ACUTE BIOLOGIC CRISIS these are the conditions that may result to patient mortality if left unattended in a brief

period of time. These are conditions that warrants immediate attention for the reversal of disea se process and prevention of further morbidity and mortality. CONDITONS 1. Cardiac Failure and Dysrythmias 2. Respiratory Failures and ARDS 3. Renal Failure and ESRD 4. Burns 5. Hepatic Coma 6. Diabetic Ketoacidosis 7. Thyroid Crisis and Adrenal Crisis 8. Multisystem Organ Failure and SHOCK RENAL FAILURE Results when the kidney are unable to remove the bodys metabolic wastes or perfor m their regulatory functions Substance normally eliminated in the urine accumulative in the body. ACUTE RENAL FAILURE Is sudden and almost complete loss of kidney function (decreased GFR) over a per iod of hours to days. Reversible Categories of Acute Renal Failure 1. Prenatal (hypoprefusion of kidneys) -volume depletion -impaired cardiac performance -vasodilation 2. Intrarenal (actual damage of kidney tissues) -prolonged renal ischema -nephrotic agents -infectious processes 3. Post renal (obstruction of urine flow) -calculi -tumors -BPH -strictures -blood clots PHASES OF ACUTE RENAL FAILURE 1. Initiation Period -begins with the initial insult and ends when oliguria develops 2. Period Oliguria -accompanied by a rise in serum concentration of substances usually excreted by the kidneys 3. Period Diuresis -gradual increase in urine output -laboratory values stop rising -observed closely for dehydration 4. Period of Recovery -signals the improvement of the renal function -3-12 months -normal laboratory values -permanent 1-3% of reduction in GFR Clinical Manifestations -edema -dry mucous membrane -uremic fetor and uremic frost -nausea and vomiting -drowsiness, headache, seizures (azotemia) -ill and lethargy -cardiac dysrhythmias

-anemia -hypertension -pruritus Diagnostic Findings -urine changes (hematuria/proteinuria) -hyperkalemia -increased BUN and creatinine level -metabolic acidosis -electrolyte imbalance -anemia -ECG changes Medical Management -determine the cause -dialysis may be indicated in severe azotemia -fluid balance-diuretic can be prescribed if edema is present -Kayexalate/Insulin/Calcium Gluconate -low dose of Dopamine -Sodium Bicarbonate -Aluminum Hydroxide High Carbohydrate, Potassium and Sodium restricted diet Nursing Management -monitoring fluid and electrolytes -reducing metabolic rate -promoting pulmonary function -preventing infection -providing skin care CHRONIC RENAL FAILURE Is a progressive, irreversible deterioration in the renal function in which the bodys ability to maintain metabolic and fluid and electrolytes balance fails, res ulting to uremia or ozotemia Kidney sustain irreversible damage -fatal without treatment Cause -diabetis mellitus (leading cause) -hypertension -Acute Glomerulonephritis -Pylonephritis -obstruction Clinical Manifestation -hypertension -edema and pulmonary edema -pruritus -uremic frost -anorexia, nausea and vomiting -altered level of consciousness, restlessness -seizure -creatinine and BUN increase (decreased GFR) -metabolic acidosis -anemia and bleeding tendencies -electrolyte imbalance -oliguria to anuria Stages of Chronic Renal Failure 1. Decrease Renal Reserve (60-89%) -asymtomatic -homeostasis 2. Renal Insufficiency (30-59%) 3. ESRD or End Stage Renal Disease (<15%) -final stage -no homeostasis

