physioloical integrity acute biologic crisis

8/10/2019 Physioloical Integrity Acute Biologic Crisis

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PHYSIOLOGICALINTEGRITY: ACUTE

BIOLOGIC CRISISIrene Shara L. Castillon


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RESPONSES TO ALTERED

RESPIRATORY

FUNCTION


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RESPIRATORY FAILURE

Failure in Gas exchange due to either

pump of heart or Lung failure or both.

Condition in which the lungs fail tooxygenate the blood adequately and

prevent carbon dioxide retention


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Ventilationthe air that reaches the

alveoli

Perfusionthe blood that reachesthe alveoli


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MECHANISMS LEADING TO

RESPIRATORY FAILURE


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Characterized by:

Hypoxemic Respiratory Failure

O2, N- CO2, Metabolic Acidosis

Hypercapnic Respiratory Failure

02, CO2, Respiratory Acidosis

Major manifestation of Respiratory Failure areHypoxemia and Hypercapnia or both


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Mechanism that can lead to

Respiratory FailureImpaired Vent i lat ion

occurs when the volume of the fresh air moving

into and out of the lungs is significantly reduced.Impaired Dif fusion

Restricted transfer of oxygen and/or carbon

dioxide across the alveolar capillary junction


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Impaired Match ing

of Vent i lat ion and

Perfusion

v/QPerfusion without

ventilation is a blocked

airway.

V/qVentilation without

perfusion is a blocked

capillary


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MANAGEMENT

Mechanical Ventilation (Negative pressure,

Positive pressure)

Endotracheal Intubation

Oxygen Therapy


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ACUTE RESPIRATORY

DISTRESS SYNDROME Cause by diffuse lung injury and leads to

extravascular lung fluid, specifically in the

alveolar capillary membrane.


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Initial Manifestation of ARDS typicallydevelop 24-48 hours after the initial insult

Manifestation:

Tachypnea Dyspnea

Deteriorating ABG levels ( 02, even with 02

delivery)

Lung Compliance

Use of Accessory Muscles


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MANAGEMENT Treat the cause

O2 therapy

Fowlers position Fluid intake Restriction

Administer Diuretics, Anticoagulants or

Corticosteroids Intubation or mechanical ventilator using PEEP


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CHRONIC OBSTRUCTIVE

PULMONARY DISEASE

Slowly progressive obstruction of the airways


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Characterized by:

EMPHYSEMAPink Puffer

It compensatesby hyperventilation. Less hypoxemia

CHRONIC BRONCHITISBlue Bloater

Hypoxemia is worst.


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MANAGEMENT

Monitor VS, Pulse Oximetry

Administer low concentration of Oxygen (1-

2L/min)

Instruct in Abdominal Breathing and pursed-lipbreathing techniques

Place the client in fowlers position and leaning

forward

Administer Bronchodilators and Corticosteroids

High protein, High Calorie intake


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RESPONSES TO ALTERED

NUTRITION AND

METABOLISM

FUNCTION


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LIVER CIRRHOSIS

Diffuse degeneration of the liver and

destruction of hepatocytes

Types

o Laennecs Cirrhosis

o Post-Necrotic Cirrhosis

o Biliary Cirrhosis

o Cardiac Cirrhosis


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COMPLICATIONS Portal Hypertension

Ascites

Bleeding Esophageal Varices Coagulation defects

Jaundice

Portal Systemic Encelophathy Hepatorenal Syndrome


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MANAGEMENT

Weight and Check Abdominal Girth Daily.

Fowlers Position Provide Supplemental Vitamins (B-complex,

Vitamins A, C and K, Folic acid and thiamine)

Restrict H20 and NA Monitor forAsterixisand Fector Hepaticus

Gastric Intubation or Balloon Tamponade for

Esophageal Varices

Monitor Coagulation Therapy

Meds: Diuretics, Lactulose, Oxazepam

Paracentesis


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DIABETIC KETOACIDOSIS

Sudden onset

Occurs in people with Type 1 DM

Precipitating FactorsInadequate Insulin dose/Infection

Characterized by:

blood glucose serum pH

ketonuria


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Manifestation

Dehydration (dry mucus membranes,

tachycardia, hypotension)

