Renal failure this condition result when the kidneys cannot remove the bodys metabolic wastes or perform

m their regulatory function. Acute Renal Failure (ARF) Is a sudden and almost complete loss of kidney function (decreased GFR) over a period of hours to days. Etiology: 1. Usually follows trauma to the kidneys or overwhelming physiologic stress (e.g. burns, septicemia, nephrotoxic drugs and chemicals, hemolytic blood transfusion reaction, sever shock, renal vascular occlusion) that decreases blood flow to the glomeruli or to the nephrons. 2. Sudden and almost complete loss of glomerular and/or tubular function 3. May cause death from acidosis, potassium intoxication, pulmonary edema or infection. 4. May progress from anuric or oliguric phase through diuretic phase to convalescent phase to return of function or may progress to chronic renal failure. Categories 1. Pre-renal condition occur as a result of impaired blood flow that lead to hypo-perfusion of the kidneys and a drop in the GFR. Causes a. Volume depletion resulting from: Hemorrhage Renal losses (diuretic, osmotic dieresis) Gastrointestinal losses (vomiting, diarrhea, nasogastric suction) b. Impaired Cardiac defieciency a. Myocardial infarction b. Heart failure c. Dysrhytmias d. Cardiogenic shock c. Vasodilation a. Sepsis b. Anaphylaxis c. Antihypertensive medication or other medication that cause vasodilation 2. Intra-renal result from actual parenchymal damage to the glomeruli or kidney tubules. Causes a. Prolonged renal ischemia a. Pigment nephropathy (associated with the breakdown of blood cells containing the pigments that in turn occlude kidney structure) b. Myoglobinuria (trauma, crush injuries, burns) c. Hemoglobinuria ( Transfusion reaction, hemolytic anemia) b. Nephrotoxic agents a. Aminoglycosides antibiotics (gentamicin, tobramicin) b. Radiopaque contrast agents c. Heavy metals (lead, mercury) d. Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic) e. NSAIDs f. ACE inhibitors c. Infectious Process

a. Acute pyelonephritis and glomerulonephritis 3. Post-Renal result from a obstruction distal to the kidney. Pressure rises in the kidney tubules eventually, GFR decreases. Causes: a. Urinary Tract Obstruction a. Calculi (stones) b. Tumors c. BPH d. Strictures e. Blood clots Phases of Acute Renal Failure 1. Initiation period begins with the initial insult and ends when oliguria develops. 2. Oliguria period accompanied by a rise in the serum concentration of substances usually excreted by the kidney (urea, creatinine, uric acid, organic acid and intracellular cations. 3. Diuresis period the patient experiences gradually increasing urine output, which signals that glomerular filtration has started to recover. 4. Recovery Period signals the improvement of renal function. It may take 3 to 12 months. Clinical findings 1. Subjective : irritability, headache, anorexia, circumoral numbness, tingling of extremities, lethargy, drowsiness that can progress from stupor to coma. 2. Objective a. Sudden drop in urinary output appearing few hours after the causative event b. Restlessness, twitching, seizures c. Nausea and vomiting d. Skin pallor, anemia, and increased bleeding time, which progress to epistaxis and internal hemorrhage e. Ammonia odor to breath and perspiration, which can progress to uremic frost on skin and pruritus f. Generalized edema, hypervolemia, hypertension, and increase venous pressure. g. Deep rapid respiration to compensate for metabolic acidosis. h. Elevated serum levels of blood urea nitrogen (BUN), creatinine, potassium; decrease serum levels of calcium, sodium, pH, carbon dioxide combining power. i. Albumin in the urine, decreased urine specific gravity. Therapeutic Interventions 1. Correct underlying cause of renal failure 2. Complete bed rest 3. Diet Therapy a. Calories adequate foe maintenance and to prevent tissue breakdown: 2000 to 2500 daily; protein low to moderate 30 to 50 g; carbohydrate relatively high for energy 300 to 400 g. fats relatively moderate 70 to 90 g b. Sodium controlled according to serum levels and excretion capacity. Vary from 1300 to 1900 mg c. Water controlled according to excretion: about 800 to 1000 ml d. Calcium intake of 100mg/day to prevent delay progression of renal osteodystrophy or demineralization of bones, which result from chronic acidosis and altered vitamin A

4. 5. 6. 7.

metabolism; phosphorus intake of less than 600mg/day to delay progression of renal insufficiency; restriction of milk, meats, poultry, fish, eggs, and cereal grains, beer and softdrinks. e. Renal diet low in water soluble vitamins, iron, zinc f. TPN and parenteral intralipid therapy. Packed RBC, electrolytes and glucose IV as necessary Exchange resins to decrease serum potassium Antibiotics to reduce possibility of infection Peritoneal dialysis, hemodialysis or hemofiltration

