Shock

1. Shock Asfand Baig AmritSandhu

2. What is the definition of shock? • Acute circulatory failure resulting in inadequate or disordered tissue perfusion and insufficient oxygen supply to cells • Low BP isn’t always a feature • Particularly in young people • Don’t wait until low BP

3. 5 types of shock • He - Hypovolaemic • Called - Cardiogenic • Me - Mechanical (obstructive) • A - Anaphylactic • Sadist - Septic Neurogenic - • Distributive shock  - anaphylactic +septic

4. Types and a short sentence on what why? • Hypovolaemic • Insufficient circulating volume • Cardiogenic • Failure of heart to pump effectively • Mechanical/Obstructive • Obstruction of blood flow outside the heart • Distributive (Septic / Anaphylactic) • Impaired utilisation of oxygen by cells

5. What causes the types of shock? • CardiogenicMI, IHD, pericarditis, digoxin toxicity • HypovolaemicBlood loss, diarrhoea, burns, urinary • Anaphylactic Allergy commonly peanut, bee stings • Septic LRTI, UTI, trauma • Mechanical/ObstructivePE, cardiac tamponade, tension pneumothorax

6. Assessing severity of shock • Table - insert

7. Stages of shock • Early - Compensated stage – BP normal • 2nd Stage – Hypotension stage - hypotension despite severe vasoconstriction. • MOF – Decompensated stage

8. Important equations • SV = • EDV – ESV • CO = • SV x HR • BP = • CO x SVR

9. Causes of hypovolaemic shock • Obvious blood loss (external) - trauma/ surgery • Internal blood loss, any major source of internal bleeding/Hidden blood loss • Intrathoracic – Central line • Intrabdominal- May come out 24 hours after if its lower GI • Liver/spleen/kidney • Retroperitoneal • Bony injury • Humerus/tibia/femur/pelvis • Other fluid losses • GIT - vomiting and/or diarrhea (norovirus) • Urinary • Cutaneous (e.g. burns)  • Into the tissues

10. What is the response of the cardiovascular system to hypovolaemic shock • Decreased circulating volume • Decreased venous return • Decreased SV and CO (starling’s law) • Decreased BP – sensed by baroreceptors • Increased sympathetic activity • Increased HR/Vasoconstriction/contractility • Reduced oxygen delivery ~CO x [Hb] x SaO2 • Impaired cellular function • BP remains normal until bottoms out by the quantity of blood loss

11. What neuroendocrine parts of the body are involved in hypovolaemic shock?  • Pituitary • Adrenal • Pancreas • Atrium

12. Coagulation cascade • Heightened in patients that are bleeding. • Vasoconstrcition- thromboxane A2

13. What is the sympatho-adrenal response in hypovolaemic shock? • Reduced stretch of aortic & carotid baroreceptors, and blood flow to chemoreceptors causes reflex increase in sympathetic tone • Increase in SVR and increase in HR • Respiratory arrest and circulatory shock (these conditions decrease arterial pO2 and pH, and increase arterial pCO2) dramatically increase chemoreceptor activity leading to enhanced sympathetic outflow to the heart and vasculature via activation of the vasomotor center in the medulla.

14. What are the effects of the sympatho-adrenal response in the case of hypovolaemic shock? • Harry - Heart - Tachycardia and Increased contractility support CO with moderate hypovolaemia - sympathetics get activated due to baroreceptors sensing low blood pressure • Ron - Redistribution - Blood flow redistributed to vital organs: brain, heart, kidneys, liver, respiratory muscles • Hermoine - Hydrostatic pressure - Reduced capillary hydrostatic pressure leads to fluid moving from ECF to blood • ICF -> • Killed - Kidney - reduced filtration and increased reabsorption restores circulating volume due to sympathetics - via RAAS =angiotensin II & aldosterone release --> vasoconstriction and fluid retention • Voldemort- Venoconstrictionincreases cardiac filling - Arteriolar constriction maintains blood pressure

15. What are the metabolic changes involved in hypovolaemic shock? • Anaerobic metabolism  • lactate & H+ production = metabolic acidosis • Hyperglycaemia • Lack of ATP leads to Na+-K+ pump failure, cell swelling, release of K+ & lysomal enzymes, entry of Ca2+ & cell death 

16. Look for external bleeding sites CONCEALED BLOOD LOSS Signs and Symptoms of hypovolaemic shock • SKIN: Cold pale clammy skin. Poor cap. Refill • Circulation • Tachycardia (NOTE: some pts on Beta blockers…what would this do?) • BP – BIPHASIC • early is increased diastolic/maintained systolic  reduced pulse pressure – thready pulse • Later HYPO • Respiration:Tachypnoea • Kidney: Oligo/Anuria • Brain: Confusion (altered GCS), restlessness, anxiety, dizziness • Metabolic: Anaerobic metabolism switch lactic acid and acidosis, hyperglycaemia, cell death (low ATP, NaK failure  cell death) • Others: Neuroendocrine, Inflammatory mediators, microcirculatory changes

17. Cardiogenic shock • Pump failure • Give examples how this could occur • Ischaemia, arrythmia, electrolyte distrubance (K), MI, valvular failure, myocarditis Backlog of blood builds up in lungs • Clinical manifestations?

