac resistance load and impedes blood ejection, such as severe valve stenosis, ventricular outflow tract obstruction, atrial ball-valve thrombus or myxoma incarceration, pulmonary artery trunk or major branch embolism, etc.
3. Sudden increase in cardiac volume load, such as trauma, acute myocardial infarction, or infective endocarditis-induced valve damage, chordae tendineae rupture, ventricular papillary muscle dysfunction, septal perforation, aortic sinus aneurysm rupture into the cardiac chamber, as well as rapid or excessive intravenous transfusion of blood or sodium-containing fluids.
4. Sudden restriction of ventricular relaxation, such as acute massive pericardial effusion or hemorrhage, rapid ectopic rhythm, etc.
5. Severe arrhythmias, such as ventricular fibrillation (referred to as VF) and other severe ventricular arrhythmias, ventricular pause, significant bradycardia, etc., causing temporary cessation of blood ejection or a significant reduction in cardiac output.
bubble_chart Clinical Manifestations
Depending on the degree, speed, and duration of the decline in cardiac output function, as well as differences in compensatory mechanisms, there are four distinct manifestations.
(1) Syncope: A transient loss of consciousness caused by reduced cardiac output leading to cerebral ischemia is termed cardiogenic syncope. When syncope lasts for several seconds, it may be accompanied by limb spasms, apnea, cyanosis, and other symptoms, known as Adams-Stokes syndrome. Episodes are mostly brief, and consciousness usually recovers immediately afterward. This is primarily seen in cases of acute obstruction of cardiac output or severe arrhythmias.
(3) Acute pulmonary edema: This is the primary manifestation of acute left-sided cardiac insufficiency or acute left heart failure. It is mostly caused by a sudden severe reduction in left ventricular output or obstruction of left atrial outflow, leading to a sharp rise in pulmonary venous and capillary pressure. When pulmonary capillary pressure exceeds plasma colloid osmotic pressure, fluid leaks from the capillaries into the pulmonary interstitium, alveoli, and even the airways, causing pulmonary edema. A typical episode involves sudden, severe dyspnea with a respiratory rate of 30–40 breaths per minute, orthopnea, paroxysmal cough, pallor, cyanosis of the lips, profuse sweating, and often frothy sputum. In severe cases, large amounts of pink frothy fluid may gush from the mouth and nose. During the episode, heart rate and pulse increase, and blood pressure may initially rise before dropping to normal or below normal. Widespread rales and wheezing can be heard in both lungs. A gallop rhythm may be audible at the cardiac apex but is often obscured by pulmonary rales. Chest X-rays may show a classic butterfly-shaped shadow spreading outward from the hilar region. In the early stage of acute pulmonary edema (acute pulmonary edema), during the interstitial phase, the typical clinical and radiographic findings may be absent, with only dyspnea, paroxysmal cough, tachycardia, apical gallop, and pulmonary wheezing. X-rays may reveal engorgement of upper pulmonary veins, blurred hilar vessels, thickened lung markings, and interlobular septal thickening. Timely diagnosis and intervention can prevent progression to alveolar pulmonary edema.
Prodromal phase: Many patients experience prodromal symptoms days, weeks, or even months before cardiac arrest, such as worsening angina, dyspnea, or palpitations, increased fatigue, and other nonspecific complaints. These prodromal symptoms are not unique to sudden cardiac death but are common before any cardiac event. Data show that 50% of sudden cardiac death victims sought medical attention within a month before death, though their complaints were not necessarily cardiac-related. Among survivors of out-of-hospital cardiac arrest, 28% reported worsening angina or dyspnea before the event. However, prodromal symptoms only indicate a risk of cardiovascular disease and cannot identify those at risk of sudden cardiac death.
