(5) nursing care plans (ncp) for cardiogenic shock
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The document provides information on cardiogenic shock, including its causes and nursing care plans. Cardiogenic shock is caused by the heart's inability to pump sufficiently due to impaired contractility. It is usually associated with conditions like myocardial infarction. The nursing care plans for cardiogenic shock involve careful assessment, monitoring of vital signs and fluid status, and adjusting medications based on assessments. Five specific nursing care plans are outlined covering impaired gas exchange, decreased cardiac output, ineffective tissue perfusion, excess fluid volume, and anxiety. The plans describe potential signs and symptoms, desired outcomes, and nursing interventions with rationales.
(5) nursing care plans (ncp) for cardiogenic shock
- 1. Prepared by Demonstrator at faculty of nursing MTI university 02 01064423095 02 01144127776 Mustafaabdalla31@gmail.com
- 2. 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 shockinvolves careful assess the client observe cardiac rhythm monitor hemodynamic parameters monitor fluid status adjust medications and therapies based on the assessment data .Here are five (5) nursing care plans (NCP) for cardiogenic shock: 1) Impaired Gas Exchange 2) Decreased Cardiac Output 3) Ineffective Tissue Perfusion 4) Excess Fluid Volume 5) Anxiety
- 3. 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. Possiblyevidenced 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 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 shockprogresses, 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.
- 4. 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 responseto 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 Pac02 and decreasing Pa02 are 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 Pa02 at 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
- 5. ventilation to the client. 2) Decreased Cardiac Output Decreased CardiacOutput: 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. Possiblyevidenced 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 Nursing Interventions Rationale Assess for any changes in Restlessness and anxiety are early signs of cerebral hypoxia while confusion and loss of consciousness
- 6. the level of consciousness. occurin 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 secondaryto vasoconstriction. Pulse pressure (systolic minus diastolic) decreases in shock. Older client have reduced responseto catecholamines; thus their responseto decreased cardiac output may be blunted, with less increase in HR. Assess the cardiac rate, rhythm, and electrocardiogram (ECG). Cardiac dysrhythmias may occurfrom 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). S3 is a classic sign of left ventricular failure and is produced during passive left ventricular filling when blood strikes a compliant left ventricle. and S4is associated with reduced ventricular compliance, which impairs diastolic filling. Assess the central and peripheral pulses. Pulses are weak, with diminished strokevolume and cardiac output. Assess capillary refill. Capillary refill is slow and sometimes absent. Assess respiratory rate, rhythm, and auscultate breath sounds. Characteristics of a shockinclude rapid, shallow respirations and adventitious breath sounds suchas 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
- 7. 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 Medication therapy is more effective when initiated
- 8. prescribed: 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 dopaminereceptors, resulting in vasodilatation. Inamrinone Inamrinone is a phosphodiesteraseinhibitor with positive inotropic and vasodilator activity. Norepinephrine (L evophed) 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 (NT G) NTG causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphateproduction resulting in a decrease in preload and blood pressure Sodium Nitropruss ide (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
- 9. 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 TissuePerfusion: 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. Possiblyevidenced 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 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 secondaryto vasoconstriction. Pulse pressure (systolic minus
- 10. 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 occurin 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 carbondioxide 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 FluidVolume: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.
- 11. Possiblyevidenced 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 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 volumewhich 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
- 12. 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 responseto diuretic therapy. Assess for distended neck veins. Jugular vein distention may indicate fluid excess. Monitor client’s electrolyte levels esp. potassium. Hypokalemia can occursince diureticspromote 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., furosem ide) as indicated. Diuretics decrease plasma volume and peripheral edema. 5) Anxiety Anxiety:Vague uneasy feeling of discomfortor dread accompanied by an autonomic response. May be related to Change in health status.
- 13. Fear of death. Guarded prognosis;mortality rate 80%. Unfamiliar environment. Possiblyevidenced 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 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. Shockcan result in an acute life-threatening situation that will producehigh 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.
- 14. 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 sourceof 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 personmay help the client feel less threatened.