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blood flow and natriuresis [34, 35]. At intermediate doses (5–10 μg/kg/min) dopamine stimulates beta‐1 adrenergic receptors, allowing for an increased stroke volume and an increased heart rate, increasing cardiac output. At high‐doses (>10 μg/kg/min) dopamine predominantly stimulates alpha‐adrenergic receptors, causing vaso‐constriction. A randomized study of 1679 patients with shock (septic, hypovolemic, and cardiogenic) assigned to dopamine or norepinephrine as the first‐line vasopressor showed more arrhythmic events in the dopamine group (24.1% vs 12.4%, p<0.001). A subgroup analysis of patients with cardiogenic shock showed that dopamine was associated with increased 28‐day mortality compared with norepinephrine [36]. An alternative is dobutamine, which is a synthetic catecholamine with strong beta‐1 and beta‐2 receptor affinity. The beta‐2 affinity of dobutamine may cause vasodilation and can cause hypotension.
Phosphodiesterase inhibitors and calcium sensitizers
Agents such as milrinone and enoximone increase the intracellular concentration of cyclic adenosine mono phosphate (cAMP) by inhibiting the action of phosphodiesterase 3 [37]. Phosphodiesterase 3 is an enzyme found in the sarcoplasmic reticulum of cardiac myocytes and vascular smooth muscle cells which breaks down cAMP into AMP. The increased intracellular concentration of cAMP increases myocardial contractility, improves diastolic relaxation, and causes vasodilation. Milrinone, the most widely used phophodiesterase inhibitor has a relatively long half‐life of 2 to 4 hours. The calcium‐sensitizer levosimendan sensitizes troponin C to calcium, thereby increasing the effects of calcium on cardiac myofilaments which increases cardiac contractility at low energy costs. Levosi‐mendan also causes vasodilatation by opening ATP‐dependent potassium channels [38, 39]. Both milrinone and levosimendan have not been tested in the setting of cardiogenic shock complicating myocardial infarction and experience with these agents in this setting is limited.
Treatment pathways for cardiogenic shock complicating myocardial infarction
A patient with CS complicating AMI should ideally be started on inotropes and vasopressors as soon as possible and be transferred to a catheterization laboratory for emergent invasive angiography. In order to better understand the etiology of CS immediate echocardiography should be performed ideally without delaying emergency angiography. A rapid bedside echo in the catheterization laboratory during preparation of the patient may suffice to evaluate left and right ventricular function and possible mechanical complications such as a ventricular septal rupture, papillary muscle rupture, or a free wall rupture. In the absence of mechanical complications, one should proceed to emergency PCI (preferably of the culprit‐lesion only) or emergency CABG if the lesions are not deemed amenable to PCI. In case of mechanical complications, surgical intervention is warranted. Short‐term percutaneous mechanical support may be considered before performing PCI as observational studies have suggested improved outcomes with early‐ rather than late initiation of mechanical support [40]. Before, throughout and after the procedure the respiratory status, blood pressure, and urine output should be monitored and mechanical ventilation, uptitration of vasopressors/inotropes, initiation or escalation of mechanical support, and renal replacement therapies should be considered. Moreover, the insertion of a pulmonary artery catheter may be considered.
Cardiogenic shock due to right ventricular failure
This entity has not been well described and devices have been used mostly anecdotally. Percutaneous right ventricular support devices (i.e. extracorporeal right atrial to pulmonary artery pump, intravenous microaxial pump, and veno‐venous ECMO) do exist and are presented in another chapter of this book. Clinical studies on patient risk stratification, hemodynamic/clinical evolution and clinical trials on outcomes are eagerly anticipated.
Cardiogenic shock due to pericardial tamponade
This entity has been traditionally treated with emergency pericardiocentesis. Echocardiography is typically used to establish the diagnosis. Although this can be performed under critical conditions with only body landmarks (needle insertion in subxiphoid area with shallow aim towards the left mid‐clavicular line), it is mostly performed with echocardiographic and fluoroscopic guidance. The echocardiographer can image the pericardial effusion from subxiphoid or apical window and identify the easiest projection to allow a straight needle track. Under local anesthesia (sedation can be rarely tolerated in such patients) and with patient positioned with a 20–40 ° upper body incline, the needle can be inserted parallel to the echo‐beam and should then be anticipated to reach the pericardial space at the depth identified by the imager. If a pressure transducer is available and zeroed at a 50 mmHg scale set‐up, it may be utilized to measure the pericardial pressure before and after fluid removal. Hemodynamic response is typically immediate upon removal of the fluid. On the other hand, shock/hypotension due to multi‐factorial cases may be associated with sizeable pericardial effusion and minor echocardiographic signs of tamponade; in such cases, the rather low and phasic pericardial pressure waveform will be indicative (to rule out a pericardial tamponade as the primary cause of hemodynamic collapse). A surgical pericardial window may be undertaken in mainly posterior effusions or in complicated cases for pericardiocentesis (or in those that a pericardial biopsy is of major diagnostic importance) [41].
Conclusions
In conclusion, the incidence of cardiogenic shock is declining, but its clinical impact remains as significant as ever. Vasopressors and inotropes can be used to improve blood pressure and cardiac output, but they cause an increase in systemic vascular resistance and an increase in pulmonary capillary wedge pressure and increase cardiac work and cardiac oxygen consumption. Therefore, the use of left‐ventricular assist devices is a promising treatment modality that is currently being investigated in larger randomized controlled trials. From clinical investigation point of view, randomized trials have been small‐sized and scarce in this subject due to the very critical presenting condition, and related enormous difficulties in appropriate screening, risk‐stratifying and consenting.
Interactive multiple choice questions are available for this chapter on www.wiley.com/go/dangas/cardiology
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