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LECTURER: IDOL L. BONDOC,M.D.,R.N.

DOC IDOL

 Life-threatening

condition in which systemic BP is inadequate to deliver oxygen and nutrients to support vital organs and cellular function.
tissue perfusion that, if untreated, results in cellular starvation, cell death, organ dysfunction progressing to organ failure, and eventual death.

 Inadequate

1. 2.

Adequate cardiac pump
Effective vasculature circulatory system Sufficient blood volume or

3.

 Almost

any patient with any disease state may be at risk of developing shock
requires assessment ongoing systematic

 Nurse

 Close

collaboration with other members of the health care team and a physician’s orders orders that need to be executed with speed and accuracy

 Anticipate

ANO KA BA? .

1. coronary or noncoronary origin 3.CARDIOGENIC SHOCK – heart has an impaired pumping ability.HYPOVOLEMIC SHOCK – decrease in intravascular volume 2. CIRCULATORY OR DISTRIBUTIVE SHOCK – maldistribution or mismatch of blood flow to the cells .

example:  Pulmonary embolism  Cardiac tamponade  Dissecting aortic aneurysm  Tension pneumothorax .4. OBSTRUCTIVE SHOCK – mechanical obstruction of blood flow through the central circulatory system despite normal myocardial function and intravascular volume.

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    Cellular edema Mitochondrial damage/swelling Increased membrane permeability Lysosomal membrane rupture   Efflux of K Influx of Na and water  Cell damage and death .

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MAP = SBP + 2 (DBP) 3  Example: patient’s BP = 125/75 mm HG  MAP = 125 + (2 x 75) 3  MAP = 92 (rounded to nearest 1/10)  .

PHYSIOLOGY/PATHOPHYSIOLOGY Precipitating cause of shock Decrease circulating blood volume Decrease cardiac output Hypotension and decrease tissue perfusion Baroreceptors stimulated Increase sympathetic stimulation and CV system Increase HR. contractility Arteriolar constriction Venous constriction Increase CO Increase BP Increase return .

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.IDOL L. BONDOC.N.M.R. .D.

CLINICAL FINDINGS IN STAGES OF SHOCK FINDINGS COMPENSATORY PROGRESSIVE IRREVERSIBLE/ REFRACTORY Blood pressure Systolic <80-90 mm Hg Requires mechanical or pharmacologic support Heart rate >100 bpm >150 bpm Erratic or asystolic Respiratory status >20 breaths/min Rapid. shallow respirations. crackles Requires intubation .

compensatory Metabolic acidosis Profound acidosis . initially Respiratory alkalosis.5 ml/kg/hr Anuric Requires dialysis Unconscious Mentation Confusion Lethargy Acid-base balance Metabolic acidosis.CLINICAL FINDINGS IN STAGES OF SHOCK FINDINGS COMPENSATORY PROGRESSIVE IRREVERSIBLE/ REFRACTORY Skin Cold. clammy Mottled Petechiae Jaundice Urinary output Decreased 0.

CLINICAL FINDINGS IN STAGES OF SHOCK FINDINGS COMPENSATORY PROGRESSIVE IRREVERSIBLE/ REFRACTORY Prognosis Good Worse Nil  Carry out Nursing  Monitor tissue  Preventing prescribed Management perfusion complications treatments (hemodynamic)  Promoting rest  Preventing  Reducing and comfort complications anxiety  Supporting  Protecting  Promoting family from injury safety members  Providing comfort .

HELLO!!! .

 Level  Vital   of consciousness signs – PP = SBP – DBP Normal PP = 30 to 40 mm Hg Narrowing PP is an earlier indicator of shock than a drop of SBP  Urinary output values – increase Na. K and  Laboratory glucose .

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RESPIRATORY EFFECTS      Rapid and shallow Crackles Increase C02 Decrease 02 Pulmonary damage progression     ARDS Acute lung injury (ALI) Shock lung Noncardiogenic edema .

CARDIOVASCULAR EFFECTS  Dysrhythmias and ischemia  HR >150 Chest pain to MI Increase cardiac enzymes – LDH. cTn-I Myocardial depression and ventricular dilation    . CPK-MB.

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NEUROLOGIC EFFECTS Dilated pupils Confusion Lethargy .

RENAL EFFECTS  ARF     Increase BUN and serum creatinine Fluid and electrolytes shift Loss of the renal-hormonal regulation of BP Decrease UO below 0.5/ml/kg per hour or below 30 ml per hour .

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LD bilirubin Elevated . ALT/SGPT.Accumulation HEPATIC EFFECTS and lactic acid of ammonia Elevated liver enzymes – AST/SGOT.

GASTROINTESTINAL EFFECTS Stress ulcers Bloody diarrhea toxin translocation Bacterial .

