Summary CCRN EXAM Cram leakage/2021 latest update/all chapters covered

CARDIOVASCULAR REVIEW CCRN Exam Cram Heart Sounds S1, S3, S4: Heard at apex S2: Heard at base S3: r/t heart failure S4: r/t MI, HTN, ventricular hypertrophy, & aortic stenosis ……………………………… Mitral stenosis is associated with atrial fibrillation due to atrial enlargement. ……………………………… Stenosis occurs with an OPEN valve. Insufficiency occurs with a CLOSED valve. ……………………………… NSTEMI: + troponin, ST depression, unrelenting chest pain. STEMI: + troponin, ST elevation, unrelenting chest pain. Prinzmetal’s (Variant) Angina: - troponin, nitroglycerin relieves chest pain and returns ST segment to normal Management of Acute Chest Pain STAT EKG done and read within 10 minutes, 325mg chewable aspirin ASAP, anticoagulant therapy, antiplatelet therapy, beta blocker administration. Use metoprolol, NOT propranolol. Treat chest pain with morphine or nitroglycerin. If symptoms have been present <12 hours, prepare for PCI. Door to balloon in 90 minutes. Door to fibrinolytic therapy in 30 minutes. ……………………………… After PCI Evidence of successful reperfusion includes chest pain relief, normalized ST segment, and reperfusion arrhythmias (VT, VF). Troponin and CK-MB remain elevated after reperfusion! Complications of PCI Monitor for signs of re-occlusion… chest pain and ST elevation similar to before PCI. Monitor for vasovagal response during sheath removal. Administer atropine and fluids, hold nitrates. Monitor for signs of retroperitoneal bleeding… back pain and hypotension. HTN Emergency BP >180/110 with evidence of end-organ damage. Needs critical care admission and emergent lowering of BP. Biggest risk is STROKE. Nitroprusside Drip: preload and afterload reducer. Assess for cyanide toxicity (thiocyanate)... mental status changes, tachycardia, seizure, need for increase in dose, metabolic acidosis. Labetalol IV Push: Intermittent IV pushes preferred over drip due to the possibility of continuing drip past max of 300mg. ……………………………… Acute Peripheral Vascular Insuciency Normal ankle-brachial index is >1. Put bed in reverse trendelenburg to increase blood flow. Do NOT elevate the extremity! Medical Management: tPA, thrombolytics, heparin, anticoagulants, antiplatelets, vasodilators. 1 QT Prolongation Normal QT interval is 0.36 to 0.4 seconds. Prolongation of the QT interval can lead to Torsades de Pointes! Treatment of Torsades de Pointes is magnesium. Drugs that prolong QT: amiodarone, quinidine, haloperidol, procainamide. Electrolytes that prolong QT: hypokalemia, hypocalcemia, hypomagnesemia. ……………………………… 3 Pacemaker Malfunctions Failure to Pace: No pacer spike when expected. Failure to Capture: Pacer spike occurs without QRS complex. Failure to Sense: Pacing in native beats. ……………………………… Heart Failure Elevated LVEDP. High intracardiac pressures & decreased CO. Systolic Heart Failure: Ejection problem, EF < 40%. Dilated ventricle. S3 heart sound. Large, dilated heart or normal heart size on CT scan. Treatment: Beta blockers, ACE/ARBs, positive inotropes. Contraindicated: Calcium channel blockers & negative inotropes. VS Diastolic Heart Failure: Filling problem, EF > 50%. Thick, hypertrophic ventricle. S4 heart sound with hypertension. Normal heart size on CT scan. Treatment: Beta blockers, ACE/ARBs, calcium channel blockers. Contraindicated: Positive inotropes (no digoxin, dopamine, or dobutamine for these patients). ……………………………… Systolic heart failure can cause valvular insufficiency r/t a dilated ventricle. Both systolic and diastolic heart failure cause pulmonary edema r/t poor ventricular emptying. Symptoms of Right-Sided Heart Failure: Hepatomegaly, splenomegaly, dependent edema, increased CVP, tricuspid insufficiency, abdominal pain. VS Symptoms of Left-Sided Heart Failure: Orthopnea, dyspnea, tachypnea, hypoxemia, tachycardia, crackles, cough with pink/frothy sputum, diaphoresis, anxiety, confusion, increased PAP & PAOP. ……………………………… NYHA Heart Failure Classification Class I: Symptoms caused by extraordinary activity. Class II: Symptoms caused by ordinary activity. Class III: Symptoms caused by minimal activity (such as walking to the bathroom). Class IV: Symptoms at rest. 2 Cardiogenic Shock Extreme decrease in stroke volume r/t systolic dysfunction. Increased PAOP r/t increased LV preload. Increased SVR r/t compensatory vasoconstriction. Decreased CO means that perfusion to organs is inadequate. Narrow pulse pressure. Treatment: Give positive inotropes! Give norepinephrine, dopamine < 10 mcg, dobutamine, or milrinone. Also, reduce preload & afterload with vasodilators in conjunction with positive inotropes, IABP, or VAD. Ventricular Assist Device (VAD) Used in the management of left ventricular heart failure, cardiogenic shock, and cardiomyopathy. Used for patients awaiting a heart transplant. Intra Aortic Balloon Pump (IABP) Inflates during diastole to increase myocardial oxygen supply. Deflates during systole to reduce left ventricular afterload. Post-Op CABG Nursing Care Monitor for complications of cardiac tamponade and pericarditis. Do not clamp or milk chest tubes, maintain dependent drainage with NO LOOPS IN TUBING . Monitor for chest tube output > 100mL for two consecutive hours. ……………………………… Valve Replacement High risk for blood clots, need anticoagulation! Avoid a drop in preload! May result in dangerous hypotension. Conduction disturbances r/t surgery near SA/AV nodes. May need a temporary or permanent pacemaker. ……………………………… Cardiac Tamponade Symptoms: Hypotension, JVD, muffled heart tones, equalization of CVP/PAOP, narrowed pulse pressure, pulsus paradoxus, enlarged cardiac silhouette. Pulsus Paradoxus is a drop in SBP during inspiration. Cardiac Trauma The aortic valve is most likely to be ruptured because it is most anterior. Pain is worse with inspiration. ST elevation present in the area of injury only. Worse outcome than pericarditis. VS Pericarditis ST elevation in ALL LEADS (aka “global” ST elevation). Pain is worse with inspiration. Dressler’s Syndrome is pericarditis that occurs after MI, surgery, or injury. ……………………………… Thoracic Aneurysms Aneurysms >6 cm needs surgery and blood pressure control with a labetalol drip. Sudden tearing, ripping pain in chest, radiating to shoulders/back, cough, and widening mediastinum on X-ray indicate a RUPTURE, which is a surgical emergency! 