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Medical-Surgical Nursing

Fluids and Electrolytes Fluids 60% of an adults body weight is water Factors affecting body fluid composi tion: 1. Age 2. Gender 3. Body fat Fluid Compartments in the body: 1. Intracellu lar space -fluid in the cells -approximately 2/3 of the total body water -primar ily located in the skeletal muscle mass

2. Extracellular Space -body fluid outside the cells -divided into: a. intravasc ular >contains plasma >approximately 3L out of 6L blood volume b. interstitial > fluid that surrounds the cells >approximately 11-12L in an average adult c. tran scellular >smallest division of the ECF >approximately 1L of fluid >CSF, synovia l, pericardial, pleural, intraocular

Electrolytes 2 types: 1. Cations -sodium, potassium, calcium, magnesium and hydr ogen ions 2. Anions -phosphate, bicarbonate, chloride 3 Pressures Important in t he Maintenance of Fluid Balance 1. hydrostatic pressure 2. osmotic pressure 3. o ncotic pressure

Regulation of Body Fluid Compartments 1. Osmosis and Osmolality 2. Diffusion 3. Filtration 4. Sodium-Potassium Pump Routes of Gains and Losses 1. Kidneys >appro ximately 1L in an average adult >1mg/kg/hour 2. Skin >may vary from 0 1000ml or more 3. Lungs >approximately at 400ml a day

4. GI tract >at 100 200ml a day Laboratory Tests for Evaluating Fluid Status 1. Osmolality serum Na x 2= glu/18 +BUN/3= Approx value of serum osmolality Osmolar ity 2. BUN 10 20mg/dl or 3.5 7 mmol/L 3. Creatinine 0.7 1.5 mg/dl or 60 130mmol/ L 4. Hematocrit males: 0.44 - 0.52 females: 0.39 - 0.47 5. Urine Sodium 50 220mE q/24 hours

Homeostatic Mechanisms 1. Kidneys -filters 170L of blood a day -excretes only 1. 5L of urine/24 hours 2. Heart and Blood Vessel Functions 3. Lungs 4. Pituitary F unction 5. Adrenal Functions 6. Parathyroid Functions 7. Baroreceptors a. high p ressure baroreceptors -in the aortic arc and carotid sinus -in the juxtaglomerul ar cells of the nephron

b. low pressure baroreceptors -in the cardiac atria (left atrium) 8. Renin - Ang iotensin - Aldosterone System Liver > Angiotensinogen > Angiotensin (kidneys) re nin Angiotensin 2 (lungs) > Aldosterone (adrenals) ACE 9. ADH and Thirst 10. Osm oreceptors 11. Atrial Natriuretic Peptide -at 20 77pg/ml (20 -77ng/L)

Third Space Fluid Shift Fluid Volume Deficit Dehydration >causes: a. inadequate intake b. abnormal fluid losses c. other causes -diabetes insipidus -osmotic diu resis -hemorrhage -coma >signs and symptoms: weight loss, poor skin turgor, olig uria, concentrated urine, postural hypotension

rapid heart rate, decreased CVP, cool clammy skin, inc temperature >assessment: BUN and Crea Hematocrit Serum elecrolytes Urine specific gravity Fluid Challenge Test >management: a. oral route of fluid replacement -preferred method b. IV ro ute -isotonic then hypotonic

c. monitoring -weight, intake and output, V/S, CVP level of consciousness, breat h sounds and skin color >nursing management: a. prevent fluid volume deficit b. correct fluid volume deficit Fluid Volume Excess -isotonic expansion of body wat er >cause: a. abnormal retention of water and sodium >s/sx: a. edema b. distende d neck veins

c. crackles g. increased CVP d. tachycardia h. increased weight e. increased BP i. increased urine output f. increased PP j. shortness of breath >assessment: BU N CXR Hematocrit Serum Osmolality Serum Electrolytes >management: a. withholding excessive administration of IVF b. diuretics c. restriction of oral fluids (sod ium)

1. Pharmacologic Therapy 2. Hemodialysis 3. Nutritional Therapy >nursing managem ent: a. preventing fluid volume excess b. detecting and controlling fluid volume excess c. teaching patients about edema Sodium Deficit -refers to serum sodium level below 135mEq/L >causes: a. vomiting d. fistulas b. diarrhea e. sweating c. diuretics f. dilutional hyponatremia

>s/sx: similar to dehydration >assessment: serum sodium of less than 135mEq/L ur ine sodium SIADH - >20mEq/L sodium loss - <20mEq/L >management: a. sodium replac ement -by mouth, NGT or through parenteral route -parenterally, must not exceed 12mEq/L in 24 hours > osmotic demyelination

b. SIADH -give Demeclocycline or Lithium c. water restriction -safer than sodium replacement

Sodium Excess -sodium level higher than 145mEq/L -can occur in patients with nor mal fluid volume or in those with FVE or FVD >causes: a. gain of sodium in exces s of water (administration of hypertonic saline) b. loss of water in excess of s odium (unconscious, cognitively impaired individuals, diarrhea,hyperventilation, burns, diabetes insipidus, heat stroke and sea water drowning) >signs and sympt oms: predominantly neurologic (cellullar dehydration)

Management: >serum sodium should be reduced at a rate of 0.51mEq/L 1. IVF Therap y -hypotonic solution or isotonic non saline solution 2. Diuretics 3. Desmopress in Acetate Nursing Management: 1. Look for the hidden sources of sodium 2. Monit or for: body temperature, thirst and level of consciousness 3. Prevent hypernatr emia 4. Correct hypernatremia

Potassium Deficit -potassium serum level <3.5mEq/L causes: >alkalosis, GI losses , hyperaldosteronism, potassium losing diuretics, other drugs (corticosteroids, amphotericin B, carbenicillin and sodium penicillin), insulin hypersecretion, in ability or unwillingness to eat a normal diet, magnesium depletion, Cushings synd rome signs and symptoms: >fatigue, anorexia, nausea, vomiting, muscle weakness, leg cramps, decreased bowel motility, paresthesias, dysrhythmias and increased s ensitivity to digitalis, glucose intolerance

Confirmatory tests: 1. Decreased serum potassium 2. ECG changes -flat or d T waves and depression of the ST segments -elevation of the U waves 3. ic Alkalosis 4. Urine potassium concentration of >20mEq/24 hours Medical ent: 1. Potassium replacement therapy -if without abnormal potassium loss, 40-80mEqs/day -oral (Kalium Durule) K chloride, K phosphate or K acetate)

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Nursing Management: 1. Monitoring for s/sx or progression of hypokalemia 2. Prev enting hypokalemia 3. Correcting hypokalemia 4. Administering IV potassium -afte r adequate urine flow -20mEqs/hour or less -30-40mEqs/L and below unless severe

Potassium Excess -less common but more severe than hypokalemia -causes: >renal f ailure, excessive intake of potassium, infection, hyporaldosteronism and Addisons disease, medications (KCl, heparin, ACE inhibitors, NSAIDS and K sparing diuret ics) and acidosis -clinical manifestations: >dysrhythmias, skeletal muscle weakn ess and paralysis >CNS and PNS involvement >Flaccid quadriplegia, respiratory an d speech muscle paralysis

Confirmatory tests: 1. ECG -peaked, narrow T waves, ST segment depression and a shortened QT interval -prolonged PR interval then absence of P wave 2. ABG 3. Se rum potassium level increase Medical Management: 1. Monitoring of serum potassiu m with ECG findings 2. Emergency pharmacologic therapy >calcium gluconate or cal cium chloride >sodium bicarbonate >insulin and glucose >beta 2 agonist 3. Dialys is

Nursing Management: 1. Monitoring 2. Preventing hyperkalemia 3. Correcting hyper kalemia Pseudohyperkalemia >use of tourniquet in an exercising muscle >marked le ukocytosis and thrombocytosis >familial pseudohyperkalemia

Calcium Deficit -less than 8.5mg/dl of calcium in the serum -causes: >hypoparath yroidism >those who received citrated blood >pancreatitis, renal failure >vitami n D deficiency, magnesium deficiency >medullary thyroid carcinoma >low albumin l evels, alkalosis and alcohol abuse -signs and symptoms: >tetany, seizures and me ntal changes -confirmatory test: >ECG- prolonged QT interval

Management: 1. Administer calcium salts -calcium carbonate, calcium chloride, ca lcium gluceptate Risks: a. Sloughing of tissues b. Bradycardia then cardiac arre st c. Digitalis toxicity 2. IVF but not normal saline or solutions containing ph osphates and bicarbonate 3. Vitamin D therapy 4. Aluminum hydroxide, calcium ace tate, calcium carbonate 5. Nutritional therapy 6. Screen for and treat hypomagne semia

Nursing Management: 1. Monitor hypocalcemia for patients at risk 2. Airway manag ement 3. Seizure precaution 4. Patient education -caffeine and alcohol decreases absorption -nicotine increases excretion -medications to decrease bone loss (al endronate, raloxifene and calcitonin)

Calcium Excess -with high mortality rate -causes: >malignancies and hyperparathy roidism >immobilization >use of Thiazide diuretics >milk-alkali syndrome >Vitami n A and D intoxication -signs and symptoms: *proportional to the elevation of se rum calcium >muscle weakness, incoordination, anorexia and constipation >cardiac arrest

>dehydration >abdominal and/or bone pain >abdominal distention and paralytic ile us >excessive urination then polyuria >s/sx of PUD >changes in the LOC and menta l status *hypercalcemic crisis Laboratory tests: 1. Serum calcium determination 2. ECG - shortening of the QT interval and ST segment - prolongation of the PR i nterval - dysrhythmias 3. Double antibody PTH test

4. X-Ray - osteoporosis 5. Sulkowitch test Management: 1. Pharmacologic therapy -dilute the serum calcium and promote its exc. (normal saline, administer phosph ates, diuretics, calcitonin) -Cancer treatment -Corticosteroid therapy > to decr ease bone turnover and tubular reabsorption -Biphosphonates (pamidronate) >cause s myalgia, pyrexia and decreased WBC -Mithramycin >causes thrombocytopenia and n ephrotoxicity and hepatotoxicity

-IV phosphates should be used with caution >Phospho-Soda, Neutra-Phos Nursing Ma nagement: 1. Monitor the s/sx 2. Increase mobility 3. Increase oral fluid intake

Chloride Deficit -serum chloride level below 96mEq/L -causes: >chloride deficien t formulas, salt restricted diets >GI tube drainage, severe vomiting and diarrhe a -signs and symptoms: >hypokalemia, hyponatremia and metabolic alkalosis (hyper excitability of muscles, tetany, hyperactivity of deep tendon reflexes, weakness , twitching, muscle cramps, cardiac dysrhythmias, seizures and coma) -lab tests: >serum chloride determination

>serum potassium and sodium determination >ABG >urine chloride level decrease (n ormal value110-250mEq/L) -medical management: >chloride replacement normal salin e and half strength saline >reevaluate the use of diuretics >nutritional therapy tomato juice, salty broth, canned vegetables, processed meats and fruits >restr iction of free water intake >ammonium chloride

-nursing management >monitoring of intake and output, ABG determination values, serum electrolyte levels, LOC, muscle strength and movement >vital signs and res piratory assessments >patient education as regards to replacement therapy

Chloride Excess -serum chloride level higher than 106mEq/L -associated with hype rnatremia, bicarbonate loss and metabolic acidosis -causes: >loss of bicarbonate (GI and/or renal) -signs and symptoms: >metabolic acidosis, hypervolemia and hy pernatremia (tachypnea, weakness, lethargy, deep rapid respirations, diminished cognitive ability and hypertension) >decrease in CO, dysrhythmias and coma -lab tests: >serum sodium and chloride determination >ABG- Bicarbonate less than 22mE q/L

-normal anion gap (8-12mEq/L) >urine chloride concentration greater than 250mEq/ L -medical management: >IVF therapy -Lactated Ringers Solution >IV sodium bicarbo nate >Diuretics >Fluids, sodium and chloride restriction -nursing management: >m onitoring V/S, ABG, I&O >assessment of neurologic, respiratory and cardiac funct ions >patient education as regards to nutrition

Normal blood pH -7.35 to 7.45 Blood pH compatible with life -6.80 to 7.80 Buffer Systems -maintains the blood pH by removing or releasing H+ ions 1. Bicarbonate -Carbonic Acid Buffer System -the major extracellular buffer system -Bicarbonate to Carbonic Acid Ratio is 20:1 2. Phosphate Buffer System 3. Plasma proteins, R BC and Hemoglobin Acid-Base Balance

Organs involved in HCO3-H2CO3 System: 1. Kidneys -activation is slower (hours to days) but more efficient -has the ability to regenerate and reabsorb or excrete bicarbonates -has the ability to retain or excrete H+ -in acidosis: excrete H+ and conserve bicarbonate -in alkalosis: retain H+ and excrete bicarbonate -canno t compensate in renal failure 2. Lungs -adjust ventilation in response to CO2 co ntent of the blood -activation is faster but less efficient

Acute and Chronic Metabolic Acidosis (Base Bicarbonate Deficit) -low pH; low pla sma bicarbonate -causes: >gain of hydrogen ions or loss of bicarbonate -2 forms: A. High Anion Gap Acidosis -due to the accumulation of the unmeasured anions (p hosphates, sulfates and proteins) B. Normal Anion Gap Acidosis (hyperchloremic a cidosis) -due to the direct loss of bicarbonates >diarrhea >diuretics >lower int estinal fistulas >renal ins.

