5 Cardiogenic Shock Nursing Care Plans

Cardiogenic shock is a condition caused by the inability of the heart to pump blood sufficiently to meet the metabolic needs of the body due to the impaired contractility of the heart. Clients usually manifest signs of low cardiac output, with adequate intravascular volume. 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 further ischemia and ventricular dysfunction.

Nursing Care Plans

The nursing care plan in clients with cardiogenic shock involves careful assess the client, observe cardiac rhythm, monitor hemodynamic parameters, monitor fluid status, and adjust medications and therapies based on the assessment data.

Here are five (5) nursing care plans (NCP) for cardiogenic shock:

1. Impaired Gas Exchange

Impaired Gas Exchange: Excess or deficit in oxygenation and/or carbon dioxide elimination at the alveolar-capillary membrane.

May be related to

- Changes in the alveolar-capillary membrane.
- Impaired ventilation-perfusion.

Possibly evidenced by

- Abnormal arterial blood gasses (ABGs).
- Abnormal respiratory rate, depth, and rhythm.
- Changes in the level of consciousness.
- Crackles.
- Cyanosis.
- Headache.
- Hypercapnia.
- Hypoxia.
- Tachycardia.

Desired Outcomes

- Client will maintain optimal gas exchange, as evidenced by ABGs within the normal range, oxygen saturation of 90% or greater, alert responsive mentation or no further reduction in the level of consciousness, relaxed breathing, and baseline HR for the client.

Nursing Interventions	Rationale
Assess the client’s respiratory rate, rhythm, and depth.	During the early stages of shock, the client’s respiratory rate will be increased due to hypercapnia and hypoxia. Once the shock progresses, the respirations become shallow, and the client will begin to hypoventilate. Respiratory failure develops as the client experiences respiratory muscle fatigue and decreased lung compliance.
Assess client’s heart rate and blood pressure.	As shock progresses, the client’s blood pressure and heart rate will decrease and dysrhythmias may occur.
Assess for any signs of changes in the level of consciousness.	Headache, restlessness are early signs of hypoxia.
Auscultate the lung for areas of decreased ventilation and the presence of adventitious sounds.	Moist crackles are caused by increased pulmonary capillary permeability and increased intra-alveolar edema.
Assess for cyanosis or pallor by examining the skin, nail beds, and mucous membranes.	Cool, pale skin may be secondary to a compensatory vasoconstrictive response to hypoxemia. Peripheral tissues become cyanotic due to impaired oxygenation and perfusion.
Monitor oxygen saturation using pulse oximetry.	Pulse oximetry is used in measuring oxygenation concentration. The normal oxygen saturation should be maintained at 90% or higher.
Monitor arterial blood gasses.	Increasing Pac0₂and decreasing Pa0₂are signs of hypoxemia and respiratory acidosis. As the client’s condition begins to fail, the respiratory rate will decrease and Pac0₂ will continue to increase.
Assist the client when coughing, and suction the client when needed.	Suction removes secretions if the client is unable to effectively clear the airway.
Place the client’s head of bed elevated.	This position facilitates optimal ventilation.
Administer oxygen as ordered.	Supplemental oxygen may be required to maintain Pa0₂at an acceptable level.
Prepare the client for mechanical ventilation if oxygen therapy is ineffective.	Early intubation and mechanical ventilation are recommended to prevent full decompensation of the client. Mechanical ventilation provides supportive care to maintain adequate oxygenation and ventilation to the client.

2. Decreased Cardiac Output

Decreased Cardiac Output: Inadequate blood pumped by the heart to meet metabolic demands of the body.

May be related to

- Cardiac muscle disease.
- Dysrhythmias.
- Increased or decreased preload or afterload.
- Impaired left ventricular (LV) contractility.
- Septal defects.
- Valve dysfunction.

Possibly evidenced by

- Changes in the level of consciousness.
- Crackles, dyspnea, and pulmonary congestion.
- Cyanosis and mottling of the extremities.
- Metabolic acidosis.
- Oliguria and/or anuria.
- Pale, cool, clammy skin.
- Respiratory alkalosis.
- Sustained hypotension with narrowing of pulse pressure.
- Tachycardia.

