THE CARDIOGENIC SHOCK TREATMENT?

WHAT IS CARDIOGENIC SHOCK?

Cardiogenic shock is a type of shock with decreased heart pumping efficiency due to damaged heart muscle. Hence blood supply to the vital organs such as the brain and heart myocardium is reduced.

The pathophysiology of cardiogenic shock is determined by tissue hypoxia resulting from severely impaired ventricular pump function in the company of adequate intravascular volume.

Definition of cardiogenic shock. http://coronary circulation

Cardiogenic shock is a life-threatening condition defined as a critical failure of the heart to maintain sufficient tissue perfusion. As an emergency, it requires immediate workup and therapeutic management. The typical patient with cardiogenic shock suffers from an acute event such as acute myocardial infarction (AMI), a mechanical complication such as papillary muscle or ventricular muscle rupture, pericardial effusion, life-threatening arrhythmia, acute myocarditis, or pulmonary embolus.

Chronic heart failure may also slowly deteriorate to a stage resembling CS. However, acute events are the leading cause of patients with cardiogenic shock, and immediate management of the underlying disease process is typically the most important therapeutic intervention.

In many cases (as in AMI), this results in further deterioration (vicious cycle or downward spiral), decreased myocardial oxygen supply, and final end-stage multi-organ damage.

CLINICAL APPROACH

Examination

• History for AMI, CAD, PE, myocarditis
• Vital signs ( systemic hypotension, tachycardia, shock index )
• Respiratory status ( SOB, tachypnoea, crackles, wheezing, pulmonary edema)
• Critical organ hypoperfusion ( level of consciousness, cool extremities, skin pallor, urine output )
• CVP ( elevated JVP )
• Emergency blood tests, especially arterial blood gases, PH, lactate, cardiac enzymes, electrolytes, glucose
• ECG (signs of AMI, LB, arrhythmias, indications of pulmonary embolism)
• Echocardiography ( left ventricular function of the aortic and mitral valve, ventricular septal defect(VSD)
• Chest x-ray ( signs of acute lung edema )

CONSIDER MONITORING

• ECG
• Arterial pressure ( for hemodynamics and continuous blood gases )
• CVP line, pulmonary wedge pressure catheter, or PICCO system. The benefit of pulmonary wedge pressure catheters has been debated. However, regardless of the system use, some information about filling pressures and CO is needed for initial evaluation and for guiding and aiming therapeutic interventions
• Urine output via the catheter.

To define patients at risk, the following definition of cardiogenic shock may be used for patients with AMI according to clinical trials –

1- Systemic hypotension ( systemic blood pressure<90 mmHg ) for at least 30 minutes and a heart rate >90 bpm or the need for positive inotropic drugs to maintain a systolic blood pressure >90 mmHg.

2- End-organ hypoperfusion ( cool extremities, altered mental status, or a urine output of <30 ml per hour ) or pulmonary edema.

3- Cardiac index <2.2 L/min/m2 and PCWP >15 mmHg or left ventricular end-diastolic pressure (LVEDP) >20 mmHg.

Caveat: the degree of impairment of left ventricular ejection fraction LVEF remains a prognostic indicator for mortality, the definition of cardiogenic shock is based mainly on clinical and hemodynamic parameters.

MANAGEMENT OF CARDIOGENIC SHOCK 7 TYPES OF THE HEART DISEASES

1- Early management

Although the initial work-up aims to elucidate the cause of cardiogenic shock, initial management should focus on the stabilization of the patients:

• Correct arrhythmias ( cardioversion, pacemaker )
• Guarantee oxygen supply ( CPAP mask or mechanical ventilation )
• Proper electrolytes and metabolic acidosis, if necessary.
• Give fluids if hemodynamics are the primary focus ( and oxygen supply is not a problem ) with continuous monitoring of MAP and CO, a test bolus of 500ml of fluid may determine if the patient benefits from further volume.
• Diuretics ( 40-80 mg of frusemide ) and low-dose nitrates may be appropriate for patients with pulmonary edema to avoid further deterioration.
• Give morphine ( 5-10 mg iv ) to reduce stress and anxiety. Any sedation or pain management may result in acute hemodynamic instability because of the adrenergic withdrawal effect ( prepare for CPR or inotropes when planning mechanical ventilation ).
• Administer inotropes or vasopressors at as low a dose as possible. In most cases, initial therapy with either dopamine or dobutamine is necessary.
• In case of an AMI give ASS ( 500 mg ), heparin ( 5000 IU ), and clopidogrel ( 600 mg ); GPllb/llla inhibitor may be considered.

2- Causal therapy

After initial management, steps toward causal therapy should be initiated. Most patients with cardiogenic shock suffer an AMI, and reperfusion therapy is the most consequential therapeutic measurement. Immediate coronary angiography and PCI have been demonstrated in a randomized trial to reduce mortality and should be considered even when not directly available on-site. The critical state of patients with cardiogenic shock should not be used as an argument against PCI. Thrombolytic therapy should only be considered for STEMI within 3 hours without access to a cath lab.

Patients with CS because of a mechanical complication ( mitral regurgitation, VSD ) should be transferred to cardiac surgery for definite therapy as soon as possible.

3- Further management with mechanical support

• IABP: intra-aortic balloon counterpulsation has been recommended in the guidelines for patients with CS despite the lack of randomized controlled trials.
• Percutaneous LVAD: all left ventricular assist devices require some interventional or surgical approach. They offer active support for failing circulation by either pumping blood from the left ventricle to the aorta or from the left atrium to the femoral artery ( tandem Heart, cardiac assist )
• Surgical implanted cardiac mechanical support: most ventricular assist devices or total artificial hearts require cardiac surgery. Which limits the use for the majority of patients with cardiogenic shock. This option should be considered for all patients who received the initial therapeutic steps, and recovered to a stable situation, but need further invasive support as a bridge to recovery or transplantation.

5- Pharmacological management

The goal of medical management of patients with cardiogenic shock is to bridge the patient for the first critical hours and days until the failing heart has recovered. MAP >60-70mmHg may be a target; however, integrative parameters such as serum lactate, oxygenation, urine output, or mental status may be more valuable targets for pharmacological management.

All positive inotropic drugs should be used at as low a dose as possible to avoid increased oxygen demand, myocardial work, and direct toxic effects of these agents. Whenever LVADs are used or MAP is sufficiently high, vasodilators are beneficial to reduce preload and afterload, thereby reducing the work of the failing heart. Tilarginine to inhibit excess nitric oxide has been tested in a large RCT with no observed survival benefit in patients with CS, despite evidence that systemic inflammatory response syndrome(SIRS) is associated with AMI and CS and SIRS might promote the vicious cycle of hypoxia in patients with CS.

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OXFORD DESK REFERENCE CARDIOLOGY, south Asia edition, Hung-Fat Tse | Gregory Y. H. Lip, Andrew J. Stewart Coats. Ross and Wilson, Anatomy and Physiology, Anne Waugh, Allison Grant.