Acute Biologic Crisis

Prepared by: Joanalain C. Cortez, RN

CRITICAL CARE NURSING 

Nurse licensed professional who provides care to meet the patient s individualized needs in response to potentially life-threatening conditions in an environment supportive of highly technological, collaborative and holistic care.

Common Problems Seen in Critical Care Setting 1. Anxiety 2. Impaired communication 3. Sleep deprivation 4. ICU psychosis

Common procedures 1. Hemodynamic monitoring 2. Circulatory assist device * IABP 3. Airway maintenance adjuncts

Complications 1.Sepsis 2.MOSF Multiple Organ System Failure 3.Shock

Nursing Interventions
1.Anxiety related to fear of death, unknown patients and significant others; ineffective coping mechanism . Tx: Family participation, biobehavioral intervention 2. Impaired communication related to barriers : ET, new TT, or trauma Tx : Acknowledge patient¶s concern ; reassurance ; alleviate common difficulties; family feedback

3. Sleep deprivation : lack of consistent REM and NREM Tx: Meds ;Family visits ; rest periods; decreased environmental stimulation ; biobehavioral intervention 4. ICU psychosis -acute confusional state sec.to CNS stimulants, narcotics, depressants, steroids/ sleep deprivation, sensory overload, F/E imbalance, dec. Oxygen, infection, head trauma, brain disorders

Hemodynamic Monitoring
1.Cardiac Output ± volume of blood that is ejected from the heart in 1 minute. - determined by the HR x SV expelled per heart beat. - NV- 4-8L/min. 2. Pre-load ± amount of stretch in the LV just before ventricular contraction at the end of diastole.

3. Afterload ± tension the ventricle must overcome to eject the blood into the arterial systems (pulmonary and aortic); measured by the systemic vascular resistance. 4. Cardiac index ± is the CO by the BSA - better indicator of the body¶s ability to perfuse the tissues effectively than CO. - - NV- 2.5 ± 4.0 L/min/m 2

PCWP-BP in the most distal peripheral capillariesof the PA. (Left Atrial Pressure) PAP-pressure exerted on the PA walls being pumped out of the RV MAP-average of S &D BP- DBP+2SBP
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CVP- blood within the heart & great vesselsof the thorax

Types of Hemodynamic Monitoring
A. Arterial lines ± provides a direct, intraarterial measurement of BP; assist in the continuous measurement of SBP, DBP and MAP. Method : a 20 g arterial catheter inserted into the radial, brachial or femoral artery connected to high pressure tubing leading to a pressure transducer and amplifier.

Nursing Management : Same mechanics in CVP reading 1.Drawing a ± blood sample ± flush A line with valve flush device to allow return of sharp arterial waveform thru a 3 way stopcock. 2. Change dressings 24-48 hrs., IV solutions and IV tubings per hosp. policy 48-72 hrs.

3. Watch out for complications : bleeding from insertion site , hemorrhage, infection- systemic , air embolus, thrombosis, occlusion of circulation with loss circulation distal to insertion site. 4. Perform Allen Test prior to radial artery insertion and freq. monitor distal pulses to decrease A/E.

B.Swan-Ganz Catheter ± Pulmonary Artery Balloon Flow provide indirect measurement of LV function for detection and treatment of CP changes.

Method : a 5 lumen, balloon tipped , flow directed catheter connected to a pressure transducer and pressurized heparin flush system is inserted thru a percutaneous or cutdown venous site and directed into the RA. Site : subclavian vein most common

Indications : a. a need to monitor PAP and or PCWP- indirectly reflect LV function. b. provide information about CO, tissue perfusion and BV. c. Obtain venous blood specimens d. Proximal orts used for continuous fluid or medication infusion.

Nursing Management : 1.Level and secure transducer at the phlebostatic axis ± 4th ICS, MAL ± serves as a reference point for the RA. 2. Taking readings ± record PA Systolic and Diastolic Pressures to obtain a PCWP or LVEDP , then inflate the catheter balloon slowly, watch for waveform changesdampening indicates wedging.

3. After reading has been recorded, allow the balloon to deflate passively and lock it out to prevent accidental wedging- take all reading at the end of expiration. 4. W/O for complications: dysrrhythmias, infection, air embolism,catheter occlusion, pneumothorax, thrombus formation.

