CARDIOGENIC SHOCK

Synonyms• cardiogenic shock• cardiac shock• global hypo perfuse• cardiac gallop

Meaning Cardiogenic shock is

characterized by a decreased pumping ability of the heart that causes a shock like state (i.e., global hypo perfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction(AMI).

Incidence

• Cardiogenic shock occurs in 8.6% of patients with ST-segment elevation

• MI with 29% of those presenting to the hospital already in shock.

• It occurs only in 2% of non–ST-segment elevation MI.

Mortality/Morbidity• Leading cause of death in AMI. • The overall in-hospital mortality rate is

57%.• Persons older than 75 years, the

mortality rate is 64.1%.• Younger than 75 years, the mortality rate

is 39.5%.• Overall mortality when revascularization

occurs is 38%. If not attempted, mortality rates approach 70%.

Race• Hispanics - 74%• African Americans - 65%• Whites -56% • Asians/others - 41%.• Indians - 43.7%Sex Women comprise 42% of all

cardiogenic shock patients.

Risk factors Pre existing myocardial

damage Diseases like diabetes Advanced age Previous AMI AMI (Q-wave, large or anterior

wall AMIs) dysrhythmia.

Etiology• Acute myocardial ischemia• Others: Beta-blocker overdose,

calcium channel blocker overdose, myocardial contusion, respiratory acidosis, hypocalcaemia, hypophosphatemia, and cardio toxic drugs (e.g., doxorubicin [Adriamycin])

Ventricular hypertrophy and restrictive Cardiomyopathy

After load - Aortic stenosis, hypertrophic Cardiomyopathy, dynamic outflow obstruction, aortic coarctation, and malignant hypertension

Valvular/structural - Mitral stenosis, endocarditis, mitral or aortic regurgitation, atrial myxoma or thrombus, and tamponade

Pathophysiology

AMI↓

Dead myocardium does not contract ↓

Marked decrease in contractility reduces the ejection fraction and

cardiac output. ↓

Increased ventricular filling pressures, cardiac chamber

dilatation↓

Univentricular or biventricular failure ↓

Systemic hypotension and/or pulmonary edema.

A systemic inflammatory response syndrome

Myocardial infections↓

Elevated levels of white blood cells, body temperature, interleukins, and C-reactive protein.

Similarly, inflammatory nitric oxide synthetase (iNOS) is also released in high levels during

myocardial stress.↓

iNOS induces nitric oxide production, which may uncouple calcium metabolism in the myocardium resulting in a stunned myocardium. Additionally,

iNOS leads to the expression of interleukins, which may themselves cause hypotension.

Myocardial ischemia↓

Decrease in contractile function↓

Left ventricular dysfunction and decreased arterial pressure

↓Exacerbate the myocardial ischemia

↓Severe cardiovascular decompensation.

Other pathophysiological mechanisms

• papillary muscle rupture leading to acute mitral regurgitation (4.4%);

• ventricular septal defect (1.5%)• wall rupture (4.1%) as a

consequence of AMI.

• Right ventricular (RV) infarct, by itself, may lead to hypotension and shock because of reduced preload to the left ventricle.

• Cardiac tamponade may result as a consequence of Pericarditis, uremic pericardial effusion, or in rare cases systemic lupus erythematosus.

Medications

• Calcium channel blockers may cause profound hypotension with a normal or elevated heart rate.

• Beta-blocking agents may also cause hypotension with or without bradycardia, or AV node block.

• Nitroglycerin, Angiotensin-converting enzyme inhibitors, opiate, and barbiturates can all cause a shock state and may be difficult to distinguish from cardiogenic shock.

Clinical manifestations• The physical examination

findings are consistent with shock.

• Patients are in frank distress• profoundly diaphoretic with

mottled extremities• visibly dyspneic

• A- Airway usually is patent initially.• B- Breathing may be labored, with

audible coarse crackles or wheezing.• C-Circulation is markedly impaired.

Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings.

• Signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present.

Diagnostic measures• History collection• General physical examination• Initial vital sign assessment • Neck examination may reveal jugular

venous distention • LV dysfunction, characterized by

pulmonary edema, can be auscultated as crackles with or without wheezing.

Careful cardiac examination may reveal mechanical causes of cardiogenic shock.

Loud murmurs may indicate a valvular dysfunction, whereas muffled heart tones with jugular venous distention and pulsus paradoxus may suggest tamponade (Beck triad).

A gallop may also be heard. The presence of an S3 heart sound is pathognomonic of congestive heart failure. The presence of pulmonary edema increases the likelihood of cardiogenic shock in the setting of hypotension.

Lab Studies• No one test is completely sensitive,

laboratory studies are directed at the potential underlying cause.

• Following are assessed in cases of suspected cardiac ischemia: Cardiac enzymes (eg, creatine kinase,

troponin, myoglobin) CBC Electrolytes Coagulation profile (eg, prothrombin time,

activated partial thromboplastin time)

An ABG may be useful to evaluate acid-base balance because acidosis .

Elevated serum lactate level is an indicator of shock.

Brain natriuretic peptide (BNP) may be useful as an indicator of congestive heart failure and as an independent prognostic indicator of survival.

A low BNP level may effectively rule out cardiogenic shock in the setting of hypotension.

Imaging Studies

Portable chest radiograph • Overall impression of the cardiac

size• Pulmonary vascularity• Coexistent pulmonary pathology • A rough estimate of Mediastinal

and aortic sizes

Other Tests• ECG Helpful if it reveals an acute injury

pattern consistent with an AMI• Echocardiogram *To reveal akinetic or dyskinetic

areas of ventricular wall motion. *To reveal surgically correctable

causes, such as valvular dysfunction and tamponade.

