1. Definition, diagnostic steps and monitoring of acute heart failure (AHF)
1.1 Definition and clinical classification of AHF
1.1.1 Definition AHF is defined as the rapid onset of signs and symptoms secondary to abnormal cardiac function, with or without prior cardiac pathology. Cardiac insufficiency is associated with systolic or diastolic insufficiency, as well as with abnormal cardiac rhythm or anterior-posterior load mismatch.AHF is often life-threatening and requires urgent treatment.AHF can present with a number of different clinical conditions.
(1) Acute decompensated heart failure with signs and symptoms of AHF that are mild and fail to meet the criteria for cardiogenic shock, acute pulmonary edema, or hypertensive crisis.
(2) Hypertensive AHF: Signs and symptoms of hypertension with heart failure, relatively preserved left heart function, and chest x-ray consistent with acute pulmonary edema.
(3) Pulmonary edema (confirmed by chest X-ray): severe dyspnea, wet rales in the lungs, telangiectatic breathing, oxygen saturation <90%. < p="">
(4) Cardiogenic shock: Cardiogenic shock is defined as inadequate tissue perfusion due to heart failure after correction of preload, with no well-defined hemodynamic parameters. Cardiogenic shock is usually characterized by a decrease in blood pressure (systolic <90 mmhg or decrease in mean arterial pressure >30 mmHg) and/or a decrease in urine output (<0.5 ml >60 bpm, with or without evidence of organ congestion.
(5) High cardiac output heart failure is characterized by high cardiac output, rapid heart rate (caused by arrhythmias, hyperthyroidism, anemia, paget’s disease, medical or other mechanisms), warm extremities, pulmonary congestion, and low blood pressure in the presence of septic shock.
(6) Right heart failure is characterized by a low cardiac output syndrome with increased jugular venous pressure, hepatomegaly, and hypotension. In the CCU and ICU, AHF is classified differently from other classifications. The killip classification is based on clinical features and chest X-ray findings; the Forrester classification is based on clinical signs and hemodynamic features, and these classifications are used for AHF after AMI. The third classification of “clinical severity” is based on clinical manifestations and is mostly used in chronic decompensated heart failure.
1.1.2 killip classification In the treatment of AMI, the killip classification is used to provide a clinical assessment of the severity of the myocardial lesion.
l Class I – no heart failure, no clinical signs of cardiac decompensation;
l Class II – heart failure with diagnostic criteria including rales, S3 gallop rhythm, pulmonary venous hypertension, pulmonary congestion, and wet rales in the lower lung fields;
l Class III – severe heart failure with significant pulmonary edema and wet rales in the entire lung field;
l Grade IV – cardiogenic shock.
1.2 Pathophysiology of AHF
1.2.1 Vicious circle of acute heart failure The last common manifestation of the AHF syndrome is the inability of the myocardium to maintain cardiac output to meet the needs of the peripheral circulation. Without consideration of the underlying etiology of AHF, the vicious cycle of AHF (without proper treatment) can lead to chronic heart failure and death. For AHF patients to respond to therapy, myocardial insufficiency must be reversible, which is particularly important in AHF due to myocardial ischemia, myocardial stenosis, or myocardial hibernation, conditions in which the insufficiently functioning myocardium can be restored to normal with appropriate therapy.
1.2.2 Myocardial stenosis Myocardial stenosis is a myocardial insufficiency that occurs after prolonged myocardial ischemia and can persist for short periods of time even after normal blood flow is restored, a phenomenon that has been described experimentally and clinically. The mechanisms of insufficiency are oxidative overload, altered Ca2+ homeostasis in vivo, decreased sensitivity of contractile proteins to Ca2+, and the action of myocardial inhibitory factors. The intensity and duration of myocardial stonewalling depends on the prior ischemic injury.
1.2.3 Myocardial hibernation Myocardial hibernation is defined as myocardial injury due to a severe reduction in coronary blood flow, but myocardial cells remain intact. By improving myocardial blood flow and oxygenation, the hibernating myocardium can regain its normal function. Hibernating myocardium can be considered as an adaptation to reduced oxygen uptake to prevent myocardial ischemia and necrosis.
Hibernating myocardium and myocardial tonus can coexist to improve hibernating myocardium when blood flow and oxygenation are reestablished, while tonus myocardium still maintains positive inotropic reserve and responds to positive inotropic stimuli. Since these mechanisms depend on the duration of myocardial injury, rapid restoration of myocardial oxygenation and blood flow is the dominant factor in reversing these pathophysiological changes.
1.3 Diagnosis of AHF
The diagnosis of AHF is based on symptoms and signs and supported by appropriate investigations such as ECG, chest X-ray, biochemical markers and Doppler echocardiography. It should be classified as systolic or diastolic insufficiency, antegrade or retrograde left or right heart insufficiency according to the diagnostic criteria.
1.4 Monitoring of patients with AHF
Monitoring of patients with AHF should be initiated as soon as possible after arrival in the emergency department. The type and level of monitoring depends on the severity of cardiac decompensation and response to initial therapy.
1.4.1 Noninvasive monitoring
Temperature, pulse, respiration, blood pressure and ECG should be routinely monitored in all critically ill patients. Some laboratory tests should be repeated, such as electrolytes, blood creatinine, glucose, markers of infection or other metabolic disturbances, and correction of hypokalemia or hyperkalemia (Class I, Level of Evidence: C).
Pulse oximetry is a simple noninvasive device to assess oxygen saturation and should be used consistently in any unstable patient (Class I, Level of Evidence: C). The use of Doppler technology enables noninvasive monitoring of cardiac output and preload (Class IIb, Level of Evidence C).
1.4.2 Invasive monitoring
1.4.2.1 Arterial catheter: An indwelling arterial catheter should be inserted when continuous monitoring of arterial pressure is required or when multiple oxygen analyses are needed (Class IIb, Level of Evidence C).
1.4.2.2 Central venous pressure catheter: A central venous pressure catheter can be used for infusion, monitoring central venous pressure, and measuring venous oxygen saturation (SVO2) in the superior vena cava and right atrium (Class IIa, Level of Evidence C).
Central venous pressure measurement is affected by severe tricuspid regurgitation and positive end-expiratory pressure ventilation (PEEP) (Class I, Level of Evidence: C).
1.4.2.3 Pulmonary artery catheter (PAC): The PAC is a balloon float catheter used to measure superior vena cava, right atrial, right ventricular, and pulmonary artery pressures, as well as cardiac output, and also to measure mixed venous oxygen saturation, right ventricular end-diastolic volume, and ejection fraction, information that allows assessment of cardiovascular hemodynamics.
PAC is also commonly used to assess PCWP, CO, and other hemodynamic variables, and can therefore guide the treatment of diffuse pulmonary disease.