C. Circulatory Assist Device ± IntraAortic Balloon Pump a counterpulsation device that assists to augment CO and to provide adequate rest and recovery Indications :
‡cardiogenic shock ‡heart failure ‡support before heart transplantation ‡ unstable angina ‡ failure to wean from CP bypass after coronary bypass surgery

Nursing Management : 1. Assist with placement as needed and maintain sterility with dressing changes. 2. Monitor and record effectiveness ± inc. CO, inc. BP, inc. U.O., inc. LOC, palpable peripheral pulses, improved ischemic EKG changes.

3. Monitor circulation, sensation and motor function in leg of insertion , keep the affected leg straight at all times. 4. Keep HOB elevated at least 30 degrees to prevent migration of the balloon. 5. Monitor Sx: hematuria ( excessive anti coagulants) excessive oozing from catheter insertion sites positive guiac in the stool abnormal PT,PTT and platelet counts

6. Complications : ‡ air/foreign body embolus if balloon should rupture ‡ thrombus formation at insertion site ‡ loss of distal circulation ‡ migration of catheter ‡ dissection of aorta ‡ sepsis ‡ complications of immobility

Common Complications in the ICU :
SEPSIS -a diffuse, inflammatory systemic response to a chemical, mechanical, bacterial or microbial assault if untreated leads to shock. -Severe sepsis : hypoperfusion,organ dysfunction, hypotension, septic shock, multi organ systemic failure, death.

Management : adeq. CO 1. ABC 2. D- disability/ drugs : Inotropics, Vasodilators 3. E-expose : V/S : CVP, ECG 4. F-fluids , nutrition 5. Cooling blankets/anti pyretics/antibiotics

MOSF-Multi Organ/ System Failute

Cause : failure of one or more body systems after a major insult to the body such as infection, trauma, severe illness, persistent hypotension and hypoxia.

4 Major Systems : 1. Pulmonary dysfunction 2. Renal dysfunction 3. CV dysfunction 4. Coagulation system failure S/Sx: per organ dysfunction leads to dec. LOC then coma with bleeding and fibrinolysis.

Dx: 1. ABG- severe acidosis 2. WBCs ± dec. platelet less than 80,000/mm 3 3. dec. fibrinogen 4. inc. PT,PTT, hgb, hct , severe anemia 5. inc. urea, BUN 6. inc. cardiac, hepatic enzymes 7. inc. serum K 8. CXR ± interstitial edema and hypoperfusion

Tx: 1. V/S,CVP 8-10 mmHg 2.ABC 3. Hemodialysis/hemofiltration 4.Nutritional suspport 5. Antibiotics 6.Bleeding control 7.Limit activities

SHOCK
-a state of imbalance between O 2 supply and demand in the body that leads to inadequate blood flow to organs, poor tissue perfusion- possibly fatal cellular dysfunction.

Classification: 1. Loss of CBV ± hypovolemic 2. Dec. pump function ± cardiogenic 3. Spinal cord injury ± Neurogenic 4. Overwhelming presence of endogenous mediators causing inflammatory response± septic Compensatory Mechanisms : 1. SNS- massive release of NE 2. Endocrine -ADH 3. RAAM

S/Sx : Early Stage: normal BP, slightly increase CR,
normal to slightly dec.U.O., slight restlessness,anxiety, thirst

Next Stage: progressive shock state ± claasic
shock sx ; cool clammy pale skin, dec. capillary refill, tachycardia, tachypnea, dec. BP, CO, temp., U.O., LOC, metabolic acidosis

Later Stage: Sx of specific organ failure : anuria,
slow thready pulse, ARDS, bleeding, coagulation dysfunction, coma.

Dx: 1. dec. hgb/hct 2. ABG- acidosis 3. inc. serum lactate and K 4. inc. cardiac hepatic GI enzymes 5. inc. BUN crea ± RF 6. initially increase glucose to decrease glucose stores 7. dec. sp. grav. urine 8. depletion of clotting studies 9. ST ischemic changes ECG

Management : 1. ABCDEFGH 2. BT, IV NSS, LR, O 2, Vasopressors, vasodilators,inotropics 3. Correct acidosis- anaphylactic and septic shock 4. Comfort measures 5. V/S,UO,,peripheral circulation, titrate meds., thorough assessment 6. Cardiac dysrythmias, coagulation dysfunction, I&O, hemodynamic status 7. dec. external stimuli, family teaching

ARDS Acute RDS
-a syndrome char. by a non-cardiac type of pulmonary edema and increasing hypoxemia despite administration of tx measures formerly known as adult resp. distress syndrome.