>excessive administration of chloride >excessive administration of parenteral so lution without bicarbonate -signs and symptoms: >headache, confusion, drowsiness >increased respiratory rate and depth >nausea and vomiting >peripheral vasodila tation and decreased CO >decreased BP, cold and clammy skin, dysrhythmias and sh ock -lab tests: >ABG - low bicarbonate level and a low pH >Serum potassium deter mination

>Anion Gap Calculation >ECG -medical management: >Eliminate excessive sources of chloride >Sodium bicarbonate -if pH is less than 7.1 -if bicarbonate is less th an 10mEq/L >Serum potassium monitoring and reversal of potential hypokalemia >Re versal of potential hypocalcemia >Sodium Bicarbonate >Dialysis

Acute and Chronic Metabolic Alkalosis (Base Bicarbonate Excess) -high pH; high p lasma bicarbonate concentration -causes: (due to gain of bicarbonates or loss of hydrogen ions) >vomiting or gastric suction- most common >diuretics- loop and t hiazides >hyperaldosteronism and Cushings syndrome >excessive alkali ingestion or administration >villous adenoma and cystic fibrosis -signs and symptoms: >decre ased calcium ionization (tingling of the fingers, toes, dizziness

and hypertonic muscles) >depressed respirations >atrial arrhythmias then ventric ular arrhythmias >decreased motility then paralytic ileus -lab tests: >ABG - pH greater than 7.45 - bicarbonate greater than 26mEq/L >Serum potassium determinat ion >Urinary chloride levels -medical management: >Chloride replacement (KCl) >I VF containing sufficient sodium and chloride >H2R antagonists- in GI suctioning

>Carbonic Anhydrase Inhibitors >I&O monitoring Acute and Chronic Respiratory Aci dosis (Carbonic Acid Excess) -pH is less than 7.35; paCO2 is higher than 42mmHg -causes: (due to inadequate excretion of CO2 > elevated plasma CO2 > elevated pl asma H2CO3) >acute pulmonary edema >sedative overdose >aspiration of foreign bod y >severe pneumonia >atelectasis >RDS >pneumothorax >MG, GBS

-signs and symptoms: >increased HR, RR, BP, mental cloudiness and feeling of ful lness in the head >ventricular fibrillation >increased intracranial pressure, pa pilledema, dilated conjunctival blood vessels >hyperkalemia -lab tests: >ABG >Se rum electrolyte determination >Chest X-Ray >ECG >Drug screen for overdose

-medical management: >Pharmacologic *bronchodilators *thrombolytics *antibiotics *anticoagulants >Pulmonary hygiene >Adequate hydration >Supplemental O2 with ca ution >Mechanical ventilation

Acute and Chronic Respiratory Alkalosis (Carbonic Acid Deficit) -arterial pH of greater than 7.45; PaCO2 of less than 38mmHg -causes: (due to hyperventilation > blowing off of CO2 > decreased plasma carbonic acid concentration) >extreme anx iety, hypoxemia, early phase of Aspirin intoxication, gram negative bacteremia a nd inappropriate ventilator settings >chronic hepatic insufficiency, cerebral tu mors -signs and symptoms: >lightheadedness, inability to concentrate

>numbness and tingling from reduced ionized calcium >tinnitus, loss of conscious ness >tachycardia, atrial and ventricular arrhythmias -lab tests: >ABG >Serum el ectrolyte determination -management: >breath slowly or into a closed system >sed atives

Acid Base Disturbances and Compensation Disorder Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosi s

Initial Event PaCO2;or N HCO3; pH PaCO2;or N HCO3;pH or N PaCO2; HCO3; pH or N PaCO2; HCO3; p Compensation Kidneys eliminate H+ & retain HCO3 Kidneys conserve H+ & excrete HCO3 Lungs elimi nate CO2 & conserve HCO3 Lungs to PaCO2, kidneys conserve H+

Burns Autograft Heterograft Homograft Carboxyhemoglobin Escharotomy Fasciotomy Rule of Nines 4 Major Goals Relating to Burns 1. Prevention 2. Institution of lifesaving measu res for the severely burned person. 3. Prevention of disability and disfiguremen t through early, specialized, individual treatment.

4. Rehabilitation through reconstructive surgery and rehabilitation programs. Bu rn Categories Burns are sustained through 1. Thermal 1. Conduction 2. Chemical 2 . Electromagnetic radiation 3. Radiation Skin destruction can lead to; 1. Increased fluid loss 2. Infection 3. Hypothermia 4. Scarring, change in body image 5. Compromised immunity 6. Changes in function Classification of burns: A. According to burn depth: 1. Superficial Partial Thic kness (Similar to First Degree Burn)

-causes: *sunburn *low intensity flash -involves the epidermis and possibly a po rtion of the dermis -signs and symptoms: *tingling *pain that is soothed by *hyp eresthesia cooling *reddened *possibly blisters *minimal or no edema -complete r ecovery within a week; no scarring -peel off

2. Deep Partial thickness (Similar to Second Degree Burn) -causes: *scalds *flas h flame -involves the epidermis, upper dermis, portion of the deeper dermis -s/s x: *pain *sensitive to cold air *hyperesthesia *blistered, weeping surface *brok en epidermis *edema -recovery in 2-4 weeks -some scarring and depigmentation con tractures -infection may convert it to full thickness

3. Full Thickness (Similar to Third Degree) -causes: *flame *prolonged exposure to hot liquids *electric current *chemical -involves the epidermis, entire dermi s and sometimes subcutaneous tissue, may involve connective tissue, muscle and b one -s/sx: *pain free *hemolysis *shock *entrance and exit wounds *hematuria *br oken skin with exposed *edema fats

-eschar sloughs -grafting necessary -scarring and loss of contour and function; contractures -loss of digits or extremity possible Physiologic Responses to Burn s Local Pathophysiologic Response -if only less than 25% of the TBSA is involved Local and Systemic Pathophysiologic Response -if more than 25% of the TBSA is i nvolved -maximal if burns cover 60% or more of the TBSA 1. Cardiovascular Respon se fluid loss > hypovolemia > decreased cardiac output > decreased BP > decrease d perfusion and oxygen delivery

> onset of burn shock > sympathetic response > peripheral vasoconstriction > fur ther decrease in the CO -the greatest volume of fluid leak occurs in 24 36 hours after the burn, peaking at 6 8 hours -basically caused by increased capillary p ermeability -diuresis occurs for several days to 2 weeks 2. Burn Edema -swelling maximal after 24 hours -begins to resolve 1-2 days post burn -completely resolv ed after 7-10 days post injury Edema > pressure on the small blood vessels and n erves of distal extremity > ischemia >

3. Effects on Fluids and Electrolytes and Blood Volume -evaporative loss through the burn wound (3-5 L) -hyponatremia (dilutional due to fluid shift from inters titial to intravascular space) -hyperkalemia due to massive cell destruction *la ter results in hypokalemia due to dilution caused by fluid shift -anemia due to blood loss and hemolysis (though may be seen as polycythemia due to excessive pl asma loss) 4. Pulmonary Response -inhalation injury > release of histamine, sero tonin and thromboxane > catecholamine release > hypoxia

-atelectasis may be present due to decreased surfactant -types of pulmonary inju ry: *upper airway injury -results from direct heat and edema *inhalation injury below the glottis -usually results from carbon monoxide poisoning -respiratory a cidosis may occur over the first 5 days after the burn -indicators of a possible pulmonary damage; *hx indicating that burn occurred in an enclosed space *burns of the face and neck *singed nasal hair *hoarseness, voice change, dry cough, s tridor *bloody sputum

*Labored breathing or tachypnea *Erythema or blistering of the oral or pharyngea l mucosa -possible consequences will be respiratory failure and acute respirator y distress syndrome 4. Other Systemic Responses -hemolysis and muscle damage > r elease of hemoglobin and myoglobin > acute tubular necrosis and renal failure -d ecreased immune response > sepsis -loss of skin tissue > altered thermoregulatio n > hypothermia > later hyperthermia due to hypermetabolism -sympathetic hyperac tivity > paralytic ileus and Curlings ulcer

Management: 1. Emergent/ Resuscitative Phase of Burn Care A. On the scene Care -airway, brea thing and circulation -disability, exposure and fluid resuscitation -duration (f rom onset of injury to completion of fluid resuscitation -priorities: *first aid *prevention of shock *prevention of respiratory distress *detection and treatme nt of concomitant injuries *wound assessment and initial care

-emergency procedures at the burn scene: *extinguish the flames *cool the burn * remove restrictive objects *cover the wound *irrigate chemical burns B. Emergency Medical Management: -transport to the nearest hospital > life-savin g measures -ABC -humidification, bronchodilation, mucolytic agents, coughing -ET tube insertion and assisted ventilation -continuous positive airway pressure -a ssessment for head and neck injuries

-burn wound management -IV access, CVP insertion -indwelling urinary catheter in sertion -baseline data -tetanus prophylaxis -adequate pain relief C. Transfer to Burn Center D. Management of Fluid Loss and Shock -fluid replacement therapy -f luid requirements Problems Associated: >Acute Resp and Renal Failure >Distributi ve Shock > Compartment Syndrome

2. Acute or Intermediate Phase of Burn Care -begins 48 to 72 hours after the bur n injury -goals: A. Infection Prevention -Staphylococcus, Pseudomonas, Proteus, E. coli, and Klebsiella -Candida is also being implicated -3 characteristics of burn wound sepsis: *100,000 bacteria/gram of tissue *inflammation *sludging and thrombosis of dermal blood vessels -early enteral feeding can be used for preven tion

B. Wound Cleaning -hydrotherapy >use of tap water >temperature of water should b e maintained at 37.8C >room temperature should be maintained at 26.6-29.4C >shou ld be limited to a 20-30 minute period C. Topical Antibacterial therapy -criteri a for choosing antibiotics: *effective against gram negative organisms *clinical ly effective

*penetrates the eschar but without systemic toxicity *does not lose its effectiv eness *cost effective, available and acceptable *easy to apply -examples: 1. Sil ver sulfadiazine 2. Silver Nitrate 3. Mafenide Acetate D. Wound Dressing E. Dres sing Changes F. Wound Debridement -2 goals: *to remove tissue contaminated by ba cteria

*to remove devitalized tissue or burn eschar in preparation for grafting and wou nd healing G. Pain Management H. Nutritional Support

Shock -types: 1. Hypovolemic Shock 2. Cardiogenic Shock 3. Circulatory Shock (Distribu tive Shock) > Septic Shock > Neurogenic Shock > Anaphylactic Shock *Obstructive Shock -Effect of shock to normal cellular functions -Vascular Responses 1. Centr al Regulatory Mechanisms 2. Local Regulatory Mechanisms

-Blood Pressure Regulation BP= CO x TPR CO= SV x HR >Maintained by: a. nervous system b. endocrine system c . chemicals >Maintain tissue/organ perfusion: a. MAP= systolic BP + 2 (diastolic BP) 3 *should exceed 70-80 mmHg -Stages of Shock 1. Compensatory Stage >BP is m aintained within normal limits due to the effect of normally functioning regulat ory mechanisms

>s/sx: *metabolic acidosis *mental status change *tachypnea >medical management: a. identify the cause of shock b. correction of shock c. support of the regulat ory mechanisms >nursing management: a. monitoring tissue perfusion *LOC *urine o utput *V/S *skin *laboratory values

b. reducing anxiety c. promoting safety 2. Progressive Stage -exhaustion of the compensatory mechanisms *myocardial depression *increased capillary permeability -assessment and dxtic findings: a. respiratory effects hypoxemia and hypercarbi a intense inflammatory response decreased surfactant production acute respirator y distress syndrome (acute lung injury, shock lung, non cardiogenic pulmonary ed ema)

b. cardiovascular effects dysrhythmias myocardial infarction cardiac depression c. neurologic effects decreased cerebral perfusion *mental status change *behavi oral change *pupillary dilation d. renal effects MAP<80mmHg acute renal failure

e. hepatic effects decreased blood flow less ability to perform hepatic function s f. gastrointestinal effects decreased blood flow *PUD *bloody diarrhea *sepsis g. hematologic DIC shock

-medical management: a. depends on the type of shock b. depends on the decompens ation of the organ systems Management Common To All Types Of Shock a. optimize i ntravascular volume b. supporting the pumping action of the heart c. improving t he competence of the vascular system Nursing Management: a. preventing complicat ions b. promoting rest and comfort c. supporting family members

