By the end of the lecture students will be able to : 1. Define shock. 2. Describe four stages of shock.

1. By the end of the lecture students will be able to: 1. Define shock. 2. Describe four stages of shock. 3. Differentiate between hypovolemic, cardiogenic and distributive shock. 4. Analyse different assessment findings of patients in a state of shock. 5. Discuss on the general and specific management of patient in shock. 6. Complete the multiple-choice questionnaire with 80% accuracy.

2. SHOCK I. Introduction Shock is an inadequate cardiac output that results in a failure of the cardiovascular system to deliver enough oxygen and nutrients to meet the metabolic needs of body cells. Low cardiac output  reduced tissue perfusion  hypoxia  affect key organs [heart/lungs]. • As a result • ·Cell membranes dysfunction • ·Cellular metabolism is abnormal • Cell death may occur

3. 3 reasons why tissue perfusion might become inadequate • A decreased circulating blood volume • A failure of the heart to pump effectively • A massive increased in peripheral vasodilation

4. Stages of shock • Initial stage • Compensatory stage • Progressive stage • Refractory stage - Irriversible 1.Initial stage Cells deprived of O2  mitochondria cannot produce ATP  anaerobic respiration  lactic acid builds up  metabolic acidosis  harmful to cells

5. Compensatory stage Body’s physiological response to overcome shock ·Hyperventillation to correct acidosis ·Hypotension detected by baroreceptors in carotid arch and aortic sinus  release of adrenaline & noradrenaline  vasoconstriction  BP & HR ·Vasoconstriction of skin, kidneys, GI tract & other organs  blood supply to the heart and brain (selfish organs) ·blood to kidneys  urine output  ologuria

6. Progressive stage • ·Compensatory mechanism fails • · perfusion of cells • ·Anaerobic metabolism continues [micro clot & DIC] • in hydrostatic pressure  leakage of fluid ·Prolonged vasoconstriction •  perfusion  vital organs compromised Refractory stage - Irriversible ·Vital organs failed ·Irreversible damage  brain damage and cell death ·Death within few hours

7. Sign & Symptoms Progressive shock Irreversible shock Neurogenic LOC, confusion, agitation, slowed speech, may be orientated,  pain response Unconscious?, reflexes absent?, disoriented, incoherent speech Pupils dilated Cardio-vascular Tachycardia(.100bmp adult,>130 child), irregular, weak, capillary refill>3sec, peripheral pulse?, skin cold, clammy, BP(systolic<90;diastolic falling) Pulse: slow, irregular, no peripheral pulses, BP(sys falling/unreadable; Dias~0 Cold clammy skin, cyanotic Respiratory Rapid (>20/min), shallow Slow, shallow, irregular (cheyne Strokes) Renal Oliguria (<0.5ml/kg/hr), >specific gravity <18ml/hr, anuria, proteinuria Thirst, hypoactive, no bowel sound,  Temp (except septic), lips & mucosa dry Other <<Temp, severe thirst if still conscious, no bowel sound

8. Classification of shock Hypovolemic, cardiogenic, Distributive [neurogenic, anaphylactic, septic]

9. Decreased Intravascular Volume Fall in cardiac output Shift of interstial fluid Release ofadrenaline/noradrenaline Release of aldosterone/ADH Increased heart rate & SVR Disengorgement of spleen Increased blood volume Increased cardiac output Fig 1: Hypovolemic shock: compensation mechanism

10. Specific management: ØRapid fluid volume replacement ØReplace blood with blood or blood products  maintain Hb levels to promote O2 delivery ØMay use autotransfusion ØControl bleeding-? Surgery

11. Fall in cardiac output Compensatory release Of adrenalin/norad Compensatory renin –aldosterone ADH Adequate/blood volume Increased SVR • preload/stroke volume • & heart rate myocardialO2 demand Pulmonary oedema Dyspnoea Furtherfall in CO Fig 2: Cardiogenic shock: compensatory mechanism