Chronic Renal Failure or End Stage Renal Disease Is a progressive, irreversible deterioration in renal function in which the bodys ability to maintain metabolic and fluid and electrolytes balance fails resulting in uremia and azotemia. Etiology 1. Occurs as a result of chronic kidney infections, developmental abnormalities, vascular disorders and destruction of kidney tubules 2. Ongoing deterioration in renal functions results in uremia. Stages 1. Reduced renal reserve characterized by a 40% to 75% loss of nephron function. The patient does not usually have symptoms because the remaining nephrons are able to carry out the normal functions of the kidney. 2. Renal Insufficiency occurs 75 % to 90 % of nephrons function is lost. At this point, the serum creatinine and blood urea nitrogen rise, the kidney loses its ability to concentrate urine and anemia develops. The patient may report polyuria and nocturia. 3. ESRD occurs when there is less than 10% nephron function remaining. All of the regulatory, excretory and hormonal functions of the kidney are severely impaired. Clinical Findings 1. Subjective: lethargy, drowsiness, headache, nausea, pruritus. 2. Objective a. Oliguria, anuria, vomiting, anemia, hypertension, anasarca, uremic frost, urochromatic pigmentation (bronze pigmentation) b. Decrease serum calcium (causing tetany) and pH (metabolic acidosis); increased serum phosphate and potassium; xray reveals renal osteodystrophy c. Kussmaul respiration, mental clouding, seizures, coma, death Therapeutic interventions 1. Fluid and sodium restrictions 2. Antihypertensive medications 3. Recombinant human erythropoietin (Epogen) to manage anemia 4. Dietary management a. Very low protein (20 g); minimal essential amino acid makes the body use own excess urea nitrogen to synthesize non essential amino acid needed for tissue protein production. b. Controlled electrolytes, especially potassium (1500 mg) 5. Continuous arteriovenous hemofiltration (CAVH); hemofiltration is based on the principle of convection, which is that some elements in plasma fluids are conveyed across semi permeable membrane as a result of differences in hydrostatic pressure in the system.

6. Peritoneal Dialysis: dialyzing solution is introduced via catheter inserted in the peritoneal cavity; the peritoneal membrane is used as a dialyzing membrane to remove toxic substances, metabolic waste, and excess fluids. a. Intermittent involves 6 48 hours several times a week b. Continuous ambulatory peritoneal dialysis (CAPD) involves approximately three or four exchanges a day, 7 days a week and can be administered home. 7. Hemodialysis the client is attached to a AV fistula or graft to a machine that pumps the blood a long a semipermeable membrane; dialyzing solution is on the other side of the membrane and osmosis and/or diffusion of wastes, toxins and fluids from the client occurs. 8. Kidney transplant from compatible donor a. Human Leukocyte antigen (HLA) tests and tissue and blood typing are done to decrease risk for rejection occurs if donor and recipient are identical twins. b. Clients own kidney is not removed unless it is infected or enlarged; new kidney is placed generally in the iliac fossa retroperitoneally and the donors ureter is attached to the bladder to prevent reflux of urine. 9. Steroids and immunosuppresives e.g azathioprine (imuran) if kidney transplant is performed. Heart Failure Often referred as congestive heart failure (CHF) Is the inability of the heart to pump sufficient blood to meet the needs of the tissue for oxygen and nutrients. Etiology 1. Inability of the heart to meet the oxygen demands of the body. 2. Pump faliure may be caused by cardiac abnormalities or condition that place increased demands on the heart such as cardiac muscles disorders, valvular defects (e.g. mitral valve prolapsed with regurgitation, aortic stenosis), hypertension, coronary atherosclerosis, hyperthyroidism, obesity and circulatory overload. 3. Heart failure maybe classifies as diastolic (impaired ventricular filling) or systolic (impaired ventricular contraction) 4. When one side of the heart fails, there is a buildup of pressure in the vascular system on that side. Right Ventricular failure will be evident on the systemic circulation while left ventricular failure will be on the pulmonary system and may cause pulmonary edema. Clinical findings 1. Left-ventricular heart failure a. Subjective: dyspnea from fluid within the lungs, orthopnea, fatigue and restlessness, paroxysmal nocturnal dyspnea. b. Objective: decreased oxygen saturation, crackles, peripheral cyanosis,cheyne-stokes respiration, frothy blood-tinged sputum, dry non-productive cough, decrease ejection fraction. 2. Right-ventricular failure a. Subjective: abdominal pain, fatigue, bloating, nausea b. Objective: jugular vein distention; dependent, pitting edema that usuallysubsides at night when feet are elevated; ankle edema is the first sign of HF, ascites from increased pressure from the portal system; hepatomegaly; anorexia; respiratory distress; increased CVP; diminished urinary output.

Therapeutic Interventions 1. 2. 3. 4. 5. 6. 7. 8. 9. Rest in Fowlers position to reduce cardiac workload Morphine sulfate to reduce anxiety and dyspnea Oxygen Therapy; in acute ventricular failure, endotracheal intubation and a ventilator Decrease cardiac workload with diuretics, vasodilators ACE inhibitors, angiotensin II receptor blockers (ARBs) and beta blockers. Increase pump performance with digitalis Potassium supplements to prevent digitalis toxicity and hypokalemia Hemodynamic monitoring through a multilumen pulmonary artery catheter Sodium restricted diet to limit fluid retention and promote fluid excretion A paracentesis is ascites exists and is causing respiratory distress.

