INTRODUCTION

Cardiogenic shock is a condition caused by the inability of the heart to pump sufficiently to
meet the metabolic needs of the body due to the impaired contractility of the heart. It is
usually associated with myocardial infarction (MI), cardiomyopathies, dysrhythmias,
valvular stenosis, massive pulmonary embolism, cardiac surgery, or cardiac tamponade. It is
a self- perpetuating condition because coronary blood flow to the myocardium is
compromised, causing ischemia and ventricular dysfunction.

DEFINITION

Cardiogenic shock is a condition of diminished cardiac output that severely impairs cardiac
perfusion.

INCIDENCE

 Cardiogenic shock occurs as a serious complication in 5% to 10% of patients

hospitalized with acute myocardial infarction.
 Historically, mortality for cardiogenic shock had been 80% to 90%, but recent
studies indicate that the rate has dropped to 56% to 67% due to the advent of
thrombolytics, improved interventional procedures, and better therapies.
 Incidence of cardiogenic shock is more common in men than in women because of
their higher incidence of coronary artery disease.

RELATED ANATOMY AND PHYSIOLOGY

The heart is a roughly cone-shaped hollow muscular organ. It is about 10 cm long and is
about the size of the owner’s fist. It weighs about 225 g in women and is heavier in men

Position

The heart lies in the thoracic activity in the mediastinum (the space between the lungs). It
lies obliquely, a little more to the left than the right, and presents a base above, and an apex
below. The apex is about 9 cm to the left of the midline at the level of the 5 th intercostal
space, i.e., a little below the nipple and slightly nearer the midline. The base extends to the
level of the 2nd rib.
Structure :

Fig. Heart
Chambers of the heart
The heart has four hollow chambers: two atria and two ventricles

 Receiving chambers. The two superior atria are primarily the receiving chambers,
they play a lighter role in the pumping activity of the heart.
 Discharging chambers. The two inferior, thick-walled ventricles are the discharging
chambers, or actual pumps of the heart wherein when they contract, blood is propelled
out of the heart and into the circulation.
 Septum. The septum that divides the heart longitudinally is referred to as either the
interventricular septum or the interatrial septum, depending on which chamber it
separates.

The heart wall is composed of three layers of tissue

 Pericardium: It is the outermost layer and is made up of two sacs. The outer sac
consists of fibrous tissue and the inner of a continuous double layer of serous
membrane.
 Myocardium: The myocardium is composed of specialised cardiac muscle found
only in the heart. It is not under voluntary control but is striated, like skeletal muscle.
 Each fibre (cell) has a nucleus and one or more branches. The ends of the cells and
their branches are in very close contact with the ends and branches of adjacent cells.
 Endocardium: This lines the chambers and valves of the heart. It is a thin, smooth,
glistening membrane that permits smooth flow of blood inside the heart. It consists of
flattened epithelial cells, and it is continuous with the endothelium lining the blood
vessels.

Associated Great Vessels

The great blood vessels provide a pathway for the entire cardiac circulation to proceed.

 Superior and inferior vena cava. The heart receives relatively oxygen-poor blood from
the veins of the body through the large superior and inferior vena cava and pumps it
through the pulmonary trunk.
 Pulmonary arteries. The pulmonary trunk splits into the right and left pulmonary
arteries, which carry blood to the lungs, where oxygen is picked up and
carbondiaoxide is unloaded.
 Pulmonary veins. Oxygen-rich blood drains from the lungs and is returned to the left
side of the heart through the four pulmonary veins.
 Aorta. Blood returned to the left side of the heart is pumped out of the heart into the
aorta from which the systemic arteries branch to supply essentially all body tissues.

Heart valves

The heart is equipped with four valves, which allow blood to flow in only one direction
through the heart chambers

 Atrioventricular valves. Atrioventricular or AV valves are located between the atrial

and ventricular chambers on each side, and they prevent backflow into the atria when
the ventricles contract
 Bicuspid valves. The left AV valve- the bicuspid or mitral valve, consists of two
flaps, or cusps, of endocardium.
 Tricuspid valve. The second set of valves, the semilunar valves, guards the bases of
the two large arteries leaving the ventricular chambers, thus they are known as the
pulmonary and aortic semilunar valves.
Flow of blood through the heart

The two largest veins of the body, the superior and inferior venae cava, empty their contents
into the right atrium. This blood passes via the right atrioventricular valve into the right
ventricle, and from there is pumped into the pulmonary artery or trunk (the only artery in the
body which carries deoxygenated blood). The opening of the pulmonary artery is guarded by
the pulmonary valve, formed by three semilunar cusps. This valve prevents the backflow of
blood into the right ventricle when the ventricular muscle relaxes. After leaving the heart the
pulmonary artery divides into left and right pulmonary arteries, which carry the venous blood
to the lungs where exchange of gases takes place: carbon dioxide is excreted and oxygen is
absorbed.

