Critical Care Final Exam PDF

Critical Care Final Exam Exam 1 Content Week 1: Conduction Disturbances and Sudden Cardiac Death Sudden Cardiac Death ○ Depolarization: systole, contraction ○ Repolarization: diastole, resting/ filling ○ Electrical Activity Precedes Mecha...

Critical Care Final Exam Exam 1 Content Week 1: Conduction Disturbances and Sudden Cardiac Death Sudden Cardiac Death ○ Depolarization: systole, contraction ○ Repolarization: diastole, resting/ filling ○ Electrical Activity Precedes Mechanical Activity ○ P wave: atrial contraction ○ QRS Complex: ventricular contraction ○ T wave: ventricular repolarization (relaxation) ○ Cardiac output = HR x SV Targeted Temperature Management (TTM) Lowers risk of neurological disability post resuscitation Cool down to 33 C for 24 hours. At 36 C start to check labs Electrolytes and BG will be low, don't treat bc they will level out Rhythm Interpretation: Assess regularity Assess rate Identify and examine waveforms Assess intervals and examine ST segment Interpret rhythm and assess clinical significance Sinus Rhythms: Normal Sinus Rhythm ○ Normal/ Expected Sinus Bradycardia ○ HR100 ○ Common causes can be anxiety, pain, fever, caffeine, stimulants. drugs, fluid overload, hypovolemic shock ○ Tx consists of treating the causes (BBs, CCBs, etc.) Atrial Rhythms Atrial Fibrillation/ Atrial Flutter ○ No defined P wave = no atrial contraction So blood sits in atrium, starts to clot, clot gets through pulmonary artery, leads to PE ○ Sx: fatigue, dizzy, SOB, decreased CO ○ Transesophageal echo (TEE) to check for clots before cardiovert ○ Cardioversion to shock at synched time ○ Check PT/INR bc of warfarin ○ EKG ○ Ablation if others don’t work ○ Meds/ Treatments: Antiarrhythmics (Amiodarone) Anticoagulants (Warfarin) Cardioversion CCBs (rhythm) Ventricular Rhythms Ventricular Tachycardia ○ “Tombstone” waveform ○ Ventricular Fibrillation ○ No pulse 1) CPR 2) Defibrillate 3) Epinephrine q3-5 mins Supraventricular Tachycardia (SVT) ○ Super fast like HR 150-250 ○ SOB, Increased RR ○ Decreased CO bc decreased Stroke volume 1) Awake pt: Valsalva maneuver  2) Not awake: Adenosine (6mg, then 12 mg) to stop heart 3) Not awake: Cardioversion Other Rhythms Asystole ○ Cannot defibrillate bc no electrical activity ○ No pulse 1) CPR 2) Epinephrine q3-5 mins Pulseless electrical activity (PEA) ○ Cannot shock Week 2: Overview of Critical Care Lol nothing worth noting here Week 3: Hemodynamic Monitoring and Cardiac Patient Hemodynamics ○ Cardiac Output: volume of blood ejected from heart/ min ○ CO = HR X SV ○ Preload: volume of blood in ventricle before systole ○ Afterload: pressure overcome on contraction ○ Contractility: force of ventricular contraction ○ Cardiac Index: CI = CO / body surface area ○ Systemic Vascular Resistance (SVR): ABP = CO X SVR ○ Mean arterial pressure (MAP) = (SBP + 2(DBP)) / 3 ○ Increased lactate = decreased cell O2 delivery- sign of sepsis Hemodynamic Monitoring ○ Phlebostatic Axis: level of R atrium- keep stopcock at this level ○ Arterial Pressure Monitoring: Radial, brachial, femoral arteries Allen’s test for radial site to ensure circulation to extremity Complications: thrombus, embolism, hemorrhage, infx Pulmonary Artery Catheter (PAC) can monitor pressure in each area ○ RAP/ CVP- RV preload. Normal = 2-6 ○ Pulmonary artery pressures ○ Continuous CO monitoring- HOB up to 45 degrees  ○ SvO2- venous O2 sat. Norm = 60-70%. Decreased w/ sepsis Coronary Artery Bypass Graft (CABG) ○ What: bypassing areas of occlusion in heart with new paths ○ Indications: MI, unstable angina, etc. ○ Risks: increased age, sex (female), number of diseased vessels, decreased EF ○ Goals: increase blood flow to