33672731 Critical Care Nursing

8/3/2019 33672731 Critical Care Nursing

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CRITICAL CARE NURSINGEncoded by/Property of: Ryan Mendoza Ecunar, SLU SN IV

The critical care environment Fast-paced Highly specialized Technical o Technologically advanced o Skilled nurses Requires various types of equipments Necessarysupplies must be easily and quickly accessible o Nurse patient ratio is 1:1 or1:2 o In RP, 1:4 Pts. Are cared for individually and uniquely In life and death

situations c supportive devices c multiple complications in intensive ttt for specific dysfxs Assessment 1. Nursing history May have direct admission CC nurse integrates data for pt and family, written hx and the transfer report o E.g. HPN-HPI Diet Smoking ROH use Stress 2. Diagnostics ECGs Respirations IntraarterialP Pulmonary artery P Venous O2 sat Body temp Continuous Airway P M o Non-invasive technique that uses a transducer cable, d P tubing & a display monitor o The waveforms produced by the system enable the clinician to continuously M the pts.Response to various modes of mechanical ventilation o d P- kinks and destructions Sources of obstructions: phlegm NR: y Look for kinks y Suction the pt o d P- cause by detached tubing, leak from the mechanical ventilator CVP M o Maybe usedin lieu of a pulmonary artery catheter when evaluation of pulmonary artery P andL sided heart failure are nor req¶d o Unit in cmH20 o 0-25 calibrations o Normal:

4-l2 cmH20 other books, 4-10 0r 6-12 cmH20 o If below: hypervolemia o If above:hypovolemia Intracranial P M o Involves placing a catheter through the skull into either the subarachnoid space or the cerebral ventricle to M changes in P within the cranial cavity o A transducer and tubing system gather the data cc are displayed on the M screens o In RP, Cushing¶s triad o If widening pulse P, Increased ICP o If narrowed pulse P, shock compensation

o Pulse Pressure= BP Systole - Diastole Cardiac Monitoring o A non-invasive procedure that poses minimal risk to pt o Placing conductive electrodes on the pts c

hest that recognizes the electrical activity of the heart and relay it to a video display screen o Review placement of electrodes o NOTE: if status post op, c breast CA, okay electrodes at the back Hemodynamic M o Invasive M of the arterialor venous system o M is accompanied through catheters that measure changes in air and fluid P o Can also be used to administer IVFs and certain arterial and/orvenous blood for lab analysis o 2 types commonly used: Intraarterial M y Catheter is inserted into an artery radial or femoral connected to a high P flush system filled c either non/heparinized saline solution y Intraarterial systems display a continuous reading of the pts BP y Transducers are connected to the systemthat interprets the air and fluid P readings and display results as waveforms oncardiac monitoring equipment Pulmonary artery M y Involves inserting a cathetervia the subclavian or internal jugular vein and advancing it into the pulmonary

artery

Teaching in the CCU is focused on the short term. The nurse communicates to thept and the family 1. 2. 3. 4. 5. rationale for the ttts, procedures and medications plans for ongoing care goals for ttt interpretations of the dx, dx tests andexpectations resources available foe financial, coping, support and other personal needs

Abdominal aortic aneurysm (AAA assoc c atherosclerosis (most common cause) and HPN common to adults 70 y/o and above ng age and smoking contributes as well 90 %develop below the renal arteries, usually where the abdominal aorta branches from the iliac arteries Risk factors HTN (more than ½ have HTN)



Genetic predisposition Caucasian race Cystic medial necrosis Athero/arterisclerosis Immunologic conditions Male four times than women Advancing age Pregnancy Congenital defects of the aortic valve Coarctation of the aorta Inflammatory aortitis Syphilis Trauma Local infection (pyrogenic or fungal) mycotic aneurysm

