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Acute Biologic Crisis

Prepared by:

Michael Magpantay

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CRITICAL CARE NURSING

nurse licensed professional who provides careto meet the

patient s individualized needs in response to potentially

life-threatening conditions in an environment supportive of

highly technological, collaborative and holistic care.

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Common Problems Seen in Critical Care Setting

1. Anxiety

2. Impaired communication

3. Sleep deprivation4. ICU psychosis

Common procedures

1. Hemodynamic monitoring

2. Circulatory assist device * IABP

3. Airway maintenance adjuncts

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Complications

1. Sepsis

2. MOSF Multiple Organ SystemFailure

3. Shock

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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 ,

newTT, or trauma

Tx : Acknowledge patients concern ; reassurance ;

alleviate common difficulties; family feedback

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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

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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 bodys ability to perfuse the tissues

effectively than CO.

- NV- 2.5

4.0 L/min/m 2

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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

-----------------

3

CVP- blood within the heart & great vesselsof

the thorax

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Types ofHemodynamic Monitoring

1. Arterial lines provides a direct, intra-arterial 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.

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Nursing Management : Same mechanics in CVP

reading1. 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 tubingsper 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 toinsertion site.

4. Perform Allen Test prior to radial artery insertion and freq.

monitor distal pulses to decrease A/E.

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2. Swan-Ganz Catheter Pulmonary Artery Balloon Flow

provide indirect measurement of LV function for detectionand 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

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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.

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4. W/O for complications : dysrrhythmias, infection, air

embolism,catheter occlusion, pneumothorax, thrombus

formation.

3. Circulatory Assist Device Intra-Aortic Balloon Pump

a counterpulsation device that assists to augment CO and

to provide adequate rest and recovery.

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Indications :

cardiogenic shock

heart failure

support before heart transplantation

unstable angina

failure to wean from CP bypass after coronary

bypass surgery

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Nursing Management :

1. Assist with placement as needed and maintain sterilit

with dressing changes.2. Monitor and record effectiveness inc. CO, inc. BP,

inc. U.O., inc. LOC, palpable peripheral pulses,

improved ischemic EKG changes.

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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

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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

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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.

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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

Cause : failure of one or more body systems after a majorinsult to the body such as infection, trauma, severe

illness, persistent hypotension and hypoxia.

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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.

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Dx; 1. ABG- severe acidosis

2. WBCs dec. platelet less than 80,000/mm 33. dec. fibrinogen

4. inc. PT,PTT, hgb, hct , severe anemia

5. inc. urea, BUN

6. inc. cardiac, hepatic enzymes7. inc. serum K

8. CXR interstitial edema and hypoperfusion

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Tx:1. V/S,CVP 8-10 mmHg

2.ABC3. Hemodialysis/hemofiltration

4.Nutritional suspport

5. Antibiotics

6.Bleeding control7.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.

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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

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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, slowthready pulse, ARDS, bleeding, coagulation

dysfunction, coma.

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Dx:

1. dec. hgb/hct

2. ABG- acidosis

3. inc. serum lactate and K

4. inc. cardiac hepatic GI enzymes5. inc. BUN crea RF

6. initially increase glucose to decrease glucose stores

7. dec. sp. grav. urine

8. depletion of clotting studies9. ST ischemic changes ECG

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Management :

1. ABCDEFGH

2. BT.IV NSS, LR, O 2, Vasopressors, vasodilators,

inotropics

3. Correct acidosis- anaphylactic and septic shock4. 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

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ARDS Acute RDS

-a syndrome char. by a non-cardiac type of pulmonaryedema 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

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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

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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

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Tx :

1. O 2

2. Neuromuscular blocking agents3. Sedation to tolerate mech. Ventilation

4. Fluid therapy- crystalloids, colloids IVC volume

5. Hemodynamic monitoring

6. Treat underlying cause of ARDS- antibiotics7. Provide nutritional support CHON balance

8. Steroid therapy stabilize cellular membrane and dec.

fluid shifts

9. Diuretic therapy10. Comfort, positioning HOB elevated

11. V/S, EKG, Neuro

12. Conserve energy-schedule activities/family teaching

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She sails on the sea shore/ coz she sells/

sea shells / by the sea shore.

Peter piper/ picked a pack of pickled

pepper/ How many packs / of pickled

pepper / did Peter Piper picked?

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Beta Bota/ bought a bit of butter

He said/ his butter was bitter, and

It will make/ my butter better So, Beta Bota / bought a bit of butter.

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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:1

5:2 for 4 cycles :1

minute1 inches compression lower1/3 sternum at a rate of100

times per minute.

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ACLS manages the airway thru ET intubation or useof an advanced airway device.