myocardium, relieve sx, prolong life ○ Complications: dysrhythmias, impaired contractility, low CO, MI, Tamponade, resp insufficiency, pain, emboli/stroke, shock, death Exam 2 Content Week 5: AKI and CKD/ GI/ Nutrition/ Endocrine Renal Failure - Partial or complete impairment of kidney function that results in inability to excrete metabolic waste products and water - Affects all body systems - Fluids, Electrolytes, & Wastes - GFR (80-125) - Reabsorption and secretion - Acid-Base Imbalance - Reabsorption of filtered bicarbonate (norm = 22-26) - Production of new bicarbonate - Excretion of small amounts of hydrogen ions - Blood Pressure Regulation - Angiotensin I - angiotensin II - aldosterone - vasoconstriction - Renin- sodium + water - increased SV - increased BP - ADH- decreased urinary output Acute Kidney Injury (AKI) - Sudden deterioration of renal function - Oliguria, Azotemia: accumulation of nitrogenous wastes - Acid base disturbances: Metabolic Acidosis  - May need IV Bicarb bc kidneys are not making it, monitor ionized calcium bc hypocalcemia can occur when pH is corrected Fluid and Electrolytes: - Hyperkalemia: low excretion - Hyponatremia: fluid retention - Hypocalcemia: low excretion of phosphorus, decreased Vit D level - Hyperphosphatemia: low excretion - Hypermagnesemia: low excretion Courses of AKI: 1) Initiation Phase (Reversible) - Time from events to signs of decreased renal perfusion - Several hours to 2 days 2) Maintenance Phase (oliguric) - BUN and Creatinine increase daily - Oliguria is common (less than 400 mL/day) - Fluid overload, electrolyte imbalances and acidosis, renal replacement therapy required 3) Recovery Phase - Return of tubular function - 4-6 months for BUN and creatinine to return to normal - Residual impairment of GFR - Early dialysis may prevent the traditional “diuretic” phase of AKI Symptoms of AKI - Altered vital signs (hyperventilation to compensate for metabolic acidosis, body temp changes, BP changes) - Volume depletion/ volume overload - General appearance: uremia (malaise, fatigue, disorientation, drowsiness), bruising, petechiae, edema, check I & Os & daily weights Types of AKI - Prerenal: Decreased blood supply - Hypoperfusion of kidney - Volume depletion, Vasodilation, Decreased cardiac output - Can progress to intrarenal  - Causes: intravascular volume depletion, decreased cardiac output, renal vasoconstriction, pharmacological agents that impair autoregulation and GFR - Decreased perfusion and decreased CO - Intrarenal: Intrinsic- failure of neurons - Kidney tissue affected directly - Acute tubular necrosis (ATN) - Ischemia, nephrotoxic agents (antibiotics, NSAIDs) - Contrast induced rhabdomyolysis - Postrenal: Obstruction of blood flow (stones) - Increased intratubular pressure leads to decreased GFR - Reverses when obstruction is removed Labs: Creatinine, BUN (affected by catabolism, bleeding, and dehydration), BUN:Creatinine ratio- normal = 10:1 to 20:1, and 24 hour urine Diagnostics: noninvasive: XR, renal ultrasound, MRI, Invasive: IV pyelogram, angiography, renal scan, renal biopsy Medical Management: Find the cause and treat the cause! - Dialysis, CRRT, dietary control, manage fluid and electrolytes, protein restriction (byproduct of protein = nitrogen) - Diuretics: hypovolemia corrected first - Dopamine: may increase renal blood flow - Acetylcysteine, fenoldopam, theophylline: prevent contrast induced AKI - Epoetin alfa: treat anemia Dietary: 25-35 calories/kg of ideal body weight per day - Restrict protein, sodium, potassium, fluid intake (output + 600-1000 mL) Chronic Kidney Disease (CKD) - Progressive, irreversible loss of kidney function - Leading causes: Diabetes, HTN, glomerulonephritis, cystic