Desired Outcomes

- Client will maintain adequate cardiac output as evidenced by strong peripheral pulses, HR 60 to 100 beats per minute with regular rhythm, systolic BP within 20 mm Hg of baseline, urinary output 30 ml hr or greater, warm and dry skin, and normal level of consciousness.

Nursing Interventions	Rationale
Assess for any changes in the level of consciousness.	Restlessness and anxiety are early signs of cerebral hypoxia while confusion and loss of consciousness occur in the later stages. Older clients are especially susceptible to reduced perfusion to vital organs.
Assess the client’s HR, BP, and pulse pressure. Use direct intra-arterial monitoring as ordered.	Sinus tachycardia and increased arterial BP are seen in the early stages to maintain an adequate cardiac output. BP drops as condition deteriorates. Auscultatory BP may be unreliable secondary to vasoconstriction. Pulse pressure (systolic minus diastolic) decreases in shock. Older client have reduced response to catecholamines; thus their response to decreased cardiac output may be blunted, with less increase in HR.
Assess the cardiac rate, rhythm, and electrocardiogram (ECG).	Cardiac dysrhythmias may occur from low perfusion, acidosis, or hypoxia, as well as from side effects of cardiac medications used to treat this condition. The 12-lead ECG may provide evidence of myocardial ischemia (ST-segment and T-wave changes) or pericardial tamponade (decreased voltage of QRS complex).
Assess the heart sounds for gallops ( S₃, S₄).	S₃is a classic sign of left ventricular failure and is produced during passive left ventricular filling when blood strikes a compliant left ventricle. and S₄ isassociated with reduced ventricular compliance, which impairs diastolic filling.
Assess the central and peripheral pulses.	Pulses are weak, with diminished stroke volume and cardiac output.
Assess capillary refill.	Capillary refill is slow and sometimes absent.
Assess respiratory rate, rhythm, and auscultate breath sounds.	Characteristics of a shock include rapid, shallow respirations and adventitious breath sounds such as crackles and wheezes.
Monitor oxygen saturation and arterial blood gasses.	Pulse oximetry is used in measuring oxygen saturation. The normal oxygen saturation should be maintained at 90% or higher. As shock progresses, aerobic metabolism stops and lactic acidosis occurs, resulting in the increased level of carbon dioxide and decreasing pH.
Monitor the client’s central venous pressure (CVP), pulmonary artery diastolic pressure (PADP), pulmonary capillary wedge pressure, and cardiac output/cardiac index.	CVP provides information on filling pressures of the right side of the heart; pulmonary artery diastolic pressure and pulmonary capillary wedge pressure reflect left-sided fluid volumes. Cardiac output provides an objective number to guide therapy.
Assess fluid balance and weight gain.	Fluid and sodium retention occurs due to the compromised regulatory mechanisms. Body weight is a good indicator of fluid and sodium retention.
Assess urine output.	The renal system compensates for low BP by retaining water. Oliguria is a classic sign of inadequate renal perfusion from reduced cardiac output.
Monitor the following laboratory: - Potassium. - Magnesium.	Hypomagnesemnia and Hypokalemia can lead to the development of dysrhythmias which can further reduce cardiac output.
Provide electrolyte replacement as prescribed.	Electrolyte imbalance may cause dysrhythmias or other pathological states.
Restrict fluids and sodium as ordered if increased preload becomes a problem.	Fluid resuscitation reduces extracellular fluid volume and decreases cardiac workload.
Administer IV fluids for clients with a decreased preload.	Optimal fluid status ensures effective ventricular filling pressure. Too little fluid reduces circulating blood volume and ventricular filling pressures; too much fluid can cause pulmonary edema in a failing heart. Pulmonary capillary wedge pressure guides therapy.
Administer oxygen as prescribed.	Oxygen may be required to maintain oxygen saturation above 90% or as indicated by order or protocol.
Administer medications as prescribed:	Medication therapy is more effective when initiated early. The goal is to maintain systolic BP greater than 90 or 100 mm Hg.
Antidysrrhythmics	Antidysrrhythmics are used when cardiac anti dysrhythmias are further compromising a low output state.
Diuretics	Diuretics are used when volume overload is contributing to pump failure.
Inotropics
- Dobutamine	Dobutamine is used in the treatment of cardiac decompensation due to depressed contractility.
- Dopamine	Dopamine stimulates beta-1 adrenergic receptors, resulting in increased cardiac output and stimulates dopamine receptors, resulting in vasodilatation.
- Inamrinone	Inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity.
- Norepinephrine (Levophed)	Norepinephrine stimulates beta1- and alpha-adrenergic receptors, resulting in increased cardiac muscle contractility, heart rate, and vasoconstriction.
Morphine	Morphine decreases pain, which reduces sympathetic stress and provides some preload reduction.
Vasodilators
- Nitroglycerin (NTG)	NTG causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production resulting in a decrease in preload and blood pressure
- Sodium Nitroprusside (Nipride)	Sodium Nitroprusside increase cardiac output by decreasing afterload and produces peripheral and systemic vasodilation by direct action to the smooth muscles of the blood vessels.
Institute an intra-aortic balloon pump (IABP) or ventricular assist device (VAD) if mechanical assistance by counterpulsation is indicated.	Mechanical assist device such as VAD or IABP temporarily helps the pumping action of the heart in order to improve cardiac output. These devices are used in client’s who do not respond to the medical management. IABP increases myocardial oxygen supply and decreases myocardial workload through increased coronary artery perfusion. The client’s stroke volume increases thereby improving perfusion to the vital organs.
Prepare the client for surgical intervention if ordered.	Acute valvular problems or septal defects often require surgical treatment.