ALERT: No deep palpation!!!Diagnostics 1. CT scan/ MRI 2. Angiography- uses contrast dye solution injectedinto the aorta or involved vessel to visualize the precise size and location ofthe Aneurysm 3. abdl UTZ- to dx AAA 4. transesophageal achocardiogram- to differentiate 5. CXR Nursing Responsibilities 1. in aortic dissection a. IV beta blockers (Esmolol) b. Na nitroprusside (similar c Dep patch) c. CCBs d. Avoid givingdirect vasodilators further destruction injury e. Post-operative anticoagulantsi. Heparin ii. Low dose ASA tx 2. Surgery a. Post-op care b. M u/o c. M FE imbalance d. M graft leaks i. Ecchymosis of the scrotum and perineum (penile area) ii. ng abdominal girth iii. Weak and absent peripheral pulses iv. Fall in Hgb andHct v. Pain over the pelvis, back and groin vi. Decreasing u/o vii. Decreasing hemodynamic M Nursing Diagnoses risk for ineffective tissue perfusion risk for in

jury anxiety Acute Respiratory Distress Syndrome Pathophysiology Pulmonary insult Chemical mediators released Damage to alveolar capillary membrane Interstitialedema alveolar edema damaged surfactantproducing cells d surfactant production

Aneurysm- abN dilation of the BVs - commonly affects aorta and peripheral arteries - may also develop in the ventricles - forms due to weakness of the arterialwall - HTN is a major contributing factor - destruction of the collagen and elastin Collagen- s tensile strength of the vessel- preventing dilation Elastin- allows recoil 1. primary component of the intimal wall and medial layers Types: 1.True Aneurysm a. brought abt by the eroding effects of atherosclerosis and HTN b. affects the 3 layers of the vessel wall and most are Fusiform or circumferential i. Fusiform- spindle shape and taper at both ends ii. Circumferential- involves the entire diameter of the vessel 2. False Aneurysm a. also known as the trau

matic Aneurysm bec of traumatic break in the vessel wall rather than weakening b. usually are saccular- like small outpouchings i. Berey Aneurysm- type of saccular Aneurysm but relatively small (2 cm in diameter) ii. Dissecting Aneurysm 1.develops when a break or tear in the tunica intima and media allows blood to invade or dissect the layers of the vessel wall 2. blood accumulates in the adventitia and thus form a saccular or a longitudinal aneurysm Aortic Dissection - a life- threatening condition a tear in the artery inner layer allows blood to dissect or split in the vessel wall manifestation is epigastric pain Clinical manifestations Asymptomatic Pulsating abdominal mass in the middle and upper abd when lying down, bruit is heard Intermittent and constant pain over the midabdominal area region and lower neck (if pain is present) Pain may range from mild discomfort to severe (depending on the size) severe pain may indicate impending rupture

Dilution of surfactants

d lung compliance, atelectasis, hyaline membrane formation d work of breathing impaired gas exchange

RESPIRATORY FAILURE Acute Respiratory Failure consequence of severe respiratorydysfx defined by arterial blood gas values o an arterial 02 level of <50-60mmHgo an arterial CO2 level of >50mmHg in COPD o acute drop in blood O2 levels



o increased CO2 levels failure of O2- hypoxemia s a rise in CO2 levels hypoventilation- hypoxemia and hypercapnia acute lung injury Mortality due to multiple organ system dysfx AKA adult hyaline membrane dse charac by noncardiac pulmonary edema and refractory hypoxemia

usually superficial involving the epidermis e.g. solar, x-rays, radioactive agents

Manifestations dyspnea tachypnea anxiety restlessness apprehension impaired judgment motor impairment tachycardia HTN Cyanosis Dysrhythmias Hypotension Decreased cardiac output Tissue hypoxia Metab acidosis Develop within 24-48hourss p initial insult Progressive respiratory distress Cyanosis does not improve c O2 adminMedications Nitric oxide reducers (nitrous oxide a free radical) Surfactants Inflammatory blockage utilizing steroids Mech vent Nutrition ± eat PO, enteral and parenteral feeding Review arachidonic acid pathway!!! Burns

An injury resulting fr exposure to heat, chemicals, radiation or electric current A transfer of energy fr a source of heat to the human body initiates a sequence of physiologic event in the most severe cases leads to irreversible tissue destruction

