Critical Care HESI Latest Version 100% Pass

Critical Care HESI Latest Version 100% Pass Acute Respiratory Distress Syndrome (ARDS) the exchange of oxygen for carbon dioxide in the lungs is inadequate for oxygen consumption and carbon dioxide production within the body's cells ARDS Characterized by: 1. Hypoxemia that persists even when 100% oxygen is given. 2. Decreased pulmonary compliance. 3. Dyspnea. 4. Non-cardiac-associated bilateral pulmonary edema. 5. Dense pulmonary infiltrates on radiography. No abnormal lung sounds are present on auscultation because the edema of ARDS occurs first in the interstitial spaces, not in the airways. HESI Hint #1 ARDS is an unexpected, catastrophic pulmonary complication occurring in a person with no previous pulmonary problems. Clients are critically ill and are managed in an ICU setting. Mortality rate is high (50%) HESI Hint #2: Interventions to prevent complications on mechanical ventilation with ARDS Elevate HOB to at least 30 degrees. Assist with daily awakening ("sedation vacation"). Implement a comprehensive oral hygiene program. Implement a comprehensive mobilization program. Common causes of respiratory failure 1. Exacerbation of COPD. 2. Pneumonia. 3. TB. 4. Contusion. 5. Aspiration. 6. Inhaled toxins. 7. Emboli. 8. Drug overdose. 9. Fluid overload. 10. DIC. 11. Shock Nursing Assessment ARDS A. dyspnea, hyperpnea, crackles (or rales). B. Intercostal retractions. C. cyanosis, pallor D. Hypoxemia: PO 50 mmHg with FiO2 60%. E. Diffuse pulmonary infiltrates seen on chest radiograph as "white-out" appearance. F. Verbalized anxiety, restlessness. Nursing Plans and Interventions ARDS A. Position client for maximal lung expansion. B. Monitor client for signs of hypoxemia and oxygen toxicity. C. Monitor breath sounds for pneumothorax. D. Provide emotional support to decrease anxiety and allow ventilatory to "work" the lungs. E. Monitor client hemodynamically with essential vital signs and cardiac monitor. F. Monitor arterial blood gases (ABGs) routinely. G. Monitor vital organ status: CNS, LOC, renal system output, and myocardium [apical pulse, BP]). H. Monitor fluid and electrolyte balance. I. Monitor metabolic status through routine lab work. HESI Hint #3 Suction only when secretions are present HESI Hint #4 Before drawing a sample for ABGs from the radial artery, perform the Allen test to assess collateral circulation. The Allen test ensures collateral circulation to the hand if thrombosis of the radial artery should follow the puncture. Respiratory Failure in Children Causes A. Congenital heart disease. B. Respiratory distress syndrome. C. Infection, sepsis. D. Neuromuscular diseases. E. Trauma and burns. F. Aspiration. G. Fluid overload and dehydration. H. Anesthesia and narcotic overdose Nursing Assessment: Respiratory Failure in Children A. Very slow or very rapid respiratory rate (tachypnea), dyspnea, apnea, gasping, stridor. B. Tachycardia. C. Cyanosis, pallor, or mottled color (connotes deterioration of systemic perfusion). D. Irritability and later, lethargy (connotes a deteriorating LOC). E. Retractions, nasal flaring, poor air movement. F. Hypoxemia, hypercapnia, respiratory acidosis. G. Lab data: values should be evaluated, keeping in mind the percentage of oxygen the child is receiving. HESI Hint #5 Cardinal sings of Acute Respiratory Failure in children are restlessness, tachypnea, tachycardia, and diaphoresis HESI Hint #6 PCO245 or PO260 on 50% O2 signifies respiratory failure. A child in severe distress should be on 100% O2. What PO2 value indicates respiratory failure in adults? PO2 below 60 mmHg What blood value indicates hypercapnia? PCO2 above 45 mmHg Identify the condition that exists when the PO2 is less than 50 mmHg and FiO2 is greater than 60%. Hypoxemai List three symptoms of respiratory failure in adults Dyspnea/tachypnea; intercostal and sternal retractions; cyanosis List four common causes of respiratory failure in children Congenital heart disease; infection or sepsis; respiratory distress syndrome; aspiration; fluid overload and dehydration What percentage of O2 should a child in severe respiratory distress receive? 100% Shock Widespread, serious reduction of tissue perfusion (lack of O2 and nutrients) that, if prolonged, leads to generalized impairment of cellular functioning Arterial pressure is the driving force of blood flow through all the organs 1. It is dependent on cardiac output to perfuse the body. 2. It is dependent on peripheral vasomotor tone to return blood and other fluids to the heart. 3. It is dependent on the amount of circulating blood. 