8 Cardiogenic Shock Nursing Diagnosis and Care Plans

The pump has failed. The heart cannot move enough blood to meet the body's demands even though the tank is full, so every organ downstream starts to starve. It feeds on itself: poor coronary flow worsens ischemia, ischemia worsens contractility, contractility drops output further. Your job is to catch the slide early, support output and oxygenation, and buy time for the definitive fix before multi-organ failure sets in.

What is Cardiogenic Shock?

Cardiogenic shock is failure of the heart to pump enough blood to meet the body's metabolic needs because contractility is impaired. The patient shows low cardiac output with adequate intravascular volume. It most often follows myocardial infarction, and also cardiomyopathies, dysrhythmias, valvular stenosis, massive pulmonary embolism, cardiac surgery, or cardiac tamponade.

Nursing Care Plans and Management

Care centers on close assessment, watching the cardiac rhythm, tracking hemodynamic parameters and fluid status, and titrating medications and therapies off the data in front of you.

Nursing Problem Priorities

Keep cardiac output up, hold hemodynamics stable while monitoring vitals for any sign of deterioration, and protect gas exchange so oxygen still reaches the tissues.

Nursing Assessment

Assess for the following subjective and objective data, and for factors driving the shock.

Track vital signs (BP, HR, RR, oxygen saturation, temperature) for hemodynamic stability. Assess cardiac status: heart sounds, murmurs or extra sounds, jugular vein distention, peripheral edema. Assess respiratory effort and lung sounds for distress. Check level of consciousness and orientation for cerebral hypoperfusion (confusion, restlessness, decreased responsiveness). Measure urine output as a read on renal perfusion.

Common drivers: dysrhythmias from electrolyte imbalance, ischemia, or structural disease; increased or decreased preload or afterload straining the pump; impaired left ventricular contractility from MI, myocarditis, or cardiomyopathy; septal defects (VSD, ASD) overloading the chambers; valve dysfunction such as severe aortic stenosis or mitral regurgitation; changes in the alveolar-capillary membrane from ARDS or pulmonary edema; ventilation-perfusion mismatch from pulmonary embolism or bronchospasm; falling renal perfusion; and sodium and water retention from renin-angiotensin-aldosterone activation, which adds preload and worsens the failure.

Nursing Diagnosis

• Decreased cardiac output

Nursing Goals

Goals and expected outcomes may include:

• The patient maintains adequate cardiac output: strong peripheral pulses, HR 60 to 100 beats per minute with a regular rhythm, systolic BP within 20 mm Hg of baseline, urine output 30 mL/hr or greater, warm dry skin, and normal level of consciousness.
• The patient maintains optimal gas exchange: ABGs within normal range, oxygen saturation 90% or greater, alert mentation or no further decline, relaxed breathing, and baseline HR.
• The patient demonstrates adequate perfusion: strong peripheral pulses, HR 60 to 100 beats per minute regular, systolic BP within 20 mm Hg of baseline, balanced intake and output, warm dry skin, alert and oriented.
• The patient reports reduced anxiety and uses effective coping.

Nursing Interventions and Actions

1. Managing Decreased Cardiac Output
2. Monitoring Diagnostic Procedures and Laboratory Studies
3. Promoting Oxygenation and Gas Exchange
4. Improving Tissue Perfusion
5. Administering Medications
6. Managing Fluid and Electrolyte Imbalance
7. Providing Perioperative Care
8. Reducing Anxiety

1. Managing Decreased Cardiac Output

1. Assess for changes in level of consciousness. Restlessness and anxiety are early signs of cerebral hypoxia; confusion and loss of consciousness come later. Older patients are especially vulnerable to reduced perfusion of vital organs.

2. Assess HR, BP, and pulse pressure. Use direct intra-arterial monitoring as ordered. Sinus tachycardia and rising arterial BP appear early as the body fights to hold output, then BP falls as the patient deteriorates. Cuff pressures may be unreliable with vasoconstriction. Pulse pressure (systolic minus diastolic) narrows in shock. Older patients respond less to catecholamines, so the HR rise may be blunted.

3. Assess cardiac rate, rhythm, and ECG. Dysrhythmias arise from low perfusion, acidosis, hypoxia, or cardiac drug effects. The 12-lead ECG can show myocardial ischemia (ST-segment and T-wave changes) or tamponade (decreased QRS voltage).