3. Irreversible Stage -severe organ damage -can no longer respond to treatment survival is less likely -medical management: a. same with the progressive stage -nursing management: a. same with progressive shock b. moral support to the fami ly c. ethical issues (living will)

Clinical Findings in the Stages of Shock Finding BP HR Compensatory normal >100bpm Progressive Systolic <80 -90mmHg >150b pm Rapid, shallow crackles Mottled, petechiae 0.5ml/kg/hr Lethargy Irreversible Mechanical or pharma support erratic, asystole Intubation Jaundice anuria, needs dialysis Coma Respiration >20 breaths/ min Skin Urine Output Mentation cold, clammy decreased confusion

Finding Compensatory Progressive Met Acidosis Irreversible Profound Acidosis A/B Balance Resp Alkalosis

HYPOVOLEMIC SHOCK -most common type of shock -characterized by decreased intrava scular volume of 15-25% -predisposing factors: External: Fluid Losses Internal: Fluid Shifts a. trauma a. hemorrhage b. surgery b. burns c. vomiting c. ascites d. diarrhea d. peritonitis e. diuresis e. dehydration f. diabetes insipidus

-medical management: >goals: a. restore intravascular volume b. redistribute flu id volume c. correct the underlying cause *pharmacologic therapy desmopressin an ti-emetic insulin anti-diarrhea -nursing management: a. administering blood and fluids safely

CARDIOGENIC SHOCK -due to cardiac failure -either coronary and non coronary Coro nary Factors Non Coronary Factors a. myocardial infarction a. cardiomyopathies b . valvular damage c. cardiac tamponade d. dysrhythmias -signs and symptoms: a. a nginal pain b. hemodynamic instability c. dysrhythmias -medical management: a. c orrection of underlying cause

b. initiation of first line treatment *supplemental oxygen *vasoactive medicatio ns *controlling chest pain *controlling HR *selected fluid support *mechanical c ardiac support c. pharmacologic therapy *dobutamine *nitroglycerine *dopamine *v asoactive meds *anti-arrhythmic meds d. fluid therapy -nursing management: a. pr eventing cardiogenic shock b. administering meds and IV fluids

c. maintaining mechanical devices d. enhancing safety and comfort CIRCULATORY SH OCK vasodilation maldistribution of blood volume decreased venous return decreas ed stroke volume decreased cardiac output decreased tissue perfusion A. Septic S hock -risk factors: a. immunosuppression

b. extremes of age d. chronic illness c. malnutrition e. invasive procedures -me dical management: a. pharmacologic therapy b. nutritional therapy -nursing manag ement: a. supportive to the medical management B. Neurogenic Shock -occurs due t o the loss of sympathetic tone -predisposing factors: a. spinal cord injury c. d epressant meds b. spinal anesthesia d. hypoglycemia

-medical management: a. restoring sympathetic tone -nursing management: a. eleva te the head of the bed 30 degrees ( in spinal/epidural anesthesia) b. immobilize the patient (in spinal cord injury) c. elastic compression stockings d. feet el evation e. heparin/low molecular weight heparin f. pneumatic compression of the legs g. passive ROM

C. Anaphylactic Shock antigen-antibody reaction brought about by severe allergic reaction provokes mast cells to release chemical mediators like histamine and b radykinin widespread vasodilatation and capillary permeability -predisposing fac tors: a. drug sensitivity c. bee sting allergy b. transfusion reaction d. latex sensitivity -medical management: a. removal of the causative agent b. restore va scular tone (epinephrine) c. antihistamines and bronchodilators

-nursing management: a. assess for previous hypersensitivity reactions b. preven tion of future exposure to antigens c. identification of new antigens d. patient education

RENAL DISEASES Terms: 1. aldosterone 2. antidiuretic hormone 3. anuria 4. bacter iuria 5. clearance 6. dysuria 7. frequency 8. GFR 9. hematuria 10. nocturia 11. oliguria 12. proteinuria 13. pyuria 14. Valsalva Leak Point Maneuver 15. vesicou reteral reflux Test of Urine Specific Gravity: 1. Osmolality 2. Specific gravity

Kidneys -retroperitoneal organs -120 170g -12cm long, 6cm wide and 2.5cm thick with 8 18 pyramids -with 4 -13 minor calyces -with 2 3 major calyces -with prote ctive structures: a. Pararenal fat b. Gerotas fascia c. Perirenal fat d. Renal ca psule

Nephron -basic structural and functional unit of the kidney

3 Processes of Urine Formation 1. Glomerular Filtration 2. Tubular Reabsorption 3. Tubular Secretion Renal function begins to decrease at a rate of 1% each year at 30. A. Acute Pyelonephritis -bacterial infection of the renal pelvis, tubule s and interstitial tissue -an ascending infection -predisposing factors: a. vesi co-ureteral reflux b. urinary tract obstruction

-enlarged kidney -with abscess on the renal capsule and at the cortico-medullary junction -s/sx: >fever and chills >costo-vertebral angle >leucocytosis tenderne ss >bacteriuria and >flank pain pyuria dysuria >inc. urinary frequency -dx: >UTZ >Nuclear scan >CT scan >IVP >Urine Culture & Sensitivity Test

Medical Management: a. uncomplicated -no dehydration, no nausea and vomiting, no sepsis >2 weeks of oral antibiotics Trimethoprim-Sulfamethoxazole Ciprofloxacin Gentamicin with or without Ampicillin Third Generation Cephalosporins >6 weeks of oral antibiotics if with relapse *urine culture 2 weeks after antibiotic ther apy b. complicated -pregnant patients >hospitalization (antibiotics from IV to o ral)

B. Chronic Pyelonephritis -repeated acute pyelonephritis >> chronic pyelonephrit is -no s/sx unless theres an acute exacerbation -kidneys scarred, contracted and non functional -signs and symptoms: fatigue polyuria headache excessive thirst a norexia weight loss -diagnosis: creatinine and BUN clearance creatinine levels i ntravenous pyelography

-complications: a. ESRD b. hypertension c. formation of renal stones -may be due to the presence of urea splitting microorganisms -medical management: a. urine culture and sensitivity guided antibiotic therapy Nitrofurantoin TMP-SMZ -nursin g management: a. monitoring -I&O b. oral fluids (3-4L/day)

c. symptomatic -antipyretics d. education -advise bed rest -prevention of UTI C. Acute Glomerulonephritis -primarily a disease of children older than 2 years ol d -may affect any age -causes: >autoimmune SLE >streptococcal Acute Post Strepto coccal Glomerulonephritis

Acute Post Streptococcal Glomerulonephritis -2 to 3 weeks after >impetigo >soret hroat -signs and symptoms: hematuria tea colored urine proteinuria inc serum BUN and c rea anemia edema hypertension headache, malaise, flank pain (+) kidney punch con gestion confusion, somnolence and seizures

Group A Beta-Hemolytic Streptococcal Infection Antigen-Antibody Reaction Deposit ion in the Glomerulus Increased Production of Epithelial Cells in the Glomerulus WBC Infiltration Thickening Scarring Decreased GFR -diagnosis: a. kidney biopsy b. electron microscopy c. immunoflourescence analysis

d. Anti-Streptolysin O Titer Anti-DNAse B Titer e. Serum Complement Determinatio n -decreased -will normalize in 2 8 weeks IgA Nephropathy -most common type of p rimary glomerulonephritis -Inc IgA; with normal serum complement -complications: a. Hypertensive Encephalopathy b. Heart Failure c. Pulmonary Edema

Rapidly Progressive Glomerulonephritis -patient deteriorates in weeks to months -course is more severe and more rapid Management To Glomerulonephritis Goals: 1. Treat symptoms 2. Preserve renal function 3. Treat complications a. antibiotics b. steroids c. cytotoxic agents d. protein restriction e. sodium restriction f. diuretics g. dialysis

D. Chronic Glomerulonephritis -components: repeated acute glomerulonephritis hyp ertensive nephrosclerosis hyperlipidemia chronic tubulo-interstitial injury hemo dynamically mediated glomerular sclerosis -contraction of the kidneys to 1/5 of its original size -deformed kidneys -may result to ESRD -signs and symptoms: may be asymptomatic hypertension inc BUN and Crea bipedal edema

retinal hemorrhages ophthalmoscopy papilledema weight loss weakness and irritabi lity nocturia GIT disturbances anemia heart failure peripheral neuropathy, decre ased DTR pulsus paradosus -diagnosis: 1. Urinalysis - fixed sp. Gravity at 1.010 proteinuria; urinary casts

2. serum chemistry -hyperkalemia -hypoalbuminemia -hyperphosphatemia -hypocalcem ia -hypermagnesemia 3. CBC -anemia 4. Chest X-Ray -cardiomegaly -pulmonary edema 5. ECG -left ventricular hypertrophy

-management: 1. treatment of hypertension 2. weight monitoring 3. give proteins of high biologic value 4. adequate calories 5. dialysis -nursing management: 1. monitoring E. Nephrotic Syndrome -components: proteinuria hyperlipidemia hypoalb uminemia

-causes: a. chronic glomerulonephritis b. diabetes mellitus c. amyloidosis d. SL E e. multiple myeloma f. renal vein thrombosis -signs and symptoms: edema (soft and pitting) -eyes, dependent area and abdomen malaise irritability headache fat igue

-diagnosis: 1. Urinalysis -proteinuria (3-3.5g/day) -inc WBC 2. Protein Electrop horesis Immunoelectrophoresis 3. Biopsy 4. AntiC1q antibodies (SLE) -complicatio ns: a. infection d. acute RF b. thromboembolism e. pulmonary emboli c. accelerat ed atherosclerosis

-management: 1. diuretics 2. ACE inhibitors 3. immunosuppressants 4. steroids 5. hypolipidemic agents 6. sodium restriction 7. CHON intake of 0.8g/kg/day low sa turated fats

Urolithiasis -stones or calculi in the urinary tract -supersaturation of substances such as c alcium oxalate, calcium phosphate and uric acid -signs and symptoms: >depends on : *the site of obstruction *edema *infection -assessment and diagnosis >IVP, Int ravenous Urography >Retrograde Pyelography >UTZ >serum chemistries and 24 urine tests

deficiency of citrate, mg nephrocalcin & uropontin dehydration infection Urolithiasis urinary stasis periods of immobility hypercalciuria and hypercalcemia

-causes of hypercalcemia and hypercalciuria: a. hyperparathyroidism b. renal tub ular acidosis c. cancers d. granulomatous disease e. excessive intake of Vitamin D f. excessive intake of milk and alkali g. myeloproliferative disease -substan ces other than calcium that may precipitate and form stones a. uric acid -5%-10% of renal stones -gout, myeloproliferative disorders

b. struvite -15% of renal stones -in persistently alkaline and ammonia rich urin e (caused by urease-splitting bacteria) -in neurogenic bladder, foreign bodies a nd recurrent UTI c. cystine -1%-2% of renal stones -hereditary defect in the ren al absorption -medicines that increases the risk of urolithiasis a. acetazolamid e d. laxatives b. Vitamin D e. high doses of aspirin c. antacids

-management: a. eradicate the stone b. determine the stone type c. prevent nephr on destruction d. control infection e. relieve any obstruction >Opioid Analgesic s NSAIDs >Hot Baths and Moist Heat to the flank area >Advise to increase oral fl uid intake (urine output of >2L/day is advisable)

-specific management: 1. Calcium stones -restrict proteins and sodium in the die t -acidify the urine using Ammonium chloride or Acetohydroxamic Acid -Cellulose sodium phosphate (binds calcium from food) -thiazide diuretics (if caused by inc PTH) 2. Uric Acid Stones -low purine diet (shellfish, mushrooms, asparagus, org an meats) -Allopurinol -alkalinize the urine

3. Cystine -low protein diet -penicillamine (to decrease excretion through the u rine) 4. Oxalate -dilute the urine -limit oxalate containing foods (spinach, str awberries, rhubarb, tea, peanuts and wheat bran) -surgical management: a. Ureteroscopy b. Extracorporeal Shock Wave Lithotripsy c . Percutaneous Nephrostomy or Nephrolithotomy

Acute Renal Failure -sudden and almost complete loss of renal function -signs and symptoms: *oliguri a *normal urine output *anuria *rising serum creatinine and BUN Categories of AR F 1. Prerenal -shock 2. Intrarenal -the result of actual parenchymal damage -use of nephrotoxic drugs (NSAIDs and ACE inh)

3. Postrenal -the result of an obstruction in the distal urinary tract Four Clin ical Phases of ARF 1. Initiation -begins with the initial insult and ends when o liguria develops 2. Oliguria -rise in the serum of waste products of metabolism -rise in serum potassium and magnesium 3. Diuresis -with gradually increasing ur ine output -renal function may still be markedly abnormal

4. Recovery Period -improvement of renal function -may take 3-12 months -with no rmal laboratory values -with permanent 1-3% reduction in GFR

Characteristics Etiology BUN value Prerenal Intrarenal Postrenal hypoperfusion parenchymal obstruction damage increased increased increased varie s, often decreased Increased, >40mEq/L Abnormal casts Increased Increased varies , may be decreased or anuria Varies, often <20mEq/L Usually normal Creatinine value increased Urine output decreased Urine sodium Decreased, <20mEq/L Normal, few hyaline casts Urinary Sediment