3 PULMONARY REVIEW CCRN Exam Cram → What is the clinical indicator of ventilation? PCO2! → What is the primary muscle of ventilation? The diaphragm! → Normal ventilation is about 4L/min. → Normal SVO2 is 60-75% → Normal PO2 is 80-100 mmHg, < 80 is hypoxemia. → The goal for most critically ill patients is O2 sat > 90%, PO2 >60 mmHG. ……………………………… Position the patient’s GOOD LUNG DOWN to prevent hypoxemia. You want to INCREASE PERFUSION to the GOOD LUNG by positioning it DOWN. ……………………………… Static Compliance: Elasticity of the lung. Dynamic Compliance: Elasticity of the airways. In asthma, static compliance is ok, dynamic compliance is decreased. Noninvasive Ventilation CPAP: For patients with hypoxemic respiratory failure. BiPAP: For patients with hypoxemic and/or hypercapnic respiratory failure. Contraindications to NIV: Hemodynamic instability or life-threatening arrhythmias, copious secretions, high risk for aspiration, impaired mental status (unable to protect airway!), suspected pneumothorax, inability to cooperate, life-threatening refractory hypoxemia. A patient with these contraindications may need INTUBATION instead of NIV! ……………………………… Carbon Monoxide Poisoning Do not use pulse oximetry to monitor O2 status, the pulse ox cannot differentiate between CO and O2! Treat with 100% FiO2 until symptoms resolve and CO level is < 10%. Status Asthmaticus Severe airway narrowing refractory to bronchodilators. Wheezing → Decreased Breath Sounds → Absent Breath Sounds… THIS IS BAD! Condition is getting worse. Starts with respiratory alkalosis r/t hyperventilation, when the patient tires out and respiratory rate drops respiratory acidosis occurs r/t hypoventilation. THIS IS BAD! Condition is getting worse. Measure presenting peak flow rate. Intubate if… respiratory acidosis, severe hypoxemia, silent chest, decrease in level of consciousness. Ventilator Management for Asthma: Use low respiratory rate to increase exhalation time. Increase inspiration:expiration ratio to 1:3-4 to allow time for optimal exhalation and prevent auto-PEEP. Use low tidal volumes to prevent auto-PEEP. 4 COPD Exhalation is HARD! Causes air trapping and auto-PEEP. V/Q mismatch r/t a problem with ventilation and increased PCO2. Treatment: Increase FiO2 to keep O2 sat > 90% or PO2 > 60. Use bronchodilators, corticosteroids, antibiotics for pneumonia, BiPAP or ventilator. ……………………………… A PULMONARY EMBOLISM results in DEAD SPACE. It responds to O2 therapy, so GIVE O2. VS ARDS is a SHUNT and will NOT respond to increased FIO2, it also needs PEEP! PEEP prevents alveolar collapse and increases alveolar recruitment. A SHUNT (ARDS!) is movement of blood from the right side of the heart to the left side without getting oxygenated. Pulmonary Embolism V/Q mismatch, increased PAP. Pulmonary angiography is the gold standard for diagnosis. Symptoms: dyspnea, tachypnea, tachycardia, cough, crackles, anxiety, respiratory alkalosis. PETECHIAE if the embolism is a FAT EMBOLISM. Treatment: Fluids! Anticoagulation (heparin drip or low-molecular weight heparin), fibrinolytic therapy for all patients with hemodynamic compromise with low risk for bleeding. ……………………………… ARDS Inflammation causes increased permeability of the pulmonary capillary membrane. Proteinaceous fluid leaks into the interstitial and alveolar spaces. Alveolar Type II cells are damaged, which results in decreased surfactant production and MASSIVE ATELECTASIS! This creates a SHUNT. FiO2 is not enough, ARDS needs PEEP! PEEP increases alveolar recruitment to treat refractory hypoxemia. Refractory hypoxemia is hypoxemia even when FiO2 is 100%. Symptoms: Bilateral infiltrates on chest X-ray. PAOP < 18 because this is a lung problem, not a heart problem. Decreased lung compliance, increased work of breathing, Decreased functional residual capacity. Pulmonary edema, crackles. Treatment: Intubate and ventilate with PEEP ≥ to 15. Monitor for barotrauma and decreased CO, but DO NOT STOP PEEP! Do not disconnect from the ventilator circuit because alveolar recruitment will be lost and is not easily corrected! Limit tidal volume to 4-6 mL/kg to prevent volutrauma! (Normal tidal volume setting is 8-10 mL/kg). Nutritional support is important! Prone positioning. Tension Pneumothorax Air unable to exit mediastinum causes a mediastinal shift AWAY FROM THE AFFECTED SIDE. 5 Symptoms: Tachycardia, distended neck veins, hypotension. Treatment: Insert chest tube to reestablish negative pleural pressure, O2 support. ……………………………… Chest Tube Management Water Seal Chamber: Tidaling with breaths is normal. Bubbling is not normal, call the MD if new bubbling occurs. Do not clamp chest tube unless changing system! No dependant loops! ……………………………… Without sufficient O2 at the cellular level, LACTIC ACID is produced, which is evidence of anaerobic metabolism, organ failure, and cell death. A patient may have a normal O2 sat and PO2 but still have an elevated lactate level. Why? O2 utilization is affected by severe sepsis/septic shock and results in anaerobic metabolism at the cellular level. Pneumonia Symptoms: Chest X-ray shows consolidation or diffuse patchy infiltrates. WBC’s can be elevated or show an increase in bands. ABG shows hypoxemia. Positive sputum and/or blood cultures. Treatment: Optimize oxygenation. Position GOOD LUNG DOWN. Bronchoscopy if necessary. Give first dose of antibiotics in ED or within 4 hours. Hydration and nutritional support. ……………………………… Aspiration Pneumonia Injury from chemical , mechanical, or bacterial factors, not just infection! Most aspiration occurs in the RIGHT LUNG because the right bronchus is shorter, wider, and less angled. Place patient in slight Trendelenburg on the RIGHT side to aid drainage. Symptoms: Tachycardia, hypoxemia, crackles, hypotension. Ventilator Management WAVEFORM CAPNOGRAPHY is the most accurate way to confirm ET tube placement. On chest X-ray the ET tube should be 3-5 cm above the carina. Get an ABG within 20-30 minutes after intubation. Start FiO2 at 100% and decrease to ≥ 50% as soon as possible. Use evidence-based confirmation of OG/NG feeding tube placement: CONFIRM with CHEST X-RAY prior to putting anything down the tube! Other feeding tube nursing tasks: Mark the exit site with a marker, assess patency Q4H, measure the pH of aspirate. Ventilator Associated Pneumonia (VAP) Prevention: Drain condensate from tubing. Prevent backflow of condensate into ET tube. Change ventilator tubing only when contaminated. Use aseptic technique for suctioning. Use oral care protocol. Keep ET tube cuff inflated. Perform subglottic suctioning before cuff deflation. Ventilator Modes: AC Mode: All breaths are machine breaths, delivered at set tidal volume. Full respiratory support. SIMV Mode: All breaths above the set rate are at the patient’s own tidal volume. Full or partial respiratory support. Reducing the SIMV rate will allow the patient to assume more work of breathing. Pressure Support Ventilation: Often used during weaning to decrease work of 6 breathing and overcome the difficulty of breathing against ET tube and ventilator circuit. Criteria for Weaning from Ventilator: Resting minute ventilation <10 L/min. Spontaneous tidal volume > 5 mL/kg. NIF > -25. Vital capacity 3-5 L. FiO2 ≥ to 50%. ABG is ok. Stop a spontaneous breathing trial if: Respiratory rate is > 35 or < 8. O2 sat < 88%. Distress, decreased LOC, or cardiac arrhythmias develop. If any of these occur the patient has failed their breathing trial! 