Myocardial infarction acute necrosis of the heart muscles caused by interruption of oxygen supply to the area (ischemia), resulting in altered functioning and decrease cardiac output. Risk Factors: Family history Increase age Gender: males and females after menopause Race: Higher risk in African American Descent Cigarette smoking contribute to vasoconstriction, platelet activation, arterial smooth muscle cell proliferation and reduced oxygen ability. Hypertension Hyperlipidemia: inc total cholesterol, inc LDL, inc ratio of LDL to HDL, dec HDL, inc triglycerides Obesity Sedentary lifestyle Diabetes Stress Metabolic Syndrome a cluster of sign including hyperlipidemia, low HDL, obesity, inc BP, and impaired glucose utilization Clinical Findings Subjective: retrosternal chestpain, pain that may radiates to the arm, jaws, neck, shoulders or back; pain is described as crushing or pressure or viselike; pain of angina is associated with activity and generally subsides with rest; palpitations, apprehensions, feeling of dread, dyspnea, nausea, Objectives 1. ECG changes may reveal ischemia (inverted T wave, elevated ST segment) or evidence of Ischemia (presence of Q wave); a holter monitoring may be used to detect changes associated with ADL. 2. Elevated serum enzymes and isoenzymes with MI a. Cardiac troponin T (cTnT) levels increase within 3 to 6 hours and remain elevated for 14 to 21 days; very accurate for assessing cardiac disease.

3. 4. 5. 6. 7.

b. Cardiac troponin L (cTnL) level rise 7 to 14 hours after an MI and remain elevated for 5 to 7 days; highly specific for myocardial damage. c. Creatinine Kinase (CK) elevated 3 to 6 hours after infarction, peaking at 24 hours and returning to normal within 72 hours. d. CK MB elevated for 4 to 6 hours after pain, peaking within 24 hours and returning to normal within 72 hours; specific for myocardial damage. e. Myoglobin: elevated in 1 to 3 hours, returning to normal within 12 hours C-reactive protein (CRP) elevation suggest inflammation of the vascular endothelium and coronary artery calcification. Doppler flow studies Cardiac nuclear scanning (thallium, MUGA) or echocardiographic studies can help determine extent of vessel involved Sympathetic nervous system response: pallor, rapid pulse, diaphoresis, vomiting Signs associated with MI: dysrhythmias and elevated temperature, sedimentation rate and WBCs

Therapeutic interventions 1. Prevention of MI a. Supervised exercise program to avoid ischemia but to promote collateral circulation and increased HDL; weight control; smoking cessation; dietary restriction of sodium, cholesterol, and total and saturated fat; management of hypertension and diabetes. b. Pharmacologic managements: nitrates, beta blocking agents, calcium channel blockers, antilipidemics, antiplatelet agents (ASA) c. Supplemental oxygen during angina attack as needed. d. Percutaneous transluminal coronary angioplasty (PTCA) e. Coronary Artery Bypass Graft (CABG) if medical regimen is not successful f. Intracoronary stent Placement g. Transmyocardial revascularization: involves creating laser channels in the myocardium to promote vascular growth 0r angiogenesis 2. Management of MI a. Improvement of perfusion 1) Administer ASA immediately. Often on way to the hospital 2) Begin beta blockers and IV nitroglycerin 3)Thrombolytic therapy within 6 hours of MI : anticoagulants 4)Antidysrhythmic to maintain cardiac functions 5)Intraaortic ballon pump that inflates during diastole and deflates during systole to decrease cardiac workload by decreasing afterload for cardiogenic shock b. Promotion of comfort and rest 1) Administer analgesic such as intravenous morphine sulfate 2) Oxygen Administration to alter tissue hypoxia 3)Maintain Bed or chair rest to decrease oxygen tissue demand 4) Diet Therapy : maybe be given 2 gram sodium diet or clear liquids, depending on presence of nausea c. Monitoring client 1) Pulse Oximetry 2)Cardiac Monitoring 3)Vital Signs 4)Swan- Ganz Catheter d. Assessment for complication of MI 1) Cardiogenic shock

2) Pulmonary Edema caused by heart failure 3)Thromboembolism 4)Extension of MI 5)Pericardial Effusion and cardiac tamponade Stroke Etiology 1. Destruction of brain cells caused by effects of a reduction in oxygen supply a. Ischemic attacks results when brain tissues are blocked from oxygen supply from thrombus or embolus: 83% of attacks are this type b. Hemorrhagic: attack results from bleeding into tissue or subarachnoid space. 2. Symptoms may depend on the affected brain involved and extent of damage; maybe ,asked or delayed because of compensatory collateral circulation through the circle of Willis. 3. Risk factors include: hypertension, hyperlipidemia, obesity, smoking, cerebral atherosclerosis, atrial fibrillation, cerebral aneurysm, advance age, African American ancestry 4. Transient Ischemic Attack (TIA) may also occur without causing permanent damage; these may last for a few minutes to 24 hours; warning sign of impending brain attack. Clinical finding Subjective : syncope, headache, changes in LOC, mood swings, unilateral paresthesias Objectives: 1. Hemiparesis or hemiplegia on side opposite the lesion. 2. Aphasia: brain is unable to fulfill its communicative functions because of damage to input, integrative or output centers. a. Expressive (motor or Brocas) aphasia: difficulty making thoughts known to others. Speaking and writing is most affected. b. Receptive (sensory or Wernickes) aphasia: difficulty understanding what others are trying to communicate; interpretation of speech and reading is most affected. c. Global aphasia: affects both expression and reception d. Dysarthia: difficulty speaking due to paralysis of muscles needed for articulation. 3. Dysphagia 4. Visual Changes a. Homonymous hemianopsia: loss of vision in half of the same visual field in both eyes b. Agnosia: disturbance in ability to recognize objects and attach meaning to them c. Ptosis and paralysis of ocular muscles (Homers syndrome) 5. Alteration in reflexes 6. Altered bladder and bowel fumction 7. CSF is bloody if cerebral or subarachnoid hemorrhage is present 8. Abnormal EEG, CT scan, MRI 9. Cerebral angiography may reveal vascular abnormalities such as aneurysm, narrowing or occlusion 10. Signs of IICP Therapeutic evaluation 1. Complete bed rest with sedation as needed.