Two pulmonary veins from each lung carry oxygenated blood back to the left atrium. Blood
then passes through the left atrioventricular valve into the left ventricle, and from there it is
pumped into the aorta, the first artery of the general circulation. The opening of the aorta is
guarded by the aortic valve, formed by three semilunar cusps.

Conducting system of the heart

The heart possesses the property of autorhythmicity, small group of specialised

neuromuscular cells in the myocardium initiate and conduct impulses, causing coordinated
and synchronised contraction of the heart muscle

Sinoatrial node (SA node): This small mass of specialised cell lies in the wall of the right
atrium near the opening of the superior vena cava. The Sinoatrial cells generate regular
impulses because they are electrically unstable. It normally set the heart rate and is called the
pacemaker of the heart. Firing of the SA node triggers atrial contraction.

Atrioventricular node (AV node): This small mass of neuromuscular tissue is situated in
the wall of the atrial septum near the atrioventricular valves. Normally, the AV node merely
transmits the electrical signals from the atria into the ventricles. There is a delay here; the
electrical signal takes 0.1 of a second to pass through into the ventricles. This allows the atria
to finish contracting before the ventricles start.

Atrioventricular bundle: This is a mass of specialised fibres that originate from the AV
node. The AV bundle, bundle branches and Purkinje fibres transmit electrical impulses from
the AV node to the apex of the myocardium where the wave of ventricular contraction
begins, then sweeps upwards and outwards, pumping blood into the pulmonary artery and
aorta.

The cardiac cycle

At rest, the healthy adult heart is likely to beat at a rate of 60-80 bpm. During with heartbeat
or cardiac cycle, the heart contracts and then relaxes. The period of contraction is called
systole and that of relaxation, diastole.

Stages of the cardiac cycle

Taking 74 bpm as an example, each cycle lasts about 0.8 of a second and consists of:

 Atrial systole – contraction of the atria

 Ventricular systole – contraction of the ventricles
 Complete cardiac diastole – relaxation of the atria and ventricles

CLASSIFICATION

 Coronary. Coronary cardiogenic shock is more common than noncoronary

cardiogenic shock and is seen most often in patients with acute myocardial
infarction.
 Noncoronary. Noncoronary cardiogenic shock is related to conditions that stress
the myocardium as well as conditions that result in an ineffective myocardial
function.

STAGES OF CARDIOGENIC SHOCK

Initial Stage

During the initial stage, the state of hypoperfusion causes hypoxia. Due to the lack of oxygen,
the cells perform anaerobic respiration. Since oxygen is not abundant, the Kreb’s cycle is
slowed, resulting in lactic acidosis (the accumulation of lactate).
Compensatory Stage

The compensatory stage is characterized by the employment of neural, hormonal, and

biochemical mechanisms in the body’s attempt to reverse the lactic acidosis. The increase in
acidity will initiate the Cushing reflex, generating the classic symptoms of shock. The
individual will begin to hyperventilate to rid the body of carbon dioxide to raise the blood pH
(lower the acidity). As a result, the baroreceptors in the arteries detect the hypotension and
initiate the release of epinephrine and norepinephrine to increase heart rate and blood
pressure.

Progressive Stage

Should the cause of the crisis not be successfully treated, the shock will proceed to
the progressive stage, in which the compensatory mechanisms begin to fail. As anaerobic
metabolism continues, increasing the body’s metabolic acidosis, the arteriolar smooth muscle
and precapillary sphincters relax. Blood remains in the capillaries, leading to leakage of fluid
and protein into the surrounding tissues. As fluid is lost, blood concentration and viscosity
increase, causing blockage of the microcirculation. The prolonged vasoconstriction will also
cause the vital organs to be compromised due to reduced perfusion. If the bowel becomes
sufficiently ischemic, bacteria may enter the blood stream, resulting in the additional
complication of endotoxic shock.

Refractory Stage

At the refractory stage, the vital organs have failed and shock can no longer be reversed.
Brain damage and cell death are occurring, and death is imminent. Shock is irreversible at
this point since a large amount of cellular ATP has been degraded into adenosine in the
absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easily
perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation,
and then is transformed into uric acid. Because cells can only produce adenosine at a rate of
about 2% of the cell’s total need per hour, even restoring oxygen is futile at this point because
there is no adenosine to phosphorylate into ATP.