It should be kept in mind that in patients with mitral stenosis or aortic regurgitation, pulmonary and occlusive lesions, high airway pressures, and left ventricular stiffness (e.g., due to left ventricular hypertrophy, diabetes mellitus, fibrosis, obesity, ischemia), PCWP does not accurately reflect left ventricular end-diastolic pressure. Severe tricuspid regurgitation (common in patients with AHF) can overestimate or underestimate the cardiac output measured by thermodilution.
PAC is recommended in hemodynamically unstable patients who do not respond to conventional therapy and in patients with both congestion and hypoperfusion. insertion of a pulmonary artery catheter in these situations is aimed at ensuring optimal ventricular fluid load and directing vasoactive and positive inotropic drug therapy (Table 1). Prolonged placement of a pulmonary artery catheter increases complications and should be removed as soon as the condition is stabilized (Class IIb, Level of Evidence C).
In cardiogenic shock and prolonged severe hypovolemic syndrome, measurement of mixed venous oxygen saturation from a pulmonary artery catheter is recommended to assess oxygen uptake (SP O2-SVO2), and SVO2 >65% should be maintained in patients with AHF.
Table 1 Guidance of AHF treatment based on invasive hemodynamic monitoring
Hemodynamic characteristics
Prompt treatment
CI
Decrease
Decrease
Decrease
Decrease
Maintain
PCWP
Low
High or normal
High
High
High
SBP(mmHg)
>85
<85< p="">
>85
Treatment
fluid replacement
vasodilators
positive inotropes, intravenous diuretics
Vasodilators and intravenous diuretics, consider positive inotropes
IV diuretics, if BP is low use vasoconstrictive positive inotropes
Note: AHF patients: low CI is <2.2L/min/m2
Low PCWP is <14 mmhg< p="">
High PCWP is >18-20mmHg
2. Treatment of AHF
2.1 General medical problems in the treatment of AHF.
Infection: Patients with severe AHF have a tendency to have concurrent infections, commonly respiratory or urinary tract infections, sepsis, or nosocomial infections. Infections (e.g. pneumonia) in elderly heart failure patients may cause worsening heart failure and respiratory distress. Increased C-reactive protein and deteriorating general condition may be the only signs of infection (may be without fever) and routine blood cultures are recommended.
Diabetes mellitus: AHF combined with metabolic disorders, hyperglycemia often occurs, glucose control with short-acting insulin should be discontinued in favor of hypoglycemic drugs, normal blood glucose improves survival in critical care combined with diabetes mellitus.
Decomposition of metabolic status: caloric deficit and negative nitrogen balance is a problem in persistent heart failure, which is associated with reduced intestinal absorption to maintain the caloric and nitrogen balance. Serum albumin concentration and nitrogen balance help monitor metabolic status.
Renal failure: There is a close interrelationship between AHF and renal failure and renal function should be closely monitored, and these patients should be considered for protection of renal function when selecting treatment strategies.
2.2 Oxygenation and assisted ventilation
2.2.1 The focus of treatment in patients with AHF is to obtain adequate oxygenation levels at the cellular level to prevent end-organ insufficiency and the development of multivisceral failure. Maintaining SaO2 in the normal range (95%-98%) is important to allow for maximal oxygen release to the tissues and tissue oxygenation. (Class I, Level of Evidence C)
Ensure that the airway is usual, increase the concentration of oxygen administered, and if this is not effective, endotracheal intubation is feasible. (Class IIa, Level of Evidence C)
There is little evidence that increasing the dose of oxygen improves regression, and what evidence there is remains controversial. Studies have demonstrated that excess oxygen reduces coronary blood flow, decreases cardiac output, increases blood pressure, and increases systemic vascular resistance. There is no doubt that oxygen concentrations should be increased in patients with hypoxemic AHF (Class IIa, Level of Evidence C). However, in patients without hypoxemia, increasing the oxygen concentration is controversial and harmful.
2.2.2 Ventilatory support without tracheal intubation (noninvasive ventilation)
Two techniques are used for ventilation support: continuous positive airway pressure (CPAP) or noninvasive positive pressure ventilation (NIPPV), which is a method of providing mechanical ventilation to the patient without endotracheal intubation.
2.2.2.1 Rationale: Application of CPAP restores lung function and increases functional residual air volume, improves lung compliance, reduces transdiaphragmatic pressure oscillations, decreases diaphragmatic activity performance, reduces respiratory work, and therefore reduces metabolic demand. mask to the patient, with an additional PEEP during inspiration leading to a CPAP mode (also called bi-level positive pressure support, BiPAP).
The physiological benefits of this mode of ventilation are the same as those of CPAP and also include inspiratory assistance, which further increases mean intrathoracic pressure, thereby increasing the benefits of CPAP, but more importantly, further reducing respiratory work and total metabolic demand.
2.2.2.2 Evidence for the use of CPAP and NIPPV in left heart failure
Five randomized controlled studies and a recent meta-analysis have been performed in patients with cardiogenic pulmonary edema comparing the use of CPAP with standard therapy. The observed endpoints in these studies were the need for tracheal intubation, mechanical ventilation, and in-hospital mortality. The results of these studies suggest that CPAP improves oxygenation, signs and symptoms, and reduces the need for endotracheal intubation and in-hospital mortality in patients with AHF compared with standard therapy alone.
In acute cardiogenic pulmonary edema, there have been three randomized controlled trials using NIPPV, and the results suggest that NIPPV appears to reduce the need for endotracheal intubation but does not translate into reduced mortality or long-term improvement in cardiac function.
2.2.2.3 Conclusions Randomized controlled trials suggest that the use of CPAP and NIPPV in patients with acute cardiogenic pulmonary edema significantly reduces the need for endotracheal intubation and mechanical ventilation (Class IIa, Level of Evidence: A).
2.2.3 Endotracheal intubation and mechanical ventilation in AHF
Invasive mechanical ventilation is not used in patients with reversible hypoxemia and can be better restored by oxygen therapy, CPAP or NIPPV. However, unlike reversible AHF-induced respiratory muscle fatigue, which is often the cause of endotracheal intubation and mechanical ventilation, AHF-induced respiratory muscle fatigue is rare and is associated with deterioration of respiratory muscle in preexisting lesions.
The most common cause of reduced respiratory muscle contractility is reduced oxygen release associated with hypoxemia and low cardiac output. Respiratory muscle fatigue can be diagnosed by reduced respiratory rate, hypercapnia, and impaired consciousness, requiring intubation and mechanical ventilation to (1) relieve respiratory distress (reduce respiratory muscle work); (2) protect the airway from gastric reflux injury; (3) improve pulmonary gas exchange and reverse hypercapnia and hypoxemia; and (4) ensure bronchial lavage to prevent bronchial embolism and pulmonary atelectasis.