Onset period: This refers to the acute cardiovascular changes leading up to cardiac arrest, typically lasting no more than 1 hour. Common manifestations include prolonged colicky heart pain or chest pain from acute myocardial infarction, acute dyspnea, sudden palpitations, persistent tachycardia, or dizziness with blurred vision. If cardiac arrest occurs instantaneously without prior warning, 95% of cases are cardiac in origin, often involving coronary artery disease. Continuous electrocardiogram (ECG) recordings from sudden cardiac death victims frequently show changes in cardiac electrical activity hours or minutes before death, most commonly accelerated heart rate and worsening ventricular premature beats. Those who die from ventricular fibrillation often experience a preceding episode of sustained or non-sustained ventricular tachycardia. Patients presenting with arrhythmias are usually conscious and engaged in daily activities before onset, with a short onset period (from symptom appearance to cardiac arrest). The predominant ECG abnormality is ventricular fibrillation. Another subset of patients presents with circulatory failure, already in an inactive or even unconscious state before cardiac arrest, exhibiting a prolonged onset period. Non-cardiac diseases often precede terminal cardiovascular changes in these cases. ECG abnormalities in this group more frequently show ventricular standstill rather than ventricular fibrillation.
Cardiac Arrest Phase: The hallmark of this phase is complete loss of consciousness. If not immediately resuscitated, it generally progresses to the death phase within minutes. Spontaneous reversal is rare.
Cardiac arrest is a marker of clinical death, and its symptoms and signs appear in the following order: ① Disappearance of heart sounds; ② Absence of palpable pulse and unmeasurable blood pressure; ③ Sudden loss of consciousness, sometimes accompanied by brief spasms. Spasms are usually generalized and often occur within 10 seconds of cardiac arrest, occasionally with eye deviation; ④ Intermittent, sighing breaths, followed by cessation, typically occurring within 20–30 seconds of cardiac arrest; ⑤ Unconsciousness, usually occurring 30 seconds after cardiac arrest; ⑥ Pupillary dilation, appearing 30–60 seconds after cardiac arrest. However, this phase has not yet reached biological death. With timely and appropriate resuscitation, recovery is possible. The success rate of resuscitation depends on: ① How soon resuscitation is initiated; ② The location where cardiac arrest occurs; ③ The type of electrical activity abnormality (ventricular fibrillation, ventricular tachycardia, electromechanical dissociation, or asystole); ④ The patient’s clinical condition before cardiac arrest. If cardiac arrest occurs in a setting where cardiopulmonary resuscitation (CPR) can be performed immediately, the success rate is higher. In hospitals or intensive care units where immediate resuscitation is possible, the success rate primarily depends on the patient’s clinical condition before cardiac arrest: if due to acute cardiac conditions or temporary metabolic disturbances, the prognosis is better; if due to advanced chronic heart disease or severe non-cardiac conditions (e.g., renal failure, pneumonia, sepsis, diabetes, or cancer), the success rate is no higher than that of out-of-hospital cardiac arrest. The latter’s success rate mainly depends on the type of electrical activity during cardiac arrest, with ventricular tachycardia having the best prognosis (67% success rate), followed by ventricular fibrillation (25%), while asystole and electromechanical dissociation have very poor outcomes. Advanced age is also a significant factor affecting resuscitation success.
Biological Death Phase: The progression from cardiac arrest to biological death depends primarily on the type of electrical activity during cardiac arrest and the timeliness of cardiac resuscitation. For ventricular fibrillation or asystole, if CPR is not administered within the first 4–6 minutes, the prognosis is very poor. If CPR is not performed within the first 8 minutes, survival is almost impossible except under special conditions such as hypothermia. Statistical data indicate that immediate CPR by witnesses and early defibrillation are key to avoiding biological death. The most common cause of death during hospitalization after cardiac resuscitation is central nervous system injury. Hypoxic brain injury and infections secondary to prolonged ventilator use account for 60% of deaths. Low cardiac output accounts for 30%, while recurrence of fatal arrhythmias accounts for only 10%. For cardiac arrest complicating acute myocardial infarction, the prognosis depends on whether it is primary or secondary: the former occurs without hemodynamic instability, while the latter follows unstable hemodynamics. Thus, primary cardiac arrest, if immediately resuscitated, can achieve a 100% success rate, whereas secondary cardiac arrest has a poor prognosis, with a resuscitation success rate of only about 30%.