4. Marked reduction in either cardiac output or peripheral vasomotor tone, without a compensatory elevation in the other, results in system hypotension. At risk for shock: Very young and very young adults. Post-MI clients. Clients with severe dysrhythmia. Clients with adrenocortical dysfunction. Persons with a history of recent hemorrhage or blood loss. Clients with burns. Clients with massive or overwhelming infection HESI Hint #7 Early signs of shock are agitation and restlessness resulting form cerebral hypoxia Hypovolemic shock related to external or internal blood or fluid loss (most common cause of shock) Cardiogenic shock related to ischemia or impairment in tissue perfusion resulting from MI, serious arrhythmia, or heart failure. All of these causes decreased cardiac output. Distributive shock results from excessive vasodilation and the impaired distribution of blood flow Anaphylactic shock related to allergens (anaphylaxis), can be acute and life threatening with respiratory distress related to bronchial constriction leading to airway obstruction; vascular collapse may follow. Neurogenic shock related to injury to the descending sympathetic pathways in the spinal cord. This results from loss of vasomotor tone and sympathetic innervation to the heart Septic shock related to endotoxins released by bacteria, which cause vascular pooling, diminished venous return, and reduced cardiac output. Obstructive shock physical obstruction related to tamponade, emboli, compartment syndrome that impedes the filling or outflow of blood resulting in reduced cardiac output. Stage 1 Hypovolemic Shock Initial Stage. Blood loss 10%. Compensatory mechanisms triggered. S/S: Apprehension and restlessness (first signs of shock), increased heart rate, cool, pale skin, fatigue. Clinical description: arteriolar constriction, increased production of ADH, arterial pressure maintained, CO usually normal, selective reduction in blood flow to skin and muscle beds. Stage 2 Hypovolemic Shock Compensatory stage. Blood volume reduced by 15-25%. Decompensation begins. S/S: Flattened neck veins and delayed venous filling time, increased pulse and respirations, pallor, diaphoresis, and cool skin, decreased urinary output, sunken, soft eyeballs, confusion. Clinical description: Marked reduction in CO, arterial pressure decline, massive adrenergic compensatory response, resulting in tachycardia, tachypnea, cutaneous vasoconstriction, and oliguria, decreased cerebral perfusion. Stage 3 Hypovolemic Shock Progressive Stage. S/S: Edema, increased blood viscosity, excessively low BP, dysrhythmia, ischemia, and MI, weak, thready, or absent peripheral pulses. Clinical description: rapid circulatory deterioration, decreased CO, decreased tissue perfusion, reduced blood volume. Stage 4 Hypovolemic Shock Irreversible stage. S/S: Profound hypotension, unresponsiveness to vasopressor drugs, severe hypoxemia, unresponsiveness to O2 administration, anuria, renal shutdown, heart rate slows, BP falls, with consequent cardiac and respiratory arrest. Clinical description: Cell destruction so severe that death is inevitable, MODS, it is the nurse's responsibility to recognize the S/S of shock. Every effort should be made to prevent the devastating clinical course that the progression of shock can take. HESI Hint #8 Severe shock leads to widespread cellular injury and impairs the integrity of the capillary membranes. Fluid and osmotic proteins seep in to the extravascular spaces, further reducing cardiac output. A vicious circle of decreased perfusion to all cellular level activities ensues. All organs are damaged, and if perfusion problems persist, the damage can be permanent. HESI Hint #9 All types of shock can lead to systemic inflammatory response syndrome (SIRS) and result in MODS. HESI Hint #10 if cardiogenic shock exists in the presence of pulmonary edema (i.e., from pump failure), position client to reduce venous return (high Fowler position with legs down) to decrease further venous return to the left ventricle. Medical Treatment for Shock Correct decreased tissue perfusion and restore cardiac output. Oxygenation and Ventilation with Shock Optimize oxygen delivery and reduce demand on heart. Increase arterial oxygen saturation with supplemental oxygenation and mechanical ventilation. Space activities that decrease oxygen consumption. Fluid Resuscitation with Shock Cause of shock dictates the type of treatment. Rapid infusion of volume-expanding fluids is the cornerstone of treatment for hypovolemic shock and anaphylactic shock. Whole blood, plasma, plasma substitutes (colloid fluids) may be used. Isotonic, electrolyte intravenous (IV) solutions such as Ringer's lactate solution and normal saline may also be use. If shock is cardiogenic in nature, the infusion of volume-expanding fluids may result in pulmonary edema. Drug Therapy with Shock Restoration of cardiac function should take priority. Drug selection is based on the effect of the shock on preload, afterload, or contractility. 