2.3 Drug therapy
2.3.1 Morphine and its analogues
Severe AHF, especially in patients with irritability and dyspnea, is indicated for the use of morphine in the early stages of treatment. (Class IIb, Level of Evidence: B).
Morphine causes venodilation and mild arterial dilation, slows heart rate, and relieves dyspnea and other symptoms in patients with CHF and AHF. The morphine dose is 3 mg IV and can be repeated if necessary.
2.3.2 Anticoagulation therapy
Anticoagulation has been used in patients with ACS with or without heart failure, and there is little evidence for the use of UFH or LMWH in the setting of AHF. In hospitalized patients with acute lesions and including heart failure, a large, placebo-controlled trial of subcutaneous enoxaparin 40 mg showed no clinical improvement but less frequent venous thrombosis. patients with AHF often have concomitant hepatic insufficiency and should be carefully monitored for anticoagulation systems. LMWH is contraindicated if creatinine clearance is <30 ml/min or used with caution and monitored for anti-Xa factor levels.
2.3.3 Vasodilators
Vasodilators are indicated in most patients with AHF and are used as first-line therapeutic agents (Table 2).
Table 2 Indications and doses of vasodilators in AHF
Vasodilator
Indication
Dose
Major side effects
Other
Nitroglycerin, isosorbide 5-mononitrate
AHF, when blood pressure is appropriate
Start at 20ug/min, increase to 200ug/min
Hypotension, headache
Tolerated with continued use
Isosorbide nitrate
AHF, when blood pressure is appropriate
Start with 1mg/h, increase to 10mg/h
Hypotension, headache
Tolerated with continued use
Sodium nitroprusside
Hypertensive crisis, cardiogenic shock, combined with intoropes
0.3-5ug/kg/min
Hypotension, cyanide poisoning
Drug is photosensitive
Nesiritide
Acute decompensated heart failure
2ug/kg IV, 0.015-0.03ug/kg/min
Hypotension
2.3.3.1 Nitrate
In AHF, especially in patients with ACS, nitrate relieves pulmonary congestion without reducing cardiac output or increasing myocardial demand for oxygen. It decreases the pre and afterload of the heart and does not reduce tissue perfusion. The effect on cardiac output depends on pre- and afterload before treatment and on the heart’s ability to respond to increased sympathetic tone induced by pressure receptors. 2 randomized trials of AHF have shown that the hemodynamically tolerated maximum dose of nitrate combined with low-dose tachyphylaxis is superior to high-dose tachyphylaxis alone. (Class I, Level of Evidence: B) In the control of severe pulmonary edema, high-dose nitrate is superior to high-dose diuretics alone.
In practice, nitrate has a U-shaped curve effect, and there may be a limited benefit to giving sub-optimal doses of vasodilators in preventing recurrence of AHF, but high doses can also reduce its benefit. Nitrates have the disadvantage of rapidly developing tolerance, especially when given intravenously at high doses, and their effectiveness is maintained for only 16-24 h.
2.3.3.2 Sodium nitroprusside
Sodium nitroprusside (0.3ug/kg/min and gradually increasing the dose to 1ug/kg/min up to 5ug/kg/min) is recommended for patients with severe heart failure and significantly increased afterload (e.g., hypertensive heart failure or mitral regurgitation). (Class I, Level of Evidence: C) Toxic reactions due to its metabolites thiocyanate and cyanide with long-term use of sodium nitroprusside, especially in patients with severe renal or hepatic failure. The dose should be gradually reduced to avoid rebound effects. Nitroglycerin is superior to sodium nitroprusside in AHF caused by ACS, because sodium nitroprusside can cause coronary steal syndrome.
2.3.3.3 Nesiritide
Nesiritide is a new class of vasodilator that has been used in the treatment of AHF. Nesiritide is a recombinant human brain peptide or BNP that is identical to endogenous hormones and is produced by the ventricle in response to increased ventricular wall tension, myocardial hypertrophy, and volume overload. Nesiritide has the property to dilate venous, arterial and coronary arteries, thereby decreasing pre and afterload and increasing cardiac output, without direct positive inotropic effects.
Intravenous infusion of Nesiritide in patients with congestive heart failure results in beneficial hemodynamic effects, leading to increased sodium excretion and inhibition of the renin-angiotensin-aldosterone system and sympathetic nervous system, relieving dyspnea. Compared to sodium nitroprusside, Nesiritide is more effective in improving hemodynamics but with fewer side effects. Experience with the clinical use of Nesiritide remains limited; the drug can cause hypotension, is ineffective in some patients, and Nesiritide does not improve the clinical regression of patients.
2.3.3.4 Calcium antagonists
Calcium antagonists are not recommended for the treatment of AHF, and the use of thioprostone, verapamil, and diisoproterenol calcium antagonists is contraindicated.
2.3.4 ACE inhibitors
2.3.4.1 ACE inhibitors are not advocated in patients with early-stage stable AHF. (Class IIb, Level of Evidence: C)
However, if these patients are at high risk, there is a role for ACE inhibitors in the early treatment of AHF and AMI. The timing of case selection and initiation of ACE inhibitor therapy remains controversial.
2.3.4.2 Benefits and mechanism of action of ACE inhibitors The hemodynamic benefits of ACE inhibitors are due to reduced AII production and increased bradykinin levels, in other words reduced total peripheral vascular resistance, reduced left ventricular remodeling and facilitated sodium excretion, short-term treatment is accompanied by reduced AII and aldosterone, increased angiotensin I and plasma renin activity.
ACE inhibitors reduce renal vascular resistance, increase renal blood flow and promote sodium and water excretion, with no change or a mild decrease in glomerular filtration rate and therefore a decrease in filtration fraction. This is due to a relatively greater effect of dilating the small outgoing than the small incoming glomerular arteries, resulting in a decrease in glomerular capillary hydrostatic pressure and glomerular filtration rate. The natriuretic effect is due to improved renal hemodynamics and reduced release of aldosterone. Bradykinin acts directly on the renal tubules and direct inhibition of angiotensin effects on the kidney.
2.3.4.3 Clinical application Intravenous ACE inhibitors should be avoided, and ACE inhibitors should be administered in small initial doses, gradually increasing the dose after early stabilization over 48 h, and monitoring blood pressure and renal function for at least 6 weeks with ACE inhibitors. (Class I, Level of Evidence: A)
ACE inhibitors should be used with caution in patients with borderline cardiac output because it significantly reduces glomerular filtration rate, and there is an increased risk of intolerance to ACE inhibitors in patients on concomitant NSAIDs and bilateral renal artery stenosis.