12. Specific management: ØRestore coronary artery blood flow to myocardium ØCardiac catheterisation + angioplasty or stenting ASAP ØCirculatory assist devices ? intraaortic balloon pump, ventricular assist device ØHaemodynamic monitoring: replace fluid cautiously ØRx- inotropic, vasodilator, diuretic, antiarrhythmic

13. Distributive shock ØCharacterised by loss of blood vessel tone ØTank being too large  blood volume remains normal  pressure cannot be maintained  CO ØLoss of vessel tone caused by: 1. sympathetic control 2.presence of vasodilator substance in blood NEUROGENIC ANAPHYLACTIC SEPTIC

14. Imbalance bet: sympathetic & parasympathetic stimulation Massive vasodilation Reduction in vascular tone Decreased SVR Inadequate CO, falling BP  Tissus perfusion of O2&nutri Impared cellular metabolism Fig 3: NEUROGENIC SHOCK

15. Antigen(allergen) meets antibody Body mounts an immune attack Release of chemicals such as Histamine, kinin, prostaglandin Increased capillary permeability Peripheral vasodilation Constriction of Smooth Muscle, Bronchospasm Laryngospasm GI tract cramps Decreased SVR Fluid leaves Intravascular space Hypovolaemia Oedema  CO  tissue perfusion Fig 4: Anaphylactic shock Impaired cellular metabolism

16. Specific management: ØDrug intervention ASAP – epinephrine  peripheral vasoconstriction, bronchodilation, blocks histamine ØAirway: oNebulised bronchodilators oAminophyllin if severe bronchoconstriction oEndotracheal, tracheostomy ØTreat hypotension aggressively  colloids, corticosteroids ØAntihistamine

17. A.Septic shock Bacterial toxins. Pathophysiology: MO invades body tissues  immune response  release of chemical mediators  vasodilation & microthrombi formation  obstruction of blood flow to tissue & organs  hypoxia  lactic acidosis Symptoms: Ø Temp,  BP,  resp, pink & warm skin Specific management Identify source  treat with antimicrobials surgical drainage Rapid infusion large amount of colloids & crystalloids If tissue perfusion poor  inotropic & vasopressor

18. PRINCIPLES OF MANAGEMENT [General] 1.identify cause 2.establish adequate ventilation & oxygenation 3.restore optimum intravascular volume 4.maintain adequate cardiac output and renal perfusion 5.maintain optimum internal metabolic environment

19. Nursing assessment and monitoring parameters 1.Arterial blood pressure 2.Cardiac function (rate, rhythm & output) – monitor & 12 lead ECG 3.Peripheral perfusion 4.Respirations (airway patency & respiratory function) ?intubation 5.Oxygenation status – pulse oxymetry, arterial blood gas ØFalse result of SPO2 in vasoconstriction - BP cuff 6.Level of consciousness – GCS 7.Temperature

20. Position-Trendelenburg's position Contra-indicated, lie flat raise legs above heart • Fluids – IV – 2 large bore – monitor CVP • Urine output – catheter • NG tube • Specific tissue/organ damage and renal function • CPK • SGOT • BUN, creatinine, billirubin, • Electrolyte status • Renal function • Hepatic function • Acid-base status • Haematological status – Hb, coagulation studies, WCC

21. Pharmaceutical interventions: • ØOxygen – High flow O2 non-rebreathing mask • ØInotropic drugs • ØCorticosteroids • ØVasopressors • ØNarcotics • ØTreat arrhythmias DO NOT FORGET: 1.Nutrition -  metabolic rate – nutritional assessment and calculation of requirements. 2.Patient may be kept NBM for surgery 3.Skin care – fluid overload – 3rd space  skin break 4.Patient & family education

22. COMPLICATIONS OF SHOCK 1.Myocardial depression 2.Acute Respiratory Distress Syndrome 3.Acute renal failure 4.Post Resuscitative Hypertension 5.Stress ulcer 6.Disseminated Intravascular Coagulation 7.Hepatic Insufficiency