Cardiogenic shock is an emergency and it needs rapid diagnosis and institution of therapy. Improved long-term outcomes require immediate diagnosis and management and if needed, transfer to a tertiary care hospital [³²].

History will usually reveal symptoms of a preceding AMI. A diagnosis of cardiogenic shock is made when myocardial dysfunction is observed in the absence of other causes such as hemorrhage, sepsis, pulmonary embolism, tamponade, aortic dissection, and preexisting valvular disease [³²]. On a physical exam (Table 3), the patient may be cyanotic with cold extremities and pulses are usually rapid and faint. If LVD is the etiology, then jugular venous distention (JVD) and rales in the lung field due to pulmonary congestion are observed. If right ventricular failure is the underlying cause then JVD and kussmaul’s sign is present and pulmonary rales are not found. Other findings include distant heart sounds and the presence of third and fourth heart sounds. Mitral regurgitation or a VSD can lead to a new systolic murmur. Arrhythmias are a frequent occurrence and need immediate attention.

64% of patients in the SHOCK trial registry, presented with hypotension and signs of hypoperfusion such as tachycardia, altered sensorium, decreased urine output and cool extremities. These patients also had signs of pulmonary congestion [³³]. A smaller proportion of patients (28%) experienced shock with no pulmonary congestion, which is also known as the silent lung syndrome. However, clinicians should be wary and refrain from incorrectly associating absence of pulmonary congestion with decreased risk [³³]. Thus, signs of hypoperfusion alone are mortality indicators regardless of the presence or absence of pulmonary congestion [³³]. Similarly, the GUSTO-I study observed increased mortality at 30 days if oliguria, cold extremities or altered sensorium were found to be present [³⁴]. Another study also ascertained oliguria and cold extremities as independent and strong mortality predictors [²⁰]. Thus, the initial clinical assessment of a patient is important in determining the future prognosis.

Tools that facilitate diagnosis (Table 4) include an electrocardiogram (ECG), cardiac enzymes, chest X ray, arterial blood gases (ABG), electrolytes, complete blood count (CBC) and/or a coagulation profile [³⁵]. Invasive hemodynamic monitoring may be required but is not a necessity. Bedside echocardiography plays a vital role in assessing the possible contributing causes [³⁶, ³⁷]. It can be used to quickly rule out or diagnose mitral regurgitation, ventricular septal or free wall tear, tamponade or a pericardial effusion so that emergent intervention can be instituted.

There is controversial evidence regarding right heart catheterization. One study claimed improved outcomes [³⁸] by using this invasive procedure while increased mortality was observed in a different study [³⁹].

Aspirin and heparin constitute the first line of treatment. Fluids may need to be given in order to rule out hypovolemic shock. These need to be instituted with continuous monitoring of clinical signs, such as urine output, blood pressure and heart rate. In right ventricular failure, fluid support is required and nitrates and morphine should be avoided, as they tend to increase hypotension. Oxygen should be given through a face mask or if the need arises, airway should be secured and mechanical ventilation started. Arrhythmias are a frequent occurrence and sustained tachyarrhythmias need to be converted electrically so as to avoid further compromise of the cardiac output. Bradyarrhythmias may require atropine or temporary pacing [³⁵].

Morphine reduces sympathetic stimulation and should be given for pain relief. It also decreases the preload and decompresses the left ventricle [³⁵]. Nitroglycerine, a venodilator, has limited use in cardiogenic shock. It is important to maintain the mean arterial blood pressure above 90 mmHg. For this purpose, inotropes and vasopressors like dopamine and catecholamines may be required. Dopamine, an inotrope and a vasopressor, is preferred initially. Another alternative is dobutamine but its use may produce vasodilation and lead to hypotension [³²]. In some situations, a combination of dopamine and dobutamine are more beneficial than the use of either agent alone [⁴⁰]. Persistently low systolic blood pressures with values such as 70 mmHg require addition of more drugs such as norepinephrine. Pressor agents should be used carefully as they increase the heart rate and may trigger arrythmias. Diuretics are added if pulmonary congestion is present to help in increasing the oxygenation [³²]. Electrolyte imbalances and metabolic acidosis need immediate treatment. Nitrates, b-blockers, and angiotensin-converting enzyme inhibitors help to improve outcomes after myocardial infarction [⁴¹]. However, beta-blockers can deteriorate the condition and are generally avoided in shock.

Intra-aortic balloon pump (IABP) is required for stabilizing patients before reperfusion therapies. It increases coronary blood flow during diastole and decreases the afterload by lowering the systemic vascular resistance during systole. However, if there is severe coronary stenosis, there is little improvement in coronary perfusion [⁴²]. The GUSTO-1 trial [⁴³], observed a decreased mortality rate at 30 days in patients treated with IABP (46%) as compared to those who did not receive this treatment (60%, P = 0.11). Similarly, in the SHOCK trial, patients who received treatment with IABP had reduced rates of mortality (50%) within hospital, versus those who did not have IABP placement (72%, P<0.0001) [⁴⁴]. It was used in both the arms of the study: medical management and revascularisation.

The American College of Cardiology/American Heart Association (ACC/AHA) STEMI guidelines [⁴⁵] give a class I recommendation for use of IABP when cardiogenic shock cannot be managed on medications alone. This allows stabilization for angiography and revascularization procedures.

Thus, in hospitals where emergent revascularization is not available, it is more appropriate to proceed with fibrinolytic therapy and IABP while arrangements are made for percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG). This might be a more realistic approach in many developing countries like Pakistan where there may be unavailability of immediate revascularization facilities in hospitals.

IABP is useful in providing mechanical support during shock. It has been observed that cardiac index can indicate if potential benefit can be derived from IABP. The use of IABP has better outcomes when used in patients with a cardiac index higher than 1.2 L/min/m² and a systemic vascular resistance less than 2100 dynes/sec/cm^–5. However, if the cardiac index is lower than 1.2 L/min/m², outcome is poor even if IABP is used. In such cases other support devices may be required [⁸⁴].

Extracorporeal life support (ECLS) has been utilized in cases of severe cardiac or pulmonary failure [⁸⁵]. Percutaneous cardiopulmonary bypass can also provide support and can be performed at the bedside through the femoral artery and vein [⁸⁶]. These two devices however, do not help in unloading the left ventricle.

Biventricular assist devices, can serve as a bridge to cardiac transplantation. This has been found to have a success rate of around 59% [⁸⁷]. Experimental percutaneous LV assist devices help to unload the left ventricle [⁸⁸] and present another option.

During the development of cardiogenic shock, the body may launch a systemic inflammatory response, which has led to investigations on inflammatory mediators. Chemical agents are being investigated for their contribution in cardiogenic shock. Nitric oxide production has also been thought to play a role in the development of cardiogenic shock and some studies indicate that inhibition of nitric oxide production may improve outcomes [^89-91].

Thus, support systems in the form of mechanical devices and medications will have an increasing role in the future as part of our management strategies.