CARDIOGENIC

SHOCK
 Cardiogenic Shock

Cardiogenic shock is the failure of the

heart to pump blood adequately to meet the
oxygenation needs of the body. It occurs when the
heart muscle loses its contractile power. It most
commonly occurs as a result of acute myocardial
infarction (AMI), and left ventricular pump failure is
the primary insult.
 Cardiogenic Shock

It is the most common cause of death in

the post-AMI patient (about 5% to 10%
of AMI patients develop cardiogenic
shock), with a resulting mortality of 50%
to 60%.
 Etiology

1 2 3
Persistent Impaired Decreased CO
hypotension contractility results in a lack of blood
causes a marked reduction and oxygen to the
with a marked systolic of
in CO and ejection fraction heart as well as other
less than 80 to 90 mm Hg
or mean arterial pressure 30 vital organs (brain
mm Hg lower than baseline and kidneys).
because of left ventricular
failure.

4 5
Lack of blood and
oxygen to the heart
muscle
Lack of blood and oxygen
to the heart muscle results
in continued damage to the
muscle, a further decline in
contractile power, and a
continued inability of the
heart to provide blood and
oxygen to vital organs.
.
Etiology
6
Myocardial Mechanical
infarction complications
MI causing extensive such as ventricular septal
damage (40% or greater) to rupture, contained
the left ventricular free wall rupture, and
myocardium is the most papillary muscle
common cause rupture are strongly
suspected in patients
with shock,
particularly a first MI
In addition to MI with or without
complications, common causes of
cardiogenic shock include:
Aortic dissection—complicated by acute
severe aortic insufficiency or MI.
Acute decompensation of heart failure.
Acute myocarditis.
Takotsubo stress-induced cardiomyopathy.
Postcardiotomy.
Cardiac tamponade.
Peripartum cardiomyopathy.
Hypertrophic cardiomyopathy with severe
outflow obstruction.
Massive pulmonary embolism.
01
ASSESSMENT FINDINGS
 Clinical Manifestations
 Confusion, restlessness, mental lethargy (because of
poor perfusion of the brain or metabolic encephalopathy).
 Low systolic blood pressure (90 mm Hg or 30 mm Hg
less than previous levels) or MAP <65 mm Hg.
 Oliguria—urine output less than 30 mL/hour for at least
2 hours (because of decreased perfusion of kidneys).
 Cold, clammy skin (blood is shunted from the peripheral
circulation to perfuse vital organs); profoundly
diaphoretic with mottled extremities.
 Weak, thready peripheral pulses, fatigue, hypotension
(because of inadequate CO).
 Dyspnea, tachypnea, cyanosis (increased left ventricular
pressures result in elevation of left atrial and pulmonary
pressures, causing pulmonary congestion).
Dysrhythmias (because of lack of oxygen to heart
muscle) and sinus tachycardia (as a compensatory
mechanism for a decreased CO).
Chest pain (because of lack of oxygen and blood to heart
muscle).
Decreased bowel sounds, nausea, or abdominal pain
(because of paralytic ileus from decreased perfusion to
GI tract).
Metabolic acidosis because of increased lactate
production and reduced clearance (caused by anaerobic
metabolism and liver dysfunction).
Hypoperfusion causes release of catecholamines, which
increase contractility and peripheral blood flow but also
may increase myocardial oxygen demand and have
proarrhythmic effects.
DIAGNOSTIC FINDINGS
 DIAGNOSTIC FINDINGS
1. Altered hemodynamic parameters (pulmonary artery wedge pressure 15 mm Hg or
greater, cardiac index (CI) less than 2.0, elevated systemic vascular resistance [SVR],
high right ventricular end-diastolic pressure (RVEDP) greater than 20 mm Hg and
decreased mixed venous oxygen saturation).
2. Chest x-ray—pulmonary vascular congestion.
3. Abnormal laboratory values—elevated blood urea nitrogen (BUN) and creatinine,
elevated liver enzymes, increased PTT and PT, elevated serum lactate, elevated brain
natriuretic peptide (BNP). BNP may be useful as an indicator of heart failure and as an
independent prognostic indicator of survival. Abnormally elevated cardiac enzymes.
4. ECG—acute injury pattern consistent with an AMI.
5. Doppler echocardiogram—reveals any ventricular wall motion or surgically
correctable cause, such as valvular dysfunction and tamponade.
6. Pulmonary artery catheterization for severely hypotensive patient.
 MANAGEMENT

Recent studies have suggested that treatment for cardiogenic shock

resulting from an AMI should focus on revascularization and thrombolytics.
Reduction in mortality related to early revascularization in patients with
STEMI is supported by research. Augmenting CO with devices (intra-aortic
balloon pump [IABP] is a method of choice) is crucial until revascularization is
established. Mechanical ventilation is supportive and left ventricular assist
device and extracorporeal membrane oxygenation may be used.
The standard treatment of beta-adrenergic blockers, ACE inhibitors,
analgesics, and nitrates after acute MI does little to treat cardiogenic shock and
may exacerbate systolic hypotension.
 PHARMACOLOGIC THERAPY

