SHOCK

Shock- Defined
 Circulatory  X-emotional state of

shock/Medical shock  LIFE THREATENING MEDICAL EMERGENCY  Inadequate oxygen consumption to meet peripheral tissue needs

shock  POSITIVE FEEDBACK MECHANISM

Stages of Shock INITIAL:  Hypoperfusion state  Cells perform anaerobic  Hypoxia  Damage of cell respiration  Build up of lactic acid membranes  Metabolic acidosis and pyruvic acid .

Stages of Shock COMPENSATORY:  Body employing  Hyperventilation  Release of adrenaline physiological mechanisms NEUROHORMONAL BIO CHEMICAL and noradrenaline  CUSHING REFLEX .

Stages of Shock PROGRESSIVE OR DECOMPENSATING:  Sodium ions build up  Potassium ions leak out  Sludging of micro  Prolonged vasoconstriction  Reduced perfusion circulation .

Stages of Shock REFRACTORY/ IRREVERSIBLE:  Vital organs have failed  Brain damage  Imminent death  ATP degraded to adenosine .

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HYPOVOLEMIC SHOCK  Most common  Insufficient circulating volume (intravascular bed)  Lack of oxygenated blood .

HYPOVOLEMIC SHOCK: CAUSES ABSOLUTE & DIRECT LOSSES  GI status  Haemorrhage  Plasma losses  Renal losses RELATIVE & INDIRECT LOSSES  Hemothorax  Sepsis  Rupture of spleen or liver .

HYPOVOLEMIC SHOCK: PATHOPHYSIOLOGY .

thready  Hypothermia  Thirs. clammy skin  Rapid. dry mouth  Fatigue  Cutis marmorata  Pupil dilation  Distracted look pulse  Cool. weak .HYPOVOLEMIC SHOCK: CLINICAL MANIFESTATIONS  Altered mental state  Hypotension  Rapid. shallow respirations .

HYPOVOLEMIC SHOCK: MANAGEMENT  Keep MAP equal or • VASOPRESSORS: • Dopamine greater to 60 mmHg MAP= Systolic BP + 2 (Diastolic BP)/3 • Crystalloids • Colloids • Levophed Never position in trendelenburg ! THREE TO ONE RULE • Blood transfusion .

SEPTIC SHOCK  Overwhelming systemic infection  Gram negative or positive bacteria  Endotoxin release producing biochemical and immunological effects .

SEPTIC SHOCK: PATHOPHYSIOLOGY Microbial infection Multi organ failure DEATH Toxins released Fever Hypotension Pulmonary edema Decreased coronary and renal perfusion Mediator released Vasodilation Edema Leukocytosis Coagulation .

SEPTIC SHOCK: MANAGEMENT  Airway (oxygenation. intubation. ventilation)  Spot checking/pulse oximeter  Antibiotic therapy  Obtain cultures  Fluid support  LABORATORY MONITORING  Trace elements. vitamins and glucose are added .

NEUROGENIC SHOCK  Spinal shock  Rarest form of shock  Trauma to spinal cord  T 6 and above spinal cord should be WOF! .

NEUROGENIC SHOCK: Pathophysiology .

NEUROGENIC SHOCK: CLINICAL MANIFESTATIONS  Bradycardia  Decreased cardiac output  Decreased PAP and PCWP  Decreased SVR  Hypotension  Hypothermia .

NEUROGENIC SHOCK: MANAGEMENT  Improve tissue perfusion  Atropine Sulfate  Transcutaneous pacemaker  Volume replacement  Vasopressors  Oxygenation  Artificial Ventilation .

CARDIOGENIC SHOCK  Inadequate pumping of blood to body tissues  Cellular destruction .

CARDIOGENIC SHOCK: PATHOPHYSIOLOGY  Caused by heart attack (MI)damaging to 40 % of ventricles .

CARDIOGENIC SHOCK: MANIFESTATIONS  Hypotension less than 90 mmHg  Weak and thready pulse  PVC’s in ECG tracing  Chest pain and tigthness  Lung and diffused crackles  Dropping of O2 saturation  Nausea .

CARDIOGENIC SHOCK: MANAGEMENT     Thrombolytic therapy Angioplasty LVAD and IABP Pharmacologic Intervention Dopamine Dobutamine Norepinephrine Milrinone Sodium Nitroprusside Nitroglycerin Diuretics .

OBSTRUCTIVE SHOCK Similar to hypovolemic shock but in addition:  Distended jugular veins  Pulsus paradoxus .

ANAPHYLAXIS & ANAPHYLACTOID REACTION  Life threatening hypersensitivity/pseudoallergic reaction IMMUNE MEDIATED CHEMICALLY MEDIATED .

medications.ANAPHYLAXIS  Antigen-antibody     reactionallergies Foods. increased capillary permeability & smooth muscle contraction  Slow reacting substance of     anaphylaxis (SRS-A) Eosinophilic chemotactic factor of anaphylaxis (ECF-A) Platelet activating factors (PAF) Kinins Prostaglandins .release of chemical mediators causing vasodilatation.Primary immune response 2nd exposure. environmental agents. blood products. IgE 1st exposure. etc can trigger an immune mediated reaction.

ANAPHYLACTOID REACTION  May occur without prior to exposure to a drug  Self limiting within 5 to 10 minutes .

giddiness w/  Laryngeal edema  Bronchoconstriction  Pulmonary edema  Dizziness  Altered state of     complaint of a sense of impending doom Vomiting Diarrhea Cramping Abdominal pain consciousness  Tachycardia  Arrythmias  Decreased SVR .ANAPHYLAXIS & ANAPHYLACTOID REACTION: MANIFESTATIONS  Pruritus  Generalized erythema  Urticaria  Angioedema  Restlesness.

3 to 0.ANAPHYLAXIS & ANAPHYLACTOID REACTION: MANAGEMENT  Discontinue causative  WOF severe laryngeal agent  Administer Epinephrine (Adrenaline) @ 0.5 ml dosage  Production of cyclic edema  Albuterol inhalation  Anti-histamines  Corticosteroids adenosine monophospate (cAMP)  ABC’s .