Differential Diagnosis• Acute coronary syndrome• Aortic Regurgitation• Cardio myopathy• Congestive cardiac failure• Mitral regurgitation• Hypovolemic or septic shock• Myocardial infarction

MANAGEMENT• Prehospital Care: aimed at minimizing

any further ischemia and shock. All patients require intravenous access, high-

flow oxygen administered by mask, and cardiac monitoring.

Twelve-lead electrocardiography, The ED physician, can thus be alerted, and may mobilize the appropriate resources.

• Emergency Department Care: Aim: making the diagnosis, preventing

further ischemia, and treating the underlying cause.

• coronary artery bypass is the treatments of choice within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation.

• If not immediately available, thrombolytics should be considered which is the second best.

Treatment begins with assessment and management of the ABCs.

• Airway should be assessed for patency. • Breathing evaluated for effectiveness and

increased work of breathing. • Endotracheal intubation and mechanical

ventilation is considered in patients with excessive work of breathing.

• Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen.

supporting myocardial perfusion and maximizing cardiac output.

• Intravenous fluids should be provided to maintain adequate preload, guided by central venous pressure or pulmonary capillary wedge pressure monitoring .

PharmacotherapyAim: To reduce morbidity and to prevent

complications.• Intravenous vasopressors provide

inotropic support increasing perfusion of the ischemic myocardium and all body tissues.

• Extreme heart rates should be avoided because they may increase myocardial oxygen consumption

1. Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption.

Dose:5-20 mcg/kg/min IV continuous infusion.

• Increase by 1-4 mcg/kg/min q10-30min to optimal response

• (>50% of patients have satisfactorily responses with doses <20 mcg/kg/min)

2.Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and after load.

Dose: 5-20 mcg/kg/min IV continuous infusion.

3. Phosphodiestrase enzyme inhibitors -improve cardiac output in refractory hypotension and shock. Milrinone and inamrinone (formerly amrinone) may be used.

• Loading dose: 50 mcg/kg IV over 10 min

• Continuous infusion: 0.375-0.75 mcg/kg/min IV

4.Natrecor (nesiritide) Should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.5.VasodilatorsSmooth-muscle relaxants and vasodilators that can reduce systemic vascular resistance, allowing more forward flow and improving cardiac output.

6. Analgesics -- Pain control is essential to quality patient care. It ensures patient comfort and promotes pulmonary toilet.

7. Natriuretic peptide Nitrates and/or morphine excessive

use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock

8.Diuretics :cause diuresis to decrease plasma volume and edema and thereby decrease cardiac output BP. •The initial decrease in cardiac output causes a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, extracellular fluid and plasma volumes almost return to pretreatment levels. •Peripheral vascular resistance decreases below that of pretreatment baseline.

Lasix: 40-80 mg/d IV/IM

Intra-aortic balloon pump (IABP) recommended for cardiogenic shock not quickly reversed with pharmacologic therapy.

It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available.

o IABP reduces LV after load and improves coronary artery blood flow.

o Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended.

o Although complications may occur in up to 30% of patients, extensive retrospective data support its use.

Complications• Cardiopulmonary arrest• Dysrhythmia• Renal failure• Multisystem organ failure• Ventricular aneurysm• Thromboembolic sequelae• Stroke• Death

Prognosis

• The prognosis is universally poor.• The mortality rate is more than

55% in patients treated medically. • At best, the rate is 38% in whom

surgical reperfusion is achieved.

NURSING MANAGEMENT

Assessment:• ABC,s, • tissue perfusion, • vital signs,• capillary refill , • skin and urinary output.

Nursing Diagnosis• Decreased cardiac output related to shock

as manifested by increased diastolic BP, tachycardia, dry mucous membrane, pallor, cyanosis, cool and clammy skin.

• Fear and anxiety related to severity of the condition as manifested by verbalization of anxiety about condition and fear of death or withdrawal with no communication, increase in heart and respiratory rate.

• High risk for organ dysfunction related to decreased tissue perfusion.

Nursing implementation• Health Promotion: Planning is

essential to help to prevent shock after a susceptible individual has been identified.

• The primary goal for the patient with an acute MI is to limit the size of the infarction.

• The nurse can modify the patients environment to provide care at intervals to increase patient’s oxygen demand.

Acute Intervention: • The role of nurse in shock involves

monitoring the patients ongoing physical and emotional status .

• Planning and implementing the nursing interventions and therapy

• Evaluating the patients response to therapy

• Providing emotional support to patient and family

• Collaborating with other members of health team.

• Neurologic status, including orientation and level of consciousness should be assessed at least every hour

• Monitor BP, HR, CVP, PAWP at least every 15 mts until patient is stable.

• Respiratory status of the patient in shock must be frequently assessed to ensure adequate oxygenation, detect complication early and provide data regarding the patients acid-base status.

• Hourly monitoring of urinary output is essential to assess adequacy of renal perfusion.

• Monitoring body temperature and skin for any change in colour indicates adequacy of perfusion

• Assessment of personal hygiene is important in shock because impaired tissue perfusion predisposes the client to skin breakdown and infection.

• Monitoring the patients anxiety and providing emotional support and comfort to the patient and family is an integral part of nursing care.

• Ambulatory and Home care:The nurse should continue to monitor the patient for indications of complications throughout the recovery period.

• Patient Education: • Early warning signs of AMI and how to

access the emergency medical system • Cardiac risk factors, particularly those that

are reversible and subject to change (eg, smoking, diet, exercise).

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