HEMATOLOGIC EFFECTS  DIC     – widespread clotting and bleeding Ecchymoses – bruises Petechiae – bleeding Prolonged PTT and PT Decreased clotting factors and platelet counts .

 Decreased  ECF IV volume = IV + interstitial (3-4x of IV)  Reduction in IV volume of 15% to 25% or loss of 750 to 1300 ml of blood in a 70-kg (154-lb) person .

HATAW YOKABABS! .

RISK FACTORS EXTERNAL: FLUID LOSSES  Trauma  Surgery  Vomiting  Diarrhea  Diuresis  Diabetes insipidus INTERNAL: FLUID SHIFTS  Hemorrhage  Burns  Ascites  Peritonitis  Dehydration .

PATHOPHYSIOLOGIC SEQUENCE OF EVENTS Decreased blood volume Decreased venous return Decreased stroke volume Decreased cardiac output/BP Decreased tissue perfusion .

READ ALOUD!!! .

MAJOR GOALS IN THE MANAGEMENT 1. Modified Trendelenberg's position . FLUID AND BLOOD REPLACEMENT/ RESUSCITATION REDISTRIBUTION OF FLUID a. 3. TREATMENT CAUSE OF THE UNDERLYING 2.

PHARMACOLOGY a. d. Insulin – if DHN is secondary to hyperglycemia Desmopressin (DDAVP) – DI Anti-diarrheal – diarrhea Antiemetic – vomiting b.4. c. .

IMPLEMENTING OTHER MEASURES a. O2 administration Direct efforts to the safety and comfort of the patient .5. b.

GRRRRR!!! .

Impaired heart’s ability to contract and to pump blood oxygen for the heart and tissues Inadequate .

RISK FACTORS CORONARY FACTORS NON-CORONARY FACTORS • Myocardial infarction • Cardiomyopathies • Valvular damage • Cardiac tamponade • Dysrhythmias .

PATHOPHYSIOLOGIC SEQUENCE OF EVENTS Decreased cardiac contractility Decreased stroke volume and cardiac output Pulmonary congestion Decreased systemic tissue perfusion Decreased coronary artery perfusion .

c. PREVENTING CARDIOGENIC SHOCK a. MONITORING STATUS HEMODYNAMIC .NURSING MANAGEMENT: 1. b. Conserving the patient’s energy Promptly relieving angina 02 supplement 2.

. 5. ADMINISTERING MEDICATIONS AND INTRAVENOUS FLUIDS MAINTAINING INTRA-AORTIC BALLOON COUNTERPULSATION ENHANCING COMFORT SAFETY AND 4.3.

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Blood volume is abnormally displaced in the vasculature a relative hypovolemia because not enough blood returns to the heart. which lead to subsequent inadequate tissue perfusion Causes .

RISK FACTORS SEPTIC SHOCK NEUROGENIC SHOCK ANAPHYLACTIC SHOCK • Immunosuppression • Spinal cord injury • Penicillin • Extreme of age (< 1 yr and >65 yr) • Malnourishment • Chronic illness • Invasive procedures • Spinal anesthesia sensitivity • Transfusion • Depressant action reaction of medications • Bee sting allergy • Glucose deficiency • Latex sensitivity .

PATHOPHYSIOLOGIC SEQUENCE OF EVENTS Vasodilation Maldistribution of blood volume Decreased venous return Decreased stroke volume Decreased cardiac output Decreased tissue perfusion .

REACTION BOYS??? .

All invasive procedures must be carried out with aseptic technique after careful hand hygiene Collaborate with other members of the health care team to identify the site and source of sepsis and the specific organisms involved 2.NURSING MANAGEMENT FOR SEPTIC SHOCK 1. .

daily weights 4. nutritional status.3. . Efforts to increase comfort if the patient experiences fever. chills. or shivering Administer prescribed IVF and medications Monitor hemodynamic status. 5. fluid I&O.

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Elevate and maintain the head of the bed at least 30 degrees – spinal or epidural anesthesia 2. mobilize or do passive exercises to prevent DVT (positive Homan’s sign) .NURSING MANAGEMENT OF NEUROGENIC SHOCK 1. Immobilization – spinal cord injury If no spinal cord injury. 3.

monitor for signs of internal bleeding that could lead to hypovolemic shock. a.4. In the immediate post-injury period. and Applying elastic compression stockings – administer heparin as ordered Elevating the foot of the bed b. Supporting cardiovascular neurologic function. . 5.

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existence 3.NURSING MANAGEMENT of ANAPHYLACTIC SHOCK 1. Advise the patient to wear or carry ID that names the specific allergen or antigen . Assess all allergies reactions to antigens Communicate the reactions or allergies or previous of 2.

Be aware of drug interaction if antibiotics is administered Identify patients at risk for anaphylactic reaction to contrast agents Explain the events to patient and family 5.4. . 6.