2.3.5 Diuretics
2.3.5.1 Patients with AHF who have symptoms of fluid retention are indications for diuretics. (Class I, Level of Evidence: B)
2.3.5.2 Benefits and mechanism of action of diuretics Diuretics increase urine output by increasing excretion of water, sodium chloride, and other ions, leading to a decrease in plasma and extracellular fluid volume, total body fluid, and sodium, a decrease in left and right ventricular filling pressures, and a decrease in peripheral vascular congestion and pulmonary edema. intravenous climbing diuretics also act as vasodilators, as evidenced by an early (5-30 min) decrease in right atrial, Pulmonary artery wedge pressure and pulmonary vascular resistance were reduced.
High-dose “bullet” injections (>1 mg/kg) are associated with a risk of reflex vasoconstriction. In contrast to long-term diuretic use, in severe decompensated heart failure, diuretics used in normal load states can reduce neuroendocrine activity in the short term, especially in patients with ACS who should be treated with low-dose diuretics.
2.3.5.3 Clinical application A loading dose given intravenously followed by a continuous intravenous drip is more effective than a “pill” injection alone. Thiazide and spironolactone diuretics can be combined with climbing diuretics, which are more effective in small doses and have fewer side effects than large doses of individual drugs. Clonidine diuretics in combination with dobutamine, dopamine, or nitrate are more effective and have fewer side effects than diuretics alone. (Class IIb, Level of Evidence: B)
2.3.5.4 Diuretic resistance Diuretic resistance is defined as a clinical state in which the response to diuretics is diminished or absent before the goal of edema relief is obtained. Diuretic resistance is associated with a poor prognosis and is more common in patients on long-term diuretic therapy for severe chronic heart failure and is also seen in acute volume depletion after intravenous climbing diuretics. Diuretic resistance is attributable to many factors (Table 3), and many therapeutic approaches have been explored to overcome diuretic resistance (Table 4), with continuous tachyphylaxis being more effective than a single “bullet” injection.
Table 3 Causes of diuretic resistance
Intravenous volume depletion
Neuroendocrine activation
Na+ uptake rebound after volume loss
Hypertrophy of the distal renal unit
Reduced renal tubular secretion (renal failure, NSAIDs)
Reduced renal perfusion (low cardiac output)
Impaired intestinal absorption of diuretics
Poor compliance with drugs or food (high sodium intake)
Table 4 Treatment of diuretic resistance
Restrict Na+/H2O intake and monitor electrolytes
Replenish blood volume deficit
Increase diuretic dose and/or frequency of administration
Intravenous “pellet” injection (more effective than oral) or intravenous drip of 5-40 mg/h (higher dose “pellet” injection more effective)
Diuretic combination therapy: tachyphylaxis + HCT; tachyphylaxis + spironolactone; metolazol + tachyphylaxis (also useful in renal failure)
Reduce ACE inhibitor dose or use very low dose ACEI
Consider ultrafiltration or dialysis if no response to the above treatment
2.3.5.5 Side effects
Although diuretics can be used safely in most patients, side effects are common and potentially life-threatening, including neuroendocrine activation, especially of the RAS and sympathetic nervous system, hypokalemia, hypomagnesia and hypochlorhydria, the latter of which can lead to severe arrhythmias, and nephrotoxicity and exacerbation of renal failure can occur with diuretics. Excessive diuresis decreases venous pressure, pulmonary artery wedge pressure, and diastolic filling of the heart, especially in patients with severe heart failure, predominantly diastolic insufficiency, or ischemic right heart insufficiency. Intravenous administration of acetazolamide (1 or 2 doses) helps to correct alkalosis.
2.3.5.6 New diuretics Several new diuretics are under investigation, including vasopressin V2 receptor antagonists, brain natriuretic peptide, and adenosine receptor antagonists. Vasopressin V2 receptor antagonists inhibit the action of vasopressin on the renal collecting duct and therefore increase the clearance of free water. The diuretic effect depends on the level of sodium and is enhanced at low sodium levels. Adenosine receptor antagonists reduce proximal tubular Na+ and water reabsorption and act as diuretics, but do not cause urinary potassium excretion.
2.3.6 Beta-blockers
2.3.6.1 Indications and rationale for β-blockers There are no studies of β-blockers in the treatment of AHF; instead, β-blockers are considered a contraindication to the treatment of AHF. Patients with ischemic chest pain ineffective to opiates, recurrent ischemia, hypertension, tachycardia, or arrhythmias should be considered for intravenous administration of beta-blockers.
2.3.6.2 Clinical Applications Patients with overt AHF and a high number of basilar wet rales should be used with caution with beta-blockers, and these patients may be considered for intravenous metoprolol (Class IIb, Level of Evidence: C) if they have progressive myocardial ischemia and tachycardia. However, β-blockers should be started early in patients with stable AMI after AHF (Class IIa, Level of Evidence: B). β-blockers should be started in patients with CHF after the acute phase (usually after 4 days) when the disease has stabilized (Class I, Level of Evidence: A).
2.3.7 Orthomolecular drugs
2.3.7.1 Clinical indications Inadequate peripheral vascular perfusion (hypotension, hyporenal function) with or without pulmonary congestion or pulmonary edema, when ineffective to the most appropriate dose of diuretics and vasodilators, is an indication for the use of positive inotropic drugs (Figure 1). (Class IIa, level of evidence: C)
AHF with systolic insufficiency
Oxygenation/CPAP
Tachypnea ± vasodilators
Clinical assessment
SBP >100mmHg
SBP 85-100 mmHg
SBP <85 mmHg
Vasodilators
(NTG, sodium nitroprusside, BNP)
Vasodilators and/or positive inotropic drugs
(dobutamine, PDEI or Levosimendan)
Volume loading? Positive inotropics and/or dopamine >5ug/kg/min and/or norepinephrine
Good response; oral tachyphylaxis, ACEI
No response: device therapy, orthomuscular drugs
Figure 1 Application of positive inotropic drugs in AHF
Orthomimetic drugs are potentially harmful because they increase oxygen demand and calcium load, and should be used with caution. In patients with decompensated CHF, whose symptoms, clinical course and prognosis depend on hemodynamics, improvement of hemodynamic parameters may become a therapeutic goal, in which case positive inotropic drugs may be useful and life-saving.
However, the beneficial effect of improving hemodynamic parameters is partially offset by the risk of arrhythmias (in some patients, myocardial ischemia) and the long-term progression of myocardial insufficiency due to excessive increase in energy depletion. However, the risk-benefit ratio is not the same for all positive inotropic drugs, and the effect of increasing cytoplasmic Ca2+ concentrations in cardiomyocytes through stimulation of β1-adrenergic receptors may be associated with a higher risk of this drug.
2.3.7.2 Dopamine
Dopamine is an endogenous catecholamine, a precursor of norepinephrine, which acts dose-dependently on 3 different receptors: dopaminergic receptors, β-adrenergic receptors, and α-adrenergic receptors.