Types of Causative agents of Burns 1. thermal most common injury dryheat: open flame moist heat: steam, hotliquids 2. chemical caused by direct skin contact c acids, strong alkali, organic compounds chemicals destroy tissue CHON leading tonecrosis e.g. inhalatory (cement) burns 3. electrical depends on the type and duration of current and amount of voltage difficult to assess because the destructive processes are concealed entry and exit wounds tend to be small, masking a widespread tissue damage underneath the wound eg. Direct and alternating current,

lightening 4. radiation usually assic c unburn and radiation fr ttt of cancer

Factors Affecting Burns Depth of the burn (layers of underlying tissue affected)o Det by the elements of the kin that have been damaged or destroyed Characs ofBurns by Depth Superficial (epidermis): skin maybe pink to red and dry usuallyheals in 3-6 days peeling of the skin is evident e.g. sunburn redness, mild edema, pain and increased sensitivity to heat desquamation is 2-3 days Partial thickness (epidermis and dermis):maybe superficial and deep partial thickness Superficial: involves the dermis and the papillae of the dermis Burn is often bright red but has a moist glistening appearance c blister formation Burnt area will blanch when P is applied; touch and pain sensation remain intact Heals in 21days c minimal or no scarring Upper 3rd of the dermis Good blood supply Blisters Nerve endings are exposed painful

Deep partial thickness: involves entire dermis but ex

tends further Sebaceous glands and epidermal sweat glands remain intact Surfaceof the skin appears pink and waxy and may be moist or dry Capillary refill is decreased and secretions to deep P is present Requires more than 21 days to heal (3-6 weeks) c scar Can proceed to full thickness due to infection, hypoxia or ischemia Contactures, hypertrophic scarring Full thickness: epidermis, dermis, underlying tissues: skin appears waxy, dry, leathery, charred Involves all layers ofthe skin, including the epidermis, dermis and the epidermal appendages It can extend to the SQ, connective tissues, muscle and bone Hard, dry, leathery escharEschar- dead tissue, must be removed Grafting to heal Deep full thickness woundsExtend beyond the skin to underlying tissues and fascia, muscles, bones and tendons Complete absence of sensation Extent of the burn (percentage of body surface area involved) o Expressed as a % of the total body surface area (TBSA) use ru

le of nines (prehosp)

Extent of Burns- expressed in % of the TBSA Rule of Nines- emergency outside the



hospital; rapid



Lund and Browder method- det surface area measurement for each body part accdg to cts. Age Parkland¶s Formula = 4 mL x TBSA x wt kgs. ABLS formula = 2- 4mL x TBSAx wt kgs.pt Curling¶s Ulcer- brought abt by stress

Classification of Burn Injuries by Extent Minor burn injuries i. excludes electr

ical and inhalational and complicated injuries such as trauma ii. partial thickness burn of less than 1% of TBSA iii. full thickness burn of less than 2% of TBSA iv. e.g 1. sunburn- exposure to UV light; most common 2. scalding burns Zone of hyperemia Zone of Stasis- with inflammatory by-products Moderate burn injuriesi. excludes electrical and inhalational and complicated injuries such as traumaii. partial thicknessof 15-25% iii. full thickness burns of less than 10% TBSAMajor burn injuries i. includes all burnsa of the hands, face, eyes, ears, feetand perineum, all electrical injuries, multiple traumas, and all cts. That are considered high risk

Burn Stages 1. Emergent/Resuscitative stage a. Fr onset of the injury through successful fluid resuscitation b. HCWs estimate the extent of burn injury c. Insti

tute 1st aid measures d. Ct may be intubated 2. Acute stage- start of the diuresis and ends c the closure of the wound, either by natural healing or by using skin grafts 3. Rehabilitative stage a. Begins c wound closure and ends when the ctreturns to highest level of H restoration, cc may take years b. CT and PT may be needed i. ROM exercises ii. Splints to prevent contracture deformities and compartment syndrome Pathophysiologic Effects of a Major Burn(Refer to Lippincott Manual of Nsg Practice 8th ed, start pp1122)