diseases, urologic diseases - Result of retained substances such as urea, creatinine, hormones, electrolytes or water - Uremia: kidney function declines so sx occur in multiple organs (usually Gfr < 15. Multiorgan failure. - Dx: Dipstick eval of protein, albuminuria, Renal ultrasound, CT, BUN/Creatinine, electrolytes, lipids, Gfr, hemoglobin and hematocrit  - Tx: mko000000000000000000000000000000000000000000000000000 - Diet/ nutrition therapy: - normal protein for stages 1-4 and HD, but increased for PD - Avoid high sodium foods - Avoid salt substitutes bc potassium - Limit potassium to 2-3g. Avoid foods high in K+ with HD - Phosphate 1g/day limit. High phosphate foods = meat + dairy - Phosphate binders essential w/ dialysis Dialysis Indications: Fluid overload, electrolyte imbalances, Acid base disturbances, Rhabdomyolysis Diffusion: movement of solutes from pt blood across semipermeable membrane (hemofilter) Ultrafiltration: removal of plasma, water, LMW particles by pressure/ osmotic gradient. Used to control fluid volume Hemodialysis: bedside in ICU. monitor for complications: volume depletion, dysrhythmias, hypoxemia, disequilibrium syndrome, vascular access infections Peritoneal Dialysis: removal of solutes and fluids using peritoneal membrane for filter. Rarely used in CC settings b/c less efficient. High risk of peritonitis. CRRT: used when too unstable for HD. Advantages: gradual removal, minimal heparin, staff nurse at bedside, flexible fluid administration. Disadvantages: bed rest, 1:1 nursing care. Diabetic Ketoacidosis (DKA) Relative/ absolute insulin deficiency- Hyperglycemia due to increased glucose production and decreased utilization Pathophysiology: Osmotic diuresis and dehydration. Hyperlipidemia d/t increased lipolysis. Metabolic acidosis. Altered potassium balance. Excess acids = increased anion gap. Altered LOC r/t acidosis and dehydration. Increase in counterregulatory hormones: glucagon, cortisol, catecholamines, growth hormone Symptoms: dehydration sx, polyuria, polydipsia, polyphagia, fruity odor to breath, hyperventilation/ Kussmauls, flushed/dry skin, lethargy/ altered LOC, N/V, BG > 250, ketonuria, wt loss.  Electrolytes: Hypokalemia bc insulin pushes potassium into cells. Phosphate depletion, mild hyponatremia, elevated BUN/Creatinine (dehydration) Meds that affect bg levels: thiazides, phenytoin, glucocorticoids, BBs, CCBs, Enteral/ parenteral nutrition. Interventions: manage airway. Fluid replacement (NS), insulin therapy, bicarb if pH less than 7.0, electrolyte replacement Acute Pancreatitis Inflammation of pancreas. Severe can lead to necrosis and hemorrhage Etiology: alcoholism, biliary tract disease, medications, trauma, idiopathic Pathophysiology: Autodigestion leads to edema, interstitial hemorrhage, necrosis. Release of histamine and bradykinin leads to increased vascular permeability, edema. Inflammation may lead to obstruction/ ischemia Sx: severe pain- epigastric or mid abdomen- radiates to back, N/V, abd distension, ascites and jaundice. Retroperitoneal hemorrhage: ○ Turner’s Sign: discoloration of flank ○ Cullen’s Sign: discoloration around umbilicus Labs: increased amylase, lipase, WBCs, glucose, LFTs, bilirubin, triglycerides. Decreased calcium, albumin, protein, potassium Dx: CT, MRI, ultrasound, UGI, Xray, ERCP Treatments: ○ Volume replacement: LR, colloids, fresh frozen plasma, packed RBCs ○ Monitor volume status: PAC, I + O, daily weights ○ Vasopressors for hypotension ○ Electrolyte replacement: calcium and potassium ○ Treat hyperglycemia ○ Rest pancreas: gastric suction, enteral feeds via jejunal route, NPO is controversial. NG tube, opiates Complications: hypovolemic