CAUSES

Cardiogenic shock can result from any condition that causes significant left ventricular
dysfunction with reduced cardiac output.

 Myocardial infarction (MI).Regardless of the underlying cause, left ventricular

dysfunction sets in motion a series of compensatory mechanisms that attempt to
increase cardiac output, but later on leads to deterioration.
  Myocardial ischemia. Compensatory mechanisms may initially stabilize the
patient but later on would cause deterioration with the rising demands of oxygen of
the already compromised myocardium.
 End-stage cardiomyopathy.The inability of the heart to pump enough blood for
the systems causes cardiogenic shock.

PATHOPHYSIOLOGY

Etiological Factors

Inadequate tissue perfusion resulting from cardiac dysfunction

Average Left Ventricular Ejection Fraction (LVEF) moderately severely depressed

Systemic Vascular Resistance (SVR) on Vasopressors

Systemic inflammatory response syndrome

Depressed Myocardial Contractibility combined with inadequate systemic vasoconstriction

Extensive Myocardial Ischemia/injury results in

Cardiogenic Shock

CLINICAL MANIFESTATIONS 

 Clammy skin. The patient experiences cool, clammy skin as the blood could not
circulate properly to the peripheries.
 Decreased systolic blood pressure. The systolic blood pressure decreases to 30
mmHg below baseline.
  Tachycardia. Tachycardia occurs because the heart pumps faster than normal to
compensate for the decreased output all over the body.
 Rapid respirations. The patient experiences rapid, shallow respirations because
there is not enough oxygen circulating in the body.
 Oliguria. An output of less than 20ml/hour is indicative of oliguria.
 Mental confusion. Insufficient oxygenated blood in the brain could gradually
cause mental confusion and obtundation.
 Cyanosis. Cyanosis occurs because there is insufficient oxygenated blood that is
being distributed to all body systems.

DIAGNOSTIC EVALUATION

 Auscultation. Auscultation may detect gallop rhythm, faint heart sounds and,

possibly, if the shock results from rupture of the ventricular septum or papillary
muscles, a holosystolic murmur.
 Pulmonary artery pressure (PAP).PAP monitoring may show increase in PAP,
reflecting a rise in left ventricular end-diastolic pressure and increased resistance
to the afterload.
 Arterial pressure monitoring. Invasive arterial pressure monitoring may indicate
hypotension due to impaired ventricular ejection.
 ABG analysis. Arterial blood gas analysis may show metabolic acidosis and
hypoxia.
 Electrocardiography. Electrocardiography may show possible evidence of acute
MI, ischemia, or ventricular aneurysm.
 Echocardiography. Echocardiography can determine left ventricular function and
reveal valvular abnormalities.
 Enzyme levels. Enzyme levels such as lactic dehydrogenase, creatine kinase.
Aspartate aminotransferase and alanine aminotransferase may confirm MI.

MEDICAL MANAGEMENT

The aim of treatment is to enhance cardiovascular status by:

 Oxygen. Oxygen is prescribed to minimize damage to muscles and organs.

  Angioplasty and stenting. A catheter is inserted into the blocked artery to open it
up.
 Balloon pump. A balloon pump is inserted into the aorta to help blood flow and
reduce workload of the heart.
 Pain control. In a patient that experiences chest pain, IV morphine is administered
for pain relief.
 Hemodynamic monitoring.An arterial line is inserted to enable accurate and
continuous monitoring of BP and provides a port from which to obtain frequent
arterial blood samples.
 Fluid therapy.Administration of fluids must be monitored closely to detect signs
of fluid overload.

Pharmacologic Therapy

Drug therapy may include:

 IV dopamine. Dopamine, a vasopressor, increases cardiac output, blood pressure,

and renal blood flow.
 IV dobutamine. Dobutamine is an inotropic agent that increase myocardial
contractility.
 Norepinephrine. Norepinephrine is a more potent vasoconstrictor that is taken
when necessary.
 IV nitroprusside. Nitroprusside is a vasodilator that may be used with a
vasopressor to further improve cardiac output by decreasing peripheral vascular
resistance and reducing preload.

SURGICAL MANAGEMENT

When the drug therapy and medical procedures don’t work, then the last option is for surgical
procedure.

 Intra-aortic balloon pump (IABP).The IABP is a mechanical-assist device that

attempts to improve the coronary artery perfusion and decrease cardiac workload
 through an inflatable balloon pump which is percutaneously or surgically inserted
through the femoral artery into the descending thoracic aorta.
 Left ventricular assist device (LVAD) is a pump that we use for patients who
have reached end-stage heart failure. We surgically implant the LVAD, a battery-
operated, mechanical pump, which then helps the left ventricle (main pumping
chamber of the heart) pump blood to the rest of the body.