Burn Wound Healing 1. Inflammatory a. Immediately ff the injury, plts. Coming in

contact c the damage tissue aggregate b. Fibrin is deposited, trapping furtherplts. And thrombus is formed (clamping) c. Hemostasis is maintained by the thrombus and vasoconstriction d. Vasodilation occurs and increases vascular permeability e. Neutrophils infiltrate (24 hours) then is replaced by the monocytes and converted to macrophages that consumes the pathogens and dead tissue f. Also stimulates the proliferation of fibroblasts g. Angiogenesis ± promoted by VEGF apoptosis 2. Proliferation a. Within 2-3 days p burn b. Granulation tissue begins c complete reepithelialization c. Epithelial cells cover the wound 3. Remodelling a.Lasts for years b. Collagen fibers laid down c. Scars contact and fade in colord. Hypertrophies scar and keloid may appear e. Hypertrophic scar i. Is an overgrowth of dermal tissue that remains within the boundaries of the wound f. Keloid-a scar that extends beyond the boundaries of the original wound

Skin Changes o Epidermis- outer layer o Dermis- 2nd layer Made up of collagen, fibers, CTs and elstic fibers Within it are BVs, sensory nerves, hair follicles,sebaceous and sweat glands Functional Changes o Evaporation o Skin can tolerateup to 40degs o 71deg C and above will cause cell destruction cc is so rapid Vascular Changes o Fluid shifts 3rd spacing due to extravasation Edema Hypovolemia Hyperkalemia Hyponatremia hemoconcentration Fluid remobilization o Diuretic stage- 48 to 72 hours o Hyponatremia o Hypokalemia o Hemodilution o Metabolic acidosis o GIVE: colloids (Zenalb- in 5% or 25 % prep) ± albumin maintains Oncotic pressure pulling P Cardiac changes Cardiac Output (CO) d circulation vasomotor rxn (vasocons) Baroreceptors stimulated stimulus Medulla oblongata impulse Release of catecholamines PNS (Epinephrine and Norepi) Effect of sympathetic response Increased Heart rate stimulus Adrenalmedulla Pulmonary changes o Cause of death (CO po

isoning) more than 60 % CO DEATH o Upper airway affected by inhaled smoke that causes edema then obstruction 10% is confusion, delirium, etc, 40% comatose Injury





Increased histamine production Increased VP EV Alveolus Congestion CO and CO2 exchange impairment GI Changes o Decreased perfusion to the GI tract o Sympatheticresponse o Curling¶s Ulcer- due to BV (compensation) increased Cardiac output epinephrine release Increased GI mobility Increased HCl release invitation Shock

y Eg. Jobst support garment Used for 6 mos to a year

state which develops where there is inadequate tissue perfusion causing the cells to be deprived of adeq 02, convert to anaerobic metabolism resulting in the production of lactate and acidosis 500 cc is adeq volume to manifest shock

Compensatory Mechanisms Inflammatory compensation Sympathetic nervous system stimulation Nursing Diagnoses Decreased cardiac output r/t altered stroke volume fran increased capillary permeability Body image disturbance Pain Impaired tissueperfusion FVD/FEI ATR- initially, hyperthermia«late, hypothermia Impaired skin integrity High risk: infection (high risk- preventable, foreseeable crisis, no s/sx yet Interventions fluid tx plasma exchange tx M o/u Management pain control te

tanus prophylaxis nutritional support prevent gastric acidity to prevent Curling¶sUlcer o PPI¶s, H2 receptor inhibitor, antacids, Antimicrobials o silver sulfadiazine o silver nitrate Surgery o Escharectomy o Debridement Removal of wound debris and eschar Has 3 types Mechanical y y Enzymatic y Surgical o Skin Grafting Autograft Homograft/allograft (cadavers) Heterograft/ xenograft (animal)- pigs Wound Mx o Dressing the wound Open- apply antimicrobial and expose Close- allocate Pdressings to prevent scar and keloids o Positioning, splints, exercise and contractures o Support garments Applied 5-7d p grafting Maintaining 10-20 mmHg to control scarring