1. Drugs that increase preload (e.g., blood products, crystalloids) or decrease preload (e.g., morphine, nitrates, diuretics). 2. Drugs that increase afterload (e.g., vasopressors, dopamine) or decrease afterload (e.g., nitroprusside, ACE-I, ARB). 3. Drugs that decrease contractility (e.g., beta blockers, calcium channel blockers) or increase contractility (e.g., digoxin, dobutamine). Monitoring with Shock Central venous pulmonary artery catheters are inserted in the operating room and ICU to monitor shock. Serial measurements of cardiopulmonary function (using electrocardiogram, pulse oximetry, end-tidal carbon dioxide monitoring, ABGs, and hemodynamic monitoring via arterial lines and/or pulmonary artery catheters), urinary output, clinical assessment (i.e., mental status) of the client are taken every 5 to 15 minutes. Following immediate attention to improvement of perfusion, attention is directed toward treating the underlying cause of the condition. Administration of drugs is usually withheld until circulating volume has been restored. Nursing Assessment of Shock A. Vital signs: Tachycardia, Tachypnea, BP decrease. B. Mental status: Early-restless, hyperalert; Late- decrease alertness, lethargy, coma. C. Skin changes: Cool, clammy skin (warm in vasogenic and early septic shock), diaphoresis, paleness. D. Fluid status (acute renal tubular necrosis can happen quickly). Urine output decreases, or an imbalance between intake and output occurs. CVP is abnormal. Urine specific gravity 1.020 indicates hypovolemia Nursing Plans and Interventions: Shock A. Monitor arterial pressure by understanding the concepts related to arterial pressure. B. Monitor BP, pulse, respirations, and arrhythmias every 15 minutes or more often, depending on stability of client. C. Assess urine output every hour to maintain at least 30mL/hr. D. Notify health care provider if urine output drops below 30mL/hr (reflects decreased renal perfusion and may result in acute renal failure). E. Administer fluids as prescribed by provider to improve preload: blood, colloids, or electrolyte solutions until designated CVP is reached. F. Remember client's bed position is dependent on cause of shock. G. Administer medication IV (not intramuscular or subcutaneous) until perfusion improves in muscles and subcutaneous tissue. H. Keep client warm; increase heat in room or put warm blankets (not too hot) on client. I. Keep side rails up during all procedures; clients in shock experience mental confusion and may easily be injured by falls. J. Obtain blood for lab work as prescribed: CBC, electrolytes, BUN, creatinine (renal damage), lactate (sepsis), and blood gases (oxygenation and ventilation). K. Provide family support. Administration of Vasopressors or adrenergic stiumlants Epinephrine, dopamine, dobutamine, norepinephrine, or isoproterenol. 1. Administer through volume-controlled pump. 2. Monitor hemodynamic status every 5-15 min. 3. Watch IV site carefully for extravasation and tissue damage. 4. Ask HCP for target mean systolic BP Administration of vasodilators hydralazine, nitroprusside, or labetalol hydrochloride to counteract effects of vasopressors. 1. Wait for precipitous decrease or increase in BP if prescribed together. 2. If drop in BP occurs, decrease vasodilator infusion rate first; then increase vasopressor. 3. If BP increases precipitously, decrease vasopressor rate first; then increase rate of vasodilator. 4. Obtain blood work as prescribed: CBC, electrolytes, BUN, creatinine (renal damage), and blood gases (oxygenation). 5. Glucose levels should be maintained at 140-180 Mean Arterial Pressure (MAP) Level of pressure in the central arterial bed measured indirectly by BP measurement. MAP=CO x total peripheral resistance=systolic BP + 2(diastolic BP)/3. In adults, usually approaches 100 mmHg. Can be measured directly through arterial catheter insertion. Cardiac output (CO) Volume of blood ejected by the left ventricle per unit of time. Stroke volume (amount of blood ejected per beat) * (heart rate (normal: 4-6 L/min) Peripheral resistance (PR) Resistance to blood flow offered by the vessels in the peripheral vascular bed Central Venous Pressure (CVP) Pressure within the right atrium; normal CVP/RAP ranges from 2-6 mmHg HESI Hint #11 All vasopressor and vasodilator drugs are potent and dangerous and require that the client be titrated prudently. Disseminated Intravascular Coagulation (DIC)