PURPOSES

 Bridge-to-transplant therapy: This is a life-saving therapy for patients awaiting a

heart transplant. Patients use the LVAD until a heart becomes available. In some
cases, the LVAD is able to restore the failing heart, eliminating the need for a
transplant. Learn more about heart transplant.
 Destination therapy: Some patients are not candidates for heart transplants. In this
case, patients can receive long-term treatment using an LVAD, which can prolong and
improve patients' lives.

RISKS

 Blood clots
 Bleeding
 Infection
 Device malfunctions
 Right Heart Failure

PROCEDURE
 Surgery will begin once the patient is under anesthesia.
 The surgeon makes a long incision on the breastbone and accesses the heart by
spreading the rib cage.
 In some cases, patients are placed on a cardiopulmonary bypass machine, which takes
over the work of the heart and lungs until the operation is complete.
 The surgeon connects one end of the LVAD tube to the heart’s left ventricle and a
tube exiting the other end of the external LVAD to the aorta. A small electrical
cord connected to the LVAD (a driveline) exits from the upper abdomen and is
connected to a power supply (either batteries or a plug-in) and a small computer
to operate the device.
 Once the device is working properly, the patient is taken off cardiopulmonary
bypass and the chest is closed with stitches.
 After surgery, patients are taken to the intensive care unit and monitored.
The length of the hospital stay depends on how quickly patients recover and can perform
some physical activity.

NURSING MANAGEMENT

Cardiogenic shock needs rapid, accurate nursing management.

Nursing Assessment

The nurse should assess the following:

 Vital signs. Assess the patient’s vital signs, especially the blood pressure.
 Fluid overload. The ventricles of the heart cannot fully eject the volume of blood
at systole, so fluid may accumulate in the lungs.

NURSING CARE PLAN

1. Impaired gas exchange related to impaired ventilation-perfusion as evidenced by

hypoxia, abnormal arterial blood gases (ABGs), cyanosis.

Intervention

 Assess the patient’s respiratory rate, rhythm, and depth

 Monitor patient’s heart rate and blood pressure
 Assess for any signs of changes in the level of consciousness
 Assess for cyanosis or pallor by examining the skin, nail beds, and mucous
membranes.
 Monitor oxygen saturation and arterial blood gases
 Provide comfortable position to the patient with head of bed elevated
 Provide oxygen therapy as ordered

2. Decreased cardiac output related to dysrhythmias, increased or decreased preload or

afterload as evidenced by crackles, dyspnea, and pulmonary congestion.

Intervention

 Assess for any changes in the level of consciousness

  Monitor vital signs and blood pressure of patient
 Assess the rate, rhythm, and electrocardiogram
 Assess capillary refill and oxygen saturation and arterial blood gases
 Administer oxygen as prescribed
 Monitor fluid balance and weight gain
 Monitor urine output
 Administer IV fluids for patients with a decreased preload

3. Anxiety related to change in health status, fear of death and unfamiliar environment as
evidence by increased questioning, uncooperative behaviour, restlessness and
agitation.

Intervention

 Assess the level of anxiety (mild, severe)

 Assess the coping techniques commonly used
 Acknowledge an awareness of the patient’s anxiety
 Encourage the verbalization of feelings
 Reduce unnecessary external stimuli by maintaining a quiet environment
 Explain all procedures as appropriate, keeping explanations basic

PREVENTION

Lifestyle changes must be made to avoid the recurrence of cardiogenic shock.

 Control hypertension. Exercise, manage stress, maintain a healthy weight, and

limit salt and alcohol intake.
 Avoid smoking. The risk of stroke is the same for smokers and non-smokers years
after you stop smoking
 Maintain a healthy weight.Losing those extra pounds would be helpful in
lowering the cholesterol and blood pressure.
 Diet. Eat less saturated fat and cholesterol to reduce heart disease.
  Exercise. Exercise daily to lower blood pressure, increase high-density
lipoproteins, and improve the overall health of the blood vessels and the heart.

COMPLICATIONS

 Cardiopulmonary arrest
 Dysrhythmia
 Renal failure
 Multisystem organ failure
 Ventricular aneurysm
 Stroke
 Death

CONCLUSION
Recent advances in the treatment of cardiogenic shock offer a mixed bag of therapies, some
very promising while others have not fulfilled their initial expectations. But one thing is clear
that an attempt is being made to accurately understand the mechanism of CS, and a multi-
pronged strategy is being applied to find out remedies which act through different and
unconventional ways. This offers us hope that the future of cardiogenic shock will not be as
dreaded as it is now.