2. Maintenance of oxygenation by oxygen therapy or mechanical ventilator 3. If ischemic type, thrombolytic therapy with recombinant tissue plasminogen activator (t-PA) within 3 hours onset 4. Maintenance of nutrition by parenteral route or nasogastric feeding if client is unable to swallow 5. Anticoagulant therapy if thrombus or embolus is present; antiplatelet therapy 6. Antihypertensive and anticonvulsant if indicated 7. Glucocorticoids may be used to reduced cerebral edema and intracranial pressure 8. Surgical Interventions a. Carotid endarterectomy to improve cerebral flow when carotid arteries are narrowed by atherosclerotic plaques. b. Performed to relieve pressure and control bleeding if hemorrhage is present Burns Etiology 1. Thermal, radiation, electrical and chemical burn; cause cell destruction and result in the depletion of fluid and electrolytes 2. Extent of the fluid and electrolytes loss directly related to extent and degree of burn a. Partial Thickness a. Superficial partial thickness burns ( first degree) affects the epidermis, causing erythema, edema and pain. Fluid loss slight, especially if less than 15 % of the body surfaced is involved. b. Deep- partial thickness (second degree) burns affects the epidermis, dermis causing erythema, pain, vesicle with oozing; fluid loss is slight to moderate, especially if less than 15 % of the body surface is involved b. Full thickness ( third degree) burn affects the entire dermis and at times the subcutaneous tissue, resulting in charred or pearly white, dry skin and absence of pain; fluid loss usually severe, especially if more than 2% of the body is involved. c. Full thickness (fourth degree) burn involves the skin, fat, muscle and bone; areas are charred or burned away. 3. Classification of burns a. Minor Burns: no involvement of the hands, face of genitalia, total partial thickness burn does not exceed 15 % b. Moderate Burns: partial thickness involvement of 15% to 25% of body; but full thickness burns does not exceed 10% of body area. c. Major Burns: involvement exceeds 25% (partial thickness) and 10%(full thickness) of body surface. Involvement of the hands, face, genitalia, or feet. This classification is also used if the client has preexisting chronic health problem, is under 18 months or over 50 years old or has additional injuries 4. Pulmonary injury should be suspected if two of the following factors are present, and expected if three or all four are present: a. Hair in nostrils singed b. Client was trapped in a closed space c. Face, nose lips burned d. Initial blood sample contains carboxyhemoglobin 5. Percentage of body surface involved is determined by Lund-Browder Chart or rule of nines 6. Curlings ulcer may occur after a burn a. The client may complain of gastric discomfort or there maybe profuse bleeding, usually occurs by the end of the first week

b. Treatment essentially the same as for gastric ulcer; however mortality after surgical repair is high because of the client debilitated state 7. Fluid shifts as a result of an osmotic gradient from vessel damage causing increase intercellular and interstitial volumes and diminished intravascular volumes Clinical Findings Subjective: extreme anxiety, restlessness, pain (depends on the severity), paresthesia, disorientation Objective a. Changes in appearance of skin indicates degree of burn b. Hematuria; blood hemolysis with subsequent rise in plasma hemoglobin may occur in full thickness burn c. Elevated hematocrit as a result of fluid loss d. Electrolyte imbalance: cellular destruction result initially in hyperkalemia, hyponatremia, and hyperuricemia e. Presence of symptoms of hypovolemic shock caused by circulatory failure, seepage of water, plasma proteins and electrolytes in burned area f. Presence of symptoms of neurogenic shock cuased by fright, terror, hysteria and pain involved in the situation. g. Evidence of renal impairment (inc BUN and creatinine) if acute tubular necrosis occur as a result of circulatory collapse. Therapeutic Interventions 1. Establishment of airway and administration of oxygen; mechanical ventilation as needed. 2. IV replacement (electrolyte solutions and colloids such as blood and plasma) to maintain circulation a. Volume of fluid replacement is based on percentage of body surface area involved and clients weight (e.g Parkland/Baxter and Brooke Army formulas) b. Half of the fluid is administered in the first 8 hours; second half is administered over the next 16 hours. 3. Reduction of total IV solution during second 24 hours depends on the urinary output, blood work and hemodynamic pressures 4. Foley catheter; hourly urinary output to monitor kidney function and influence fluid replacement. 5. Insertion of central line to monitor hemodynamic pressures (CVP, PCWP) 6. Vital signs monitored every 15 minutes 7. Serum electrolytes and blood gases to observe for levels and assist in deciding replacement therapy. 8. Tetanus toxoid booster administration: tetanus human immune globulin for passive immunity 9. NPO except for mineral water for the first 24 hours. Clear liquid as tolerated after 2 days high protein, carbohydrates, fat and vitamin as tolerated, 10. Maintenance of surgical asepsis 11. Daily hydrotherapy; water temperature should be tepid (100of or 37.8OC ) 12. Skin grafting to limit fluid loss, promote healing and prevent contractures a. Heterograft (xenograft) skin from animals, usually pigs (porcine graft) b. Homograft (allograft) skin from other person or cadaver c. Autograft: skin from another part of the clients body i. Mesh Graft: machine used to mesh skin obtained from a donor site so it can be stretched to cover a large area of burn