Small doses (<2ug/kg/min) of dopamine act only on peripheral dopaminergic receptors, directly and indirectly reducing peripheral vascular resistance, with the most pronounced dilatation of renal, visceral, coronary and cerebrovascular beds, improving renal blood flow, glomerular filtration rate, diuresis and sodium excretion rate, and increasing the response to diuretics in patients with renal hypoperfusion and renal failure.
Larger doses (> 2ug/kg/min, IV) of dopamine directly and indirectly stimulate β-adrenergic receptors and increase myocardial contractility and cardiac output. Doses > 5ug/kg/min act on α-adrenergic receptors to increase peripheral vascular resistance, which worsens heart failure due to increased left ventricular afterload, pulmonary artery pressure, and vascular resistance.
2.3.7.3 Dobutamine Dobutamine is a positive inotropic drug that acts primarily through stimulation of β1 and β2 receptors (3:1 ratio), and its clinical effects are the result of direct dose-dependent positive inotropic effects and increased heart rate, secondary to adaptation to increased cardiac output, such as decreased sympathetic tone in patients with heart failure, resulting in decreased vascular resistance. Small doses of dobutamine cause mild arterial dilation and increase cardiac beat volume by decreasing afterload, while high doses of dobutamine cause vasoconstriction.
Heart rate usually increases in a dose-dependent manner, with a smaller increase in heart rate than with other catecholamines. However, the increase in heart rate is more pronounced in patients with atrial fibrillation because of the accelerated atrioventricular conduction. Arterial pressure in the body circulation usually increases mildly, but may remain unchanged or decrease. Similarly, pulmonary artery pressure and pulmonary capillary wedge pressure are usually decreased, but may be unchanged or even increased in individual patients with heart failure.
2.3.7.4 Clinical Applications In patients with heart failure with hypotension, dobutamine may be used as a positive inotropic agent (>2ug/kg/min), and in patients with heart failure with hypotension and oliguria, small doses (≤2-3ug/kg/min) of intravenous dobutamine are used to improve renal blood flow and diuresis, and treatment may be discontinued if there is no response (Table 5). (Class IIb, level of evidence: C)
Table 5 Application of positive inotropic drugs
Intravenous push injection
Intravenous drip
Dobutamine
None
2-20ug/kg/min (β+)
Dopamine
None
< 3ug/kg/min: renal effect
3-5 ug/kg/min: positive muscle power (β+)
>5 ug/kg/min: vasopressure (α+)
Milrinone
25-75ug/kg, >10-20min
0.375-0.75 ug/kg/min
Enoximone(Enoximone)
0.25-0.75mg/kg
1.25-7.5 ug/kg/min
Levosimendan
12-24ug/kg, >10min
0.1ug/kg/min, can be reduced to 0.05 or increased to 0.2ug/kg/min
Norepinephrine
None
0.2-1.0ug/kg/min
Adrenaline
1mg at resuscitation, iv, repeated 3-5min later, no benefit from intratracheal administration
0.05-0.5ug/kg/min
Dobutamine is used to increase cardiac output and is usually started at 2-3ug/kg/min intravenously, then the dose is adjusted according to symptoms, diuretic response or hemodynamic monitoring. The hemodynamic effect is proportional to the dose and can be increased to 20ug/kg/min. The drug is rapidly excreted after discontinuation of the infusion and is very easy to use.
In patients treated with the beta-blocker metoprolol, the dose of dobutamine can be increased to 15-20ug/kg/min to restore its positive inotropic effect. The effect of dobutamine is different in patients receiving carvedilol: when the dose of dobutamine is increased to 5-20ug/kg/min, it leads to an increase in pulmonary vascular resistance.
Based on hemodynamic data alone, the positive inotropic effects of dobutamine are additive to those of phosphodiesterase inhibitors (PDEI), and the combination of the two is stronger than the positive inotropic effects of each drug alone.
Prolonged dobutamine infusion time (24-48 h) is associated with resistance and partial loss of hemodynamic effects. Withdrawal of dobutamine may be difficult because of recurrence of hypotension, congestion, or renal insufficiency. This can sometimes be resolved by gradual reduction of dobutamine dosage (i.e., 2ug/kg/min every other day) and optimal oral vasodilator therapy, such as hydrazidiazide and/or ACE inhibitors.
Intravenous dobutamine increases the incidence of atrial and ventricular arrhythmias, an effect that is dose-related and more common than with phosphodiesterase inhibitors, and should be rapidly supplemented with potassium salts when diuretics are used intravenously. Tachycardia also limits its use, and dobutamine can provoke chest pain in patients with coronary artery disease. In patients with hibernating myocardium, a short-term increase in myocardial contractility in conditions of damage to the myocardium and recovery from loss of myocardium.
Pulmonary edema when there is peripheral tissue hypoperfusion (hypotension, hyporenal function) with or without congestion or ineffective to the most appropriate dose of diuretics and vasodilators is an indication for the use of dobutamine. (Class IIa, Level of Evidence: C)
2.3.7.5 Phosphodiesterase inhibitors (PDEIs) Type III phosphodiesterase inhibitors block the degradation of cAMP to AMP. milrinone and enoximone are two PDEIs used clinically. when used in severe heart failure, these drugs have significant positive inotropic and peripheral vasodilatory effects, increase cardiac stroke volume and cardiac output, and decrease pulmonary artery pressure, pulmonary artery wedge pressure, and systemic and pulmonary vascular resistance .
Patients with evidence of peripheral tissue hypoperfusion, with or without congestion, ineffective to optimal doses of diuretics and vasodilators, and normal blood pressure are indications for the use of type III PDEIs. (Class IIb, Level of Evidence: C)
PDEI is preferable when dobutamine is used concomitantly with beta-blockers and/or when there is a poor response to dobutamine. (Class IIa, Level of Evidence: C)
Milrinone and enoximone are less likely to cause thrombocytopenia than amrinone.
2.3.7.6 Vasopressin for cardiogenic shock Because of the combination of cardiogenic shock with elevated vascular resistance, increased afterload on the failing heart and further reduction in end-organ blood flow, any vasopressin should only be used with caution for short periods of time.
2.3.7.7 Epinephrine Epinephrine is a catecholamine with high affinity for β1, β2, and α receptors. When dobutamine is ineffective and blood pressure remains low, epinephrine 0.05-0.5ug/kg/min intravenously can be used. The use of epinephrine requires direct monitoring of arterial pressure and monitoring of hemodynamic response with PAC.
2.3.7.8 Norepinephrine Norepinephrine is a catecholamine with a high affinity for alpha receptors and is commonly used to increase systemic vascular resistance. Norepinephrine induces a milder increase in heart rate than epinephrine and is administered at the same dose as epinephrine. Norepinephrine is often used in combination with dobutamine to improve hemodynamics. Norepinephrine improves end-organ perfusion.