Classification of Shock 1. Hypovolemic shock- extremely lowered ciculating bloodvolume (due to hemorrhage, internal andextravascular loss) 2. Cardiogenic shocka. inability of the myocardium to pump an adeq cardiac output to maintain tissu

e perfusion b. happens when myocardial fx is depressed, several compensatory mechanism are activated c. sympathetic stimulation increases heart rate and contractility, and renal fluid retention increases preload (tachycardia and effects ofRAA mechanism) and cause selewctive vasoconstriction d. Renin-angiotensin-Angiotensinogen System Cardiac output kidneys ( perfusion) juxtamedullary nephrons Renin secreted fr the kidneys Aldosterone Na and water retention Increased BV Increased BP Angiotensin 1 ACE in lungs Angiotensin II VC Increased BP

Causes/Etiology of Cardiogenic shock most common cause is the loss of 40-50% ofviable myocardial tissue Mechanical Px o Valvular heart dses o Perforated intraventricular septum o Papillary muscle dysfx/rupture o Myocardial rupture o Syphilis a spirochete destroys myofilaments Shock and aneurysm o Cardiomyopathies o Hypovolemia o Metabolic dysfx o Vasomotor dysfx o Microcirculatory dysfx 3. Extracardiac obstructive shock- physical condition to flow (ie. Tension Pneumothorax,dissecting AA and pulmonary embolus) 4. Distributive shock a. abN distribution of intravascular vol. b. includes the ff i. Septic shock 1. more on G- bacteria a. blows off O2 increased RR resp alkalosis 2. endogenous pyrogenes EARLY/ WARM stage Hypothalamus



progresses LATE/ COLD stage

Increased temp friction ability

Dilation, etc 3rd spacing Decreased cardiac output Metabolic acidosis 3. Coagulating fx XI- Hageman factor Complement sys kinin sys fibrinolytic cascade clotting Interferons serotonin Protrombin and thrombin (natural antiviral) bradykinin h

istamine ii. Anaphylactic shock iii. Neurogenic shock Manifestations 1. Compensatory Phase a. tachycardia (compensation 2 sympathetic stimulation and RAA systemb. bounding pulse c. tachypnea (compensation for hypoxia and excessive amountsof CO2) d. restlessness and irritability (resulting fr cerebral hypoxia) e. decreased U/O, cool and pale skin (vasoconstriction) f. epinephrine SNS tachycardiaBP 2. Progressive stage a. HPoN (failing compensatory mech) i. MAP <60mmHg but manifestation of HPoN reveals if arterial P is <40mmHg b. Narrowed pulse P c. Decstroke vol- weak, rapid and thready pulse saused by decreased cardiac output d.Shallow resp e. Weakness progresses f. Dec renal output g. Respiratory acidosis3. Irreversible stage a. Unconsciousness reflexes (A_B/ Electrolyte imbalance)b. HPoN worsens (decreased cardiac output) c. Slow, Cheyne-stokes respiration (2to resp center depression) d. Anuria (renal failure) i. Diff: oliguria- 100-400

cc/24 hours vs. ii. Anuria- 5-10 cc/24hours Diagnostic Examinations CBC- hct (concentration of compositions, plasma) levels may be d due to hemorrhage o d Hctnay mean DHN o d overload ESR- if elevated- due to injury and inflammation, indicates infection BUN and Creatinine clearance- elevated due to d renal perfusion Lactate- elevated sec to anaerobic metabolism Glucose levels- elevated due to release of glycogen sec to sympathetic response ABGs o Resp alka in early stages assoc c tachypnea

Resp acidosis in later stages due to respiratory depression o Metabolic acidosisin later stages sec to anaerobic metabolism Urinalysis- increased specific gravity due to effects of ADH CXR- pulmonary congestion latter stages ECG- dets MI (elevation of ST segment, widening of QRS complex, overriding U) heart rate and ischemic changes o