ii. Postage stamp graft: earlier method in accomplishing the same goal as mesh graft; donor skin is cut into small pieces and applied to the burn iii. Sheet grafting: large strips of skin placed over the burn as close together as possible iv. Cultured epithelial autografting is used for massive burn treatment d. Synthetic coverings 13. Surgical, mechanical or enzymatic debridement 14. IV antibiotics (based on C&S) and topical antibiotics (mafenide acetate ointment, silver nitrate solution and silver sulfadiazine, neomycin sulfate, bactricin, polymyxin B) 15. Opioids to reduce pain and sedatives to decrease anxiety, given IV or orally because of decreased muscle absorption.

Electrocardiogram it is a graphic record of the electrical potentials produced by the cardiac tissue. Standard 12 Lead ECG Limb Leads RA Red LA yellow LL green RL black Chest Leads V1 RED 4TH ICS RPSB V2 YELLOW 4TH ICS LPSB V3 GREEN MIDWAY BETWEEN V2 & V4 V4 BROWN 5TH ICS MIDCLAVICULAR LINE V5 BLACK LAAL LATERAL AND HORIZONTAL TO V4 V6 VIOLET LMAL LATERAL AND HORIZONTAL TO V5 Waves and Segment Morphology P Wave Represents the electrical forces generated from atrial activation Duration(seconds): 0.08 0.11 seconds (less than 3 boxes) Amplitude (mm): baseline to top (or bottom) of P wave. <2,5 mm (2.5 small boxes) positive in limb leads <1.5 mm positive (tall and < 1mm negative in V1 PR interval Intraatrial, intermodal and His purkinje conduction Duration 0.12 to 0.20 or 0.22 sec Q Wave Represents the start of the ventricular depolarization

Duration: >/= 0.04 second Amplitude: >/= of the R wave QRS Complex Represents ventricular depolarization Duration is 100 msec QRS interval should be less than 0.10 sec or two and one-half small boxes ST Segments represents interval between end of ventricular depolarization (QRS complex) and the beginning of repolarization ( T wave) T waves Upright in I, II, V3-V6 Inverted in aVR, and V1 Maybe upright, flat or biphasic in III, aVL, aVF, V1, V2 Amplitude usually <6mm in limb leads and </= 10mm in precordial leads Determine the Axis To determine the axis use the limb leads I, II, III, aVR, aVL, aVF Normal axis is defined as ranging from -30 to +90 AXIS Normal axis (0 90) Normal axis (0 90) Left axis (0-90) Right Axis (0-90) Right Superior (indeterminant) axis (-90 to +180) Legend + represents positive net of QRS voltage - represents negative net QRS voltage TACHYARRHYTMIAS Sinus Tachycardia Sinus node fires at a rate between 100 to 180 beats/min but maybe higher in extreme exertion. Gradual onset and termination Usually physiologic: due to increase adrenergic tone or withdrawal of parasympathetic activity. SUPRAVENTRICULAR ARRHYTMIAS Atrial tachycardia Has an atrial rate of generally 150 to 200 beats/min with P waves looking differently from the sinus P wave Usually occurs in short, recurrent episodes with spontaneous episodes. The rhythm can sometimes be irregular Atrial Flutter Produces an atrial rate between 250 to 400 BPM LEAD I + + + aVF + + LEAD II + -

P waves: flutter waves resembles SAWTOOTH or PICKET FENCE

Atrial Fibrillation Is characterized by random, chaotic atrial depolarization without effective atrial contractions. The chaotic nature of AF results grossly irregular rhythm. The rhythm is considered controlled of the rate is less than 100BPM; uncontrolled if rate conducts greater than 100 BPM. Drugs such as flecainide, sotalol and amiodarone can terminate and prevent atrial fibrillation. Drug therapy can be used before or after cardioversion to maintain sinus rhythm. Paroxysmal Supraventricular Tachycardia Reentry tachycardia in the AV node is characterized by a tachycardia with a QRS complexes of supraventricular in origin, with onset and termination generally rates between 150 and 250 beats/min and with regular rhythm. a. AV nodal reentry tachycardia b. AV reentry tachycardia VENTRICULAR TACHYCARDIA Premature Ventricular Complexes PVC is characterized by the premature occurrence of a QRS complex that is abnormal in shape and has a duration exceeding >120msec, the T wave is commonly large and opposite in the direction of the major T deflection of the QRS. Isolated PVCs Multi focal PVCs more than one shape Couplet PVCc occurs in pairs Bigeminal PVCs occurs every other beat Triplet PVCs occurs in a group of three BRADYARRHYTHMIAS Sinus Bradycardia Is a benign arrhythmia where the sinus nodes discharges a lower rate slower than 60 bpm. This results from excessive vagal and/or decreased sympathetic tone. Most cases of symptomatic sinus bradyarrhythmia result from medication. Right Bundle Branch Block QRS duration >120msec Broad notched R waves in V1 and V2 Wide and deep S wave in V5 and V6 Left Bundle Branch Block QRS duration > 120msec Broad, notched R waves in V5 and V6 and usually leads I and aVL Small or absent initial r waves in V1 and V2 followed by deep S waves. Absent septal q waves in V5 and V6