7 NEUROLOGY REVIEW CCRN Exam Cram Most Important Cranial Nerves for CCRN I: Olfactory (Smell). Function may be lost with basilar skull fracture. II: Optic (Sight, but NOT pupillary function!) III: Oculomotor (Pupillary function). This is the nerve you are checking when you check pupils. V: Trigeminal (Corneal reflex). VIII: Vestibulocochlear (Doll’s Eyes test and Cold Caloric test). IX: Glossopharyngeal (Swallow, gag reflex). X: Vagus (Pharyngeal, laryngeal movement). ……………………………… Brain Function and Anatomic Location Frontal Lobe: Personality, abstract thought, and long-term memory. Temporal Lobe: Hearing, taste, smell, interpretations. Parietal Lobe: Object recognition and body part awareness. Occipital Lobe: Vision and reading comprehension. Cerebellum: Gait, balance, and coordination. ……………………………… Broca’s area controls SPEECH. ……………………………… Flaccid muscles are a symptom of MEDULLA dysfunction. ……………………………… Symptoms of a PONTINE problem are apneustic breathing, pinpoint pupils, and parasympathetic innervation. Look for the P’s to help you remember! ……………………………… Decorticate Posturing: Flexed arm posturing. Indicates hemispheric dysfunction. Decerebrate Posturing: Straight arm posturing. Indicates a midbrain or pons dysfunction. This has a WORSE outcome than decorticate posturing. Reflex Tests Babinski Reflex: Toes flair up and out when the bottom of the foot is stroked. POSITIVE BABINSKI IS BAD. The babinski reflex will occur contralateral to the problem. If the brain problem is on the right side, the babinski will be positive on the left foot. Doll’s Eyes Test: Eyes turn opposite of the side the head is turned. If the head is turned to the right, eyes look to the left. POSITIVE DOLL’s EYES IS GOOD! Remember the phrase, “It’s good to be a doll.” Cold Caloric Test: Ice water is injected into the ear canal. The eyes should turn toward the side the water was injected into. POSITIVE COLD CALORIC IS GOOD! ……………………………… Homonymous Hemianopia: Loss of vision in HALF the field of each eye. Indicates damage to cranial nerve II, the OPTIC nerve. Occurs contralateral to the side of the brain that has a problem. If the problem is on the right side of the brain, the patient will have left homonymous hemianopsia. 8 FOR NEURO PROBLEMS REMEMBER: → Eyes deviate TOWARD the problem. For a right side brain injury the eyes deviate to the right. → Homonymous Hemianopia occurs on the OPPOSITE side of problem. A right side brain injury will cause left homonymous hemianopsia. → Motor changes and positive Babinski’s occur on the OPPOSITE side of the problem. A right side brain injury will cause left sided weakness and a positive Babinski on the left foot. ……………………………… Consciousness depends on an intact cerebral cortex and reticular activating system (RAS). ……………………………… Glasgow Coma Scale: Scored on the patient’s BEST response. 15 is the best score. A score < 8 indicates a poor prognosis. ……………………………… Change in level of consciousness is always the FIRST sign on a neurologic problem EXCEPT in EPIDURAL HEMATOMA when PUPILS CHANGE FIRST! Cushing’s Triad: A sign of BRAIN HERNIATION. Increased SBP. Decreased HR. Decreased RR. ……………………………… Central Brain Herniation Swelling on BOTH sides of the brain creates a DOWNWARD herniation. Change in LOC is the first sign! Positive Babinski reflexes BILATERALLY because BOTH sides of the brain are involved. Usually related to diffuse edema, slower development. VS Uncal Brain Herniation Swelling on ONE side of the brain creates a LATERAL SHIFT. Change in PUPILS is the first sign, then change in LOC afterward. Why? Because uncal herniation is usually caused by an EPIDURAL HEMATOMA. Positive Babinski reflex on the side OPPOSITE of brain involvement. Encephalopathy Diffuse disease of the brain that alters its structure and function. Can be hypoxic, metabolic, hepatic, or caused by drugs or infection. Encephalopathy can cause increased intracranial pressure! Symptoms: Memory loss, decreased cognitive ability, personality changes, agitation, seizures, coma, brain death. Treatment: Identify and treat the underlying cause (hypoxia, liver failure, infection), seizure precautions and safe environment, prevent conditions that cause increased intracranial pressure. ……………………………… Stroke Right Sided Stroke: Causes emotional lability Left Sided Stroke: Causes aphasia Stroke Treatment: Rule out hypoglycemia first! CT scan within 25 minutes of arrival to hospital. Do not treat acute blood pressure unless BP is >220/120. Lowering BP will decrease cerebral perfusion. 9 tPA Treatment for Stroke Inclusion Criteria: Onset < 4.5 hours. CT scan negative for hemorrhage. No contraindications. Goal blood pressure in the first 24 hours after tPA is < 180/105. Labetalol is the drug of choice for BP control. The worst complication of tPA is INTRACEREBRAL HEMORRHAGE! Monitor for change in level of consciousness. ……………………………… The Basilar Artery and Middle Cerebral Artery are NOT part of the Circle of Willis. ……………………………… Subarachnoid Hemorrhage Caused by aneurysm rupture, usually the Middle Cerebral Artery. Hydrocephalus may develop because chorionic villi are blocked from reabsorbing CSF. Complications are REBLEED and VASOSPASM. Avoid hypotension to prevent vasospasm. Vasospasms can also be prevented with Nimodipine, a calcium channel blocker. Subarachnoid hemorrhage rebleeds can be prevented with Amicar, an anti-fibrinolytic agent. Classic symptoms of aneurysm rupture: Sudden and explosive headache, decreased level of consciousness, nuchal rigidity and Kernig’s sign, prominent U-wave on EEG. ……………………………… A-V Malformation A congenital vascular anomaly that shunts arterial blood to the venous side without connecting capillaries. Symptoms: Hemorrhage, seizures headache, neuropsychiatric manifestations. Treatment: Surgery, radiation for small malformations, embolization prior to surgery or radiation to decrease the risk of bleeding. HEPARIN is given during embolization to PREVENT CLOTTING. ……………………………… Increased Intracranial Pressure (ICP) There are many causes of increased ICP (medical, surgical, trauma), so ANY patient with a NEURO PROBLEM can develop increased ICP! The FIRST sign of increased ICP is CHANGE IN LOC! Normal ICP is 0-10 mmHg. 10-20mmHg is moderately high, >20mmHg is INCREASED ICP. HYPOTENSION WITH INCREASED ICP IS BAD! The brain will not be adequately perfused! Symptoms: Altered LOC first, then pupil changes, restlessness, agitation, headache, nausea, vomiting, seizures, cranial nerve palsies, visual dysfunction, papilledema, motor dysfunction, and Cushing’s Triad (increased SBP, decreased HR, decreased RR). ……………………………… ICP Monitoring Level transducer at the external auditory meatus (the Foramen of Monro). Three types of ICP waves: A-waves are “awful.” B-waves are “bad.” C-waves are “common.” Cerebral vasospasm results in “awful” A-waves and increased ICP! Remember that Nimodipine is used to prevent vasospasms. 