Characteristics Prerenal Urine osmolality Increased to 500mOms Urine specific In creased gravity Intrarenal Abnormal casts and debris Low normal, 1.010 Postrenal Usually normal Varies

-associated problems: *metabolic acidosis *hyperphophatemia and hypocalcemia *an emia -prevention: *prevention of exposure to nephrotoxic drugs -aminoglycosides, cyclosporine, amphotericinB *serum BUN and creatinine monitoring -management: a . restore chemical balance and prevent complications b. identification and treat ment of the underlying cause c. maintain fluid balance -BP, CVP, serum and urine elect., fluid loses

d. monitoring for over hydration -dyspnea, crackles, distended neck veins -Furos emide, Ethacrynic Acid e. dialysis -to prevent serious complications *hyperkalem ia *severe metabolic acidosis *pericarditis *pulmonary edema f. pharmacologic -c ation exchange resin (sodium polystyrene sulfonate-kayexalate)

-retention enema -diuretic therapy -low dopamine dose (1-3g/kg) -phosphate bindi ng agents (AlOH) g. nutritional therapy -give additional proteins (1g/kg/day dur ing the oliguric phase) -high potassium and phosphate foods are restricted (bana na, citrus and coffee) -potassium restricted to 20-40mEq/day -sodium restricted to 2g/day -may require parenteral nutrition

-nursing management: a. monitoring fluid and electrolyte balance b. reducing met abolic rate -bed rest, prevention of fever and infection c. promoting pulmonary function -assistance in changing positions -advise to cough and deep breath d. p reventing infection -asepsis -avoid inserting an indwelling urinary catheter e. providing skin care f. providing support

Chronic Renal Failure -is a progressive irreversible deterioration in renal func tion -with uremia or azotemia (severity of build up will be proportional to the severity of s/sx) -prognosis will be determined by the presence or absence of hy pertension and proteinuria -causes: *diabetes mellitus- most common *hypertensio n *chronic glomerulonephritis *obstruction of the urinary tract *polycystic kidn ey disease *infections

- stages: Stage 1 -Reduced Renal Reserve -40%-75% loss of nephron function -usua lly asymptomatic Stage 2 -Renal Insufficiency -75%-90% loss of nephron function -increase in serum BUN and creatinine -inability to concentrate urine -anemia ma y develop -with polyuria and nocturia

Stage 3 -End Stage Renal Disease -<10% of nephron function remaining -regulatory , excretory and hormonal functions are lost -requires dialysis -signs and sympto ms: cardiovascular *hypertension *pulmonary edema *heart failure *pericarditis d ermatologic *pruritus *uremic frost (deposit of urea crystals) GI and Neurologic s&sx

-assessment and diagnosis a. glomerular filtration rate creatinine clearance b. serum electrolytes c. ABG d. CBC -complications a. Hyperkalemia b. Pericarditis, Pleural Effusion and Cardiac Tamponade c. Hypertension d. Anemia e. Bone Diseas e

-medical management: a. maintain kidney function and homeostasis b. treat the un derlying cause and contributory factors >medications >dialysis >diet therapy 1. Pharmacologic Therapy a. antihypertensives > includes intravascular volume contr ol *fluid restriction *sodium restriction b. sodium bicarbonate c. erythropoieti n >will achieve a Hct of 33%-38%

>IV or SC 3x a week >takes 2-6 weeks to increase Hct >A/R: *hypertension *increa sed clotting of vascular access sites *seizures *depletion of body iron stores d . iron supplementation e. antiseizure agents >Diazepam >Phenytoin f. antacids

>aluminum based antacids neurologic symptoms osteomalacia >calcium carbonate 2. Nutritional Therapy -regulation of protein intake -regulation of fluid intake (5 00-600ml more than the previous days 24 hour UO) -regulation of sodium intake -re gulation of potassium -adequate calories and vitamins 3. Dialysis -to prevent hy perkalemia

-nursing management: a. avoid the complications of reduced renal function b. ass ess fluid status c. identify potential sources of the imbalance d. implement a d ietary program e. encourage self care and independence

Cardiovascular System Definition of Terms 1. Preload venous blood return; degree of stretch of cardiac muscle fibers at the end of diastole 2. Afterload BP in a rtery; amt of resistance to ejection of blood from ventricle 3. Depolarization a ctive; caused by entry of Na while K exits cell 4. Repolarization rest; caused b y reentry of K to the cell while Na exits 5. Systole blood supply to all except the heart; ventricular contraction from ejection of blood from ventricles to pul monary artery and aorta

6. Diastole blood supply to the heart; period of ventricular relaxation resultin g in ventricular filling 7. Cardiac Output blood volume per minute; normal = 5L/ min (resting adult heart) 8. Stroke Volume blood volume per contraction; normal = 70mL (resting heart) 9. Baroreceptors nerve fibers located in the aortic arch and carotid arteries that are responsible for reflex control of BP 10. Postural/ Orthostatic Hypotension result to syncope (blood drops to brain = faint); usual ly 10mmHg systolic or more

Anatomy and Physiology 1. Heart Valves 2. Heart Chambers 3. Coronary Arteries 4. Cardiac Muscle 5. Cardiac Conduction System 6. Cardiac Hemodynamics >Cardiac Pr essures *right ventricular systole (15-25mmHg) *PA diastolic pressure (8-15mmHg) *left v entricular systole (110-130mmHg) *resting aortic pressure (80mmHg)

*4-12mmHg on both ventricles and atria at the end of diastole 7. Cardiac Output preload afterload stroke volume contractility baroreceptors heart rate Gender Differences 1. resting rate 2. stroke volume 3. ejection fraction higher in women

4. conduction time is briefer in women 5. arteries occlude more easily in women with atherosclerosis 6. effects of estrogen in cardiovascular system of women -r egulation of vasomotor tone -response to vascular injury -good liver function -i ncreased coagulation proteins -decreased fibrinolytic substances Diagnostic Work -ups Purposes: 1. to aid in the diagnosis of diseases 2. for prognostication 3. to screen patients at risk of diseases

4. monitor serum concentration of meds 5. monitor therapeutic effects of meds A. Cardiac Enzymes >Creatine Kinase (CK) *MB -most specific enzyme for MI -first e nzyme level to rise in MI *MM and BB -other isoenzymes >Lactate Dehydrogenase -p eaks 2-3days after MI >Myoglobin -starts to increase 1-3hours after MI; 4-12hour s (peak)

>Troponin I -contractile proteins found in cardiac muscles only -starts to rise 3-4 hours after MI -peaks in 4-24 hours and remain elevated for 1-3 weeks B. Blo od Chemistry >Lipid Profile *Total Cholesterol -should be less than 200mg/dl *Se rum Lipoproteins LDL - should be less than 130mg/dl HDL - should be 35-65mg/dl i n men - should be less than 35 to 85mg/dl in F TAG - should be 40-150mg/dl

Factors that may elevate TAG level: 1. obesity 2. alcohol use 3. diabetes Factor s that contribute variations in cholesterol level: 1. age 4. exercise 7. tobacco use 2. gender 5. genetics 8. stress level 3. diet 6. menopause Factors that low er HDL level 1. smoking 4. physical inactivity 2. diabetes 3. obesity

>Serum Electrolytes >BUN and Creatinine >Serum Glucose Level C. Coagulation Stud ies >PTT -effects of Heparin therapy -intrinsic pathway -1.5 to 2.5x of their ba seline values >PT -effects of Warfarin therapy -extrinsic pathway -2.5-3.5x (INR )

D. Hematologic Studies >CBC -WBC monitoring in immunocompromised patient after h eart transplantation -associated anemia will aggravate CAD E. Chest X-Ray -for t he evaluation of the size, position and contour of the heart -cardiac and perica rdial calcification F. ECG >Continuous ECG Monitoring a. Hardwire Cardiac Monito ring b. Telemetry c. Transtelephoning

G. Cardiac Stress Testing a. Exercise Stress Test -by using a treadmill or stati onary bike b. Pharmacologic Stress Test -by using Dipyridamole or Adenosine c. E motional Stress Test Purposes of Cardiac Stress Test >to evaluate CAD >to determ ine the cause of chest pain >to assess the functional capacity of the heart afte r MI or surgery >to evaluate the effectiveness of anti-anginal drugs >to evaluat e dysrhythmias after physical exercise >to determine specific goals for a fitnes s program

H. Echocardiography -to determine: a. pericardial effusions b. etiology of heart murmurs c. function of prosthetic heart valves d. chamber size e. ventricular w all motion *Transesophageal Echocardiography -with 6 hours of fasting prior -IV line -with local anesthetic and sedation -BP and ECG monitoring

-after the study: extension of fasting for another 4 hours monitoring for 30 60 minutes sorethroat for the next 24 hours I. Radionuclide Imaging >to evaluate: a . coronary artery perfusion b. myocardial ischemia and infarction c. left ventri cular function >uses: Thallium 201 emits gamma rays Technetium 99m detected by s cintillation camera

>types: a. Myocardial Perfusion Imaging b. Computed Tomography c. Positron Emiss ion Tomography d. Magnetic Resonance Imaging J. Cardiac Catheterization -cathete r advancement guided by fluoroscopy -to measure oxygen saturation and pressures on right and left side of the heart -needs: a. IV line b. BP and ECG monitoring c. resuscitation equipment at bedside -uses contrast agent (iodine based)

-complications: (right sided cardiac catheterization) a. dysrhythmias d. cardiac perforation b. venous spasm e. cardiac arrest c. infection -complications: (lef t sided cardiac catheterization) a. dysrhythmias d. systemic embolization b. MI c. perforation -nursing interventions (pre-op) 1. fasting for 8 12 hours 2. expl ain that the procedure will take 2 hours or less 3. with mild to moderate sedati on 4. explain the anticipated sensations (flushing,

5. ask the patient to breath deeply or hold the breath >to lower the diaphram fo r better visualization >ask the patient to cough (to disrupt a dysrhythmia and t o clear the contrast agent from the arteries) -nursing interventions (post-op): 1. observe the site for bleeding and hematoma 2. assess peripheral pulses on the same ext q 15mins for 4 hours then q 1 2 hours 3. evaluate temperature and colo r of the affected extremity 4. ask the patient to report signs and symptoms of a rterial insufficiency (pain, numbness and tingling)

5. monitor for dysrhythmias and vasovagal reaction *bradycardia >may be *hypoten sion precipitated by a *nausea distended bladder >prompt interventions: -raise t he feet and legs -administer IVF and IV atropine 6. explain that the patient sho uld be in supine position for 2 6 hours 7. analgesics 8. report chest pain, blee ding and sudden discomfort 9. increase fluid intake to flush out the dye 10. wat ch out for orthostatic hypotension

Hemodynamic Monitoring 1. Central Venous Pressure 2. Pulmonary Artery Pressure 3 . Intra-arterial BP Monitoring Central Venous Pressure -pressure in the vena cav a or right atrium is used to: a. assess right ventricular function b. venous blo od return to the right side of the heart -nursing interventions: a. application of dry, sterile dressing -should be dry and occlusive b. chest x-ray to confirm placement c. daily inspection for signs of infection (complication)

d. watch out for air embolism (complication) e. maintenance of the transducer in phlebotactic axis *normal range: 0 8 mmHg >>> Pressure Monitoring System 3 8 cm H2O >> Water Manometer System Pulmonary Artery Pressure Monitoring -assessment o f left ventricular function -etiology of shock -response to vasoactive medicatio ns -can measure: 1. CVP or right atrial pressure 2. pulmonary artery systolic an d diastolic pressure (25/9 mmHg)

3. Mean Pulmonary Artery Pressure (15mmHg) 4. Pulmonary Artery Wedge Pressure (4 .5 to 13 mmHg) -nursing interventions: a. Maintenance of the transducer at phleb otactic axis b. Watch out for complications: -infections -pulmonary artery ruptu re -pulmonary thromboembolism -pulmonary infarction -catheter kinking -dysrhythm ias -air embolism

Intra-arterial BP Monitoring -direct and continuous BP measurements -ABG measure ments -to obtain blood samples *after selection of an area (site)>> assess colla teral circulation a. Allens test b. Doppler test -nursing interventions: a. obser ve asepsis b. watch out for complications: -local obstruction with distal ischem ia -external hemorrhage -massive ecchymosis

-dissection -air embolism -blood loss -pain -arteriospasm -infection Hypertension -terms related: >hypertensive emergency >hypertensive urgency >rebound hypertens ion -types: a. Primary Hypertension b. Secondary Hypertension

-BP monitoring: *normal BP >> *high normal >> *first stage >> *second stage >> * third stage >> -as a sign -as a risk factor -as a disease -risk factors: a. smok ing b. dyslipidemia c. diabetes mellitus recheck in 2 years recheck in 1 year confirm in 2 months confirm in 1 month conf irm immediately d. age older than 60 years e. gender (men) f. family history of CVD