3. Ineffective Tissue Perfusion

Ineffective Tissue Perfusion: Decreased in the oxygen resulting in the failure to nourish the tissues at the capillary level.

May be related to

- Reduction/cessation of blood flow.

Possibly evidenced by

- Abnormal ABG’s.
- Altered mentation
- Capillary refill longer than 3 seconds.
- Cyanosis.
- Dysrhythmias.
- Dyspnea.
- Oliguria.

Desired Outcomes

- Client will demonstrate increased perfusion as individually appropriate as evidenced by strong peripheral pulses, HR 60 to 100 beats per minute with regular rhythm, systolic BP within 20 mm Hg of baseline, balanced intake and output, warm and dry skin, and alert/oriented.

Nursing Interventions	Rationale
Assess the client’s HR, BP, and pulse pressure. Use direct intra-arterial monitoring as ordered.	Sinus tachycardia and increased arterial BP are seen in the early stages to maintain an adequate cardiac output. BP drops as condition deteriorates. Auscultatory BP may be unreliable secondary to vasoconstriction. Pulse pressure (systolic minus diastolic) decreases in shock.
Assess for any changes in the level of consciousness.	Restlessness and anxiety are early signs of cerebral hypoxia while confusion and loss of consciousness occur in the later stages.
Assess capillary refill.	Capillary refill is slow and sometimes absent.
Monitor oxygen saturation and arterial blood gasses.	Pulse oximetry is used in measuring oxygenation concentration. The normal oxygen saturation should be maintained at 90% or higher. As shock progresses, aerobic metabolism stops and lactic acidosis occurs, resulting in the increased level of carbon dioxide and decreasing pH.
Restrict the patient’s activity, and maintain the client on a bed rest.	Minimize oxygen demand by maintaining bed rest and limiting the client’s activity.
Provide oxygen therapy as indicated.	Oxygen is administered to increase the amount of oxygen carried by available hemoglobin in the blood.
Administer IV fluids as ordered.	Sufficient fluid intake maintains adequate filling pressures and optimizes cardiac output needed for tissue perfusion.

4. Excess Fluid Volume

Excess Fluid Volume: Increased isotonic fluid retention

May be related to

- Decrease in renal organ perfusion.
- Increased sodium and water retention.
- Hydrostatic pressure increase or decrease plasma proteins.