10 Strategies to Lower ICP: Decrease vascular volume with mannitol, lasix, or 3% saline. Upright positioning to facilitate venous drainage from the brain. Prevent acidosis. Acidosis causes dilation of cerebral blood vessels. BUT do NOT hyperventilate the patient! Keep pH at about 7.35, the low end of normal. Reduce CSF with a ventriculostomy. Prevent agitation and pain. Using propofol for sedation decreases ICP. AVOID restraints, restraints cause increased ICP in most patients. AVOID PEEP, fever, and low serum protein levels. Feed the patient to keep serum protein levels up and keep fluid in the vascular space. Do not give any hypotonic fluids (D5W, 1/2NS)! ……………………………… Intracranial Hematomas: Three types: Epidural, Subdural, and Intracerebral. Epidural Hematoma: Always acute. Develops rapidly. Usually caused by a Meningeal artery bleed. Remember: Change in level of consciousness is always the FIRST sign on a neurologic problem EXCEPT in EPIDURAL HEMATOMA when PUPILS CHANGE FIRST! Symptoms: Change in pupils occurs first, then change in LOC. Also, headache, irritability, confusion, vomiting, and hemiplegia. Treatment: Burr hole for emergent evacuation of the hematoma. Monitor for and treat increased ICP. VS Subdural Hematoma: May be acute, subacute, or chronic. Symptoms: Change in LOC occurs first, then change in pupils. Symptoms may develop slowly. Treatment: Surgery to evacuate the hematoma. Monitor for and treat increased ICP. VS Intracerebral Hematoma Caused by stroke, depressed skull fractures, gunshots, and whiplash injuries. Patients with intracerebral hematomas may or may not have increased ICP. Treatment: Surgery for large hematomas or if neurologic status is deteriorating. ……………………………… Skull Fractures: Linear skull fractures do not require surgery. Depressed skull fractures need surgery if they are > 5mm. Basilar skull fractures cause a meningeal tear! The signs of a basilar skull fracture are Raccoon Eyes, Battle’s Sign, otorrhea, and rhinorrhea. The patient may also damage Cranial Nerve I and lose their sense of smell! Raccoon Eyes: Periorbital discoloration. Battle’s Sign: Discoloration at the back of the ear. Otorrhea: Fluid leaking from ear. Rhinorrhea: Fluid leaking from nose. Nursing Treatment for basilar skull fractures: Check fluid draining from ear/nose to see if it is CSF. If it is positive for glucose, it is CSF! If it makes a clot surrounded by a yellow halo (“halo sign”) when placed on 11 gauze, it is CSF! Cover the ear or nose with dry sterile gauze, but DO NOT PACK IT IN! Just tape a gauze pad under the nose or over the ear. DO NOT INSERT AN NG TUBE IN THESE PATIENTS! An NG tube can displace into the brain if a basilar skull fracture is present. Use an OG tube instead. Do NOT let the patient blow their nose! These patients are at risk of developing meningitis, monitor for symptoms. Surgery is only necessary if CSF leakage is persistent. ……………………………… Meningitis Bacterial Meningitis has CSF with very high protein, low glucose, very high WBCs , and purulent CSF. Viral Meningitis has slightly elevated protein, normal glucose, slightly high WBC’s, and clear CSF. Both bacterial and viral meningitis have symptoms of meningeal irritation: headache, nuchal rigidity, positive Brudzinski’s sign, and positive Kernig’s sign. Brudzinski’s Sign: Severe neck stiffness causes the patient’s hips and knees to flex when the neck is flexed. Kernig’s Sign: Severe stiffness of the hamstrings causes pain in the neck when the hip is flexed 90 degrees. ……………………………… Seizures: STOP seizures with lorazepam (Ativan) or diazepam (Valium). PREVENT seizures with phenytoin (Dilantin) or phenobarbital. What if the Dilantin level is therapeutic and the patient still has a seizure? Administer lorazepam! ROMAZICON reverses benzodiazepines. Status Epilepticus: Seizure activity for 5 minutes. Can be a single seizure or a string of seizures without return of consciousness between them. Status Epilepticus is not responsive to the usual drug interventions and can cause hyperkalemia, hypoglycemia, arrhythmias, and rhabdomyolysis. Cerebral blood flow is not able to meet the brain’s demands. Death is due to cerebral hypermetabolism. Guillain-Barré Syndrome Ascending paralysis caused by a viral agent. Diaphragmatic involvement may result in respiratory failure. Monitor vital capacity for signs of impending respiratory failure. Monitor urine output for urinary retention. Treatment: Immunoglobulin, steroids, plasmapheresis exchange. Myasthenia Gravis An autoimmune disorder that causes progressive skeletal muscle weakness and paralysis. Treatment with pyridostigmine, steroids, removal of the thymus gland, plasmapheresis, or IV immune globulin. Treatment depends on whether the patient is having a myasthenic crisis (caused by under-treatment and deficiency in acetylcholine) or a cholinergic crisis (caused by over-treatment and excess of acetylcholine. Tensilon Test: The patient is given 2mg of IV Tensilon. If the patient improves, it was a myasthenic crisis. If the patient experiences increased muscle weakness, salvation, lacrimation, or GI distress, it was a cholinergic crisis. 12 GASTROINTESTINAL REVIEW CCRN Exam Cram Esophageal Varices: Caused by portal hypertension r/t liver disease. Hepatic cirrhosis prevents normal drainage through the liver, pressure backs up into the esophageal vein. Treatment: Endoscopy with bandy or sclerosing of varices. Esophageal Balloon Tamponade: Performed with a SengstakenBlakemore Tube inserted through the nose or mouth. The gastric balloon is inflated inside the stomach to compress and reduce blood flow to varices. A balloon can also be inflated to help stop bleeding. If the esophageal balloon displaces UP the airway may occlude! CUT THE BALLOON WITH SCISSORS if respiratory distress occurs. Scissors should ALWAYS be kept at the bedside of patients receiving esophageal balloon tamponade! Acute Pancreatitis: Inflammation and autodigestion of the pancreas. Pancreatitis is NOT always caused by an infection! Symptoms: Boring abdominal pain that radiates to all quadrants and lumbar area. Nausea, vomiting, rigid abdomen, decreased or absent bowel sounds, low-grade fever, increased serum amylase, increased serum lipase, increased serum glucose. Decreased serum calcium (assess for Trousseau’s Sign, long QT, and seizures). Presence of Cullen’s Sign and Grey-Turner’s