- ET placement check

- Venous access peripheral IV g 16-18Drugs:

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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 only3. 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 IV7. Na HCO3- 1 MEQ/kg/IV bolus

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Asystole: pulseless electrical activity

1. Epinephrine

2. At SO 4

3. CPR/ transcutaneous pacing

Bradycardia

1. At SO 4

Ventricular fibrillation

-chaotic rhythm, rapid disorganized depolarization of

ventricles

Tx: defibrillation 200-300-360 joules / O 2 / CPR /

Epinephrine lidocaine amniodarone

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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

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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

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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 IVP3. Verapamil Isoptin 2.5-5mg Iv over 2 mins.

4. Synchronized Cardioversion

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Nursing Role During a Code :

Call Code

CPR, paraphernalia

Determine team leader

Serial assessments and documentationCrowd control

Psychosocial needs of family, room mates and staff

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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.

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Etiology : As the need for cellular fuel grows more critical ,

the body begins to draw on its fat and CHON

stores for energy. 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 B-

hydroxybutyrate---- severe acidosis

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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.

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4 Pathologic events in DKA

1.Incomplete lipid metabolism

2. DHN

3. Metabolic acidosis

4. Electrolyte imbalance

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S/Sx :

- hyperglycemia

glycosuria polydipsia

ketonemia

ketonuria

metabolic acidosis

Kussmauls respiration acetone breath-dec. acetone combining power

DHN

dry skin

sunken eyeballs

flushed face

electrolyte imbalance

tachycardia

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Management : Prevent complications

1. Adequate ventilation

2. Fluid replacement-NaHCO3,NaCl,K

3. Insulin4. Indwelling FC

5. IVF,D5050 IV

6. Hgt ,ABG,CXR,12 lead EKG

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HHNK-Hyperglycemic Hyperosmolar

Nonketotic Coma

-a condition resulting from elevated concentration of blood

glucose

- level which increases the osmolarity of blood without

significant ketoacidosis.

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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

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THYROID STORM

-one of the 3 major complications of Graves ds.:

exophthalmos, heart ds., thyroid storm.

-Sometimes fatal, acute episodes of thyroid overactivity

char. By high fever , severe tachycardia, DHN and extreme

irritability.

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Causes :

1. Increased amounts of thyroid hormones

2. With Graves ds., undergoes sudden stress or developsan infection

3. A pregnant woman enters labor

4. individuals inadequately prepared for thyroid surgery

5. Unrecognized hyperthyroidism

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S/Sx:

1. increased temp. 41 C

2. DHN

3. irritability

4. frustration5. cardiac dysrythmias

6. CHF

7. delirium

8. diarrhea/N/V

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HEPATIC ENCEPHALOPATHY

-encompasses a spectrum of CNS disturbances

such as severe liver injury, liver failure orportal shunt.

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Pathology :

1.Increased NH3 levels in the blood and CSF

-many unusual cpds. Begin to form Octopamines :

false neurotransmitters

2. Failure of the liver to perform a function due to liver celldamage and necrosis.

3. Shunting of blood from portal system directly into the

systemic venous circulation bypassing the liver.

4. CNS disturbances- hepatic coma death

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S/S x :

1.impairs memory, attention, concentration and rate of

response

2.sleep pattern reversal

3. significant changes in handwriting and speech4. 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- depressedconfusedcoma

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Dx:

1. Serum NH3 level, electrolytes, CSF

2. ABGs,EEG, Hepatic Function Tests bilirubin, albumin,

prothrombin, enzymes

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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.

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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

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RENAL FAILURE

-state of total or nearly total loss of the kidneys ability to

maintain F/E balance and excrete waste products.

-inability of the kidney to function normally or effectively.

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Renal Insufficiency

-designates significant loss of renal function but witha 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.

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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.

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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.

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2. Stage of renal insufficiency metabolic wastes beginto accumulate in the blood and there is a slight increase

in BUN.

3. Stage of uremia the kidney loses its ability to maintainhomeostasis.U.O. is usually scanty, electrolyte balance

is severely disturbed and nitrogenous wastes accumulate

in high concentrations.

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S/Sx : 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

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Management :

1. Diet: Giordano Giovanetti Regimen- dec. CHON,

essential amino acid, -controlled K1,500mg, 20g

very low CHON, minimal essential AA.2. Tx of Infection : unnecessary surgery and instrumentation

are avoided; antibiotics

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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.

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-Ca gluconate- as an emergency measure when the K level isdangerously 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 theserum K.

-Na HCO 3 treat acidosis.

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Aggressive Mgmt :

1. Hemofiltration/Hemodialysis

2. Peritoneal Dialysis

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End of acute biologic crisis!