-hypothesis: a. increased sympathetic activity b. renin-angiotensin-aldosterone system c. increased absorption of chloride d. decreased vasodilation of arteriol es -complications: a. myocardial infarction b. heart failure c. renal failure d. stroke/ cerebro-vascular accident e. impaired vision -gerontologic consideratio ns: a. accumulation of atherosclerotic plaque

b. fragmentation of arterial elastins c. increased collagen deposits d. impaired vasodilatations -diagnosis: a. urinalysis f. creatinine clearance b. blood chem istry g. renin level c. 12-lead ECG h. 24 hour urine protein d. chest x-ray e. e chocardiography -medical management: a. pharmacologic therapy b. dietary therapy

-nursing interventions: a. patient education >avoid risk factors >promote health y lifestyle

Peripheral Arterial Occlusive Disease -usually involves the segment of the aorta below the renal artery to the popliteal artery -risk factors: a. age (elderly) b. diabetes mellitus -clinical manifestations: a. intermittent claudication b. c oldness or numbness of the affected extremity c. skin and nail changes d. ulcera tions and gangrene e. bruits f. diminished to absent peripheral pulses g. muscle atrophy

-medical management: a. pharmacologic therapy *Pentoxyphylline -increases RBC fl exibility and decreases blood viscosity *Cilostazol -inhibits platelet aggregati on -increases vasodilatation -inhibits smooth muscle proliferation *Aspirin, Tic lopidine, Clopidogrel -antiplatelets b. surgical management: vascular grafting e ndarterectomy

-nursing management: a. maintain circulation *doppler *pulses *color q 1 hour x 8 hours *temperature q 2 hours x *capillary refill 24 hours *motor and sensory b . monitoring for potential complications *urine output *CVP & PR *mental status *hematoma

c. avoidance of leg crossing or dependency of the lower extremity d. reduce edem a -elevate the affected extremity -exercise e. stockings -may not be necessary U pper Extremity Arterial Occlussive Disease -due to: a. atherosclerosis b. trauma -clinical management: a. forearm claudication b. poor motor function

-diagnosis a. difference of 20mmHg of BP between 2 arms b. duplex ultrasonograph y c. transcranial doppler evaluation -management: a. surgery *PTA *carotid to su bclavian artery bypass *axillary to axillary bypass *autogenous reimplantation o f the subclavian to carotid artery Aneurism Aortic Dissection Raynauds Phenomenon

Deep Vein Thrombosis Venous thrombosis Thrombophlebitis/ Phlebothrombosis -of unknown cause -with predisposing factors: (Virchows triad) A. stasis of blood >heart failure >vasodilators >shock >immobility B. vessel wall injury >trauma > chemical irritation C. altered blood coagulation >abrupt withdrawal from anticoa gulants

>OCP >severe blood dyscrasias -manifestations: a. nonspecific b. phlegmasia ceru lea dolens >massive iliofemoral venous thrombosis >entire extremity is massively swollen, tense, painful and cool to touch *deep vein involvement -edema of the affected extremity -affected extremity is warmer to touch -tenderness

*superficial vein involvement -pain -redness -tenderness -warmth -assessment a. history >varicose veins >obese >hypercoagulation >elderly >neoplastic disease >O CP >cardiovascular disease >recent major surgery b. physical assessment -prevent ion a. application of elastic compression stockings

b. use of intermittent pneumatic compression device c. positioning d. exercise medical management 1. anticoagulation therapy a. unfractionated heparin -sc or i v (intermittent infusion) for 57days -given with Warfarin -coagulation study mon itoring b. low molecular weight heparin -with longer half life

-can be used in pregnant women -less toxic c. thrombolytic therapy -alteplase, r eteplase, t-PA streptokinase -should be given within the first three -effects le ss significant after 5 days -surgical management >when pharmacologic therapy is contraindicated a. thrombectomy b. vena cava filter -nursing management a. asses sing and monitoring anticoagulant therapy

b. monitoring and managing potential complications >bleeding >thrombocytopenia > drug interactions c. provide comfort >bed rest >elevation of the leg >elastic co mpression stockings >analgesics >application of warm moist packs d. intermittent pneumatic compression devises >with 35 to 55 mmHg

e. positioning >feet higher than the heart f. exercises >passive then active exe rcises >deep breathing exercises >early ambulation *avoid sitting for more than 2 hours *walking for at least 10minutes every after 2 hours

Varicose Veins -abnormally dilated, tortuous, superficial veins caused by the incompetent venou s valves -may occur in the lower extremities and esophagus -predisposing factors >old age >pregnancy >prolonged standing >genetic predisposition -has 2 types: a . primary -without involvement of the deep veins

b. secondary -resulting from the obstruction of the deep veins -manifestations > dull aches >increased muscle >muscle cramps fatigue >ankle edema >feeling of hea viness -assessment a. duplex scan b. air plethysmography c. venography

-prevention a. avoidance of wearing tight socks or constricting panty girdle b. avoidance of crossing the thighs c. avoidance of prolonged standing d. frequent position changes e. elevating the affected extremity when tired f. walking 1 to 2 miles each day g. using the stairs instead of elevators h. elastic compression stockings i. weight reduction planning -management >surgery

>sclerotherapy -with application of elastic compression bandages for 5 days

Acquired Valvular Disorders Mitral Valve Prolapse ve balloons back into tomatic -palpitations n -dizziness -anxiety s -usually produces no symptoms -mostly in women -mitral val the left atrium during systole -signs and symptoms: -asymp -shortness of breath -syncope -light headedness -chest pai -diagnosis: -mitral clicks -murmur of mitral regurgitation

-medical management: a. symptomatic b. elimination of stimulants c. anti-arrhyth mic meds d. beta blockers/ calcium channel blockers -nursing management: a. cond ition can be genetically transmitted b. use of prophylactic antibiotics -for pat ients with systolic click and a murmur c. instruct to avoid stimulants d. diet, activity and sleep

Mitral Regurgitation -signs and symptoms: a. chronic- asymptomatic b. acute - se vere congestive heart failure dyspnea fatigue most common symptoms weakness palp itations shortness of breath on exertion cough -diagnosis: a. systolic murmur b. echocardiography

-medical management: similar to congestive heart failure Mitral Stenosis -causes rheumatic endocarditis -signs and symptoms: >dyspnea on exertion >fatigue (low cardiac output) >hemoptysis >cough -diagnosis: >weak pulses

>diastolic murmur -low pitched rumbling sound at the apex >echocardiography >ECG and cardiac catheterization with angiography -to determine the severity of mitr al stenosis -medical management: a. prophylactic antibiotics b. anticoagulants c . treatment of CHF d. surgery -valvuloplasty -valve replacement

Aortic Regurgitation -causes: >endocarditis >syphilis >dissecting aneurism >dete rioration of an aortic valve replacement -signs and symptoms: >asymptomatic >for ceful heart beat (head and neck) exertional dyspnea and fatigue signs of left ve ntricular failure -diagnosis: >diastolic murmur (high pitched blowing sound)

>widened pulse pressure >water hammer pulse >echocardiography, ECG, MRI and card iac catheterization -medical management: a. antibiotic prophylaxis b. valvulopla sty or valve replacement Aortic Stenosis -cause: *rheumatic endocarditis -signs and symptoms: >asymptomatic

>exertional dyspnea >dizziness due to left ventricular failure >syncope >chest pain -diagnosis: >systolic murmur -loud, rough -crescendo-decres cendo >12 lead ECG > echocardiography

-management: a. antibiotic prophylaxis b. valvuloplasty c. valve replacement

Cardiac Dysrhythmias Sinus Node Dysrhythmias 1. Sinus Bradycardia -causes: *lowe r metabolic needs (hypothyroidism, hypothermia, sleep) *vagal stimulation (vomit ing, suctioning, extreme pain) *medications (calcium channel blockers, beta bloc kers) *increased intracranial pressure *myocardial infarction -treatment: *atrop ine sulfate *catecholamines

2. Sinus Tachycardia -causes: *acute blood loss *pain *anemia *hypermetabolic st ate *shock *fever *hypervolemia *anxiety *hypovolemia *sympathomimetic meds *con gestive heart failure -decreased diastolic filling decreased cardiac output -syn cope -acute pulmonary edema -decreased BP

-management: a. Ca channel blockers b. Beta blockers 3. Sinus Arrhythmias -no si gnificant hemodynamic effects -not treated usually Atrial Dysrhythmias 1. Premat ure Atrial Complex -begins before the next impulse of the SA node -causes: >caff eine, alcohol nicotine >stretched atrial myocardium

>anxiety >hypokalemia >hypermetabolic state >atrial ischemia, injury or infarcti on -management: >directed toward the cause 2. Atrial Flutter -only at the atrium at a rate of 250-400/minute -therapeutic block at the AV node -causes: >advance d age >hypertension >valvular heart disease >cardiomyopathy >coronary artery dis ease >hyperthyroidism

>pulmonary disease >acute moderate to heavy ingestion of alcohol (holiday heart syndrome) >aftermath of open heart surgery -signs and symptoms: *chest pain *low BP *shortness of breath -management: >electrical cardioversion >if stable -digi talis -beta blockers -calcium channel blockers

3. Atrial Fibrillation -rapid, disorganized and uncoordinated twitching of atria l musculature -with decreased stroke volume -with decreased diastole >> decrease d coronary artery perfusion >> increase the risk of myocardial ischemia -increas ed risk of thrombus formation within the atria >> embolism -2 to 5x increased ri sk of stroke -same causes as with atrial flutter -s/sx: *irregular palpitations *malaise

-treatment: >same as with atrial flutter >cardioversion (if present in less than 48 hours unless the patient is on anticoagulant treatment) >anti-arrhythmic med s: -amiodarone, flecainide, ibutilide >adenosine (treatment and diagnosis) >pace maker insertion Ventricular Dysrhythmias 1. Premature Ventricular Complex -an im pulse that starts at the left ventricle and is conducted through the ventricles before the next normal sinus impulse -causes: *caffeine, nicotine and alcohol

*cardiac dysrhythmias and infarction *increased workload to the heart (exercise, fever, hypervolemia, heart failure, tachycardia) *digitalis toxicity *hypoxia, acidosis *electrolyte imbalances (hypokalemia) -with danger of ventricular tachy cardia if with MI -bigeminy, trigeminy -signs and symptoms: >asymptomatic >with s kipped beats -treatment: >treat the cause Lidocaine- short term and immediate th erapy

2. Ventricular Tachycardia -3 or more PVCs in a row occurring at a rate exceedin g 100 beats/minute -causes are similar to PVCs -usually associated with CAD prec eding to PVC -an emergency: pulseless and unresponsive -treatment: >if stable: attach to ECG >if unstable: -cardioversion or defibrillation 3. Ventricular Fibr illation -rapid but disorganized ventricular rhythm -no atrial activity

-causes: >electrical shock >brugada syndrome -normal heart, few or no risk facto r for CAD, and a family history of sudden cardiac death -signs and symptoms: >no heartbeat >no pulse >no respiration -management: >immediate defibrillation >vas oactive meds >anti-arrhythmic meds 4. Ventricular Asystole

HEMATOLOGY Hematologic System 1. Blood a. Plasma -albumin -globulin -fibrinogen -electrolyt es -waste products b. cellular component -RBC -WBC -platelets 2. Reticulo-endoth elial -liver -spleen -bone marrow

Functions of the blood a. carrier -oxygen and nutrients -waste products b. hemos tasis Hematopoiesis a. intramedullary b. extramedullary RBC -approximately 8 mic rometers -flexible, can pass through a small blood vessel -made up of hemoglobin (95% of cell mass)

Erythropoietin -response to low RBC count -stimulate the BM -for erythropoiesis >requires iron, folic acid, pyridoxine and cyanocobalamin Iron Stores and Metabo lism -diet: >10-15 mg of elemental iron/day in a well balanced diet >only 0.5 to 1 mg is absorbed >> transferrin >> normoblast >> hemoglobin -total body iron co ntent: >3 grams

-normal concentration value: >75-175ug/dl for males >65-165 ug/dl for females Vi tamin B12 and Folic Acid Metabolism -required in the synthesis of DNA ANEMIA 3 B road Causes: 1. loss of RBC 2. inadequate production 3. increased destruction 1. Types of Anemia due to decreased production of RBC a. Iron Deficiency Anemia C. Folate Deficiency b. Vitamin B12 deficiency D. Dec. Erythropoietin

2. anemia due to blood loss 3. Types of anemia due to increased destruction (hem olytic) a. altered erythropoiesis >sickle cell anemia >thalassemia >hemoglobinop athies b. hypersplenism c. drug induced anemia d. autoimmune anemia Clinical man ifestations: (fatigue- most common) >severity depends on: 1. speed with which an emia has developed