Pathophysiologies of Shock 1 Marked d cardiac output Cardiac index (% cardiac output dist to systemic circu) < 1.8 L/m/m2 d coronary blood flow Compensatory mechanism occur (increase VR and catecholamine) Increased pload inc contractility

ISCHEMIA 2 L vent and diastolic P Pulmonary P s Pulmonary edema cavity distention dec pload

endocardial ischemia

Increased arterial hypoxemia pulmonary artery P cellular acidosis Ischemia and RVent failure fluid retention may increase volume to the pt where pulmonary congestion and hypoxemia occur iscgemia also s ventricular diastolic compliance, further elevating L atrial P worsening pulmonary congestion

Effects of Vasoconstriction vasoconstriction cc is the effect of systemic vascular resistances, increases myocardial pload, further impairing cardiac performance and increasing myocardial o2 demand further causing worsening ischemia and further to pts. demise vasoconstriction to maintain BP can compromise multisystematically (renal, splanchnic and cutaneous perfusion) Medical Mx id underlying cause if possible o Streptokinase and Urokinase Thrombolytics Intubation, mech ventand suppl O2 to increase oxygenation Improve O2 content (Hgb and arterialO2 sat) Continuous cardiac M- detects changes in heart rate and rhythm Two (2) IV linesc large gauge needles (g 14-16, in RP only 18 is available) for fluid and drugadmin IV fluids (crystalloids) to maintain and Increase intravascular volume Med

ications Inotropics- increases heart contractility and cardiac output o Dopamine(has Calcium) o Dobutamine and Epinephrine Vasodilators





o o

Given c vasopressors to decrease the ventricular workload Only for cardiogenic shock Nitroglycerine and nitroprusside Has vasodilatory effects towards peripheral circulation Decreased vascular resistance

Decreased stroke volume Thrombolytic Tx o For coronary revascularization to allow restoration of coronary artery blood flow o Streptokinase/ Urokinase o NOTE: If MI lasted already for 12 or 6 hours, don¶t give T tx anymore because the myocardium is already dead! Diuretics- If c fluid overload to decrease ventricular workload For septic shock: o Give antibiotics o Antipyretics due to fever vasodilatory effects o BT whole blood and its by-products PRBC WB Plt. Concentrate FFP also has cryoppts and plt (for DICcryoppts has clotting factors 10-20 cc to be used) o Osmotic diuretic maybe needed to increase renal bloodflow and U/O

Adenohypophysis/ Anterior Pituitary Gland: FAT-LPG-Me o F- Follicle-stimulatinghormone o A- Adrenocorticotropic hormone o T- Thyroid-stimulating hormone o L- L

uteinizing hormone o P- Prolactin o G- Growth hormones o M- Melanocyte stimulating hormone Posterior hypophysis/ Posterior pituitary gland: Anti-Oxy o A- Antidiuretic Hormone o O- Oxytocin

Nursing Management MVS q 15min o <80 mmHg usually results in inadequate coronaryartey blood flow (incr in O2 flow if blood P is <80 mmHg then notufy the physician immediately) M ECG tracings continuously Hemodynamic M o CVP, RV P, Pulmonary artery P, Pulmonary wedge P, L atrial P and CO M U/O Maintain patent airway and adequate ventilation M serum levels M skin color and temp and note changes o Cold clammy skin is maybe a sign of continuing peripheral vascular constriction,indicating progressive shock M arterial blood samples o to increase ABG levels o

ABG results are the determinant for O2 manipulation Provide psychological support- reassuring ct. to relieve apprehension and keep family advised Minimize factors contributing to shock o Elevate lower extremities to 45 degs to promote venous return o Avoid trendelenburg position bec it increases respiratory impairmento Just position the pt to modified trendelenburg position : PILLOW o Promote adequate rest by using energy conservation measures and maintaining a restful andquiet env¶t. Mneumonic of Hormones and their Origin