Diagnosing acute cardiac insufficiency is not difficult based on typical symptoms and signs. The main challenge lies in differentiating it from syncope, shock, and pulmonary edema caused by other factors (especially vascular insufficiency). Syncope can be ruled out as cardiac in origin if there is no significant bradycardia, tachycardia, irregular rhythm, or pauses during the episode, and if there is no underlying heart disease predisposing to acute cardiac insufficiency. Cardiogenic shock is distinguished from other types of shock by elevated venous pressure and end-diastolic ventricular pressure. When pulmonary edema is accompanied by wheezing, it should be differentiated from bronchial asthma; in such cases, a gallop rhythm at the cardiac apex supports the diagnosis of pulmonary edema. Pulmonary edema caused by other factors—such as changes in pulmonary vascular permeability due to chemical or physical agents (e.g., infection, hypoalbuminemia, allergies, toxic gas inhalation, or radiation pneumonitis), impaired interstitial lymphatic drainage (e.g., cancerous infiltration of pulmonary lymphatics), increased negative intrathoracic pressure (e.g., rapid or excessive thoracentesis), or impaired bronchial drainage (e.g., aspiration of fluid into the bronchi or loss of cough reflex)—can usually be distinguished from cardiac pulmonary edema based on relevant medical history and signs. However, it is important to note that cardiac patients may develop non-cardiogenic pulmonary edema, and cases where other causes of pulmonary edema coexist with cardiogenic pulmonary edema are not uncommon. A comprehensive assessment is necessary for accurate diagnosis.
bubble_chart Treatment Measures
First, provide appropriate treatment based on the disease cause.
(1) Treatment of Cardiogenic Syncope Cardiogenic syncope is mostly brief but may recur. Treatment should include prevention of episodes. For syncope caused by obstructed cardiac blood flow, rest in a supine or knee-chest position, warmth, and oxygen administration often provide relief. If the atrioventricular valve orifice is blocked by a thrombus or tumor, changing body position during an episode may reduce the obstruction or stop the episode. For syncope caused by severe arrhythmias, rapid control of the arrhythmia is necessary (see "Arrhythmias"). Definitive treatment involves addressing the disease cause, such as surgically relieving outflow tract obstruction, removing thrombi or tumors, or controlling arrhythmias.
(2) Treatment of Cardiogenic Shock Refer to "Shock" and "Myocardial Infarction."
(3) Treatment of Acute Pulmonary Edema Acute pulmonary edema is a medical emergency requiring prompt and effective treatment.
1. Treatment Principles ① Reduce left atrial pressure and/or left ventricular filling pressure. ② Increase left ventricular stroke volume. ③ Reduce circulating blood volume. ④ Decrease fluid infiltration into alveoli to ensure gas exchange.
2. Specific Measures
(1) Position the patient in a sitting or semi-recumbent position with legs dangling to reduce venous return from the lower extremities.
(2) Oxygen Therapy: Pulmonary congestion and reduced lung compliance increase respiratory effort and oxygen consumption in pulmonary edema patients, while mucosal congestion and edema impair gas exchange in terminal respiratory units. Mask oxygen delivery is more effective than nasal cannula. Positive-pressure oxygen not only corrects hypoxia but also reduces fluid infiltration into alveoli and decreases venous return by increasing alveolar and intrathoracic pressure. Increased venous resistance also raises peripheral venous pressure, facilitating fluid shift from blood vessels into interstitial spaces, thereby reducing circulating blood volume. However, excessive alveolar pressure may impair right ventricular output, leading to reduced stroke volume and hypotension. Adjust oxygen pressure, shorten positive-pressure duration, and extend intervals for optimal results.