S/Sx : 1. labored respirations 2. restlessness 3. dry, non productive cough 4. cyanosis 5. pallor 6. adventitious breath sounds with used of accessory muscles with retraction

Dx : 1. CXR ± white out due to bilateral diffuse infiltrates 2. PFT ± dec. in compliance , lung capacity 3. Increase peak inspiratory pressures 4. ABG- initially resp. alkalosis due to hyperventilation then acidosis. 5. Inc. hemodynamic monitoring ± PA Systolic and Diastolic Pressures with normal PCWP and LVEDP

Pathology : 1. Primary Insult 2. Chemical mediators released 3.Interstitial edema 4. Alveolar edema 5. Damaged surfactant producing cells 6. Dec. lung compliance 7. Atelectasis, hyaline membrane formation 8. Inc. work of breathing 9. Impaired gas exchange 10. Respiratory failure

Tx : 1. O 2 2. Neuromuscular blocking agents 3. Sedation to tolerate mech. Ventilation 4. Fluid therapy- crystalloids, colloids ± IVC volume 5. Hemodynamic monitoring 6. Treat underlying cause of ARDSantibiotics

7. Provide nutritional support ± CHON balance 8. Steroid therapy ± stabilize cellular membrane and dec. fluid shifts 9. Diuretic therapy 10. Comfort, positioning HOB elevated 11. V/S, EKG, Neuro 12. Conserve energy-schedule activities/family teaching

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CARDIOPULMONARY RESUSCITATION BCLS ± to recognize cardiac or resp. arrest and re establish or provide airway breathing pattern and effective circulation until the client responds or until another type of life support is initiated. HT / CL maneuver, jaw thrust maneuver LLF M-M/ ambu bag Closed CC Adult one rescuer: 15:2 for 4 cycles : 1 minute 1 ½ inches compression lower 1/3 sternum at a rate of 100 times per minute.

ACLS ± manages the airway thru ET intubation or use of an advanced airway device. - ET placement check - Venous access peripheral IV g 16-18 Drugs: Asystole: pulseless electrical activity 1. Epinephrine 2. At SO 4 3. CPR/ transcutaneous pacing Bradycardia 1. At SO 4

Fibrillation, Pulseless Vtach : 1.Epinephrine 1mg repeated 3-5 min, IV; tracheal adm. 2-2.5mg in 10 ml NSS 2. Vasopressin ±Pitressin 40 U or ET single dose once only 3. Amiodarone- Cordarone 300mg IV 4. Lidocaine-Xylocaine-1-1.5mg/kg IV 5. Lidocaine drip 1-4 mg/min for maintenance infusion 6. Procainamide 20mg/min IV 7. Na HCO3- 1 MEQ/kg/IV bolus

Ventricular fibrillation
-chaotic rhythm, rapid disorganized depolarization of ventricles Tx: defibrillation ± 200-300-360 joules / O 2 / CPR / Epinephrine lidocaine amniodarone

Ventricular Tachycardia
-rapid ventricular contraction 100bpm above VR ± 150-250 bpm QRS more than .12 sec. wide, bizarre Tx : hemodynamically stable: O 2 / lidocaine amniodarone to dec. irritability

PVC
-ectopic beats occur earlier than expected followed by a compensatory pause. Salvos: 1. more than 6/min PVC 2. paired 3. multifocal ±differing shapes 4. R on T Tx: Lidocaine

SVT
-more than 100 bpm originating above the ventricle but not in the sinus node. -AR more than 140 bpm VR depends on degree of block Tx : 1. Attempt vagal nerve stimulation 2. Adenosine 6 mg rapid IVP 3. Verapamil± Isoptin 2.5-5mg IV over 2mins. 4. Synchronized Cardioversion

Nursing Role During a Code : Call Code CPR, paraphernalia Determine team leader Serial assessments and documentation Crowd control Psychosocial needs of family, room mates and staff

Diabetic Ketoacidosis
-a complication of IDDM, a condition arising from a lack of insulin resulting in a derangement of CHO, CHON and fat metabolism with DHN and electrolyte imbalance. Ketoacidosis occurs when FA are broken down to ketone bodies because of absoloute or relative deficiency of insulin.