Sign indicates hemorrhagic pancreatitis. Cullen’s Sign: Bruising and bluish discoloration around the umbilicus. Grey-Turner’s Sign: Bruising of the flanks. Acute pancreatitis can cause SIRS (Systemic Inflammatory Response Syndrome). This causes increased vascular permeability, vasodilation, vascular stasis, and microthrombosis. Pancreatitis causes PULMONARY COMPLICATIONS! →LEFT lobe atelectasis →LEFT pleural effusion →Bilateral crackles →Elevation of diaphragm →ARDS r/t destruction of Type II Alveolar Cells that produce surfactant. Treatment: NG to suction, fluid and electrolyte replacement, PPI’s and H2 blockers to decrease gastric pH, pain management with morphine, glucose control, enteral feeding below duodenum. MONITOR FOR PULMONARY COMPLICATIONS! Liver Failure : Never give Lactated Ringer’s to a patient in liver failure! LR increases lactic acidosis in these patient’s. Anything that increases ammonia (NH3) can cause hepatic encephalopathy and may increase ICP! Restrict protein ONLY if hepatic encephalopathy is present. Give lactulose to treat high ammonia. Give neomycin to kill gut bacteria that produce ammonia. Keep in mind that a complication of this treatment is vitamin K deficiency. Give acetylcysteine (Mucomyst) for suspected acetaminophen overdose. 13 Lab Values: Increased ammonia (NH3), decreased protein and albumin, increased PT and PTT, increased AST and ALT, increased bilirubin, decreased blood sugar. Physical symptoms: Mental status changes r/t hepatic encephalopathy and increased ammonia. Asterixis r/t increased ammonia. Ascites r/t decreased albumin and protein, Jaundice r/t increased bilirubin. Liver is enlarged first, then becomes non-palpable as hepatic necrosis progresses. Management: Prevent anything that increases ammonia! Also, monitor blood sugar, administer clotting factors, monitor neuro status. What increases ammonia? → Hypokalemia: use aldactone to treat ascites because it is potassiumsparing. → High BUN → Lactic acidosis: Lactated Ringer’s causes lactic acidosis in these patients because the liver cannot convert it into bicarb. → GI bleeding: breakdown of protein in the digestive system increases ammonia. “TIPS” Transjugular Intrahepatic Porto-Systemic Shunt: Procedure to treat liver failure. A complication of this procedure is hepatic encephalopathy.The liver is bypassed, which decreases detoxification of the blood. Spleen: The patient with a history of splenectomy has reduced immune function Signs of splenic rupture: sharp pain referred to the left shoulder (Kehr’s Sign). Diaphragmatic irritation causes this referred pain. Also, abdominal distention with absent bowel sounds. Abdominal Trauma: Ecchymosis over upper left quadrant = splenic injury. Ecchymosis around umbilicus = Cullen’s Sign = intraperitoneal bleeding. Ecchymosis of flank = Grey Turner’s Sign = retroperitoneal bleeding. Left shoulder pain = Kehr’s Sign = ruptured spleen. Absence of bowel sounds with abdominal distention = visceral injury. Bowel Infarction : Decreased blood flow to mesenteric vessels with prolonged ischemia causes edema of the intestinal wall. Necrosis, perforation, and peritonitis occur. Insert an NG tube for gastric decompression. Monitor for sepsis. Treatment is a bowel resection. ……………………………… Bowel Obstruction: Small Bowel: Sharp episodic pain, vomiting early, high pitched bowel sounds, hypokalemia. VS Large Bowel: Dull pain, vomiting late, lowpitched bowel sounds, abdominal distention, change in bowel habits. In bowel obstruction, bowel sounds are hyperactive early and hypoactive late. Treatment: NG tube, tube feeding distal to obstruction, fluids to treat hypovolemia (hypovolemia can be life-threatening), treat pain, monitor for infection. 14 Bowel Perforation: Symptoms: Rigid, boardlike abdomen. Rebound tenderness, decreased or absent bowel sounds, free air in peritoneum on KUB. Treatment: Needs surgery! ……………………………… Enteral Nutrition: Enteral nutrition is preferred over TPN. Start enteral feedings EARLY! Within 24-48 hours after admission. Advance to goal feeding rate over 48-72 hours. If the patient is hemodynamically unstable, hold enteral nutrition until the patient is fully resuscitated. In the ICU, the presence of bowel sounds is NOT required to start enteral nutrition. Evidence of resolution of ileus is NOT required to initiate enteral nutrition. Considerations: Keep HOB at least 30 degrees. Obtain chest X-ray to confirm NG/OG tube placement. If the gastric residual is > 250mL after a second residual check, consider a pro-motility agent. If residual is > 500mL, hold feeding and reassess tolerance. ……………………………… Parenteral Nutrition (PN): In a patient who was healthy before ICU admission, PN should be initiated only after the first 7 days. Malnourished patients may have PN initiated ASAP after adequate resuscitation. 15 RENAL REVIEW CCRN Exam Cram Key Points: The best indicator of GFR is a 24-hour urine collection for creatinine clearance. GFR is inversely related to the serum creatinine. Normal urine specific gravity is 1.010 - 1.020. Extremely elevated serum CK is an indicator of rhabdomyolysis. Metabolic acidosis = intrarenal failure. Proteinuria is an important indicator of early diabetic neuropathy. Low serum albumin decreases oncotic pressure and causes third spacing. Nephrotoxic Substances: Antibiotics, NSAIDs, ACE/ARBs, antineoplastics, contrast media, overused diuretics. Acute Tubular Necrosis/Intrarenal Failure: Destruction of the tubular basement membrane. Usually caused by prolonged hypoperfusion to the kidneys (hypotension, sepsis, CABG, vascular surgery). May also be caused by infections (strep, hepatitis, or varicella), Lupus, drugs, or contrast dye. ……………………………… Contrast Medium Nephropathy: Patients are at increased risk for contrast medium nephropathy if they take NSAIDs, ACEs, or metformin. Also, if they are elderly, have a history of diabetes/heart failure/renal insufficiency, or if they receive large doses of contrast. Prevent nephropathy by hydrating patients with IV fluids before and after receiving contrast. ……………………………… Rhabdomyolysis: Release of K+, CK, and myoglobin = obstruction of renal tubules. Symptoms: Decreased urine output and tea-colored urine. Causes: Crush injuries prolonged immobility, hyperthermia, DT’s, compartment syndrome. Treatment: Give fluids! Treat hyperkalemia, give bicarb to alkalize urine. ……………………………… Acute Intrarenal Failure: Give Lasix! Attempt to convert oliguric acute intrarenal failure to non-oliguric. INFECTION is the highest cause of mortality in these patients. Address anemia, prevent bleeding. Administer epogen and platelets. ……………………………… Prerenal Failure BUN : Creatinine ratio 20-40 : 1 Concentrated urine High specific gravity Low urine sodium Responds to Lasix VS Intrarenal