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
with a marked systolic of causes a marked blood and oxygen
less than 80 to 90 mm reduction in CO and to the heart as
Hg or mean arterial ejection fraction well as other vital
pressure 30 mm Hg organs (brain and
lower than baseline kidneys).
because of left
ventricular failure.
 Etiology
4 5 6
Lack of blood and Myocardial Mechanical
oxygen to the infarction complications
heart muscle MI causing extensive such as ventricular
Lack of blood and damage (40% or greater) septal rupture,
oxygen to the heart to the left ventricular contained free wall
muscle results in myocardium is the most rupture, and
continued damage to common cause papillary muscle
the muscle, a further rupture are
decline in contractile strongly suspected
power, and a continued in patients with
inability of the heart to shock, particularly
provide blood and a rst MI
oxygen to vital organs.
.
In addition to MI with or
without complications,
common causes of cardiogenic
shock include:
Aortic dissection—complicated by acute
severe aortic insu ciency or MI.
Acute decompensation of heart failure.
Acute myocarditis.
Takotsubo stress-induced
cardiomyopathy.
Postcardiotomy.
Cardiac tamponade.
Peripartum cardiomyopathy.
Hypertrophic cardiomyopathy with
severe out ow 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
ow but also may increase myocardial oxygen
demand and have proarrhythmic e ects.
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 e ect.
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 uid
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 ow 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 brinolytic 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 ow 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


bene ts.
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
 COMPLICATIONS

 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.
1. Observe for presence of central and peripheral cyanosis.
2. Observe for development of edema and cool extremities.
3. Identify signs and symptoms indicative of extension of MI—recurrence of chest pain,
diaphoresis.
4. Identify patient’s and signi cant 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.




Ine ective Tissue Perfusion (renal, cerebral,
cardiopulmonary, GI, and peripheral) related to
decreased blood ow.




Anxiety related to intensive care environment and
threat of death.

NURSING
INTERVENTION
S


 NURSING INTERVENTION
1. Administer oxygen by face mask or arti cial airway to ensure adequate
oxygenation of tissues and adjust oxygen ow rate as blood gas measurement
indicates.
2. Administer diuretic with caution if ordered to increase renal blood ow 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
e ectiveness 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 in ltrates 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 ow through coronary vessels is inadequate
with MAP less than 65 mm Hg).
 Measure and record urine output every hour from indwelling catheter and uid 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 elds 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.
 1.
Relieving Anxiety
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. O er 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 elds.

Normal sensorium; urine output
adequate; skin warm and dry.

THANK YOU
FOR
LISTENING