2.3.7.9 Cardiac glycosides Cardiac glycosides inhibit myocardial Na+/K+ ATPase, thus increasing Ca2+/Na+ exchange and producing a positive inotropic effect. In CHF, cardiac glycosides reduce symptoms and improve clinical status and reduce the risk of hospitalization for heart failure, but have no effect on survival. In AHF syndrome, cardiac glycosides caused a mild increase in cardiac output and a decrease in filling pressures. In addition, in patients with myocardial infarction and AHF, digitalis is a predictor of life-threatening arrhythmogenic events and therefore prednisone is not recommended for use in AHF, especially after myocardial infarction.
The indication for the use of cardiac glycosides in AHF is tachycardia-induced heart failure, where the ventricular rate of atrial fibrillation cannot be controlled with other drugs (e.g., beta-blockers). effective control of the ventricular rate of tachyarrhythmias in AHF can control the symptoms of heart failure. Contraindications to cardiac glycosides include bradycardia, second- and third-degree AV block, sick sinus node syndrome, carotid sinus syndrome, pre-excitation syndrome, hypertrophic obstructive cardiomyopathy, and hypokalemia and hypercalcemia.
2.4 Underlying diseases of AHF
2.4.1 Coronary heart disease
AHF induced or complicated by coronary artery disease can manifest as antegrade failure (including cardiogenic shock), left heart failure (including pulmonary edema), or right heart failure. reperfusion therapy with AMI significantly improves or prevents AHF. cardiogenic shock due to ACS should be treated with coronary angiography and revascularization as soon as possible (Class I, Level of Evidence: A). Metabolic support with high-dose glucose, insulin, and potassium salts is not recommended (Class IIa, Level of Evidence: A).
Left ventricular assisted pump mechanical support should be considered when all measures to obtain a stable hemodynamic status have failed, especially in patients awaiting cardiac transplantation.
Emergency management of left heart failure/pulmonary edema is similar to that of other causes of pulmonary edema, where positive inotropic drugs may be harmful and intra-aortic balloon counterpulsation (IABP) should be considered.
Long-term treatment strategies include coronary revascularization, RAAS inhibitors, and β-blockers.
2.4.2 Heart Valve Disease
Acute aortic or mitral valve insufficiency or aortic or mitral stenosis, prosthetic valve thrombosis, or aortic coarctation can cause AHF. However, infective endocarditis is a common cause of AHF, and severe acute aortic or mitral regurgitation should be treated with early surgery.
Emergency surgical intervention does not improve the prognosis if there is prolonged mitral regurgitation and a decrease in cardiac index to <1.5 L/min/m2 and ejection fraction <35%. Endocarditis complicated by severe acute aortic regurgitation is an indication for urgent surgery. < p="">
2.4.3 Treatment of AHF due to prosthetic valve thrombosis
The treatment of AHF due to prosthetic valve thrombosis (PVT), which has a high mortality rate, remains controversial, with thrombolytic therapy feasible in patients at high risk for right heart prosthetic valves and surgery and surgical treatment preferred for left heart prosthetic valve thrombosis (Class IIa, Level of Evidence: B).
Emergency surgery in critically ill patients with hemodynamic instability (NYHA class III/IV, pulmonary edema, hypotension) has a high mortality rate, but thrombolytic therapy is not effective until 12 h. This delay can lead to further deterioration, and failure of thrombolytic therapy increases the risk of reoperation.
Patients with NYHA class I/II or non-obstructive thrombosis have a low surgical mortality rate, and recent data from non-randomized trials suggest that long-term antithrombotic and/or thrombolytic therapy has the same efficacy in these patients. Thrombolytic therapy is ineffective when fibrous tissue grows into the thrombus (vascular opacification). Very large and/or active thrombi, where thrombolytic therapy is associated with a high risk of major embolism and stroke, should be treated surgically as an option in all these patients. Transesophageal ultrasound is used to rule out vascular opacity formation or structural defects of the prosthetic valve before deciding on surgical treatment.
Thrombolytic therapy: tPA 10 mg IV push followed by 90 mg IV drip over 90 min; streptokinase 250-500,000 IU IV over 20 min followed by 1-1.5 million IU IV drip over 10 h. After thrombolysis all patients should be treated with IV plain heparin (control aPTT at 1.5-2.0 times); urokinase 4400 IU/kg/h. continuous IV drip for 12h without heparin or 2000 IU/kg/h continuous IV drip for 24h with heparin.
2.4.4 Aortic coarctation
Acute aortic coarctation (especially type I coarctation) may present with symptoms of heart failure with or without pain. AHF is usually associated with hypertensive crisis, aortic valve closure insufficiency, or myocardial ischemia.
2.4.5 AHF and hypertension
AHF is one of the known acute complications of hypertension, the latter being defined as a state in which immediate lowering of blood pressure (not necessarily to normal values) is required to prevent or limit organ damage including encephalopathy, aortic coarctation, or acute pulmonary edema.
Epidemiological data on hypertension-induced pulmonary edema show that it is usually seen in older adults (especially women >65 years of age) with a long history of hypertension, left ventricular hypertrophy, or inadequate treatment. The clinical signs of AHF associated with hypertensive crisis are almost exclusively signs of pulmonary congestion, which can be mild or very severe to acute pulmonary edema in both lungs, and because it occurs rapidly, it is called “lightning Because of its rapid onset, it is called “flash” pulmonary edema and requires rapid management.
The goals of treatment of acute pulmonary edema with hypertension are to reduce left ventricular preload and afterload, reduce myocardial ischemia and maintain adequate ventilation. Treatment should be started immediately with: oxygenation, CPAP or non-invasive ventilation, mechanical ventilation if necessary, usually for a shorter period of time, and intravenous administration of anti-hypertensive drugs.
The goal of antihypertensive therapy is to rapidly (within minutes) reduce systolic or diastolic blood pressure by 30 mmHg, followed by further reduction to pre-critical levels (which takes several hours); do not attempt to return to normotension, as this can cause inadequate organ perfusion.
If hypertension persists, the following drugs may be administered alone or in combination.
(1) Intravenous climbing diuretics, especially in patients with a long history of CHF and significant fluid retention;
(2) Intravenous nitroglycerin or sodium nitroprusside to reduce venous preload and arterial afterload and to increase coronary blood flow;
(3) use of calcium channel blockers (e.g., nicardipine), as these patients often have diastolic insufficiency and increased afterload. Nicardipine can cause adrenergic activation (tachycardia), increased intrapulmonary shunts (hypoxemia) and central nervous system complications.
In the presence of coexisting pulmonary edema, beta-blockers are not recommended among the drugs used to treat hypertensive crisis. However, in some cases, particularly hypertensive crisis associated with pheochromocytoma, slow intravenous labetalol (Labetalol) 10 mg with monitoring of heart rate and blood pressure followed by an intravenous drip of 50-200 mg/h may be effective.