Complications 1. Hyperkalemia 2. Pericarditis, pericardial effusion 3. Anemia 4. Bone disease 5. Hypertension Medical Management 1. Pharmacologic Therapy -Antacids- aluminum based antacids -calcium carbonate -avoid magnesium based antacids -anti hypertensive -diuretics -epogen 2. Nutritional Therapy -protein restricted diet -potassium restricted diet -regulate sodium and fluid intake -vitamin supplement 3. Other Therapy -dialysis -Kayexalate -kidney transplant Nursing Management The same with Acute Renal Failure HEPATIC ENCEPHALOPATHY and COMA A life threatening complications of liver disease Results from the accumulation of ammonia and other toxic metabolites in the bloo d Hepatic Coma represents the most advanced stage of hepatic encephalopathy Amonia accumulation Enters the blood stream Passes to the blood brain barrier Brain dysfunction and damage HEPATIC ENCEPHALOPATHY Clinical Manifestations Earliest Symptoms 1. Minor mental changes and motor disturbance 2. Confused and unkept 3. Altered sleep patterns, restlessness 4. Fetor hepaticus -fruity, musty breath odor -similar to tha of freshly mowed grass,acetone or old wine 5. Asterixis or liver flap 6. Constructional apraxia 7. With further progression of the disorder, the patient lapses into coma a nd may have seizure MedicalManagement 1. Lactulose (Duphalac) -to reduce serum ammonia levels -draws the ammonia from the blood into the colon and removed from the body -changes fecal flora to organisms that do not produce ammonia from urea -2-3 stools per day

-NURSING ALERT Patient receiving lactulose is monitored closely for the development of watery d iarrheal stools because they indicate a medication overdose 2. I.V. Administration 3. Neomycin Sulfate -decrease the normal flora in the intestines to reduce bacterial activity on pro tein Nursing Management 1. Neurologic status is assessed frequency a daily record of handwriting sp ecimen is kept. 2. Maintaining safe environment. 3. Provide small, frequent meals and an evening snacks of complex CHO to av oid CHON overloading. 4. Monitor intake and output 5. Monitor serum ammonia level as ordered. 6. Protein diet restriction. 7. Limit activity. 8. Prevent GI bleeding. 9. Monitor for side effects of mediations. DISORDERS OF THE ADRENAL GLANDS ADDISON DISEASE Occurs when the adrenal glands do not produce enough of the hormone cortisol and , in some case, the hormone aldosterone -hyposecretion of the adrenal cortex hormones -90% of the gland is destroyed The disease is also called adrenal insufficiency or hypocortisolism Either primary or secondary can progress to adrenal to adrenal crisis Adrenal Crisis (Addisonian Crisis) is a deficiency of mineralocorticoid and gluc ocorticoid that requires immediate treatment ADDISON CRISIS Life threatening disorder caused by acute renal insufficiency precipitated by st ress, infection, trauma or surgery Causes: hyponatremia, hypoglycemia, hyperkalemia and Shock Given Glococorticoids IV: e.g.hydrocortisone Na succinate (Solu-cortex), mineral ocorticoids e.g. fludrocortisone (Florinef) Severe generalized muscle weakness,severe hypotension, hypovolemia,shock (vascul ar collapse), irritability and confusion, hypoglycemia, increased BUN, rapid res piratory rate, rapid weak pulse Check BP and electrolyte levels Strict bed rest in quiet environment and protect from infection CUSHINGS SYNDROME/CUSHING DISEASE Hypersecretion of glucocorticoids from the adrenal cortex CUSHINGS DISEASE Is a metabolic disorder characterized by abnormally increased secretion endogeno us of cortisol caused by an increased amounts of ACTH secreted by the pituitary gland. Etiology -adrenal tumor -ectopic ACTH production by malignancies -long steroid usage ASSESSMENT Subjective -generalized muscle weakness and wasting -moonface, buffalo hump -truneal obesity with thin extremities -Hirsutism -hypokalemia -hypertension -pendulous abdomen, purple straea easy bruising