4. Assess heart sounds for gallops (S3, S4). S3 is a classic sign of left ventricular failure, produced during passive filling when blood strikes a stiff ventricle. S4 reflects reduced ventricular compliance that impairs diastolic filling.

5. Assess central and peripheral pulses. Pulses are weak with diminished stroke volume and output.

6. Assess capillary refill. Refill is slow and sometimes absent.

7. Assess respiratory rate, rhythm, and breath sounds. Shock brings rapid shallow respirations and adventitious sounds such as crackles and wheezes.

8. Administer IV fluids for a decreased preload. The right fluid status keeps ventricular filling pressure effective. Too little drops circulating volume and filling pressure; too much floods a failing heart and causes pulmonary edema. Pulmonary capillary wedge pressure guides the fluid.

9. Administer medications as prescribed. Drug therapy works best started early. The goal is systolic BP above 90 to 100 mm Hg. See Medications.

2. Monitoring Diagnostic Procedures and Laboratory Studies

1. Monitor oxygen saturation by pulse oximetry. Hold saturation at 90% or higher.

2. Monitor arterial blood gases. Rising PCO2 and falling PaO2 signal hypoxemia and respiratory acidosis. As the patient fails, the respiratory rate drops and PaCO2 keeps climbing.

3. Monitor CVP, pulmonary artery diastolic pressure (PADP), pulmonary capillary wedge pressure, and cardiac output/cardiac index. CVP reflects right-sided filling pressures; PADP and wedge pressure reflect left-sided volumes. Cardiac output gives an objective number to titrate against.

4. Monitor magnesium and potassium. Hypomagnesemia and hypokalemia drive dysrhythmias that cut output further.

3. Promoting Oxygenation and Improving Gas Exchange

1. Assess respiratory rate, rhythm, and depth. Early on the rate rises with hypercapnia and hypoxia. As shock progresses respirations turn shallow and the patient hyperventilates. Respiratory failure follows as the muscles fatigue and lung compliance drops.

2. Assess heart rate and blood pressure. As shock progresses, BP and HR fall and dysrhythmias may appear.

3. Assess for changes in level of consciousness. Headache and restlessness are early signs of hypoxia.

4. Auscultate for areas of decreased ventilation and adventitious sounds. Moist crackles come from increased pulmonary capillary permeability and intra-alveolar edema.

5. Assess for cyanosis or pallor at the skin, nail beds, and mucous membranes. Cool pale skin reflects compensatory vasoconstriction to hypoxemia. Peripheral cyanosis follows impaired oxygenation and perfusion.

6. Assist with coughing and suction as needed. Suction clears secretions the patient cannot.

7. Elevate the head of the bed. This eases ventilation.

8. Administer oxygen as ordered. Supplemental oxygen keeps PaO2 at an acceptable level.

9. Prepare for mechanical ventilation if oxygen therapy is not enough. Early intubation and ventilation head off full decompensation and support oxygenation and ventilation.

4. Improving Tissue Perfusion

1. Assess HR, BP, and pulse pressure. Use direct intra-arterial monitoring as ordered. Early tachycardia and rising BP give way to falling BP as the patient deteriorates. Cuff pressures may be unreliable with vasoconstriction, and pulse pressure narrows in shock.

2. Assess for changes in level of consciousness. Restlessness and anxiety are early signs of cerebral hypoxia; confusion and loss of consciousness come later.

3. Assess capillary refill. Refill is slow and sometimes absent.

4. Monitor oxygen saturation and arterial blood gases. Hold saturation at 90% or higher. As shock progresses, aerobic metabolism stops and lactic acidosis sets in, raising carbon dioxide and dropping pH.

5. Keep the patient on bed rest and limit activity. Bed rest minimizes oxygen demand.

6. Provide oxygen therapy as indicated. Oxygen raises the amount carried by available hemoglobin.

7. Administer IV fluids as ordered. Adequate fluid keeps filling pressures up and optimizes the output that perfuses tissue.

5. Administering Medications

1. Antidysrhythmics. Used when a dysrhythmia is further compromising a low-output state.

2. Diuretics. Used when volume overload is contributing to pump failure.

3. Inotropes.

• Dobutamine treats cardiac decompensation from depressed contractility.
• Dopamine stimulates beta-1 adrenergic receptors to raise output and dopamine receptors to produce vasodilation.
• Inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity.
• Norepinephrine (Levophed) stimulates beta1- and alpha-adrenergic receptors, raising contractility, heart rate, and vasoconstriction.