Diabetic Ketoacidosis Causes infection Illness Surgery Stress Insufficient or absent insulin Assessment Findings Kussmaul¶s breathing Fruity breath odor 3 P¶s Wt loss Muscle wasting Leg cramps Treatment rehydration PNSS IV insulin M blood glucose Assess LOC and patent airway MVS ± for DHN restoration of acid-base balance andelectrolyte balance

control of glucose level (insulin drip) or sliding scale

fo

r Hyperkalemia: o Kayexalate tx (Enema) ± excretion of K o Gics solution ± admin ofhyperosmolar solution plus insulin in D50-50 o Aerosol tx (salbutamol)- a sympatomimetic drug Excretes K (no need for resting) Adequate contraction of the heartBronchodilation Addison¶s Disease primary adrenocortical insufficiency, hypofx ofthe adrenal cortex causes decreased production of hormones Assessment fatigue,muscle weakness anorexia, N/V, wt loss hypoglycemic reactions hypotension, weakpulse decreased capcity to deal c stress low cortisol levels bronzelike pigmentation of the skin ± common to 2o Secondary:ACTH and low adrenal gland fx Sugar Sexsalt Primary: ACTH px AG fx Sugar Sex salt Nursing responsibilities: Hormone replacement o Glucucorticoids Decadron (dexamethasone) hydrocortisone o Mineralocorticoids (fludrocortisones acetate) MVS and I&O



Decrease stress in the env¶t Prevent exposure to infxn and heat (hot weather) Restperiods, prevent fatigue Weigh daily Provide small freq feedings (high in CHO,Na and CHON) to prevent hypoglycemia and hyponatremia

Addisonian Crisis severe exacerbation of adddison¶s dse caused by acute adrenal in

sufficiency Precipitated by o Strenuous activities o Infxn (pneumonia) o Traumao Stress and failure to take meds o Iatrogenic: surgery on pituitary gland or adrenal glands, rapid cdrawal of exogenous long time steroid use Assessment severegeneralized muscle weakness hypotension hypovolemia shock due to vascular collapse Nursing responsibilities admin glucucorticoids (hydrocortisone) and IVFs tomaintain hydration abt 3-5 liters of saline strict bedrest and eliminate all forms of stressful activities MVS and I&O, weigh daily Protect fr infxn Assess forfluid balance (increase in fluid intake during the hot weather due to increase in perspiration) Thyroid Storm uncontrolled life threatening hyperthyroidism caused by excessive release of thyroid hormone commonly caused by stress, infectionand unprepared thyroid surgery S/Sx o Apprehension o Restlessness o Extremely high temp of abt 40 deg C o Tachycardia o CHF o Resp distress o Delirium o Coma Nu

rsing responsibilities maintain a patent airway and adequate ventilation O2 andIV tx Admin anti thyroid drugs, sedatives and cardiac drugs Give INDERAL Controlfever c non ASA drugs (it competes c thyroxine site storm) Pancreatitis inflameprocess c varying degrees of pancreatic edema inflame of the pancreas that mayresult to autodigestion of the pancreas by its own enzymes leading to hemorrhageand necrosis occurs most often in men in the middle ages Alcoholism is the mostcommon cause Other causes: o Biliary tract dse o Trauma o Drugs

Etiology and Risk factors 1. ROH abuse- causes physiochemical alteration of CHONthat plugs the pancreatic ductules (sphincter of Oddi) 2. Gallstones- when a stone migrates through the ampulla of Vater 3. abdl trauma 4. hyperlipedemia 5. hypercalcemia 6. familial causes 7. Pancreatic trauma 8. pancreatic ischemia Assessment LUQ pain mid-epi of the LUQ that radiates to the back and L shoulder and L