shock, atelectasis, ARDS, DIC, pseudocyst, renal failure, high bg and triglycerides, low calcium Ranson’s Criteria: Severity of Illness- GALL ETOH. Glucose, Age, Leukocytosis, LFT, Electrolyte (Ca+), Third spacing/ increased BUN, Oxygen, Hematocrit Peptic Ulcer Disease (PUD) Duodenal vs gastric Risk Factors: Smoking, H. pylori, NSAIDs, ASA, steroids, alcohol Duodenal and gastric ulcers are the most common cause of PUD. ulcer is crater surrounded by inflamed cells Tx: hemodynamic stabilization, gastric lavage, PPIs, antacids, H2 receptor blockers, antibiotics, surgery Week 6: CAD and Structural Heart Disease Coronary Artery Disease: progressive narrowing of coronary arteries by atherosclerosis Risk factors: age, family hx, smoking, inactivity, overweight, high cholesterol, DM, HTN Dx: holter monitor, exercise tolerance test, stress test, Xray, echo Labs: CBC, Na, K, Ca, Mg, troponin, cholesterol Tx: diet low cholesterol low salt, exercise, wt loss, stop smoking, manage DM and HTN, statins, lipid lowering, Zetia blocks cholesterol absorption, meds affecting platelets Angina: Stable: (chronic, exertional) T wave inversion Tx = nitroglycerin and rest Unstable: (acute) more often and more severe. Tx = nitro, rest, drugs affecting platelets, revascularization Variant: Prinzmetal’s (vasospasms) ST elevation during pain. Tx = CCBs Acute Coronary Syndrome: umbrella term Ischemia with myocardial cell death Imbalance of O2 supply and demand Includes unstable angina, stable angina, and acute MI Causes: atherosclerosis, emboli, blunt trauma, spasm Acute MI STEMI: ST elevated NSTEMI: non ST elevated Sx: midsternal chest pain- severe, crushing, squeezing, pressure. Pain may radiate, unrelieved with nitrates. Pale and diaphoretic, dyspnea, tachypnea, hypoTN, syncope, feeling of impending doom, N/V, dysrhythmias Dx: signs and symptoms, EKG, elevated troponin  Medical Management: pain relief: morphine and nitro, oxygen, prevent platelet aggregation, fibrinolytic therapy, Meds: nitrates, BBs, ACEs Complications: dysrhythmias, sudden death, HF, cardiogenic shock, ventricular aneurysm, pericarditis Treatment AMI: CABG, stent Heart Failure Inability of the heart to generate adequate flow and to meet the metabolic demands of the body Systolic: impaired contractility Diastolic: impaired filling Pathophysiology: LHF- decreased pumping, blood backup, fluid in lungs, backflow leads to RHF. RHF leads to systemic sx. Brain natriuretic peptide (BNP)- cardiac hormone secreted by ventricular myocytes in response to wall stretch- normal = 100 Sx: JVD, edema, perfusion status, lung sounds Treatment: ○ Improve pump function: diuretics, ACEs, ARBs, BBs (carvedilol), Digoxin ○ Nesiritide citrate for acute decompensation of HF ○ Reduce cardiac workload: intra aortic balloon pump, biventricular pacing, rest, cardiac rehab ○ Optimize gas exchange: airway assessment, semi-fowlers, O2, diuresis, control Na and fluid retention, daily wt, VTE prophylaxis Inflammatory Heart Disease Pericarditis: can lead to infusion, tamponade, scarring. From MI, uremia, cancers. SX: friction rub, pulsus paradoxus, initial ST elevation. TX: pericardiocentesis Endocarditis: can lead to valvular dysfunction, vegetation. SX: high fever, shaking chills, night sweats, cough, wt loss, malaise, weakness, fatigue, new murmurs, symptoms of HF, skin abnormalities, janeway lesions. DX: echo, TEE. TX: antibiotics, rest. Prevention: antibiotic prophylaxis before procedures Week 7: Acute Respiratory Failure and Ventilation Week 8: Shock, Sepsis, and MODS Exam 3 Content Week 10: Emergency and Disaster Nursing Week 11: TBI, SCI, and Stroke Week 12: Hematologic and Vascular Dysfunction New Content Week 14: Issues in Transplant Nursing