Possibly evidenced by

- Changes in mental status.
- Cough.
- Crackles.
- Dyspnea.
- Edema.
- Jugular vein distention.
- Oliguria.
- Orthopnea.
- Pulmonary congestion.
- Shortness of breath.
- Weight gain.

Desired Outcomes

- Client will have stable fluid volume as evidenced by balanced intake and output, stable weight, vital signs within normal limits, and absence of edema.

Nursing Interventions	Rationale
Monitor urine output, observe its color and amount.	Urine output may be concentrated and scanty due to decreased renal perfusion.
Auscultate the lung for the presence of adventitious breath sound such as crackles, wheezing. Note for presence of cough, dyspnea, or orthopnea.	These may indicate pulmonary edema from a worsening pulmonary congestion and intervention must be done immediately.
Monitor client’s intake and output.	Decreased cardiac output may lead to decreased renal perfusion and impairment with excess fluid volume which causes water and sodium retention and oliguria.
Assess for edema.	Edema (usually pitting edema) that starts in the feet and ankles and gradually lead to weight gain.
Assess fluid balance and weight gain.	Fluid and sodium retention occurs due to the compromised regulatory mechanisms. Body weight is used to detect response to diuretic therapy.
Assess for distended neck veins.	Jugular vein distention may indicate fluid excess.
Monitor client’s electrolyte levels esp. potassium.	Hypokalemia can occur since diuretics promote renal potassium secretion.
Monitor client’s Chest x-ray.	Review chest radiographs to evaluate the client’s progress or a worsening lung condition.
Place the client in a semi position.	Semi fowler’s position increases renal filtration and decreases the production of ADH thus promoting diuresis.
Frequently change the client’s position at least every 2 hours.	Repositioning promotes enhanced breathing, decreases pressure ulcer and mobilization of secretions.
Instruct the client to have a low sodium diet.	Low sodium diet can decrease fluid and electrolyte retention.
Administer diuretics (e.g., furosemide) as indicated.	Diuretics decrease plasma volume and peripheral edema.

5. Anxiety

Anxiety: Vague uneasy feeling of discomfort or dread accompanied by an autonomic response.

May be related to

- Change in health status.
- Fear of death.
- Guarded prognosis; mortality rate 80%.
- Unfamiliar environment.

Possibly evidenced by

- Agitation.
- Avoid looking at equipment or keeps vigilant watch over equipment.
- Increased questioning.
- Increased awareness.
- Sympathetic stimulation.
- Verbalized anxiety.
- Uncooperative behavior.

Desired Outcomes

- Client will use effective coping mechanisms.
- Client will describe reduction in level of anxiety experienced.

Nursing Interventions	Rationale
Assess previous coping mechanism used.	Anxiety and ways of decreasing perceived anxiety are highly individualized. Interventions are most effective when they are consistent with the client’s established coping pattern. However, in the acute care setting these techniques may no longer be feasible.
Assess the client’s level of anxiety.	Shock can result in an acute life-threatening situation that will produce high levels of anxiety in the client as well as in significant others.
Explain all procedures as appropriate, keeping explanations basic.	Information helps reduce anxiety. Anxious clients unable to understand anything more than simple, clear, brief instructions.
Encourage the client to verbalized his or her feelings.	Talking about anxiety-producing situations and anxious feelings can help the client perceive the situation in a less threatening manner.
Acknowledge an awareness of the client’s anxiety.	Acknowledgement of the client’s feelings validates the client’s feelings and communicates acceptance of those feelings.
Reduce unnecessary external stimuli by maintaining a quite environment. If medical equipment is a source of anxiety, consider providing sedation to the client.	Anxiety may escalate with excessive conversation, noise, and equipment around the client.
Maintain a confident, assured manner while interacting with the client. Assure the client and significant others of close, continuous monitoring that will ensure prompt intervention.	The staff’s anxiety may be easily perceived by the client. The client’s feeling of stability increases in a calm and non-threatening atmosphere. The presence of a trusted person may help the client feel less threatened.

References and Sources : nurseslabs.com

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