Etiology : As the need for cellular fuel grows more critical , the body begins to draw on its fat and CHON stores for energy.
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Increase fatty acids are metabolized from adipose tissue cells and transported to the liver. Liver in turn, accelerates the rate and produces ketone bodies ( KETOGENESIS ) for catabolism by other body tissues particularly muscle. As increase metabolism- increase ketone bodies ± accumulate in the blood ( KETOSIS ); spill into urine ( KETONURIA ); metabolic acidosis develops develops from acidic effect of ketoacetoacetate and Bhydroxybutyrate---- severe acidosis

Precipitating Factors :
1. taking too little insulin 2. omitting doses of insulin 3. failing to meet increased for insulin due to surgery, trauma pregnancy puberty or febrile illness. 4. developing insulin resistance owing to insulin antibodies or severe emotional stress.

4 Pathologic events in DKA 1.Incomplete lipid metabolism 2. DHN 3. Metabolic acidosis 4. Electrolyte imbalance

S/Sx :
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- hyperglycemia glycosuria polydipsia ketonemia ketonuria metabolic acidosis Kussmaul¶s respiration acetone breath-dec. acetone combining power DHN dry skin sunken eyeballs flushed face electrolyte imbalance tachycardia

Management : Prevent complications 1. Adequate ventilation 2. Fluid replacement NaHCO3, NaCl,K 3. Insulin 4. Indwelling FC 5. IVF,D5050 IV 6. Hgt ,ABG,CXR,12 lead EKG

HHNK-Hyperglycemic Hyperosmolar Nonketotic Coma -a condition resulting from elevated concentration of blood glucose - level which increases the osmolarity of blood without significant ketoacidosis.

Causes : 1. large NaHCO3 infusion as in CPR 2. marked hyperglycemia 3. uremia with increased BUN 4. Na retention from adrenal steroid Tx: 1. Insulin 2. F/E 3. Dialysis

THYROID STORM -one of the 3 major complications of Grave¶s ds.: exophthalmos, heart ds., thyroid storm. -Sometimes fatal, acute episodes of thyroid overactivity char. By high fever , severe tachycardia, DHN and extreme irritability.

Causes : 1. Increased amounts of thyroid hormones 2. With Grave¶s ds., undergoes sudden stress or develops an infection 3. A pregnant woman enters labor 4. Individuals inadequately prepared for thyroid surgery 5. Unrecognized hyperthyroidism

S/Sx: 1. increased temp. 41 C 2. DHN 3. irritability 4. frustration 5. cardiac dysrythmias 6. CHF 7. delirium 8. diarrhea/N/V

Tx:
1. hypothermic blankets,anti-pyretics 2. oral/parenteral anti thyroid drug PTU -to block thyroid hormone secretion followed one hour later by K iodide. 3. corticosteroid prev. adrenal insufficiency- inhibit T4 (thyroxine)-T3(triiodothyronine) conversion rxn decreasing fever and maintain BP 4. beta adrenergic blocking agents- Propranolol,Quinidine ± block the overactive sympathetic nervous functions and relieve cardiac dysrthmias 5. barbiturates- agitation 6. antibiotics 7. caloric intake , B complex ± inc. catabolic rate

HEPATIC ENCEPHALOPATHY

-encompasses a spectrum of CNS disturbances such as severe liver injury, liver failure or portal shunt.

Pathology : 1.Increased NH3 levels in the blood and CSFmany unusual cpds. Begin to form Octopamines: false neurotransmitters 2. Failure of the liver to perform a function due to liver cell damage and necrosis. 3. Shunting of blood from portal system directly into the systemic venous circulation bypassing the liver. 4. CNS disturbances- hepatic coma ± death

S/S x : 1.impairs memory, attention, concentration and rate of response 2.sleep pattern reversal 3. significant changes in handwriting and speech 4. flapping tremors- liver flap or asterixis 5. hyperventilation with resp. alkalosis 6. fetor hepaticus ± presence of methylmercaptans causing the odor char. 7. lab results : inc.NH3 and glutamine 8. dec. LOC- depressed²confused²coma