Diagnosis -24 hours urine cortisol -ACTH levels determination -Serum Na, K -FBS/HGT -radiographic studies -CT scan/MRI Nursing Management -Promote comfort: protect from trauma -prevent complication: monitor fluid balance, glucose, metabolism, and hypertens ion -health teachings a. DIET: increased protein, potassium, increased calories, sodium b. MEDS: -Cytoxic Agents: aminoglutethimide (cytaden), trilostane (Modrastane), m itotane (Lysodren) to decrease cortisol production -replacement hormones as needed c. Signs and symptoms of progression of disease d. Prepare client for adrenalectomy DIABETIC KETOACIDOSIS Is an acute complication of hyperglycemia crisis It is life threatening complication of DMs Causes: a. Infection/illness b. Surgery c. Stress d. Insufficient or absent insulin Pathophysiology Absence of endogenous insulin Decreased glucose cellular uptake Hyperglycemia Body breaks down fats Fatty acid Ketone bodies Diabetic ketoacidosis ------------- hyperkalemia COMA Clinical Manifestations 1. Drowsiness 2. Coma 3. Severe dehydration 4. Fruity breath odor 5. Rapid and deep breathing 6. Polyuria, polyphagia, polydipsia 7. Weight loss 8. Muscle wasting 9. Vision changes 10. Recurrent infections 11. Abdominal cramps 12. Nausea and vomiting 13. Leg cramps Diagnostic Evaluation -serum glucose: 200-800 mg/dl

-positive urine acetone -arterial blood gas analysis -serum potassium -electrocardiogram (tall tented T-waves, widened QRS) -flattened T-wave and presence of U-wave Medical Management 1. IV administration CARDIOVASCULAR DISORDER The Heart -enclosed within the inferior mediastinum -enclosed by a double sac of serous membrane Pericardium Serous Fluid -lubricating fluid that is produced by the serous pericardial membranes -allow heart to beat easily Pericarditis -decreased in the amount of serous fluid adhesion Interfere with the heart movement 3 Layers of the Heart Walls 1. Epicardium -tightly hugs the external surface of the heart 2. Myocardium -consists of thick bundles of cardiac muscle -contracts 3. Endocardium -thin, glistening sheet of endothelium that lines the heart chambers Chambers of the Heart 4 CHAMBERS 1. ATRIA (2) -receiving chambers -not important in the pumping activity 2. VENTRICLES (2) -inferior, thick walled -discharging chamber -contraction propulsion of blood circulation VALVES Allows the blood flow in only one direction through the heart chambers 1. Atrioventricular Valves -between the atrial and ventricular chamber on each side -prevents the backflow of blood into the atria during ventricular contraction Bicuspid Valve- mitrial valve (left) Tricuspid Valve-right AV Chordae Tendinae-anchor the AV valve flaps in a closed position -open during heart relaxation and closed ventricular contraction 2. Semilunar Valves -guards the bases of the two large arteries -pulmonary and aortic semilunar valves -closed during heart relaxation and open during ventricular contraction CORONARY ARTERY DISEASE It is a heart disease due to impaired coronary blood flow Disrupts the blood rich in oxygen and nutrients Most common cause is ATHEROSCLEROSIS Etiology Non-modifiable factors -age -gender -family history Modifiable Factors

-hyperlipidemia -hypertension -cigarette smoking -diabetes mellitus -physical inactivity -obesity ATHEROSCLEROSIS Abnormal deposit of fatty substances and fibrous tissue in the intima of the blo od vessels Pathophysiology Injury in the endothelial lining Allows entry of lipids to the intima Recruits monocytes and promote expression of inflammatory mediators Monocytes differentiate macrophages and ingest LDL Fatty streak or foam cells formation Stimulates release of growth factors Fibrous plague formation Foam cells increases in size becomes rigid calcified and fragile Intimal ulceration Platelet aggregation further increasing the plaque Narrowing of blood vessel lumen Obstruction of blood flow No or decrease blood supply ANGINA PECTORIS Clinical syndrome usually characterized by episodes of pain and pressure in the anterior chest Increase oxygen demand and decrease oxygen supply Usually a result of atherosclerosis Types of Angina Pectoris 1. Stable Angina -a consistent pain that occurs on activity and is relieved by rest 2. Unstable Angina -increasing frequency, duration and intensity of pain at lower level of activity 3. Prinzmetal Angina -result of coronary vasospasm 4. Silent Angina -ischemia occurs without at all Clinical Manifestations 1. Pain 2. Shortness of breath 3. Diaphoresis 4. Pallor 5. Weak or numbness of arm 6. Dizziness or lightheadedness 7. Feeling of impending doom 8. Choking or strangling sensation 9. Anxiety