ATRIO VENTRICULAR BLOCKS Heart block is a disturbance in the conduction of impulse that may be permanent or transient. This exists when an atrial impulse is conducted with a delay or is not conducted to a ventricle. With AV blocks, the disruption of impulse conduction can occur at the level of the AV node, His bundle, or bundle branches. Classification 1. First degree AV Block conduction time is delayed but all atrial impulses are conducted to the ventricles. 2. Second degree AV Block Type I (Weckenbach) progressive lengthening of impulse conduction time until an impulse is not conducted. 3. Second degree AV Block Type II (Mobitz) indicates occasional or repetitive sudden block of conduction without prolongation of conduction time. 4. Third degree AV Block no impulse is conducted. Asystole / Agonal Rhythm Absence of any ventricular electrical activity Sometime, occasional P or wide QRS escape beats (agonal beats) may occur. Cardiac Pacemaker Insertion Artificial pacemakers replace natural electric stimulation of the heart and are indicated in the treatment of third degree AV block, Second degree AV block and Adam stokes syndrome. Nursing Care 1. Observe cardiac monitor before, during, and after the procedure to verify pacemaker capture and observe dysrhythmias; note stimulation threshold; have emergency medications (lidocaine, atropine sulfate) available; stand by defibrillator; monitor incision for infection and hematoma. 2. Teach client how to take pulse, to keep a diary of pulse, to notify the physician immediately if the rate falls below the set on the pacemaker and to remain under physicians supervision because batteries must be replaced periodically. 3. Encourage the client to wear a Medic alert bracelet or carry a medical alert card. 4. Teach client to avoid high magnetic fields such as high tension wires and hand held screening device and magnetic resonance imaging. Cardioversion Elective procedure in which current is administered to the myocardium in a synchronized fashion to depolarized all cells simultaneously, allowing SA node to resume pacemaker function; maybe useful in treating tachydysrhythmias, AF, Supraventricular Tachycardias and V-Tach Nursing Care 1. Obtain informed consent 2. Maintain NPO and ascertain IV line 3. Ensure that no one is touching the bed or client when shock is delivered. 4. Monitor cardiac status for dysrhythmias for several hours after procedure. Cardiopulmonary Resuscitation (CPR) Institution of artificial ventilation and circulation with rescue breathing and external cardiac compression. Nursing Care

1. Assess LOC: shake victims shoulder and shout. Are you OK?; of no response, call for help or activate EMS 2. Assess and establish airway; use head-tilt or jaw-thrust maneuver; determine whether air is being exchanged by looking to see whether the chest is moving; listening whether air can be heard during exhalation and be felt during exhalation. 3. Initiate rescue breathing; maintain the head-tilt or jaw-thrust maneuver and pinch victims nostrils: give two slow breaths using pocket mask or mask bag. 4. Assess circulation: palpate carotid pulse. 5. Deliver external cardiac compression; the victim should be in supine position and in firm surface. Place heel of the hand over lower half of the body of the sternum interlock hands and compress the chest 3.8 to 5cm. 6. Maintain ventilation/compression ratio: one or two rescuers two breaths every 15 compressions 7. Defibrillate using AED 8. Place in a recovery position if pulse and respiration resume 9. Terminate CPR as indicated: return of cardiac rhythm and spontaneous respirations; rescuer exhaustion; physician ordered cessation. Hemodynamic Monitoring with Pulmonary Artery Catheter Catheter that us used to measure pulmonary capillary wedge pressure (PCWP), pulmonary artery pressure (PAP), right atrial pressure (CVP) A double-lumen catheter with a balloon tip is inserted into a vein and advanced through the superior vena cava into the right atrium and ventricle, then into the pulmonary artery; the catheter is guided further until when the balloon is inflated, it is wedged in the distal arterial branch. The catheter yields information on the clients circulatory status, left ventricular pumping action and vascular tone. Nursing care: 1. Assist physician with catheter insertion into the jugular or subclavian vein using sterile technique; obtain CXR to check for placement and complication of pneumothorax 2. Observe the site for inflammation 3. Observe the line for patency and air bubbles 4. Take readings with client in supine position if possible with transducer at the level of the clients sterna notch. 5. Provide site care. 6. Notify physician if the waveform changes or pressure readings are altered. 7. Normal Readings a. PCWP 5 to 13 mmHg b. PAP systolic 16-30 mmHg; diastolic 0-7 mmHg c. RAP 2 to 6 mmHg; less than 2 suggest low blood volume; greater than 6 suggest fluid overload. 8. Keep emergency medications and defibrillator available. Arterial Blood Gases To assess ventilation and acid-base balance Radial artery is the common site for withdrawal of blood specimen Allens Test is done to assess for adequacy of collateral circulation of the hand. Use 10 ml pre-heparinized syringe to draw blood specimen. Place specimen in a container with ice to prevent hemolysis.