flank Pain is continuous and is worsened by lying down in supine position FETALPOSITION is the most comfortable position for them Wt loss due to N/V Steatorhhea Abdominal assessment o Generalized jaundice o Cullen¶s sign ± grey blue discoloration of the flank o Low bowel sounds due to paralytic ileus o Abdominal tenderness, rigidity and guarding the peritoneum o VS ± M impending shock Laboratories serum amylase-2-12 hours fr onset of the mainifestations serum lipase- on of the most specific indications bec it is solely the Pancreatitis (7h-2d) WBC- above 10,000mm3 Hyperglycemia hypocalcemia Types of Pancreatitis 1. Acute Pancreatitis a.apigastric pain radiating to the back b. Cullen¶s Sign (purpura around the umbilicus) c. Turners sign (violet discoloration/ ecchymosis at the L flank) d. Elevated pancreatic enzymes (lipase and amylase) e. MX: i. NPO ii. IVF iii. NGT iv. TPN as a last resort most common compli of this is hyperglycemia v. Avoid ROH 2. Chronic Pancreatitis a. Abdl pain or tenderness (LUQ) b. DM c. Mx: i. High calorie diet, low fat ii. Avoid ROH iii. Admin pancreatic enzymes iv. glucoseMx Pathophysiology Trypsin by HCl Protelytic enzymes and lipolytic enzymes Prematurely activated in the pancreas Tissue damage Interventions



Comfort Measures o Knee chest position or side lying position c pillow pressed against the abd TPN During the recovery phase when food is tolerated give small freq feeding mod to high CHO, high CHON, low fat meals Food shld be bland c liitle spice Caffeine (tea, etc._ shld be avoided GI irritants ENSURE (directly absorbed amino acids) AVOID ROH Fasting- to rets the pancreas and dec Pancreatic enzy

me action IV- for rehydration Meperidine- drug of choice Morphine- contraindicated because spasm of the sphincter of Oddi can potentiate parenchymal injury Ca and MgSO4 ± IV replacement Gastric decompression- prevents gastric digestive juicesfr flowing into the duodenum NGT drainage and suction- for continuous V/ give DEMEROL Food in the duodenum CCU cells PZ cells Stimulated Gallbladder Release bile Bile salts pancreas release enzymes Pancreatitis

Renal Failure and End-stage Renal Dse early sign is albuminuria (cloudy in appearance) N, K and CHON are absorbable in kidneys Acute Renal Failure is the rapiddecline of renal fx c azotemia (presence of urine by-products in the blood) andfluid and electrolyte imbalance onset is sudden (hours to days) % of nephron involvement : 50 % Duration is 2-4 weeks to less than 3 months Prognosis- good if n

ephron of renal fx c supportive care, high mortality in some situations Causes Renal infection o take full course antibiotics and drink at least 3L of h2o everyday ± prevents ARF (abt 8-10 glasses) NSAIDS o vs COX1 dec BV dec CO tissue hypoxia (give Na and H20 tx) DM o High glucose level inc tonicity of the circulation dec perfusion formation of plaques in the intimal wall of glomerolus dec GRF RF HTN Glomerulonephritis Types of ARF 1. Pre-renal failure- inadequate kidney perfusion a. due to heart failure, etc 2. Intrarenal or intrinsic renal failure ± damage to the glomeruli, interstitial tissues or tubules a. DM b. Pyelonephritis (cloudy or whitish urine output) c. Presence of stones 3. Post-renal Failure ± obstruction in the urine flow a. Tumor in kidney bladder b. Testicular carcinoma c. Cystolithiasis Other lecture:, refer to brown paper«

Nursing Dx: imbalance nutrition: LTBR Hepatic Encephalopathy inability of the li

ver to convert ammonia to urea that accumulates causing neurologictoxic manifestations causes: o liver cirrhosis o hepatitis o Pancreatitis o gallstones ammonia(crosses the BBB blood brain barrier) CHON AA Intestine thru E coli Ammonia Liver Urea Kidneys Ammoniacal odor of the urine Management admin enemas c intestinal antibiotics eg. Aminoglycosides gentamicin and lactulose (increases the osmolality incr fluid soft stool « attracts the fluids to feces, absorbs NH4 to be disposed in the feces) as ordered restrict dietary CHON in the diet: provide a high CHO intake and Vit K supplements

RYAN M. ECUNAR, SLU SN IV Saint Louis University College of Nursing Baguio City



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33672731 Critical Care Nursing