Diagnostic Tests 1. ECG 2. 2D echocardiogram 3. Cardiac enzymes 4. CBC, ESR 5. Lipid levels 6. Exercise stress test 7. Cardiac catheterization and angiography Medical Management 1. Oxygen therapy 2. Pharmacological treatment -nitrates -beta-adrenergic blocker -calcium channel blocker -antiplatelet drugs -antilipidemics 3. Surgical management -CABG -PTCA -Laser angioplasty atherectomy Nursing Management 1. Lifestyle modification 2. Careful monitoring during angina episodes 3. Keep nitroglycerine available for immediate use 4. Complete bed rest 5. Provide stress reduction activity MYOCARDIAL INFARCTION Coronary occlusion, heart attack, and MI are used synonymously, but the preferre d term is MI. Characterized by the ischemic death of the myocardium due to the reduced of abse nce of blood flow. Causes 1. Atherosclerosis 2. Complete occlusion of an artery by an embolus or thrombus 3. Vasospasm of a coronary artery (constriction or narrowing) 4. Decreased oxygen supply (acute blood loss, anemia, or low blood pressure ) 5. Increased demand for oxygen (from rapid HR thyrotoxicosis, or ingestion of cocaine Pathophysiology Occlusion/vasospasm Decreased diameter of the arterial wall Reduced/decreased blood supply Decreased oxygen supply to the myocardium NECROSIS Clinical Manifestations 1. Sudden persistent chest pain 2. Anxious and restless 3. Cool, pale and moist skin 4. Tachycardia and tachypnea 5. Epigastric pain 6. Disorientation and confusion 7. Fainting and weakness Diagnostic Evaluation

1. ECG 2. 2D echocardiogram 3. Coronary angiography 4. Myocardial perfusion imaging with thallium 5. serial serum cardiac markers 6. creatinine kinase (CK) 7. lactic dehydration (LDH) 8. myoglobin 9. troponin T and 1 Medical Management Goal: reperfusion of the necrotized area a. to minimize myocardial damage b. to preserve myocardial function c. to prevent complication 1. oxygen therapy 2. pain control -opiate analgesic a. Morphine Sulfate (DOC) -vasodilation b. Nitroglycerine -anxiolytic therapy -benzodiazepine 3. Other pharmacologic therapy -thrombolytic To dissolve and lyse the thrombus in the coronary artery (thrombolysis) allowing blood flow through coronary artery -do not affect the atherosclerotic lesions -Must be administered ASAP after the onset of symptoms the indicate an AMI a. Streptokinase -increase the amount of plasminogen activator thus increasing the amount of both circulating and clot-bound plasminogen -made from bacteria (risk of allergic reaction) -vasculitis is noted up to 9days after administration -not used if the patient received streptokinase in the past 6-12 months b. Tissue Plasminogen Activator (t-PA) -activates theplasminogen on the clot -heparin can be used (to prevent another clot from forming at the same lesion si te because t-PA dose not decrease the clotting factors) -anticoagulants/antiplatelet -beta-adrenergic blockers -anti dysrhythmic -ACE inhibitors 4. Surgical Management -PTCA -CABG Nursing Interventions 1. Relieving chest pain 2. Improving respiratory function 3. Promoting adequate tissue perfusion 4. Reducing anxiety 5. Managing and monitoring potential complications CARDIAC TAMPONADE Is a rapid, unchecked increase in pressure in the pericardial sac compressing th e heart, impairing the diastolic filling reducing cardiac output. Causes 1. Effusion 2. Hemorrhage due to trauma 3. Hemorrhage due to non-traumatic causes 4. Chronic renal failure