Step I. Remember the normal values Blood ph 7.35 7.45 paO2 80-100 mmHg paCO2 35 45 mmHg HCO3 22 26 mEq/L O2 Sat 95 100% BE/BD (Base excess / Base deficit) - -2 to +2 Step II. Look at the pH. Does it indicate the presence of academia, alkalemia or normal pH? pH low ACIDOSIS pH high ALKALOSIS Step III. Look at PaCo2 (respiratory indicator) PaCO2 high respiratory acidosis PaCO2 low respiratory alkalosis Step IV. Look at the HCO3 (bicarnonate) HCO3 high metabolic alkalosis HCO3 low metabolic acidosis Step V. Determine the primary ACID-BASE disturbance Use ROME Step VI. Look at the degree of compensation When the acid base balance is compensated but the pH is Abnormal: partial compensation. When the acid base balance is compensated but the pH is Normal: Complete compensation. Uncompensated When the CO2 and HCO3 levels move towards opposite direction. When paCO2 is abnormal and HCO3 remains normal and vice versa

Shock - defined as a condition in which widespread perfusion to the cells is inadequate to deliver oxygen and nutrients to support vital organs and cellular function . Stages of shock

Etiology 1. Hypovolemic shock occurs when there is a loss of fluid resulting in inadequate tissue perfusion caused by excessive bleeding, diarrhea or vomiting fluid loss from fistula or burns. 2. Cardiogenic shock occurs when pump failure causes inadequate tissue perfusion caused by heart failure, myocardial infarction, cardiac tamponade 3. Neurogenic shock caused by rapid vasodilation and subsequent pooling of blood within the peripheral vessels caused by spinal anesthesia, emotional stress, drugs that inhibit sympathetic nervous system, spinal injury. 4. Anaphylactic shock - caused by an allergic reaction that causes the release of histamine and subsequent vasodilation. 5. Septic reaction to bacterial toxins (generally gram-negative infections) which causes the leakage of plasma into tissues resulting in hypovolemia. Clinical Findings Subjective: apprehension, restlessness, paresis of extremities Objective: weak, rapid, thread pulse, diaphoresis, cold clammy skin, pallor, decrease urine output, progressive loss of consciousness, decrease mean arterial pressure (normal 80 120 mmHg) Therapeutic Interventions 1. Correction of the underlying cause 2. Fluid and blood replacement 3. Vasoconstricting drugs to increase blood pressure 4. Cardiac or hemodynamic monitoring 5. Adrenergic blockage: prevents the effect of prolonged vasoconstriction, causes loss fluid from vascular compartment. 6. Cardiotonics for cardiogenic shock 7. Antihistamine such as diphenhydramine (Benadryl) for anaphylactic shock 8. Antibiotics for septic shock based on blood culture 9. Elevation of lower extremities to ensure circulation to vital organs 10. Intraaortic balloon pump may be used to aid failing heart. 11. MAST or pneumatic antishock garments causes resistance in the vessel and reduces vessels diameter in the legs and abdomen Poisoning - ingestion of a toxic substance or an excessive amount of substance Did you know? More than 90% of poisoning occurs at home Highest incidence occurs in children under 4 Improper storage is the major contributing factor to poisoning Increased Intracranial Pressure Normal ICP is 10-20 mmHg ICP is measured in the lateral ventricles The rigid cranial vault contains brain tissue (1400g), blood (75ml), and CSF (75ml) Causes: head injury, brain tumors, subarachnoid hemorrhage, toxic and viral encephalopathies.

Clinical Manifestations: Early signs Disorientation, restlessness, increased respiratory effort, purposeless movement, and mental confusion (brain cells are responsible for cognition which are sensitive to decreased oxygenation. Pupillary changes and impaired extraocular movements ( increase pressure displaces the brain against the oculomotor and optic nerve. Weakness in one extremity or one side of the body (IICP compresses the pyramidal tracts) Headaches that is constant, increasing in intensity and aggravated by movement of straining (causes pressure and stretching of venous and arterial vessels in the base of the brain) Later signs Decreasing LOC Pulse rate and respiratory rate decrease or become erratic and blood pressure and temperature rise. Widened pulse pressure Altered respiratory pattern Projectile vomiting (IP on the reflex center in the medulla) Hemiplegia or decorticate or decerebrate posturing (IP in the brain stem) Loss of brain stem reflexes, including papillary, corneal, gag and swallowing reflexes. Diagnostics: Cerebral angiogram, CT scan, MRI, PET scan. Transcranial Doppler studies detection of cerebral blood flow LP is avoided because sudden release of pressure can cause herniation of the brain. Complication 1. Brain stem Herniation results in the excessive increase in ICP 2. Diabetes Insipidus result in the decrease secretion of antidiuretc hormone 3. SIADH result of increased secretion of antidiuretic hormone. Treatment: fluid restriction Management 1. Monitoring ICP Purpose: 1. Identify increased pressure before cerebral damage occur 2. Quantify the degree of elevation 3. Initiate appropriate treatment 4. Provide access to CSF sampling and drainage 5. Evaluate effectiveness of treatment a. Ventriculostomy ventricular catheter monitoring a fine bore catheter is inserted into a lateral ventricle usually the non dominant hemisphere of the brain. The catheter is connected to a transducer, which records the pressure in electrical impulse. subarachnoid bolt (or screw) is a hollow device inserted through the skull and dura mater into the cranial subarachnoid space