2. duration of anemia 3. metabolic requirements of the individual 4. presence of other disorders Complications: 1. Congestive Heart Failure 2. Paresthesia 3. Co nfusion Nursing Diagnosis: 1. Activity Intolerance related to Fatigue, Weakness and Generalized Malaise 2. Altered Nutrition: Less than body Requirements relate d to Inadequate Intake of Essential Nutrients 3. Altered Tissue Perfusion r/t In adequate Blood Volume

Nursing Interventions: 1. Managing fatigue -the most frequent symptom and compli cation -profound impact on ones level of functioning and quality of life 2. Main tain adequate nutrition -well balanced diet -avoidance of alcohol -dietary teach ing -dietary supplements 3. Maintain adequate perfusion -transfusion -supplement al oxygen/vital signs monitoring

4. Complying with prescribed therapy 5. Monitoring and managing potential compli cations a. CHF b. paresthesia c. confusion Hypoproliferative Anemias Iron Defici ency Anemia -causes: >decreased dietary intake of iron >blood loss *menorrhagia *PUD (alcoholics)

-clinical manifestations: >smooth, sore tongue >brittle and ridged nails >angula r cheilosis -diagnosis: a. BMA b. serum ferritin/TIBC c. peripheral blood smear (dec MCV) d. CBC (dec Hgb and Hct) -management: a. Iron supplementation (Ferrous SO4, Ferrous Fumarate or Ferrous Gluconate) -should be taken for 6-12 months

*if oral iron preparation is not tolerated, give iron g Management: 1. Diet -should take foods rich in iron vegetables *beans *raisins -should take foods rich in an empty stomach -if with GI distress, take with food creased by 50%) -liquid oral iron preparation

dextran (IM or IV) -Nursin *organ meats *green leafy vitamin C -take iron with (but absorption will be de

Anemia in Renal Disease -ESRD: >less likely to develop unless serum creatinine e xceeds 3mg/dl -Dialysis: >may lose blood into the dializer >> folic acid deficie ncy and iron deficiency -Management: 1. Recombinant Erythropoietin >A/R: HPN- ma y inc Hct by 33-38% (dose needs to be titrated and administer antiHPN) 2. Oral i ron and folic acid supplementation

Anemia of Chronic Diseases -due to chronic disease of inflammation, infection an d/or malignancy -mild to moderate anemia -insidious onset over a period of 6-8 w eeks -Hct seldom less than 25% -Hgb seldom less than 9 g/dl -erythropoietin leve ls are low -moderate shortening of the RBC lifespan -management: >no need >treat ment of the underlying cause

Aplastic Anemia -may lead to pancytopenia -damage to the BM stem cells -replacem ent of the marrow with fat -also has neutropenia and thrombocytopenia -forms: >c ongenital >idiopathic >acquired -clinical manifestations: (insidious onset) >inf ection >anemia >bruising

-causes: 1. chemicals -pesticides -glue 2. medications -antimicrobials (Chloramp henicol) -gold compounds -sulfonamides -assessment and diagnosis: 1. BMA -medica l management: 1. BM transplant or Peripheral Stem Cell Transplant 2. Immunosuppr essive therapy

3. Withdrawal of the offending agent 4. RBC and platelet transfusion Megaloblast ic Anemia -may lead to pancytopenia -due to vitamin B12 and Folic Acid Deficienc y (abnormal DNA synthesis) -Hgb may be as low as 4-5 gm/dl -WBC count may be as low as 2000-3000/mm3 -platelet count of less than 50000/mm3 -RBC (increase in MC V) Folic Acid Deficiency -causes: *depletion in 4 months time without sufficient folic acid in the diet (green leafy vegetables and liver) *increased folic acid requirement (pregnancy,

alcoholism and chronic blood loss) Cyanocobalamin deficiency -causes: *strict ve getarians (no meat or dairy products) *absence of intrinsic factor *faulty absor ption in the ileum Clinical manifestations: a. Hemolytic s/sx -unique to vit B12 def b. GI and Nervous system effects Assessment and Diagnostic Findings: a. Sch illing Test

-medical management: a. increase folic acid in the diet and take 1 mg of folic a cid daily (IM for patients with malabsorption) b. Vit B12 replacement -oral supp lements -fortified soy milk *if with intrinsic factor deficiency and malabsorpti on, monthly IM injection of cyanocobalamin at a dose of 1000ug -nursing manageme nt: a. mild jaundice b. vitiligo c. premature graying of the hair

d. smooth, red and sore tongue e. unstable gait f. impaired position and vibrati on sense Myelodysplastic Syndrome -is a group of disorder of myeloid stem cells causing dysplasia of one or more cell types -most common feature is the dysplasi a of the RBCs >> macrocytic anemia (WBC & platelets may be affected) -may evolve into Acute Myeloid Leukemia -types: a. Primary >more than 80% (elderly) b. Seco ndary

-clinical manifestations: a. variable -assessment and diagnosis: a. CBC >RBC, WB C & platelets are decreased b. decreased serum erythropoietin -medical managemen t: a. bone marrow transplantation b. blood transfusion (needs chelation of iron) c. platelet transfusion d. growth factors (G-CSF) e. erythropoietin

-nursing management: 1. prevention of infection 2. instructions on the risks of bleeding *chelation therapy is best administered as a subcutaneous infusion over 10-12 hours often at night *close monitoring of lab values for anticipation of transfusion and determination of response to growth factors Hemolytic Anemias Sickle Cell Anemia -a result of inheritance of sickle hemoglobin gene -sickled H gb *crystal formation when exposed to low oxygen tension, deformed, rigid and si ckled RBC > ischemia & infarction

-sickling process is intermittent (with exposure to low oxygen tension and cold environment) -assessment and diagnostic findings >sickle cell trait: *normal RBC *normal WBC *normal platelets >sickle cell anemia *decreased Hct *sickled cells on smear -confirmatory test: Hemoglobin electrophoresis

-clinical manifestations: *Hgb 7-10mg/dl *jaundice *enlargement of the bones of the face and the skull *tachycardia, cardiac murmurs and enlarged heart *dysrhyt hmias and heart failure *susceptible to infection primarily pneumonia and osteom yelitis *chronic hemolysis and thrombosis >> ischemia and necrosis of organs wit h slowed circulation (spleen, lungs and CNS) -complications: 1. stroke

2. infection 3. renal failure 4. impotence 5. heart failure 6. pulmonary hyperte nsion Sickle Cell Crisis -3 types: 1. Very painful sickle cell crisis > due to t issue hypoxia and necrosis 2. Aplastic crisis > due to infection of human parvov irus > Hgb decreases rapidly that the BM cannot compensate

3. Sequestration Crisis >pooling of sickled cells in an organ *spleen >> splenic infarction >> autosplenectomy Acute Chest Syndrome -decreased hemoglobin and he matocrit (rapid) -fever -tachycardia -bilateral chest film infiltrate -causes: diagnostic tests: *infection *CXR *fat embolism *incentive spirometry -treatment : *bronchoscopy *antibiotics *phospholipase A2 det

*fluid restriction *corticosteroid *transfusion >decreases phospholipase A2 -pro gnosis: >usually diagnosed during childhood -medical management: >3 treatment mo dalities: a. BM transplantation b. Hydroxyurea *increases the concentration of f etal Hgb *decreases vaso-occlusive crisis c. Long term RBC transfusion

Adverse Effects of Hydroxyurea 1. chronic suppression of WBC formation 2. terato genesis 3. potential for later development of pregnancy Complications of Transfu sion 1. Iron Overload -needs chelation therapy 2. poor venous access 3. alloimmu nization due to repeated transfusion *exchange transfusion Treatment: 1. Support ive >pain management

*folic acid supplementation 2. Prompt use of antibiotics -nursing diagnosis: 1. Pain related to tissue hypoxia 2. Risk for infection 3. Powerlessness related to illness induced powerlessness 4. Knowledge deficit regarding prevention of cris is -goals: 1. Relief of pain 2. Decreased incidence of crisis 3. Enhanced self e steem and power 4. Absence of complications

-nursing interventions: 1. Management of pain 2. preventing and managing infecti ons 3. promoting coping skills 4. Minimizing knowledge deficit 5. Monitoring and managing potential complications -leg ulcers -priapism leading to impotence -ch ronic pain and substance abuse Thalassemias -a hereditary disorder associated wi th defective hemoglobin chain synthesis -characterized by microcytosis and hypoc hromia

-imbalance in the configuration of hemoglobin >> increased rigidity of RBC >> he molysis -2 types: (according to the globin chain diminished) a. alpha thalassemi a -milder and often without symptoms b. beta thalassemia -more severe and lethal Alpha Thalassemia Clinical Syndromes: 1. Silent Carrier -asymptomatic -deletion of a single alpha globin gene

-barely detectable reduction in alpha globin gene synthesis 2. Alpha Thalassemia Trait -deletion of 2 globin gene -minimal or no anemia and no abnormal physical signs 3. Hemoglobin H Disease -deletion of the 3 out of 4 alpha globin gene -he moglobin H has extremely high O2 affinity and therefore not useful for O2 exchan ge -with moderately severe anemia 4. Hydrops fetalis -most severe form -deletion of the 4 alpha globin gene

-in the fetus > gamma globin chains in excess form tetramers (hemoglobin Bart) > extremely increased oxygen affinity > unable to deliver oxygen to the tissues > severe anoxia Beta Thalassemia Clinical Syndromes: 1. Thalassemia Major -lead t o severe transfusion dependent anemia -severe anemia and first become manifested 69mos after birth (hemoglobin synthesis switches from HgbF to HgbA) -if untrans fused, Hgb may range between 36gm/dl (with marked anisocytosis and microcytic, h ypochromic anemia)

-aggregated alpha chains are taken up by the spleen -increased reticulocytes but erythropoiesis is ineffective -clinical course: short or brief because of death at an early age 2. Thalassemia Minor -resistant against falcifarum malaria -asy mptomatic and anemia is mild if present G6PD Deficiency (G6PD is essential for m embrane stability) -would result to chronic hemolytic anemia -hemolysis only whe n under stress, infection or due to the use of certain medications (oxidant drug s) -inherited as X-linked disease

-oxidant drugs: >anti-malarial agents >sulfonamides >nitrofurantoin >analgesics (ASA, Phenacetin) >thiazides >chloramphenicol >para-amino-salisylic acid >vitami n K -clinical manifestations: >s/sx of hemolysis *reticulocytosis *jaundice *hem oglobinuria *pallor

-presence of Heinz bodies (taken up by the spleen) -assessment and diagnostic fi ndings: >qualitative assay for G6PD -medical management: a. withdrawal of the of fending agent b. transfusion -only in severe hemolytic states c. health educatio n -avoid triggering factors Hereditary Spherocytosis -Is also a type of hemolyti c anemia -Abnormal permeability of RBC membrane > spherocytosis > taken up by th e liver > hemolysis

-treatment: >surgical removal of the spleen (splenectomy) Immune Hemolytic Anemi a -due to exposure of RBCs to antibodies formation of alloantibodies destruction of RBCs (intravascular hemolysis) -usually result from hemolytic transfusion re actions -RBCs may be destroyed also because of poor level of suppressor lymphocy tes > antibody formation (IgG) -2 types: 1. warm body antibodies >bind to RBCs m ost active in warm conditions

>most common (IgG usually but sometimes IgA) >mostly extravascular 2. Cold-body Antibodies >react in cold environment >usually IgM >usually occur acutely during recovery from viral infections, chronically with lymphoproliferative disorder > self limited intravascular hemolysis -clinical manifestations: (variable dependi ng on the severity) a. splenomegaly in 80% of cases b. hepatomegaly c. lymphaden opathy d. jaundice

-assessment and diagnostic findings: a. CBC -decreased Hgb and Hct b. peripheral blood smear -increased reticulocytes c. serum chemistry -increased serum biliru bin -medical management: a. withdrawal of the offending agent b. increased doses of corticosteroids (1 mg/kg/day) c. blood transfusions -slowly and cautiously ( 10-15ml for 2030mins) d. splenectomy

e. immunosuppressive therapy -if splenectomy and steroids fail -cyclophosphamide (more rapid effect but more toxic) -azathioprine (less rapid effect but less to xic) f. Immunoglobulin administration -nursing management: a. prevention of infe ction *after splenectomy; during steroid and immunosuppressive therapy Hereditar y Hemochromatosis -deposition of excessive iron in the liver, myocardium, testes , thyroid and pancreas

-women are less affected than men -signs and symptoms: a. weakness b. lethargy c . arthralgia d. weight loss e. loss of libido f. skin hyperpigmentation g. cardi ac dysrrhythmias and cardiomyopathy > edema and dyspnea h. endocrine involvement *hypothyroidism *diminished libido *hypogonadism may lead to Hepatocellular Car cinoma

-diagnosis: a. liver biopsy -definitive test -medical management: a. therapeutic phlebotomy -removing whole blood from a vein -every 13 year period -nursing mana gement: a. diet low in iron is not that important b. prevent liver injury such a s alcoholism c. alpha feto-protein determination -serial screening test for hepa toma d. monitor for signs and symptoms of organ dysfunction