Failure BUN : Creatinine ratio 10-15 : 1 Dilute urine Low specific gravity 16 High urine sodium No response to lasix → In general, when the renal tubules are still able to function the urine sodium may be low and the osmolality high. The tubules are still able to hold onto Na+ and concentrate urine! ……………………………… Electrolyte Relationships: Sodium & Potassium: INVERSE relationship (low Na+ = high K+) Calcium & Phosphorus: INVERSE relationship (low Ca+ = high Phos) Magnesium & Calcium: SIMILAR relationship (low Mg+ = low Ca+) Magnesium & Potassium: SIMILAR relationship (low Mg+ = low K+) ……………………………… Hyponatremia: Risk of seizures! Hypocalcemia: Assess for Chvostek and Trousseau Signs. Hypophosphatemia: Decreased diaphragmatic movement can cause hypoventilation. Chvostek sign: Tapping the skin over the facial nerve causes a spasm of the lip and cheek. Trousseau sign: Inflating a blood pressure cuff on the patient’s arm causes flexion of the wrist and hand. 17 ENDOCRINE REVIEW CCRN Exam Cram Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH): Too much ADH = too much water retention! Urine is concentrated. →Decreased urine output. →Decreased serum sodium because the blood is DILUTED (hypo-osmolar). →Biggest danger is SEIZURE r/t hyponatremia. Treatment: Give DILANTIN to inhibit ADH secretion. Put the patient on a fluid restriction. ……………………………… Diabetes Insipidus: Not enough ADH = too much water lost! Urine is diluted! →Increased serum sodium because the blood is concentrated (hyper-osmolar). →Can be caused by taking Dilantin. → Complications include hypovolemia and hypovolemic shock. Treatment: Give VASOPRESSIN (synthetic ADH) and administer IV fluids. When giving vasopressin, monitor for coronary artery ischemia. ……………………………… DKA vs HHS/HNK Diabetic Ketoacidosis (DKA): More common in younger patients. BS > 250mg/dL Develops quickly 4-6L fluid loss No insulin produced. Positive ketones Normal or increased serum osmolality Kussmaul breathing GIVING INSULIN IS THE FIRST PRIORITY, then giving fluids is the second priority. Serum K+ is normal or increased, but TOTAL BODY K+ IS LOW! Infection is the most common cause. VS Hyperglycemic Hyperosmolar Syndrome (HHS) (aka HNK): More common in older patients. BS > 600mg/dL Develops slowly (weeks) 6-9 L fluid loss… YIKES! Some insulin produced. Small amount of ketones HIGH osmolality> 320 mOsm/kg. Fast, shallow breathing, GIVING FLUIDS IS THE FIRST PRIORITY, then giving insulin is the second priority. Serum K+ is high HHS patients are NOT acidotic! ……………………………… → When treating DKA and HHS 50 to 100 mg/dL/hr the goal is to decrease blood sugar by and add dextrose to IV fluids when blood sugar is about 250 for DKA or 300 for HHS. → Differentiation of DKA and HHS is best done by evaluation SERUM OSMOLALITY! Remember… in HHS/HNK serum osmolality will be > 320mOsmkg! 18 → In DKA, decreased LOC is r/t hypovolemia and intracellular dehydration of brain cells. ………………………… Hypoglycemia: Remember that Beta Blockers mask the symptoms of hypoglycemia, so the first sign may be decreased LOC. 19 HEMATOLOGY REVIEW CCRN Exam Cram Disseminated Intravascular Coagulation (DIC): Activation of clotting consumes all of the clotting factors. DIC is primarily a CLOTTING PROBLEM , not a bleeding problem! DIC is ALWAYS secondary to another problem. → endothelial damage from sepsis, ARDS, AAA, cardiac arrest. → Trauma, OB emergencies, dissecting aneurysm, malignancies. → Acute pancreatitis, liver disease. →massive transfusions, pulmonary embolism. Symptoms: Decreased platelets, fibrinogen, and hematocrit. Increased fibrin split products, D-dimer, and antithrombin 3. Increased PT, PTT, and INR. Increased FIBRIN SPLIT PRODUCTS is THE DEFINITIVE TEST for the presence of DIC! D-dimer must also be elevated, but it is NOT definitive for diagnosis of DIC. Treatment: → Identify and eliminate the underlying cause. → Give Vitamin K. → Give blood products. → Give low dose heparin to treat overactive clotting. → Maintain hemodynamic stability. ……………………………… Heparin Induced Thrombocytopenia (HIT): A reaction to heparin that results in thrombosis and consumes platelets. Symptoms: → Platelets suddenly < 150,000 OR a drop by 30-50%. → Petechiae is an EARLY sign. →Clots may lead to PE, MI, STROKE, or AMPUTATION. Treatment: → STOP ALL HEPARIN IMMEDIATELY!!! → Start ARGATROBAN, a direct-thrombin inhibitor!!! → Start warfarin. → Monitor PTT. → If platelets are < 10,000, monitor for decreased LOC r/t intracranial bleeding. 20 HEMODYNAMIC REVIEW CCRN Exam Cram Important Normal Hemodynamic Values: Measures of Preload: CVP: 2-6 mmHg. CVP is a measure of right ventricular preload. PAOP: 8-12 mmHg. PAOP is a measure of left ventricular preload. Measures of Afterload: PVR: 50-250 dynes/s/cm-5. PVR is a measure of right ventricular afterload. SVR: 800-1200 dynes/s/cm-5. SVR is a measure of left ventricular afterload. CO: 4-L/min CI: 2.5-4 L/min/m2 SV: 50-100 mL/beat PAP: 20-30/8-15 mmHg CAPP: 60-80 mmHg SvO2: 60-75%. Mixed venous O2 sat. ……………………………… SvO2 measures mixed venous oxygen saturation. It is the most sensitive indicator of cellular oxygenation. Normal SvO2 is 60-75%. Too high OR too low is bad! If SvO2 is increased, cells are not extracting and using oxygen from the bloodstream effectively (sepsis, septic shock, hypothermia. If SvO2 is decreased, cells are requiring and using more oxygen than normal OR cardiac output may be low (hypoxemia, hypotension, hypovolemia, fever, arrhythmias). ……………………………… Hemodynamic Comparison of Shock States: Cardiogenic Shock: BP ↓ CVP ↑ PAP ↑ PAOP CO/CI ↓ SVR ↑ SvO2 ↓ Hypovolemic Shock: BP ↓ CVP ↓ PAP ↓ PAOP ↓ CO/CI ↓ SVR ↑ SvO2 ↓ Septic Shock: BP ↓ CVP ↓ PAP ↓ PAOP ↓ CO/CI ↑ SVR ↓ SvO2 ↑ Important points to keep in mind about shock states: SvO2 only goes ↑ in septic shock! This is because the cells are not using O2 from the bloodstream effectively, so the venous O2 is higher. CO/CI only goes ↑ in septic shock! The HR increases to compensate, which increases CO/CI up to a point. In late septic shock, this compensation mechanism will begin to fail. SVR is how you tell the difference between hypovolemic and septic shock! It is ↓ in septic shock and ↑ in hypovolemic shock. It is ↓ in septic shock because of acute systemic vasodilation. It is ↑ in hypovolemic shock because the vessels are constricting to compensate for the loss of blood volume. In septic shock everything is ↓ except CO/CI and SvO2! In hypovolemic shock everything is ↓ except for SVR! 21 Medications for Hemodynamic Instability: To increase preload: Crystalloids Colloids Vasopressors To decrease preload: Diuretics Vasodilators (Nitrates, Nitroprusside, Nesiritide) To increase afterload: Norepinephrine Phenylephrine Epinephrine High-dose dopamine (>10 mcg/kg/min) To decrease afterload: Nitroprusside ACE inhibitors Hydralazine Ca+ Channel Blockers IABP High doses of nitroglycerin To increase contractility: Positive inotropes! Dobutamine Dopamine (5-10 mcg/kg/min) Milrinone Epinephrine To decrease contractility: Negative inotropes! Beta blockers Ca+ channel blockers Remember that dopamine at 5-10 mcg/kg/min is a positive inotrope, but at > 10 mcg/kg/min it becomes a vasoconstrictor! ……………………………… Regarding the PAOP waveform when the pulmonary artery catheter is wedged: If you see the phrase “giant V-waves” the problem is MITRAL VALVE INSUFFICIENCY. This is associated with acute inferior wall MI and papillary muscle rupture. ……………………………… Hemodynamic Monitoring Hints: Dynamic Response Test (aka Square Wave Test): Do this test at the beginning of each shift, after zeroing the line, and whenever you are questioning your reading. Use the flush device and look for your “square wave.” Over-dampened wave can be caused by air/clot in the system, loose connections, kinked tubing, pressure bag needs pumped up. Under-dampened wave can be caused by a defective transducer, add-on tubing, pin-point air bubbles. Dicrotic Notch: Represents the closing of the aortic valve. Oxyhemoglobin Dissociation Curve: Shows the relationship between PaO2 and SaO2. 2,3-DPG is an organic compound found in RBCs that affects the affinity of hemoglobin for oxygen. Decreased 2,3-DPG makes hemoglobin hold on to oxygen. Increased 2,3-DPG makes hemoglobin release oxygen. The curve can shift to the LEFT or shift to the RIGHT. ….. LEFT SHIFT… Remember the L’s! Left shift Low 2,3-DPG hoLds onto O2, so the O2 sat goes up. aLkalosis coLd Causes of LEFT SHIFT: Multiple blood transfusions, hypophosphatemia, hypothyroidism. Result of LEFT SHIFT: O2 saturation on pulse oximetry is high, but less O2 is available to the tissues. ….. RIGHT SHIFT… REMEMBER THE R’S! Releases more O2 into the tissues, O2 sat goes down. Raised 2,3-DPG 22 Causes of RIGHT SHIFT: Chronic hypoxemia (COPD), anemia, hyperthyroidism, fever, acidosis, increased PCO2 (COPD). Result of RIGHT SHIFT: O2 sat on pulse oximetry is low, but more O2 is available to the tissues. 23 MULTISYSTEM REVIEW CCRN Exam Cram Risks of Blood Product Administration: - Hemolytic and non-hemolytic reactions. - Transfusion Related Acute Lung Injury (TRALI) - Hypothermia r/t administration large amounts of blood products that have not been warmed… use a blood warmer! - Coagulopathy… make sure to provide plasma and platelets in addition to PRBCs! - Hypocalcemia and hypomagnesemia… citrate in transfused blood binds ionized calcium and magnesium. - Banked blood does not have adequate 2,3-DPG , which causes a left shift of the oxyhemoglobin dissociation curve and less O2 is available to tissues. In Massive Transfusion Protocol, you must prevent the TRIAD OF DEATH: 1. Hypothermia 2. Acidosis 3. Coagulopathy Sepsis: SIRS: 2 or more of the following criteria... 1. Temperature ≥38 °C or < 36 °C. 2. HR >90 3. RR >20 or PaCO2 < 32. 4. WBC > 12,000 or < 4,000 You can have SIRS without sepsis (pancreatitis and burns are good examples). SEPSIS: Meets the criteria for SIRS and has a suspected or documented infection. SEVERE SEPSIS: Meets the criteria for sepsis and has markers of organ dysfunction (hypotension, hypoxemia, decreased urine output, lactate > 2, decreased LOC, coagulopathy). SEPTIC SHOCK: Meets the criteria for severe sepsis plus one of the following… 1. MAP < 65 despite adequate fluid resuscitation. 2. MAP > 65 requires a vasopressor. Remember from Hemodynamic Concepts: In septic shock everything is ↓ except CO/CI and SvO2! SvO2 is ↑ because cells are unable to extract and use O2 from the bloodstream effectively. CO/CI is ↑ because the heart is pumping harder and faster to compensate. SVR is ↓ because of acute systemic vasodilation. Sepsis Treatment: - Fluid resuscitation 30 mL/kg. - If the patient is still hypotensive start a vasopressor! Norepinephrine is the 1st choice. Add epinephrine if a second vasopressor is needed. Vasopressin can be used if still need additional BP support. - Begin antibiotics ASAP! - Get 2 sets of blood cultures. - Begin dobutamine as a positive inotrope for patients with low CO. Sepsis Goals: Goal SvO2 is ≥ 65% Goal CVP is 8-12 mmHg Goal MAP is > 65 mmHg Goal urine output is 0.5 mL/kg/hr ……………………………… Sedation in Critical Care: The patient who is agitated should receive an analgesic first, before receiving and anxiolytic or sedation. IV opioids are the first choice for treatment of pain in critical care. Prevent pain by pre-medicating before procedures and using non-pharmacological interventions. 24 Maintaining a light level of sedation is associated with better clinical outcomes than heavier levels of sedation. When sedation is PRN, there is less possibility of oversedation than with a continuous infusion. Give DAILY sedation vacations to patients on continuous infusions! Also, use a light target level of sedation. A patient fails their daily sedation vacation if any of these signs are observed: - Dangerous agitation - Sustained tachypnea or increased work of breathing - O2 sat < 90% - Acute arrhythmia - Hypotension Romazicon (Flumazenil) is the antidote to benzodiazepines. Reversal effects may wear off before the benzo’s, so monitor for re-sedation. ……………………………… Therapeutic Hypothermia : Inclusion Criteria: - Cardiac arrest with ROSC. - Unresponsive and not following commands. - Witnessed arrest with down-time < 60 minutes. 1. Start induction ASAP, 33°C. 2. Maintenance at 33°C for 24 hours. 3. Rewarming slowly to 36.5°C. Systemic Considerations: Cooling Phase: - Hyperglycemia - Decreased serum K+ during cooling - Electrolyte and fluid shifts - Platelet dysfunction Maintenance Phase: - May need insulin drip. - Monitor train-of-four if a paralytic is used with goal twitch 1-2. Rewarming Phase: - Increase temperature of 1°C per hour. - Stop all K+ administration 8 hours prior to warming because rewarming causes REBOUND HYPERKALEMIA. ……………………………… Toxic Ingestion : If comatose, give Dextrose 50%, thiamine 50-100mg, and naloxone 2mg. This covers multiple causes of unresponsiveness. If acetaminophen overdose is suspected give N-acetylcysteine. If aspirin overdose is suspected, give charcoal and prepare for DIALYSIS . If opioid overdose is suspected, support the airway and give naloxone. If cocaine ingestion is suspected, give activated charcoal and fluids. If methamphetamine use is suspected, give fluids and provide cooling. Give benzodiazepines, haloperidol. 