5. Connective tissue disorder 6. Acute myocardial infarction Pathophysiology Accumulation of fluid in the pericardial sac Obstruction of blood flow into the ventricles Increase pressure in the pericardial sac Decreased venous return Reduce the amount of blood that can be pumped out Reduced cardiac output Clinical Manifestations 1. Feeling of fullness within the chest (from stretching of the pericardial ) 2. Elevated CVP with jugular vein distention (increased venous pressure) 3. Shortness of breath 4. Pulsus paradoxus 5. Muffed heart sounds 6. Narrowed pulse pressure 7. Orthopnea 8. Diaphoresis anxiety and restlessness 9. Cyanosis 10. Weak, rapid peripheral pulses Diagnostic Test 1. Chest x-ray 2. ECG 3. Echocardiogram 4. CT-scan or MRI Medical Management Goal: to relieve intrapericardial pressure and cardiac compression 1. Pericardiocentesis 2. Pericardiotomy 3. Insertion of a drain the pericardial sac 4. Inotropic drugs 5. Blood transfusion 6. Protamine Sulfate (heparin induced tamponade 7. Vit. K administration (warfarin induced tamponade) Nursing Responsibilities 1. Monitor the cardiovascular and hemodynamic status frequently 2. Monitor for pulsus paradoxus 3. Watch closely for signs of increasing tamponade, increasing dyspnea and arrhythmias 4. Infuse IV solution and inotropic drugs 5. Administer oxygen therapy 6. Monitor respiratory status 7. Prepare for pericardiocentesis or thoracotomy 8. Assess renal function status closely 9. Monitor capillary refill time, LOC peripheral pulses, and skin temperatu re for evidence of diminished tissue perfusion. CONGESTIVE HEART FAILURE Is the inability of the heart to pump enough blood to meet the metabolic needs o f the body Results intravascular and interstitial volume overload and poor tissue perfusion Most commonly occurs with disorders of cardiac muscle that result in decreased c ontractile properties of the heart Categories

a. Left-sided failure b. Right-sided failure c. Systolic dysfunction d. Diastolic dysfunction Causes 1. Myocardial Dysfunction -coronary artery disease -ischemia -myocardial infarction 2. Arterial hypertension 3. Valvular heart disease Etiologic Factors 1. Increased metabolic rate 2. Hypoxia 3. Anemia 4. Respiratory and metabolic acidosis 5. Cardiac dysrhythmias Pathophysiology 1. Myocardial Dysfunction a. CAD b. Ischemia blood flow to c. Dilated Cardiomyopathy myocardium Hypoxia ------acidosis Necrosis contractility CHF 2. Arterial Hypertension workload of the heart

Hypertrophy of myocardial muscle fibers contractility of the myocardium ability of the heart to fill amount of resistance 3. Valvular Heart Disease moving forward ejection of the blood pressure within the heart myocardial contractility pulmonary and venous congestion -left and right sided dysfunction: word format Compensatory Mechanism: -all types of the heart failure reduced cardiac output Triggers compensatory mechanism difficulty of blood in during diastole

at the expense of increased Ventricular work a. Increased symphatetic activity b. Renin-angiotensin aldosterone system c. Ventricular dilatation Clinical Manifestation (LEFT SIDED CARDIAC FAILURE 1. Dyspnea 2. Paroxysmal nocturnal dyspnea 3. Orthopnea 4. Cough 5. Pulmonary crackle 6. Lower than normal oxygen saturation level 7. Restlessness and anxiety 8. Tachycardia/palpitations 9. Easily fatigue 10. Insomnia RIGHT SIDED CARDIAC FAILURE 1. Depended edema 2. Weight gain 3. Hepatomegaly 4. Distended neck veins 5. Ascites 6. Anorexia and nausea 7. Nocturia 8. Weakness Diagnostic Exam 1. Chest x-ray 2. ECG 3. Liver and renal function test 4. ABG 5. Echocardiogram