macam2 syok ok

Preview:

DESCRIPTION

macam2 syok

Citation preview

SHOCK, SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS),& MULTIPLE ORGAN DYSFUNCTION SYNDROME (MODS)

JOAN M. PINO-TALBOT

FALL 2005

SHOCK

A condition that occurs when the cardiovascular system fails to adequately perfuse the body’s tissues.

Inadequate tissue perfusion occurs when there is an imbalance between O2 supply and the demand

BEST TREATMENT OF SHOCK IS PREVENTION

SHOCK SYNDROME

Best defined as a generalized systemic response to inadequate tissue perfusion. Cyclic, self-perpetuating

Regardless of the cause and clinical manifestations…all types of shock result in ineffective tissue perfusion acute circulatory failure or shock syndrome:

Cellular hypoxia Impaired cellular metabolism= tissue damage—Organ

failure-- Death

Shock Syndrome

Etiology 4 Classifications

Hypovolemic Cardiogenic Distributive

Septic, Anaphylactic or Neurogenic

Shock Syndrome

Pathophysiology Initial Stage Compensatory Stage Progressive Stage Refractory Stage

COMPENSATORY STAGE

The body’s attempt to increase O2to tissues. initiate three types of responses:

Neural: increased: HR, contractutility,and venous vasconstriction

Chemical: hyperventilation toneutralized lactic acid Hormonal: vasconstriction,Na &H2O retention

increased blood glucose levels

PROGRESSIVE STAGE

Compensatory mechanism begin to fail. Energy from anaerobic metabolism not

sufficient to maintain cellular functioning & irreversible damage begins: Na/K pump begins to fail---cell & organelles swell Mitochondria the “powerhouse” of the cells

ruptures…cellular energy production ceases: O2 delivery is futile-no longer able to utilize Destructive enzymes leak into cell leading to auto-

digestion leading to cell death

REFACTORY STAGE

Shock now is irreversible at this stage. Unresponsive to medical thearpies… organ systems

fails

MODS occurs MODS is defined as the failure of two or more

interrelated organ systems. Death is imminent !!!! Death as a result of the original problem: ineffective

tissue perfusion---inability to meet cellular O2 demands

Shock Syndrome

Assessment and DiagnosisSBP below 90 mm HgTachycardia or bradycardiaAltered mental statusVaries with specific shock

syndromes

Shock Syndrome

Medical Management Improvement of tissue perfusion Adequate pulmonary gas exchange Adequate cardiac output Optimal metabolic environment Nutritional support

Shock Syndrome

Understanding of pathophysiologyFamily support

Hypovolemic Shock

Hypovolemic Shock Description Etiology

Absolute Relative

Pathophysiology Loss of circulating blood volume

Hypovolemic Shock

Hypovolemic Shock Assessment and Diagnosis

Initial stage Compensatory stage Progressive stage Refractory stage

Hemodynamic Assessment

Hypovolemic Shock

Hypovolemic Shock Medical Management

Correct hypovolemia Restore tissue perfusion

Management Prevention of hypovolemic shock Minimize fluid losses Enhance volume replacement

Cardiogenic Shock

Cardiogenic Shock Description

Failure of heart to pump blood effectively Etiology

Primary ventricular ischemia Structural problems Dysrythmias

Cardiogenic Shock

Cardiogenic Shock Pathophysiology

Impaired ability of ventricle to pump blood

Caused by a “heart” problem Assessment and Diagnosis

Low CO and low BP Compensatory mechanisms develop

Hemodynamic Assessment

Cardiogenic Shock

Card Cardiogenic Shock iogenic Shock Medical Management

Correct underlying cause of pump failure

Increase myocardial oxygen supplyDecrease myocardial demandRestore tissue perfusion

Cardiogenic Shock

Cardiogenic Shock Management

Prevention of cardiogenic shock Limit myocardial oxygen consumption Enhance oxygen supply Knowledge of side effects of interventions

Inotropes, Vasodilators,

Anaphylactic Shock

Anaphylactic Shock Description

Distributive shock Etiology

Antigen-antibody reaction Pathophysiology

Immunologic stimulation Peripheral vasodilation

Anaphylactic Shock

Anaphylactic Shock Assessment and Diagnosis

CV Respiratory Cutaneous Neurologic GI Subjective Hemodynamic

Anaphylactic Shock

Anaphylactic Shock Medical Management

Remove antigen Reverse effects of biochemical mediators Fluid replacement Oxygen Epinephrine

Anaphylactic Shock

Anaphylactic Shock Management

Prevention of anaphylactic shock Note all allergies Facilitate ventilation Enhance volume replacement Promote comfort Hemodynamic monitoring

Neurogenic Shock

Neurogenic Shock Description

Distributive shock Etiology

Disruption of SNS Pathophysiology

Lack of sympathetic tone

Neurogenic Shock

Neurogenic Shock Assessment and Diagnosis

Hypotension Bradycardia Hypothermia Warm dry skin

Hemodynamic Assessment

Neurogenic Shock

Neurogenic Shock Medical Management

Remove cause of neurogenic shock Restore tissue oxygenation and perfusion

Management Prevention of neurogenic shock Immobilization of spinal cord injuries DVT prevention

Septic Shock

Septic Shock Description

Distributive shock Etiology

Septic originIntrinsic factorsExtrinsic factors

Septic Shock

Septic Shock Pathophysiology

Stimulation of immune / inflammatory system

Systemic response

Septic Shock

Septic Shock Assessment and Diagnosis

Initial stage: Massive vasodilation HR: Increases to compensate for

hypotension Lungs: Ventilation / perfusion mismatch

ABG Neuro: LOC decreases WBC: Elevates

Septic Shock

Septic Shock Medical Management

Control and eliminate infection

Reverse pathophysiologic responses

Support CV system

Fluid administration

Provide oxygenation and ventilation

Initiate nutrition

Pharmacologic therapy

Septic Shock

Septic Shock Management

Prevention of septic shockSupport all body systemsProvide comfortPrevent secondary complications

Septic Shock

Septic Shock Pathophysiology

Stimulation of immune / inflammatory system

Systemic response

SIRS & MODS

Multiple Organ Dysfunction Syndrome Nursing Management

Multidisciplinary collaboration Infection (prevention, detection,

treatment) Tissue oxygenation Nutritional / metabolic support

SIRS & MODS

Multiple Organ Dysfunction Syndrome Pathophysiologic Mechanisms

Platelet Activating Factor (PAF) Arachidonic Acid Metabolites (AA) Proteases Complement

SIRS & MODS

Multiple Organ Dysfunction Syndrome Organ-Specific Manifestations

GI Dysfunction

Hepatobiliary Dysfunction

Renal Dysfunction

CV Dysfunction

Coagulation Dysfunction Thrombotic Hemorrhagic