25 BEHAVIORAL REVIEW CCRN Exam Cram Delirium: Delirium results in increased length of stay and an increase in 6-month mortality. Prevention and appropriate treatment of delirium improves patient outcomes. Biggest risk factors for delirium: Pre-existing dementia History of hypertension History of alcoholism Critical illness Coma Benzodiazepines Do not attempt to assess for delirium if your patient is unresponsive or heavily sedated. Criteria for delirium: Must have an acute onset with fluctuating course AND patient must exhibit inattention. If your patient has an acute onset with fluctuating course, continue the assessment and test for inattention. If your patient is positive for inattention, continue the assessment and test for either of these criteria: Altered level of consciousness OR disorganized thinking. If the patient has either of these characteristics they are positive for delirium. How to prevent delirium: Promote orientation with communication, hearing aids/glasses, familiar objects from the patient's home, consistency of caregivers, television or music per patient preference. Keep lights off at night and keep lights on during the day, control excess noise, avoid restraints, minimize tubes and wires. Maintain hemodynamic stability. Assess for substance abuse, treat symptoms of withdrawal. How to prevent delirium in patients who are sedated with the ABCDE bundle: Awakening trials Breathing trials Communication and collaboration among interdisciplinary staff Delirium management with proven tools Early progressive mobility ……………………………… Interventions for Depression: - Do not isolate - Assess suicide risk - Minimize stimulation - Encourage expression of feelings - Do not force decision making - Involve support system - Psychiatric referral (*A patient with POOR SELF-ESTEEM benefits from being provided with choices because it encourages patient control and decreases passivity. However, a DEPRESSED patient should not be forced to make decisions.) ……………………………… Suicide Intent Interventions: - One-on-one observation - Remove hazards from room - Screen personal belongings - Paper/plastic dietary service - Make sure patient swallows medications - Room patient close to nurse’s station ……………………………… Alcohol Withdrawal: Initial signs appear in the first 6-36 hours without alcohol. Tremors, anxiety, headache, diaphoresis, palpitations, GI upset. Seizures can occur in the first 48 hours. Hallucinations can occur in the first 12-48 hours. Visual, auditory, tactile hallucinations. 26 DT’s can occur in the first 48-96 hours. Delirium, agitation, tachycardia, hypertension, fever, diaphoresis. Treatment of alcohol withdrawal: Benzodiazepines like Ativan, Valium, and Librium. Assess patient with CIWA scale for alcohol withdrawal or RASS scale for agitation-sedation. Give glucose and thiamine to prevent Wernicke’s encephalopathy and Korsakoff syndrome. Give multivitamins with folate. Treat potassium, magnesium, and phosphate deficiencies. Give IV fluids to correct volume deficits. Wernicke’s encephalopathy: Gait disturbances, nystagmus, eye muscle paralysis. Caused by a thiamine deficiency. Korsakoff syndrome: Amnesia, memory loss, decreased spontaneity. Caused by a thiamine deficiency. ……………………………… Abuse: Interview the patient privately. Provide support, do not judge. Document your assessment and referrals. Refer to social services. Elder abuse must be reported to adult protective services by law. 27 PROFESSIONAL CARING AND ETHICS REVIEW CCRN Exam Cram AACN Practice Alerts r/t Professional Caring: Family Presence During Resuscitation and Invasive Procedures: This practice alert states that family presence during resuscitation and invasive procedures is BENEFICIAL and helps meet the psychosocial needs of patients and families. ….. Family Visitation in the Adult ICU: This practice alert states that family visitation is beneficial and supports UNRESTRICTED visitation of a support person or persons in the adult ICU. ……………………………… Advocacy and Moral Agency: The nurse advocates from the patient/family point of view. The nurse works with his/her manager to amend rules for the benefit of the patient/family. Never go against hospital policy, but work with management to secure permission for the family. For example: If the family wishes to burn sage at the patient’s bedside in accordance with their religious practices, but the hospital has a policy against open flames, the nurse would advocate for her patient with hospital management to secure permission for this religious practice to be carried out. If the family wants to use an herbal remedy consult with a pharmacist first, then allow them to use it if it is safe. The nurse always considers the patient’s support system in the plan of care. The nurse empowers the patient to speak for themselves. The nurse ensures that ALL patients understand palliative options are available to relieve suffering at the end of life. The nurse initiates collaboration and doesn’t wait for other clinicians to initiate it first. The nurse appreciates differences in race, culture, ethnicity, lifestyle, education, values, and beliefs and incorporates them into the plan of care. The nurse finds opportunities TO TEACH and to BE TAUGHT. The nurse questions and evaluates clinical practice, reads professional literature, and shares his/her knowledge of best practices. ……………………………… AACN Patient Characteristics: Consider these characteristics when planning patient care: Resiliency: The capacity to return to a restorative level of functioning by using compensatory coping mechanisms; the ability to bounce back quickly after injury. Vulnerability: Susceptibility to stressors. Stability: Ability to maintain equilibrium. Complexity: The involvement of 2 or more body systems. Resource Availability: Social, psychological, monetary, technological, etc. Participation in Care: Extent to which the patient and the patient’s family engage in aspects of care. Participation in Decision Making: Extent to which patient and patient’s family engage in decision making. 28 Predictability: A characteristic that allows one to expect a certain course of events or course of illness. ……………………………… When answering Professional Caring and Ethical Practices questions THINK… Is there an opportunity for the nurse to teach? Follow the hospital policy! Advocate for your patient’s preferences within the hospital system. Listen and put the patient’s needs first. Collaborate with other clinicians. Communicate with the physician to ensure your understand their orders and plan of care. Be transparent… if there is an error the nurse should report it. Professionalism and professional growth important. Request education if you need it to care for patients safely during your shift. Ensure that the patient and their family understand the information/teaching provided to them. Contan! Yo ma it to te en of te CN Exa Cra! ……………………………… This CCRN Exam Cram review is for personal use only. Please do not reproduce, copy, or distribute it without permission. Thanks! CornflowerBlueStudio 29