Polycythemia Polycythemia Vera or Primary Polycythemia -may lead to Acute Myeloi d Leukemia -myeloid stem cells have escaped normal control mechanisms -Increased RBC count (predominating sign) involvement of the spleen in hematopoiesis fibro sis of the bone marrow (burnt or spent phase) -signs and symptoms: >ruddy comple xion >splenomegaly >pruritus (due to histamine)

>headache >dizziness >tinnitus >paresthesias >fatigue due to an increased blood volume >blurred vision >angina >claudication due to increased blood >dyspnea viscosity >thrombophlebitis >erythromyalgia - burning sensation of the fingers and toes

-assessment and diagnostic findings: 1. increased RBC mass (nuclear medicine pro cedure) -normal in erythropoietin 2. normal oxygen saturation level 3. enlarged spleen -other signs: 1. increased WBC and Platelet count 2. increased vitamin B1 2 3. increased alkaline phosphatase -complication 1. thrombosis - may lead to st roke or MI 2. bleeding

-medical management: 1. therapeutic phlebotomy >500ml once or twice weekly >to r educe the blood cell mass 2. radioactive phosphorus >to suppress marrow function but may increase the risk of leukemia -nursing management: 1. patient education >avoid Aspirin to decrease the risk >minimize alcohol of bleeding >cool or tepi d water bath -for itchiness -antihistamines are not effective

Secondary Polycythemia -due to excessive production of erythropoietin as a react ion to: >smoking >COPD >cyanotic heart disease >increased altitude -medical mana gement: 1. Therapeutic Phlebotomy Leukopenia and Neutropenia -may result from: * ionizing radiation *long term use of steroids

*uremia *neoplasms -diagnosis: Absolute Neutrophil Count = % neutrophils + % ban ds X total WBC count 100 -clinical manifestations: infections -medical managemen t: 1. withdrawal of the offending agent 2. corticosteroids 3. withholding or dec reasing the dose of chemotherapy or radiotherapy 4. culture of blood, urine and sputum; CXR > monitoring

-nursing management: 1. infection control Bleeding Disorder -vascular in origin >> localized -platelets or coagulation factor defects >> widespread Primary Thro mbocythemia -also called essential thrombocythemia -stem cell disorder in the bo ne marrow -platelet count >> 600,000/mm3 >> size is abnormal increased RBC incre ased WBC

-clinical manifestations: >usually asymptomatic >hemorrhage or vasooclusion of t he microvasculature >painful, burning, warmth and redness on the localized area of the extremity (due to an increased platelet ct.) -diagnosis: >CBC and other b lood tests (not necessary to perform BMA and biopsy) *median survival is 10 year s -medical management: (controversial) 1. Low Dose Aspirin -in young patient wit hout aggravating factors like atherosclerosis, smoking and peripheral vascular d isease

2. Hydroxyurea -chemotherapeutic agents to lower down the platelet count Anagrel ide -more specific than Hydroxyurea -side effects: severe headache Alpha Interfe ron -lower the platelet count by unknown mechanisms -sc 3x a week -very expensiv e -side effects: >fatigue >dizziness >weakness >anemia >memory defects >liver dy sfunction

3. Platelet Pheresis -to reduce platelets with transient effects -nursing manage ment: 1. Patient education >risk of bleeding and thrombosis >signs of bleeding a nd thrombosis (visual changes, tingling and weakness) Secondary Thrombocytosis increased platelet production -an increase above 1 M count is rare -platelet funct ion is normal >survival time is normal or increased

-triggering factors: >chronic inflammatory disorders >iron deficiency >acute hem orrhage >malignant disease >splenectomy Idiopathic Thrombocytopenic Purpura -aff ects all ages -more common to children and women -2 types: a. acute >predominant ly in children >often 1-6 weeks after a viral illness >self-limited (remission w ithin 6 months)

b. chronic -hypothetical causes: a. exposure to sulfa drugs, quinine b. SLE c. p regnancy d. autoimmunity -signs and symptoms: a. platelets >less than 20,000/mm3 or even less than 5,000/mm3 b. bruising, heavy menses and petechiae on the extr emities and trunk

*2 types of purpura a. dry purpura -simple bruising or petechiae -tend to have f ewer complications b. wet purpura -GIT bleeding -hemoptysis -intracranial bleedi ng -assessment and diagnostic findings: decreased platelet count decreased megak aryocytes

-management: a. safe platelet count -risk of bleeding starts at a platelet count of 10,000/mm3 and below b. withdrawal of the offending agent c. immunosuppressi ve therapy to inc -mainstay of short term treatment plt ct -to block the binding receptors in macrophages *Prednisone 1mg/kg -effective in 75% of cases -can be used also for maintenance at a dose of 2.5 to 10mg QOD *Cyclophosphamide

*Azathioprine *Dexamethasone *Vincristine d. intravenous immunoglobulin -binding the receptors on the macrophages -1g/kg for 2 days (very expensive) e. splenect omy -effective in 50% of cases -at risk of sepsis (should receive vaccines) *Pne umovax should be given *Haemophilus influenzae B within 2-3 wks *Meningococcal v accines prior to proc

-nursing management: a. history taking -viral infection -intake of sulfa contain ing drugs b. neurologic assessment -in addition to physical examination -vital s igns: dont use the rectal route c. patient education -s/sx of bleeding -whom to c ontact in case of emergency -avoidance of sulfa containing drugs -compliance to pharmacologic therapy (tapering) -frequency of monitoring the platelet count

d. avoid the risk of bleeding -no constipation -use electric razors only -use so ft bristled tooth brush -refrain from vigorous sexual intercourse e. education o f the disadvantages of corticosteroid treatment -osteoporosis should receive Ca -proximal muscle wasting and vit D -dental caries supplements -cataract formatio n

Pulmonary Disorders Acute Respiratory Distress Syndrome -characteristics: (in the absence of LV Fail ure) *sudden or progressive pulmonary edema *increasing bilateral infiltrates on CXR *hypoxemia refractory to oxygen supplementation *reduced lung compliance -w ith a high mortality rate as high as 50-60% -multiple organ system failure with sepsis (most common cause of death)

acute lung injury alveolar capillary leak a. pulmonary edema surfactant b. hyali ne membrane defect c. microatelectasis decreased V/Q mismatch compliance right t o left shunt pulmonary hypertension dyspnea hypoxemia increased dead space incre ased work of increased minute ventilation breathing microvascular obstruction

-causes: *aspiration (gastric acid) *drug ingestion and overdose *hematologic di sorders -DIC, massive transfusion *prolonged inhalation of high concentrations o f O2, smoke or corrosive substance *localized infection *metabolic disorders (pa ncreatitis) *shock *major surgery *fat or air embolism *sepsis

-signs and symptoms: *rapid onset of dyspnea -12 to 48 hours after the initiatin g event *arterial hypoxemia not responsive to O2 therapy *pulmonary edema -quick ly worsen -assessment and diagnostics: *history and physical exam -retractions a nd crackles *CXR *pulse oximetry *ABG

-management: a. identification and treatment of the underlying condition b. aggr essive, supportive care -intubation and mechanical ventilation c. circulatory su pport -IVF d. nutritional support (35-45kcal/kg/day) e. O2 inhalation f. PEEP (p ositive end expiratory pressure) -critical in ARDS -improves the oxygenation -in crease the functional residual capacity

h. pharmacologic therapy -interleukin-1 receptor antagonist (anakinra) -neutroph il inhibitors -pulmonary specific vasodilators -surfactant replacement therapy antisepsis therapy -antioxidant therapy -corticosteroids -nursing management: a. close monitoring b. respiratory modalities -O2 inhalation, nebulizer therapy, c hest physiotherapy, ET intubation, suctioning, mechanical ventilation and bronch oscopy

c. positioning -to improve ventilation d. reduce anxiety and agitation -explain all procedure and provide care in a calm and reassuring manner e. continuous ass essment (ventilator setting) -presence of tube blockade by kinking or retained s ecretions -acute respiratory problems (pneumothorax) -sudden hypoxemia -ventilat or malfunction f. sedation -to decrease the patients O2 consumption

-to allow the ventilator provide full respiratory support -to decrease anxiety g . administration of neuromuscular blocking agents -alternative to sedation Acute Respiratory Failure -is a sudden life threatening deterioration of the gas exchange function of the lung -fall in arterial oxygen tension to less than 50m mHg and a rise in CO2 tension to more than 50mmHg and with an arterial pH of les s than 7.35 -mechanisms: *alveolar hypoventilation *V/Q mismatch *diffusion abno rmalities *shunting

-causes: a. decreased respiratory drive -severe brain injury -brainstem lesions -use of sedatives -metabolic disorders (hypothyroidism) b. dysfunction of the ch est wall -diseases of the muscles, nerves, spinal cord and neuromuscular junctio n c. dysfunction of the lung parenchyma -pleural effusion -upper airway obstruct ion -pneumothorax

-signs and symptoms: *all related to hypoxemia and hypoxia restlessness dyspnea fatigue air hunger headache tachycardia and inc BP confusion, lethargy, tachycar dia, tachypnea, central cyanosis respiratory arrest -management: a. correct the underlying cause b. restore adequate gas exchange (ET with ventilator)

surfactant replacement therapy antiseptic agents antioxidant therapy corticoster oids c. nutritional therapy Chronic Obstructive Pulmonary Disease -airflow limit ation not fully reversible -types: a. chronic bronchitis b. emphysema A. Chronic Bronchitis -cough with sputum for at least 3 months in each of 2 consecutive ye ars

Smoke/environmental pollutants Hypersecretion of mucus and inflammation B. Emphy sema Destruction of the walls of distended alveoli Impaired gas exchange -2 type s: 1. panlobular >respiratory bronchiole, alveolar duct and alveoli are destroye d 2. centrilobular >destruction of the center of the secondary lobule -risk fact ors: 1. environmental >cigarette smoking

>prolonged and intense exposure to occupational dusts and chemicals >indoor air pollution >outdoor air pollution 2. host >alpha-1-antitrypsin deficiency -3 prim ary symptoms: a. cough b. sputum c. dyspnea on exertion -assessment and diagnosi s: >spirometry -complications: a. respiratory failure

b. respiratory insufficiency -medical management: a. risk reduction b. pharmacol ogic therapy *bronchodilators >MDI >nebulization >oral (pill or liquid) beta adr energic agonist anticholinergic agents methylxanthines *corticosteroids oral or IV (Beclomethasone, Fluticasone)

*vaccines >influenzae and pneumococcal *alpha-1-antitrypsin augmentation therapy *antibiotics *mucolytics *antitussives c. surgical management: *bullectomy *lun g volume reduction surgery *lung transplantation -nursing management: a. patient education *breathing exercises

*inspiratory muscle training *activity pairing *self care activities *physical c onditioning *oxygen therapy *nutritional therapy *coping measures

Asthma -a reversible chronic inflammatory disease of the airways -triad: *airway hyperresponsiveness *mucosal edema *excessive mucus production -signs and sympt oms: *cough *wheezing *chest tightness *dyspnea -causes: a. allergy- strongest p redisposing factor >seasonal (weed pollens, grass >perennial (molds, dust, roach es)

b. airway irritants (perfumes, smoke, cold, heat) c. exercise d. stress or emoti onal upset e. sinusitis f. medications g. viral respiratory tract infections h. gastro-esophageal reflux -pathophysiology bronchospasm mucosal edema exc mucus secretion bronchial muscle mucosal gland en largement hypertrophy thick tenacious secretions alveolar hyperinflation

chronic asthma (chronic airway inflammation) airway subbasement membrane fibrosi s airway narrowing irreversible airflow limitation -signs and symptoms: *cough usually at night or early in the *dyspnea morning du e to circadian *wheezing variations *diaphoresis *hypoxemia *tachycardia *centra l cyanosis *widened pulse pressure

-types according to severity: A. Mild Intermittent -symptoms <2 times a week -as ymptomatic and normal PEF between exacerbations -exacerbations are brief; intens ity may vary -night time symptoms <2 times a month B. Mild persistent -symptoms >2 times a week but <1 time a day -exacerbations may affect activity -night time symptoms >2 times a month C. Moderate Persistent -daily symptoms -daily use of inhaled short acting beta2 agonist

-exacerbations affect activity -exacerbations >2 times a week; may last days -ni ght time symptoms >1 time a week D. Severe Persistent -continual symptoms -limit ed physical activity -frequent exacerbations -frequent night time symptoms

-assessment and diagnostics: *clinical history and physical assessment *sputum/b lood tests >eosinophilia *serology >elevated IgE *ABG >hypoxemia >hypocapnia the n hypercapnia *pulse oximetry >hypoxemia -prevention: a. identificaton and avoid ance of allergens

-complications: a. status asthmaticus b. respiratory failure c. pneumonia d. ate lectasis -medical management: a. Long Acting Medications *corticosteroids -most potent and effective -inhaled preparations commonly causes oral thrush -fluticas one, beclomethasone, budesonide