Pharmacologic therapy may need to be discontinued or its use

decreased when a patient has gone into cardiogenic shock.
Standard therapy for a failing heart includes:
1. Positive inotropic drugs (epinephrine, dopamine,
dobutamine, amrinone, milrinone) stimulate cardia
contractility. Dobutamine, amrinone, and milrinone may
lower BP because of vasodilatory effect.
2. Vasodilator therapy.
Decreases the workload of the heart by reducing venous return
and lessening the resistance against which the heart
pumps (preload and afterload reduction).
CO improves, left ventricular pressures and pulmonary
congestion decrease, and myocardial oxygen consumption
is reduced.
 PHARMACOLOGIC THERAPY
3. Vasopressor therapy may be needed to maintain adequate
perfusion pressure (MAP 70 mm Hg or greater). These
medications are norepinephrine, epinephrine, vasopressin, and
phenylephrine. These should be used in the lowest possible
dose. Higher vasopressor doses are associated with poor
survival.

4. Diuretic therapy is used to reduce plasma volume and peripheral

edema. The reduction in extracellular fluid and plasma volume
associated with diuresis may initially decrease cardiac output
and, consequently, blood pressure, with a compensatory
increase in peripheral vascular resistance. Continuous renal
replacement therapy has been considered for patients in
cardiogenic shock if unable to diurese because of low renal
perfusion.
 REPERFUSION THERAPY
Revascularization in cardiogenic shock patient may increase the patient’s survival rate.

1. Percutaneous cardiac interventions (PCI)—prompt restoration of blood flow can lead to

improved left ventricular function, thus salvaged ischemic myocardium. Timing of
revascularization less than 90 minutes of door-to-door angioplasty after onset of
symptoms provides better survival rates of CS patients.
Antithrombotic therapy such as antiplatelets and anticoagulation is a mainspring during PCI.
They showed to reduce mortality of cardiogenic shock patients following an acute MI.
2. Thrombolytics—use of fibrinolytic drugs lead to improved left ventricular systolic function
and survival in patients with myocardial infarction associated with either ST-segment elevation
or left bundle-branch block. Limitation to its use due to contraindication generally because of
allergy and bleeding concerns such as recent hemorrhagic stroke.
COUNTERPULSATION THERAPY

 Improves blood flow to the heart muscle and

reduces myocardial oxygen needs.
 Results in improved CO (1.5 L/minute increase)
and preservation of viable heart tissue.
 Should be instituted as quickly as possible to
increase survival because of its overall benefits.
CIRCULATORY AND MECHANICAL
SUPPORT
 Left ventricular assist device (LVAD) or
right ventricular assist device may be used
as bridge to recovery in some patients.

 Extracorporeal life support (ECMO)-

circulates blood using a membrane
oxygenator which relieves both left and right
heart and the lungs of part of their workload.
EMERGENCY CARDIAC SURGERY

 Bypass graft
 Heart transplantation
 COMPLICATION

S
Neurologic impairment/stroke.
 Acute respiratory distress syndrome.
 Renal failure.
 Cardiopulmonary arrest.
 Dysrhythmia.
 Ventricular aneurysm.
 Multiorgan dysfunction syndrome.
 Bowel ischemia.
 Limb ischemia.
 Death.
 NURSING
ASSESSEMENT
 NURSING ASSESSEMENT
Clinical assessment begins with attention to the airway/breathing/circulation and vital signs.
1. Identify patients at risk for development of cardiogenic shock.
2. Assess for early signs and symptoms indicative of shock:
Restlessness, confusion, or change in mental status.
Increasing heart rate and decreasing blood pressure.
Decreasing pulse pressure (indicates impaired CO).
Presence of pulsus alternans (indicates left-sided heart failure).
Decreasing urine output, weakness, fatigue.
3. Observe for presence of central and peripheral cyanosis.
4. Observe for development of edema and cool extremities.
5. Identify signs and symptoms indicative of extension of MI—recurrence of chest pain,
diaphoresis.
6. Identify patient’s and significant other’s reaction to crisis situation.
NURSING
DIAGNOSES
Decreased Cardiac Output related to impaired contractility
because of extensive heart muscle damage.

Impaired Gas Exchange related to pulmonary congestion

because of elevated left ventricular pressures.

Ineffective Tissue Perfusion (renal, cerebral,

cardiopulmonary, GI, and peripheral) related to decreased
blood flow.