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epidural monitor uses a pneumatic flow sensor that functions on a nonelectrical basis. This pneumatic epidural ICP monitoring system has a low incidence of infection and complications and appears to read pressures accurately. fiberoptic monitor, or transducer-tipped catheter - reflects pressure changes, which are converted to electrical signals in an amplifier and displayed on a digital monitor. Decreasing Cerebral Edema a. Osmotic diuretics (mannitol) may be given to dehydrate the brain tissue and reduce cerebral edema. They act by drawing water across intact membranes, thereby reducing the volume of brain and extracellular fluid. b. Corticosteroids (eg, dexamethasone) help reduce the edema surrounding brain tumors when a brain tumor is the cause of increased ICP. c. fluid restriction - Limiting overall fluid intake leads to dehydration and hemoconcentration, drawing fluid across the osmotic gradient and decreasing cerebral edema. Conversely, overhydration of the patient with increased ICP is avoided, as this will increase Maintaining Cerebral Perfusion - The cardiac output may be manipulated to provide adequate perfusion to the brain. Improvements in cardiac output are made using fluid volume and inotropic agents such as dobutamine hydrochloride. The effectiveness of the cardiac output is reflected in the cerebral perfusion pressure, which is maintained at greater than 70 mm Hg. Reducing CSF And Intracranial Blood Volume - CSF drainage is frequently performed because the removal of CSF with a ventriculostomy drain may dramatically reduce ICP and restore cerebral perfusion pressure. Caution should be used in draining CSF because excessive drainage may result in collapse of the ventricles. Controlling Fever - Preventing a temperature elevation is critical because fever increases cerebral metabolism and the rate at which cerebral edema forms. Strategies to reduce temperature include administration of antipyretic medications, as prescribed, and use of a cooling blanket. Maintaining Oxygenation - Arterial blood gases must be monitored to ensure that systemic oxygenation remains optimal. Hemoglobin saturation can also be optimized to provide oxygen more efficiently at the cellular level. Reducing Metabolic Demands a. Cellular metabolic demands may be reduced through the administration of high doses of barbiturates when the patient is unresponsive to conventional treatment. The mechanism by which barbiturates decrease ICP and protect the brain is uncertain, but the resultant comatose state is thought to reduce the metabolic. b. administration of pharmacologic paralyzing agents. The patient who receives these agents cannot move, decreasing the metabolic demands and resulting in a decrease in cerebral oxygen demand.

Patients receiving high doses of barbiturates or pharmacologic paralyzing agents require continuous cardiac monitoring, endotracheal intubation, mechanical ventilation, ICP monitoring, and arterial pressure monitoring. Pentobarbital (Nembutal), thiopental (Pentothal), and propofol (Diprivan) are the most common agents used for high-dose barbiturate therapy. Serum barbiturate levels must be monitored.

Surgical Management A craniotomy involves opening the skull surgically to gain access to intracranial structures. This procedure is performed to removea tumor, relieve elevated ICP, evacuate a blood clot, and control hemorrhage. The surgeon cuts the skull to create a bony flap, which can be repositioned after surgery and held in place by periosteal or wire sutures. One of two approaches through the skull is used: (1) above the tentorium (supratentorial craniotomy) into the supratentorial compartment, or (2) below the tentorium into the infratentorial (posterior fossa) compartment. A transsphenoidal approach through the mouth and nasal sinuses is used to gain access to the pituitary gland.

Diabetic Ketoacidosis (DKA) is caused by an absence or markedly inadequate amount of insulin. This deficit in available insulin results in disorders in the metabolism of carbohydrate, protein, and fat. The three main clinical features of DKA are Hyperglycemia Dehydration and electrolyte loss Acidosis

Pathophysiology

Clinical Manifestation polyuria and polydipsia (increased thirst) blurred vision, weakness, and headache gastrointestinal symptoms such as anorexia, nausea, vomiting, and abdominal pain acetone breath (a fruity odor), which occurs with elevated ketone levels hyperventilation (with very deep, but not labored, respirations) may occur mental status in DKA varies widely - may be alert, lethargic, or comatose Management 1. Rehydration - fluid replacement enhances the excretion of excessive glucose by the kidneys. The patient may need as much as 6 to 10 L of IV fluid to replace fluid losses caused by polyuria, hyperventilation, diarrhea, and vomiting. Plasma Expanders can also be used to correct hypotension. 2. Electrolyte Restoration - The major electrolyte of concern during treatment of DKA is potassium.

3. Reversing Acidosis - Ketone bodies (acids) accumulate as a result of fat breakdown. The acidosis that occurs in DKA is reversed with insulin, which inhibits fat breakdown, thereby stopping acid buildup. Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) is a serious condition in which hyperosmolarity and hyperglycemia predominate, with alterations of the sensorium (sense of awareness). - occurs most often in older people (50 to 70 years of age) who have no known history of diabetes or who have type 2 diabetes. Clinical Manifestation hypotension profound dehydration (dry mucous membranes, poor skin turgor) tachycardia variable neurologic signs (eg, alteration of sensorium, seizures, hemiparesis). Management The overall approach to the treatment of HHNS is similar to that of DKA: fluid replacement, correction of electrolyte imbalances, and insulin administration.