2.4.6 Renal failure
Heart failure and renal failure often coexist, with heart failure causing renal hypoperfusion through activation of neuroendocrine mechanisms. Concomitant therapy (e.g., diuretics, ACEI by dilating the small outflowing arteries; non-steroidal anti-inflammatory drugs by inhibiting dilation of the small incoming arteries) also contributes to the development of renal failure. Initially, hypoperfusion to the kidney can be compensated by self-regulation of renal blood flow and small efferent artery constriction, but in later stages, renal function in patients with severe heart failure is largely dependent on incoming blood flow to the point where renal failure and oliguria are common.
Urinalysis findings depend on the etiology of renal failure and are characterized by a urinary Na +/K+ ratio < 1 when renal failure is secondary to hypoperfusion. Acute tubular necrosis can be diagnosed based on increased urinary sodium, decreased urinary nitrogen concentration and typical urinary sediment findings.
Mild-moderate renal impairment is usually asymptomatic and well tolerated, but even mild-moderate increases in serum creatinine and/or decreases in glomerular filtration rate are independently associated with a poor prognosis.
Administration of ACEI to patients with renal failure increases the incidence of severe renal failure and hyperkalemia, and serum creatinine >3.5 mg/dl (>266 umol/L) is a relative contraindication to continuous ACEI therapy.
Moderate-to-severe renal failure (i.e., blood creatinine >2.5-3 mg/dl (190-226 umol/L) is also associated with a reduced response to diuretics – a clear predictor of death in patients with HF, such patients may require increasing doses of climbing diuretics and/or adding a diuretic with a different mechanism of action diuretic with a different mechanism of action (e.g., metozatone), but this may be combined with hypokalemia and a further decrease in glomerular filtration rate.
Patients with severe renal insufficiency and intractable fluid retention may require continuous veno-venous hemofiltration (CVVH), and CVVH combined with positive inotropic agents may increase renal blood flow, improve renal function, and restore the diuretic effect. Loss of renal function may require dialysis treatment, especially with hyponatremia, acidosis and uncontrolled significant fluid retention. The choice between peritoneal dialysis, hemodialysis or hemofiltration depends on the available techniques and the underlying blood pressure.
Patients with heart failure are at the highest risk of renal damage after contrast administration, which is attributable to reduced renal perfusion and direct tubular damage from the contrast agent. Other methods to prevent contrast-induced renal failure and concomitant HF that are better tolerated by patients include the use of minimal doses of isotonic contrast media, avoidance of nephrotoxic drugs such as NSAIDs, and the use of selective DA1 receptors. anti-inflammatory drugs and the selective DA1 receptor antagonist fenoldopam.
Perioperative hemodialysis is effective in preventing nephropathy in patients with severe renal insufficiency. (Class IIb, Level of Evidence: B)
2.4.7 Cardiac arrhythmias and AHF
2.4.7.1 Bradyarrhythmias Bradycardia in patients with AHF is commonly associated with AMI, especially with right coronary artery occlusion. Treatment of bradyarrhythmias is initially with atropine 0.25-0.5 mg intravenously and can be repeated if needed. In patients with atrial separation with low ventricular reactivity, intravenous isoprenaline 2-20ug/min should be avoided in patients with myocardial ischemia.
Atrial fibrillation with slow ventricular rate can be treated with intravenous aminophylline 0.2-0.4 mg/kg/h. If there is no response to drug therapy, a temporary pacemaker should be implanted, and myocardial ischemia should be treated as soon as possible before and after pacemaker implantation (Table 6). (Class IIa, level of evidence: C)
2.4.7.2 Supraventricular tachycardia Supraventricular tachycardia can cause AHF. Atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia are occasionally seen in AMI, and delayed (>12 h) arrhythmias are usually associated with more severe heart failure (60% are killip class III or IV).
2.4.7.3 Treatment recommendations for paroxysmal supraventricular tachycardia in heart failure Controlling the ventricular rate in patients with AF and AHF is important, especially in patients with diastolic insufficiency (Table 6). (Class IIa, level of evidence: A)
Patients with AHF and atrial fibrillation should be anticoagulated. Paroxysmal AF should be considered for pharmacologic or electrical resuscitation, and anticoagulation should be used for 3 weeks and medications to obtain an optimal heart rate if AF persists >48 h before resuscitation. If hemodynamically unstable, urgent electrical resuscitation should be performed and thrombus should be excluded by transesophageal ultrasound prior to resuscitation.
Acute atrial fibrillation should be avoided with isoptin and thiazepam, as they can worsen heart failure and cause third-degree atrioventricular block. Amiodarone and beta-blockers may be used to control heart rate and prevent recurrence (Class I, Level of Evidence: A).
Rapid digitalisization may be considered, especially in atrial fibrillation secondary to AHF. Verapamil may be considered for the treatment of supraventricular tachycardia in patients with only mild systolic hyposystole, atrial fibrillation or narrow QRS waves. Class I antiarrhythmic agents should be avoided in patients with low ejection fraction, especially in wide QRS waves. Among the pharmacological resuscitators, dofetilide is a promising new drug, but further studies on its efficacy and safety are still needed.
If beta-blockers are tolerated, it can be tried in supraventricular tachycardia. Patients with wide QRS wave tachycardia can be terminated with intravenous adenosine, and electrical cardioversion can be considered in patients with AHF with hypotension. patients with AHF with AMI and diastolic heart failure cannot tolerate tachyarrhythmias. Serum potassium and magnesium levels should be monitored, especially in patients with ventricular arrhythmias. (Class IIb, Level of Evidence: B)
2.4.7.4 Treatment of life-threatening arrhythmias Ventricular tachycardia or ventricular fibrillation requires immediate electrical cardioversion (Table 6), and amiodarone and β-blockers prevent these arrhythmias from occurring (Class I, Level of Evidence: A).
Table 6 Treatment of arrhythmias in the presence of AHF
Ventricular fibrillation or ventricular tachycardia without pulsation
200-300-360 J defibrillation (preferably with 200 J biphasic defibrillation) or, if ineffective for the first shock, intravenous epinephrine 1 mg or pressin 40 IU and/or amiodarone 150-300 mg
Ventricular tachycardia
If the condition is unstable, electrical resuscitation can be performed, if the condition is stable, drug resuscitation with amiodarone or lidocaine can be performed.
Sinus tachycardia or supraventricular tachycardia
β-blockers when clinically and hemodynamically tolerated: metoprolol 5mg IV (repeat if tolerated); esmolol 0.5-1.0mg/kg IV for 1 min followed by 50-300ug/kg/min IV or labetalol 1-2mg IV followed by 1-2mg/min IV (total 50-200mg). 200mg). Labetalol may also be used for AHF associated with hypertensive crisis or pheochromocytoma, 10mg IV, 300mg total.