Dx: 1.Serum NH3 level, electrolytes, CSF 2. ABGs,EEG, Hepatic Function Tests ± bilirubin, albumin, prothrombin, enzymes

Management : 1.Reduce CHON in the intestine- CHON restriction 20-40gms/day, assess GI bleeding, cathartics/enemas 2. Reduce bacterial production of NH3 ± Neomycin and Lactulose Neomycin-not absorbed into the circulation but exerts a powerful effect on the intestinal bacteria responsible for NH 3 production. Lactulose ± a combination of galactose and fructose that passes through the intestine unchanged.

3. Eliminate : a. hypovolemia- F/E imbalance b. hypoxia c. concurrent infection d. hypokalemia-diuretics,I&O e. depressants except phenobarbital 4. Maintain function in the unconscious person- immobility/injury Complication : death

RENAL FAILURE -state of total or nearly total loss of the kidney¶s ability tomaintain F/E balance and excrete waste products. -inability of the kidney to function normally or effectively.

Renal Insufficiency -designates significant loss of renal function but with a function requiring to maintain a normal environment provided no additional stress is added. Azotemia -accumulation of nitrogenous wastes within the blood,not life threatening without a decreased output. Uremia -an azotemia progressing to a symptomatic state.

Types of Renal Failure :
A.Acute RF -a sudden, complete or nearly complete loss of kidney function which develops rapidly over a period of day or few weeks. Output drops suddenly to less than 400ml/day.

3 Phases : 1.Oliguric Phase ± begins shortly after injury and is char. By gradually decreasing U.O. 2.Anuric Phase ± there is total absence of urine production. 3. Polyuric Phase ± recovery , there is marked diuresis, there may be rather marked wasting of various electrolytes, esp. Na, K, HCO3.

Causes :
1. Pre-renal ± when the lesion or cause is before the kidney. - shock, mismatch BT 2. Renal ± when the lesion is found in the kidney itself. - nephritis,nephrotoxic infection 3. Post renal ± reached the kidney - obstruction of the urinary tract : renal calculi.

B. Chronic RF
-gradual deterioration of kidney function occurring over months or years.

3 Stages:
1. Stage of diminished renal reserve- renal function is impaired but metabolic wastes do not accumulate in the blood and the BUN remains normal.

2. Stage of renal insufficiency ± metabolic wastes begin to accumulate in the blood and there is a slight increase in BUN. 3. Stage of uremia ± the kidney loses its ability to maintain homeostasis.U.O. is usually scanty, electrolyte balance is severely disturbed and nitrogenous wastes accumulate in high concentrations.

3 Causes :
1. Pre-renal -gout,DM,sub acute endocarditis 2. Renal -SLE,pyelonephritis,GN 3.Post renal -prostatic obstruction

S/Sx :
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alteration in U.O. weak,easily fatigued becomes increasingly drowsy HA and slight breathlessness and lethargic restlessness and insomnia dry, skin and mucous membrane halitosis- urineferous breath loss of appetite, intractable N/V CNS manifestation- anxiety, irritability, hallucination, mental wandering, muscle twitching, coma HPN anemia edematous, tend to bruise easily

Management :
1. Diet: Giordano Giovanetti Regimen- dec. CHON, essential amino acid, -controlled K 1,500mg, 20g very low CHON, minimal essential AA. 2. Tx of Infection : unnecessary surgery and instrumentation are avoided; antibiotics

3. Tx of alterations in Body Chemistry -limit CHON metabolism and K ; -hyperkalemia ±peaked T wave, depressed ST segment, flaccid paralysis,slow respiration, anxiety, convulsions Tx: Kayexalate ±contain Na in a compound absorbed by the GIT. While in the GIT, the Na exchange places with serum K ; and K becomes part of the non absorbable compound.

-Ca gluconate- as an emergency measure when the K level is dangerously high and cardiac arrythmias are imminent. -Glucose and insulin- insulin causes glucose to go into cell; as glucose moves into the cell, it takes with it and reduce the serum K. -Na HCO 3 ± treat acidosis.

Aggressive Mgmt : 1. Hemofiltration/Hemodialysis 2. Peritoneal Dialysis

Thantk ou!

Thank you!