*mast cell stabilizer -for mild to moderate asthma only (prophylaxis) - cromolyn sodium and nedocromil *beta 2 agonist -to control symptoms especially at night -prophylaxis of exercise induced asthma -salmeterol, albuterol, formoterol *meth ylxanthines -mild to moderate bronchodilator -mainly for the relief of night tim e sx (theophylline as mild anti-inflammatory)

*leukotriene modifiers (inhibitors) -may be added or be used as an alternative t o inhaled corticosteroids -zafirlukast, montelukast, zileuton B. Quick Relief Me dications *short acting beta 2 agonist -to relieve acute symptoms -to prevent ex ercise induced asthma -may be combined with an anticholinergic -salbutamol, comb ivent (salbutamol+ipratropium bromide) >management of asthma exacerbation -early treatment and education of the patient

*quick relief medications *corticosteroids *O2 inhalation *serial measurement of lung function -peak flow meter (FEV) Status Asthmaticus -severe and persistent asthma that does not respond to conventional therapy -may last longer than 24 ho urs -causes: *infection *dehydration *anxiety *inc adrenergic blockage *nebulize r abuse *irritants (aspirin)

-pathophysiology: similar to bronchial asthma *hypoxemia and respiratory alkalos is >>> respiratory acidosis -signs and symptoms: similar to asthma (extent of wh eezing does not indicate the severity of attack) -assessment and diagnosis: *pul monary function study -most accurate *ABG -respiratory alkalosis (most frequent finding)

-medical management: *short acting beta adrenergic agonist and steroid *O2 inhal ation *IVF *mechanical ventilation Bronchiectasis -is a chronic irreversible dil ation of the bronchi and bronchioles -causes: *airway obstruction *diffuse airwa y injury *pulmonary infections and complications

*genetic disorders (cystic fibrosis) *abnormal host defense (ciliary dyskinesia) *idiopathic causes -pathophysiology: chronic airway inflammation bronchial wall damage bronchial obstruction (due to thick sputum) bronchial distention and dis tortion (localized; segmental/lobar-lower lobes usually) inflammation of the per ibronchial tissues alveolar collapse pulmonary scarring/fibrosis

-signs and symptoms: *chronic cough *excessive production of purulent sputum *he moptysis *clubbing of the fingers *repeated pulmonary infections -assessment and diagnosis: *history and physical assessment -prolonged history of productive co ugh *sputum exam -consistently negative for tubercle bacilli *CT scan -bronchial dilatation

-medical management: a. bronchial drainage -to clear excessive secretions -to pr event or control infection *postural drainage *bronchodilators *bronchoscopy *ch est physiotherapy b. smoking cessation c. infection control -antimicrobial thera py (year round) -vaccination (influenza and pneumococcal pneumonia)

d. surgery -for patients who continue to expectorate large volume of phlegm -for patients with repeated bouts of pneumonia and hemoptysis *segmental resection * lobectomy *pneumonectomy -complications: *atelectasis *bronchopleural fistula *p neumonia *empyema

-nursing management: a. supportive and symptomatic b. assistance to clear secret ions c. patient education -smoking cessation -infection prevention -postural dra inage -activity/rest -nutrition

Pulmonary Edema -abnormal accumulation of fluids in the lung tissue and/or alveo lar space -a severe, life threatening condition -causes: *left ventricular failu re *hypervolemia *sudden increase in the intravascular pressure in the lungs (po st operative pneumonectomy) >flash pulmonary edema

*rapid re-inflation of the lungs after the removal of air from a pneumothorax or evacuation of fluid from a large pleural effusion >re-expansion pulmonary edema -signs and symptoms: >increasing respiratory distress -dyspnea -central cyanosi s -hunger -confusion/stupor >foamy, frothy, and often blood tinged secretions

-assessment and diagnostic findings: a. physical examination >crackles -initiall y in the base and posterior part of the lungs -progress toward the apices >tachy cardia b. chest x-ray >increased interstitial markings c. pulse oximetry d. arte rial blood gas determination -medical management: a. correction of the underlyin g cause b. vasodilators

c. inotropic agents d. afterload or preload agents e. contractility meds f. diur etics and fluid restriction g. oxygenation and mechanical ventilation h. morphin e -nursing management: supportive to the medical management Pulmonary Hypertensi on -systolic pulmonary artery pressure exceeding 30mmHg -mean pulmonary artery p ressure exceeding 25mmHg -2 Types: 1. Primary Pulmonary Hypertension

-with no evidence of pulmonary or cardiac disease or pulmonary embolism -more co mmon in women 20-40 y/o -high mortality within 5 years of diagnosis 2. Secondary Pulmonary Hypertension -more common -secondary to existing cardiac and pulmonar y disease (hypoxemia) -

Hypoxemia Hypercapnia Pulmonary Embolism Pulmonary Artery Constriction Increased Pulmonary Vascular resistance Increased Right Ventricular Workload Right Ventri cular Hypertrophy Right Ventricular Failure -signs and symptoms: *dyspnea -main symptom initially with exertion then eventua lly at rest *substernal chest pain *weakness *syncope *fatigue *occasional hemop tysis

*right sided heart failure -peripheral edema, ascites, neck vein engorgement, li ver engorgement, crackles -assessment and diagnosis: *clinical history and physi cal examination *CXR *pulmonary function studies -normal, or slight decrease in VC and compliance -mild decrease in diffusing capacity *electrocardiogram -right ventricular hypertrophy -right axis deviation -tall peaked T waves (inferior le ads) -tall R waves, ST segment depression, T wave inversion (anterior leads)

*echocardiogram -can assess the progression of the disease *ventilation perfusio n scan -defects in the pulmonary vasculature such as pulmonary emboli *cardiac c atheterization -elevated pulmonary arterial pressure *lung biopsy -through thora cotomy or thoracoscopy -medical management: Goal: 1. to manage the underlying ca rdiac or pulmonary condition

A. Supplemental Oxygen -reverses vasoconstriction -reduces pulmonary hypertensio n B. Pulmonary Vasodilators (calcium channel blockers, IV prostacyclin) -reduces pulmonary vascular resistance -increases the cardiac output C. Anticoagulants i f with cor D. Fluid Restriction pulmonale E. Diuretics F. Cardiac Glycosides G. Heart-Lung Transplantation

-nursing management: 1. identify high risk patients -COPD, pulmonary emboli, con genital heart disease, mitral valve disease 2. monitor s/sx 3. administer oxygen therapy appropriately 4. home use oxygen supplementation Cor pulmonale -charact erized by: a. right ventricular enlargement b. pulmonary congestion -causes: a. COPD -most frequent

b. deformities of the thoracic cage c. massive obesity d. primary embolism e. di sorders of the nervous system f. disorders of the respiratory muscles g. disorde rs of the chest wall h. disorders of the pulmonary arterial tree Lung Disease Hy poxemia and Hypercapnia Pulmonary Hypertension Increased Work Load to the Right Ventricles Right Sided Heart Enlargement Right Sided Heart Failure

-signs and symptoms: *s/sx of the underlying pulmonary disease *s/sx of right si ded heart failure -management: goals: 1. improvement of ventilation 2. treatment of the underlying lung disease 3. treatment of the manifestations of the heart A. Continuous 24 Hour O2 Therapy -improvement may require 4-6weeks of O2 therapy -monitor pulse oximetry and ABG

B. Chest Physiotherapy and Bronchial Hygiene Maneuvers C. Bronchodilators D. ET Intubation and Mechanical Ventilation E. Bed Rest F. Sodium Restriction G. Diure tic Therapy H. Digitalis Therapy I. ECG Monitoring -nursing management: *support ive to the medical management

Pulmonary Embolism -obstruction of the pulmonary artery or one of its branches b y a thrombus or thrombi -causes: *venous thrombosis *atrial fibrillation Occlusi on of the Pulmonary Artery Increased Alveolar Dead Space Ventilation/Perfusion I mbalance Hypoxemia and Hypercapnia Pulmonary Hypertension Right Ventricular Fail ure Shock

-signs and symptoms: *dyspnea -most frequent symptom *tachypnea -most frequent s ign *chest pain -sudden and pleuritic -mimics angina pectoris *anxiety, fever, t achycardia, apprehension, cough, diaphoresis, hemoptysis, syncope -less than 10% progresses to pulmonary infarction -assessment and diagnosis: a. Ventilation Pe rfusion Scan (test of choice) b. Pulmonary Angiography (gold standard)

c. CXR -infiltrates -atelectasis -pleural effusion -elevation of the diaphragm d . ECG -sinus tachycardia -PR interval progression -non specific T wave changes e . Peripheral Vascular Studies f. ABG -prevention: *prevention of DEEP VEIN THROM BOSIS

-management: a. Emergency Management *Nasal O2 Therapy *IV access *Perfusion Sca n, ABG, Hemodynamic Measurements *Dobutamine or Dopamine *ECG *Digitalis Glycosi des, IV Diuretics and Antiarrhythmics when appropriate *Blood Studies *ET Intuba tion and Mechanical Ventilation *Indwelling Urinary Catheter Insertion *Small Do ses of Sedatives or Morphine

b. General Management *O2 therapy *elastic compression stockings *intermittent p neumatic leg compression *elevation of the leg c. Pharmacologic Management *Anti coagulation Therapy Heparin (IV bolus of 5T to 10T U then infusion of 18U/kg/hour not to exceed 600U/hour) Warfarin (begun within 24 hours after initiating Hepari n therapy) *Thrombolytic Therapy Urokinase, Streptokinase, Alteplase

CVA w/in the past 2 months active bleeding w/in the past 10 days recent labor & delivery severe hypertension d. Surgical Management: *embolectomy *interruption of the inferior vena cava Teflon clips -nursing management: a. Minimizing the ri sk of pulmonary embolism b. Preventing thrombus formation c. Assessing for poten tial pulmonary embolism d. Monitoring thrombolytic therapy CI:

e. managing pain f. managing O2 therapy g. relieving anxiety h. monitoring for c omplications i. post op nursing care

Diabetic Ketoacidosis -is caused by an absent or markedly inadequate amount of i nsulin -results in disorder in the metabolism of carbohydrate, protein and fat 3 main clinical features of DKA: *hyperglycemia *dehydration and electrolyte los s *acidosis -assessment and diagnostic findings: *blood glucose level -300 to 80 0 mg/dl *serum bicarbonate -0-15mEq/L

*serum pH -low: 6.8-7.3 *PCO2 -low: 10-30mmHg -reflects respiratory compensation for acidosis *ketone bodies -elevated in the blood and in the urine *electrolyt e depletion *BUN, creatinine, hgb and hct -elevated due to water loss

-lack of insulin increased breakdown of fat increased fatty acids increased keto ne bodies -acetone breath -poor appetite -nausea -blurred vision acidosis -nause a -vomiting -abdominal pain increasingly rapid respirations -decreased utilization of glucose by muscle, fat and liver -increased production of glucose by liver hyperglycemia polyuria dehydration -weakness -headache increased thirst

-prevention: a. full compliance to the medical treatment of diabetes mellitus b. good hydration c. good nutrition d. monitoring of blood and urine ketones every 3-4 hours -management: a. rehydration >6-10 L of IVF >plain NSS or half strengt h saline b. restoring electrolytes >ECG monitoring

*reversing acidosis: -insulin -nursing management: *same as in DM

Addisons Disease Sugar Salt Sex Physical Appearance Hypoglycemia, hyperkalemia Hy ponatremia Decreased libido Not seen, more on symptoms Cushings Syndrome Hyperglycemia,hypokalemia Hypernatremia Sexual urge not merely affected Buffalo hump, moonface, pitting edema, hirsutism, breast atrophy, purpl e striae on abdomen, easy bruising, facial flushing, acne, hyperpigmentation Diet High Na, CHON, Low Na, CHO, fats but high CHO intake except K CHON and K intake

Hyperthyroidism (Thyroid Crisis) Graves Disease; inc. amt. of T3&T4 Inc. appetite wt. loss due to inc. metabolism, heat intolerance, all VS increase, exopthalmos -pathognomonic symptom, amenorrhea Inc. caloric diet; watch out for thyrotoxicos is (triad): b. Tachycardia c. Hyperthermia d. agitation Meds: SSKI (Lugols soluti on), PTU prophylthiuracil Hypothyroidism (Myxedema Coma) Dec. T3T4; causes in adult myxedema, child cretin ism Dec. appetite wt. gain due to decreased. metabolism, all VS decrease, decrea sed menstruation Dec. caloric diet, force fluid Meds: Levothyroxin (T4) synthroid

DKA Acute complication of type1 DM due to severe hyperglycemia, leading to CNS depre ssion & coma HHNS Hyperglycemia w/o ketosis is commonly on DM type2 Polyuria, Polydipsia, Hypotension, extreme thirst, Polyphagia, Glycosuria, dehyd ration, tachycardia, Pathognomonic hypokalemia, hyponatremia Sx: >acetone breath fruity odor >kussmuls respiration rapid, shallow breathing Mx: monitor VS; I/O Med s: Insulin therapy (IV), counteract acidosis Na HCO3 Tx: give insulin, inc. flui d