(3) Sedation: Intravenous injection of 3–5 mg morphine rapidly dilates systemic veins, reduces venous return, and lowers left atrial pressure. It also alleviates dysphoria, anxiety, and dyspnea while reducing peripheral vascular resistance, thereby decreasing left ventricular afterload and increasing cardiac output. Subcutaneous or intramuscular injection may not ensure full absorption in patients with significant peripheral vasoconstriction.
(4) Sublingual or intravenous nitroglycerin can rapidly reduce pulmonary wedge pressure or left atrial pressure, often providing significant symptomatic relief but may cause hypotension. After confirming systolic blood pressure ≥13.3 kPa (100 mmHg), administer 0.3 mg sublingually, reassess blood pressure after 5 minutes, and repeat with 0.3–0.6 mg. If systolic pressure drops to ≤12 kPa (90 mmHg), discontinue.
For intravenous nitroglycerin, start at 10 μg/min and increase by 5–10 μg/min every 5 minutes under blood pressure monitoring until symptoms resolve or systolic pressure falls to ≤12 kPa (90 mmHg). Maintain the effective dose, then taper gradually to avoid rebound symptoms upon abrupt discontinuation.
(5) Intravenous injection of 40 mg furosemide or 50 mg ethacrynate sodium (diluted in 50% glucose solution). Furosemide reduces left atrial pressure and alleviates dyspnea by dilating the venous system before diuresis begins. Diuresis starts within 15–30 minutes, peaks at 60 minutes, and further reduces left atrial pressure by decreasing blood volume. Use cautiously in hypotensive patients, especially those with acute myocardial infarction or aortic stenosis, to avoid hypotension or shock.
(6) Other adjuvant treatments: ① Intravenous injection of aminophylline 0.25g (diluted with 40ml of 50% glucose and injected over 15–20 minutes) can relieve bronchospasm and alleviate dyspnea. It may also enhance myocardial contraction, dilate peripheral blood vessels, and reduce pulmonary stirred pulse and left atrial pressure. ② Digitalis preparations are highly effective for pulmonary edema caused by supraventricular tachyarrhythmias. Digitalis slows atrioventricular conduction, reducing ventricular rate and thereby improving left ventricular filling and lowering left atrial pressure. For intravenous injection of lanatoside C or digoxin, the initial dose for patients who have not used digoxin within the past week is lanatoside C 0.6mg or digoxin 0.5–0.75mg; for those who have used digoxin within the past week, it is advisable to start with a smaller dose. Intravenous digitalis preparations can constrict resistance vessels and increase afterload, making them less suitable for pulmonary edema patients with sinus rhythm. ③ For pulmonary edema caused by hypertensive heart disease, intravenous infusion of sodium nitroprusside can rapidly and effectively reduce cardiac preload and afterload, as well as lower blood pressure. The initial dosage is 15–20μg/min, increased by 5–10μg/min every 5 minutes until symptoms are relieved or systolic blood pressure drops to 13.3kPa (100mmHg) or below. Maintain the effective dose until the condition stabilizes, then gradually reduce and discontinue the medication. Sudden withdrawal may cause rebound. Long-term use can lead to cyanide and thiocyanate toxicity, so it has increasingly been replaced by nitroglycerin in recent years. Intravenous infusion of phentolamine at 0.1–1mg/min can also rapidly lower blood pressure and reduce afterload, but it may cause tachycardia and has a weaker effect on preload, making it less commonly used in recent years. ④ For pulmonary edema patients with hypotension, it is advisable to first administer dopamine intravenously at 2–10μg/kg/min to maintain systolic blood pressure at 13.3kPa (100mmHg), followed by vasodilator therapy. ⑤ Venipuncture to withdraw 300–500ml of blood can be used for pulmonary edema patients unresponsive to the above treatments, especially those caused by massive rapid fluid or blood transfusion.