Anxiety related to intensive care environment and threat of

death.
NURSING
INTERVENTION
S
 NURSING INTERVENTION
1. Administer oxygen by face mask or artificial airway to ensure adequate oxygenation of
tissues and adjust oxygen flow rate as blood gas measurement indicates.
2. Administer diuretic with caution if ordered to increase renal blood flow and urine output.
3. Monitor and record blood pressure, pulse, respiratory rate, and peripheral pulse every 1 to 5
minutes until the patient stabilizes. Record hemodynamic pressure readings according to
hospital protocol.
4. Monitor ABG values, complete blood count, and electrolyte levels.
5. To ease emotional stress, allow frequent rest periods as possible.
6. Allow family members to visit and comfort the patient as much as possible.
7. During therapy, assess skin color and temperature and note any changes. Cold and clammy
skin may be a sign of continuing peripheral vascular constriction, indicating progressive
shock.
 Improving Cardiac Output
1. Establish continuous ECG monitoring to detect dysrhythmias, which increase myocardial oxygen
consumption.
2. Monitor hemodynamic parameters continually with pulmonary artery to evaluate effectiveness of
implemented therapy.
 Obtain pulmonary artery pressure (PAP), pulmonary artery wedge pressure, and CO readings, as
indicated.
 Calculate the CI (CO relative to body size) and SVR (estimation of afterload).Cautiously titrate
vasoactive drug therapy according to hemodynamic parameters.
3. Be alert to adverse responses to drug therapy.

 Dopamine may cause an increase in heart rate, which may result in ischemia.

 Vasodilators, such as nitroglycerin and nitroprusside, may worsen hypotension.

 Dobutamine may result in dysrhythmias.

 Diuretics may cause hyponatremia, hypokalemia, and hypovolemia.

 Improving Cardiac Output
 Administer vasoactive drug therapy through central venous access (peripheral tissue necrosis can occur if
peripheral IV access infiltrates and peripheral drug distribution may be lessened from vasoconstriction).
 Monitor blood pressure and MAP with intra-arterial line continuously during active titration of
vasoactive drug therapy.
 Maintain MAP greater than 65 mm Hg (blood flow through coronary vessels is inadequate with MAP less
than 65 mm Hg).
 Measure and record urine output every hour from indwelling catheter and fluid intake.
 Obtain daily weight.
 Evaluate serum electrolytes for hyponatremia, hypomagnesemia, and hypokalemia.
 Be alert to incidence of chest pain (indicates myocardial ischemia and may further extend heart damage).

 Report immediately.

 Obtain a 12-lead ECG; check cardiac enzymes—CK, CK-MB, myoglobin, and troponin.

 Anticipate use of counterpulsation therapy.

 Anticipate pump failure; evaluate need for surgical intervention (ie, ventricular assist device,
extracorporeal membrane oxygenation).
 Improving Oxygenation
1. Monitor rate and rhythm of respirations every hour.
2. Auscultate lung fields for abnormal sounds (coarse crackles indicate severe pulmonary congestion)
every hour; notify health care provider.
3. Evaluate arterial blood gas (ABG) levels and correlate with oxygen saturation.
4. Administer oxygen therapy to increase oxygen tension and improve hypoxia.
5. Elevate head of bed 20 to 30 degrees, as tolerated (may worsen hypotension), to facilitate lung
expansion.
6. Reposition patient frequently to promote ventilation and maintain skin integrity.
7. Observe for frothy pink sputum and cough (may indicate pulmonary edema); report immediately.
 Maintaining Tissue Perfusion
1. Perform a neurologic check every hour using the Glasgow Coma Scale.
2. Report changes immediately.
3. Obtain BUN and creatinine blood levels and monitor urine output to evaluate
renal function.
4. Auscultate for bowel sounds every 2 hours.
5. Evaluate character, rate, rhythm, and quality of arterial pulses every 2 hours.
6. Monitor temperature every 2 to 4 hours.
7. Use sheepskin foot and elbow protectors to prevent skin breakdown.
8. Obtain serum lactate to evaluate tissue perfusion and acidosis.
 Relieving Anxiety
1. As with the above, always evaluate signs of increasing anxiety and/or new-onset anxiety
for a physiologic cause before treating with anxiolytics.
2. Explain equipment and rationale for therapy to patient and family. Increasing knowledge
assists in alleviating fear and anxiety.
3. Encourage patient to verbalize fears about diagnosis and prognosis.
4. Explain sensations patient will experience before procedures and routine care measures.
5. Offer reassurance and encouragement.
6. Utilize social worker or pastoral care for support.
7. Provide for periods of uninterrupted rest and sleep.
8. Assist patient to maintain as much control as possible over environment and care.
Develop a schedule for routine care measures and rest periods with patient.
Make sure that a calendar and clock are in view of patient.
 Patient Education and Health Maintenance
1. Assess patient’s readiness to learn.
2. Teach patients taking digoxin the importance of taking their medication as
prescribed, taking pulse before daily dose, and reporting for periodic blood
levels.
3. Teach signs of impending heart failure—increasing edema, shortness of breath,
decreasing urine
4. Teach patient importance of keeping follow-up appointments with his or her
primary care physician and cardiologist.
5. Have dietitian teach patient and family about a low-sodium, low-fat diet, and
reiterate the importance of adhering to this diet.
6. Explain to the patient the need to work with a physical and occupational
therapist—especially if the patient has low ejection fraction—for energy
conservation.
 EVALUATION:
EXPECTED
OUTCOMES
CO greater than 4 L/minute; CI greater
than 2.2; PCWP less than 18 mm Hg.
Respirations unlabored and regular;
normal breath sounds throughout lung
fields.
Normal sensorium; urine output
adequate; skin warm and dry.
Verbalizes lessened anxiety and fear.
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