Fruity odor to breath:Acetone

Acidosis: Kussmaul breathing, change in

consciousness

Signs of infection: fever, oropharyngeal

erythema, boils on skin

Electrolyte Loss


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Management

Fluid Replacement

Insulin Administration

Electrolyte Imbalance correction


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NON-KETOTIC

HYPERGLYCEMIC

HYPERSOMOLAR SYNDROME Onset is gradual

Occurs in people with type 2 DM

Precipitating FactorsPoor fluid intake or infection

Characterized by:

Plasma Osmolarity >340 mOsm/L

Greatly elevated blood glucose (>600mg/dL)

Altered LOC


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Management

Fluid Replacement

Insulin Administration Electrolyte Imbalance correction


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Responses to Altered

ELIMINATIONFUNCTION


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ACUTE RENAL FAILURE

Reversible

Characterized by accumulation of

nitrogenous wastes in the blood andalterations in body fluids


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Has 3 Causes

PRERENAL FAILUREConditions affecting before reaching the

nephrons

INTRARENAL FAILUREConditions affecting nephron itself.

POSTRENAL FAILURE

Conditions affecting beyond the nephron or the

urinary tract.

Obstruction of the urine collecting system


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3 STAGES OF ARF Oliguric/Anuric Phase

lasts between 8-14 days

Great reduction in the GFR

Increased BUN/Creatinine

Electrolyte abnormalities (hyperkalemia,

hyperphosphatemia and hypocalcemia)

Metabolic acidosis


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Diuretic Phase

source of obstruction has been removed but

the residual scarring and edema of the renal

tubules remains

last 7-14 days and is characterized by:

Increase in glomerular filtration rate (GFR)

Urine output as high as 2-4 L/day

Urine that flows through renal tubules

Renal cells that cannot concentrate urine


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Recovery Period Phaselast from several months to over a year

Condition is getting back to normal function

(if damage was significant, BUN andCreatinine may never return to normal

levels)

GFR has usually returned to 70% to 80% ofnormal.


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Diagnostic Test

Urinalysis

Serum Creatinine and BUN

Serum Electrolytes

ABG

CBC

Renal Ultrasonography

CT- Scan

Intravenous Pyelography

Renal Biopsy


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Management

Fluid Restriction

Dietary Management

Medication Administration

Diuretic (Loop and Osmotic Diuretic)

Electrolyte Replacement (Calcium,

Potassium)

Erythropoietin

Dialysis


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CHRONIC RENAL FAILURE

Progressive irreversible kidney injury.

When kidney function is too poor to sustain

life, CRF is termed End-stage renal disease

80% of nephrons stop working before

symptoms show up, a silent disease


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ManifestationUremic Frost

Uremia

AnemiaHypertension

Uremic Fretor (Urine-like breath)

Renal EncepalophathyCNS Manifestation


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Stage 1: Reduced Renal Reserve a 40-75% loss of nephron function, no

symptoms

Polyuria/ Nocturia- First sign of CHF. Fromthe loss of nephron functioning and

kidneys can not concentrate the urine


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Stage 2: Renal Insufficiency

78-80% nephron function is lost and

replaced by scare tissue. Symptoms begin CLINICAL SIGN: Hyponatremia, increased

BUN and Creatinine.


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Stage 3: Final Stage

End Stage Renal Disease ESRD only 10% of

nephrons remain functioning


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Management

Fluid Regulation

Dietary Management Skin Care

Potassium and Phosphorous restriction

MedicationsDiuretics

Electrolyte Imbalances Corrections

Insulin Administration

Folic Acid/Ferrous Sulfate


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LONG-TERM MANAGEMENT

Dialysis

Kidney Transplant


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Reference

Ignatavicius D. and Workman, M. (2006) Medical-surgical nursing

(Fifth edition).United states of America: Elsevier saunders

Porth, C. (2005) Pathophysiology (seventh edition). Philadelphia:

Lippincott Williams and Wilkins Lemone, P. and Burke, K. (2004) Medical surgical nursing (third

edition). New Jersey: Pearson Education, Inc.

physioloical integrity acute biologic crisis

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