Atrial fibrillation or atrial flutter
If possible then resuscitation, digoxin 0.125-0.25mg IV or beta-blockers or amiodarone to slow atrioventricular conduction. Amiodarone induces pharmacologic resuscitation without impairing left ventricular hemodynamics. Patients should be heparinized.
Bradycardia
Atropine 0.25-0.5 mg intravenously for a total of 1-2 mg. as a temporary measure, isoprenaline 1 mg in 100 ml of saline intravenously for a maximum of 75 ml/h (2-12ug/min). In case of atropine resistance, temporary transcutaneous or transvenous pacing may be used. For atropine-resistant AMI patients use glycopyrrolate sodium 0.25-0.5 mg/kg IV followed by 0.2-0.4 mg/kg/h.
2.4.8 Perioperative AHF
Perioperative AHF is usually associated with myocardial ischemia. Perioperative cardiac complications including myocardial infarction and death are approximately 5% in patients with at least 1 of the following cardiovascular risk factors: age >70 years, angina pectoris, history of infarction, congestive heart failure, treated ventricular arrhythmias, treated diabetes mellitus, limited exercise tolerance, hyperlipidemia, or smoking. The highest incidence is seen within the first 3 days postoperatively. Most importantly, postoperative coronary instability is usually of the silent type, i.e., not combined with chest pain.
2.5 Surgical treatment of AHF
2.5.1 AHF associated with complications of AMI
2.5.1.1 Free wall rupture: The incidence of free wall rupture after AMI is 0.8-6.2%, usually due to pericardial tamponade or electro-mechanical separation within minutes of sudden death, and the diagnosis is rarely obtained before death. However, in some cases presenting as subacute cases (thrombotic or adhesive closure of the rupture) there is an opportunity for intervention.
Most of these patients present with cardiogenic shock, sudden hypotension and/or loss of consciousness, and some have chest pain, malignancy, vomiting, or ST-segment re-elevation or T-wave changes in infarct-related leads prior to rupture. All these patients should undergo immediate echocardiography, and the diagnosis can be established based on the clinical presentation, depth of pericardial effusion >1 cm, and ultrasound density of the effusion. Temporary hemodynamic stabilization can be achieved by treatment with pericardiocentesis, fluid replacement and positive inotropic drugs. Free wall rupture is also a rare complication of echocardiographic dobutamine loading test after AMI.
2.5.1.2 Post-myocardial infarction septal rupture (VSR): VSR occurs in approximately 1-2% of AMI patients and usually occurs in the first 1-5 days after MI. The main sign is the presence of a holosystolic murmur at the left lower border of the sternum. Echocardiography provides a definitive diagnosis and assessment of ventricular function, identifying the site of VSR, the area of the left-to-right shunt, and coexisting mitral valve insufficiency (Class I, Level of Evidence: C).
Patients with hemodynamic compromise should be treated with intra-aortic balloon counterpulsation, vasodilators, positive inotropic drugs, and assisted ventilation. Coronary angiography is usually performed because several small retrospective studies have shown that concomitant revascularization improves late cardiac function and survival.
Virtually all medically treated patients die, and most patients should undergo surgery immediately after definitive diagnosis. In-hospital mortality in patients undergoing surgical repair of VSR is 20-60%, with improved prognosis recently reported due to improved surgical and myocardial protection. The current consensus is that surgical treatment should be performed rapidly after the diagnosis is made, as the rupture can suddenly enlarge and lead to cardiogenic shock. (Class I, Level of Evidence: C)
Transcatheter occlusion of VSR has been used in stable patients with good results, but more experience is needed to recommend its use.
Recently, left ventricular outflow tract obstruction with compensatory hyperdynamic cardiac basal ganglia has been reported as a new cause of systolic murmur and cardiogenic shock in patients with anterior wall apical myocardial infarction.
2.5.1.3 Acute mitral regurgitation: Severe acute mitral regurgitation after AMI is seen in about 10% of patients in cardiogenic shock; it occurs 1-14 days (usually 2-7 days) after infarction, and most acute mitral regurgitation due to complete rupture of the papillary muscle dies in the first 24 h after onset if not treated surgically.
Partial rupture of the papillary muscle is more common and has a higher survival rate than complete rupture. In most patients, acute mitral regurgitation is secondary to papillary muscle insufficiency rather than rupture. Endocarditis is also a cause of severe mitral regurgitation and requires surgical repair.
Severe acute mitral regurgitation presents with pulmonary edema and/or cardiogenic shock. Patients with severe mitral regurgitation due to papillary muscle rupture and markedly elevated left atrial pressures may not have a characteristic apical systolic murmur. Chest x-ray shows pulmonary congestion (possibly unilateral).
Pulmonary artery catheterization is used to rule out VSR, pulmonary capillary wedge pressure scans show large regurgitant V waves, and ventricular filling pressures may be used to guide patient management (Class IIb, Level of Evidence: C).
Prior to cardiac catheterization and angiography, most patients require intra-aortic balloon counterpulsation (IABP) for stabilization. When a patient develops acute mitral regurgitation, early surgical treatment is indicated because of the sudden deterioration and other complications that can occur. Severe acute mitral regurgitation, pulmonary edema, or cardiogenic shock require emergency surgery (Class I, Level of Evidence: C).
2.6 Mechanical Assist Devices and Heart Transplantation
2.6.1 Indications
Patients with AHF who do not respond to conventional therapy, or as a bridge to heart transplantation, or where intervention may lead to significant recovery of cardiac function are indications for temporary mechanical assisted circulation (Class IIb, Level of Evidence: B).
2.6.1.1 Intra-aortic balloon counterpulsation pump (IABP): In cardiogenic shock or severe acute left heart failure, intra-aortic balloon counterpulsation has become an integral part of standard therapy: (1) in patients who do not respond to rapid rehydration, vasodilators, and positive inotropic drug support; and (2) in acute left heart failure complicated by significant mitral regurgitation or septal rupture, the use of IABP to obtain hemodynamic stability to allow for definitive diagnostic testing or treatment; (3) left heart failure with severe myocardial ischemia, for which IABP can be used to prepare for coronary angiography or angioplasty.
IABP can dramatically improve hemodynamics, but its use is limited to patients whose underlying lesions can be corrected (e.g., coronary revascularization, valve replacement, or heart transplantation) or who can recover spontaneously (e.g., very early post-AMI myocardial stenosis, myocarditis). IABP is contraindicated in patients with aortic coarctation or significant aortic valve insufficiency, and should not be used in patients with severe peripheral vascular disease, heart failure whose etiology cannot be corrected, or multiple organ failure. or in patients with multiple organ failure (Class I, Level of Evidence: B).