4. Morphine. Cuts pain, which lowers sympathetic stress and reduces preload.

5. Vasodilators.

• Nitroglycerin (NTG) relaxes vascular smooth muscle by raising intracellular cyclic guanosine monophosphate, dropping preload and blood pressure.
• Sodium nitroprusside (Nipride) raises output by reducing afterload and produces peripheral and systemic vasodilation by direct action on vascular smooth muscle.

6. Managing Fluid and Electrolyte Imbalance

1. Monitor urine output, color, and amount. Output may be concentrated and scant from reduced renal perfusion.

2. Auscultate for crackles and wheezing; note cough, dyspnea, or orthopnea. These point to pulmonary edema from worsening congestion and call for immediate action.

3. Monitor intake and output. Low output cuts renal perfusion, causing water and sodium retention and oliguria.

4. Assess for edema. Pitting edema starts at the feet and ankles and builds into weight gain.

5. Assess fluid balance and weight. Fluid and sodium retention follows compromised regulation. Daily weight tracks the response to diuretics.

6. Assess for distended neck veins. Jugular vein distention points to fluid excess.

7. Monitor electrolytes, especially potassium. Hypokalemia follows because diuretics promote renal potassium loss.

8. Monitor the chest x-ray. Films track progress or a worsening lung picture.

9. Place the patient in semi-Fowler's position. This raises renal filtration and lowers ADH to promote diuresis, and it helps lung expansion against pulmonary congestion.

10. Reposition at least every 2 hours. Turning improves breathing, mobilizes secretions, and prevents pressure ulcers.

11. Instruct the patient on a low-sodium diet. Cutting sodium reduces fluid and electrolyte retention, since high sodium holds water in the bloodstream and pushes fluid into the tissues.

12. Administer diuretics (for example, furosemide) as indicated. Diuretics drop plasma volume and peripheral edema. Watch for fluid and electrolyte imbalances. See Medications.

7. Providing Perioperative Care

1. Institute an intra-aortic balloon pump (IABP) or ventricular assist device (VAD) when counterpulsation is indicated. These devices take over part of the pump's work to raise output when drugs are not enough. The IABP increases myocardial oxygen supply and lowers myocardial workload through better coronary perfusion, raising stroke volume and perfusion to vital organs.

2. Prepare for surgical intervention if ordered. Acute valve problems or septal defects often need surgery.

8. Reducing Anxiety and Promoting Coping

1. Assess previous coping mechanisms. Anxiety and the ways to ease it are individual. Build on the patient's established pattern, though some methods are not feasible in acute care.

2. Assess the patient's level of anxiety. A life-threatening shock state produces high anxiety in the patient and the family.

3. Explain procedures simply. Anxious patients take in only brief, clear instructions.

4. Encourage the patient to verbalize feelings. Naming the fear makes the situation feel less threatening.

5. Acknowledge the patient's anxiety. Acknowledgment validates the feeling and communicates acceptance.

6. Cut unnecessary stimuli and keep the environment quiet. Excess conversation, noise, and equipment escalate anxiety. If equipment is the trigger, consider sedation as ordered.

7. Stay calm and assured at the bedside. Staff anxiety reads to the patient. A calm, confident presence and the promise of close, continuous monitoring steady the patient and family.

Evaluation

Expected outcomes include preventing recurrence of cardiogenic shock, monitoring hemodynamic status, administering medications and IV fluids, and maintaining intra-aortic balloon counterpulsation.

Discharge and Home Care Guidelines

Lifestyle changes lower the chance of recurrence. Control hypertension with exercise, stress management, a healthy weight, and limited salt and alcohol. Stop smoking; years after quitting, stroke risk drops back toward that of someone who never smoked. Lose extra weight to bring down cholesterol and blood pressure. Eat less saturated fat and cholesterol. Exercise daily to lower blood pressure, raise HDL, and improve the health of the heart and vessels.

Documentation Guidelines

Document baseline and subsequent hemodynamic parameters, heart and breath sounds, ECG pattern, peripheral pulses, skin and tissue status, renal output, and mentation. Record respiratory rate, breath sound character, secretions, cyanosis, and lab findings. Note conditions limiting oxygen supply or driving fluid retention, intake and output, fluid balance, pulses and BP, the patient's pain response and acceptable level, prior medication use, the plan and teaching plan, responses to interventions, status at discharge, progress toward outcomes, and any changes to the plan.