18. Cardiogenic shock features • Clinical features • Reduced contractility • Low CO  shock • Murmurs • High LVEDP  • Pulmonary congestion/ oedema • Dyspnoea • Crackles/wheeze • Pulmonary oedema and pleural effusion • RV failure • JVP – elevated CVP • Rx – look at cardio pharm • Note: Diuretics should be considered when using IV fluids (fluid titration)

19. What is the response of the cardiovascular system to cardiogenic shock? • Damage to LV • Decreased contractility • Decreased CO • Increased EDV • Pulmonary congestion/oedema • RV failure

20. Diagnosis and Management • E.g. if MI… • History, ECG, Trop T, angiography • Morphine, Oxygen, Nitrates, Aspirin • Thrombolysis

21. Mechanical Shock • 3 causes • Pulmonary embolism (PE): Overloading of RV and hypovolaemia of LV • Tension pneumothorax: in the pleural space pushes the mediastinum to the opposite hemi-thorax  kinked great veins and tamponade • Pericadialtamponade: prevent filling of heart - trauma, cardiac surgery, MI, ureamia • All present with features of shock, fix underlying cause • Elevated CVP

22. 51yr old Julie Heskin presents to A&E with sudden onset shortness of breath and pleuritic chest pain. There’s nothing remarkable in her Hx except that she has recently returned from visiting her daughter in Australia. • what is your suspected diagnosis Pulmonary Embolism • What investigations will confirm your diagnosis • CT Pulmonary angiogram – gold standard. • D-dimer assay – gives a hint  • How will you treat • Anti-coagulants • Thrombolysis if severe

23. 22yr old Claire Marchal presents with sudden onset and progressively worsening shortness of breath. Examination reveals poor chest expansion on 1 side and deviation of her trachea and absent breath sounds on the same side. • What is your suspected diagnosis • Tension pneumothorax • What is you immediate action • Decompression of thorax – chest tube

24. Mechanical shock caused by a tension pneumothorax. How does it work? How is it treated? • Valve mechanism allows air into pleural space, but not out.  • leads to: • - Increasing pressure collapses lung, then pushes mediastinum and heart to other side. • - Raised intrathoracic pressure and kinked great veins prevents venous filling. • - Features of shock + high venous pressure  • Immediate decompression with needle, then chest drain with underwaterseal

25. 28yr old Alex Heskin presents with sharp stabbing chest pain, and shortness of breath and feeling light-headed following receiving a kick to the chest in a kickboxing match. And also Pulsusparadoxuswhich is exaggerated reduction in strength of pulse (or fall in BP on inspiration) • What is your suspected diagnosis • Cardiac tamponade – pericardium filling with blood • How will you confirm • Echocardiogram • How will you treat • Sub-xiphoidpericardiocentesis

26. Mechanical shock caused by a cardiac tamponade.  Explain the mechanism. How is it treated? • Fluid collects within the indistensible pericardial sac, which compresses the heart. Heart cannot fill, leads to features of shock + high venous pressure. • - Sub- xipoidpericardiocentesis- Sugical exploration

27. What is the response of the cardiovascular system to anaphylactic shock • Inflammatory mediators • Vasodilation and IV coagulation = decreased volume • Leaky capillaries • Blood pools in peripheries • Decreased venous return • Decreased CO • Decreased BP

28. What is the response of the cardiovascular system to septic shock • Endotoxin release = inflam mediators • Vasodilation and IV coagulation = decreased volume • Leaky capillaries • Blood pools in peripheries • Decreased venous return • Decreased CO • Decreased BP

29. Septic Shock • Infection of the blood results in systemic inflammatory response and mass vasodilation – fluids leaks out. • Risk factors – insert • Signs • toxic look –warm/flushed • Hyperdynamic circulation • Low diastolic pressure • Tachycardic/hypotensive • Altered GCS • Peripheral cyanosis • Multi-organ failure (ARDS, Myocardial depression, renal failure) • What is SIRS?

30. Septic shock • Overwhelming sepsis leads to the release of loads of inflammatory mediators.  • These causes vasodilation, intravascular coagulation and loss of circulating fluid (leaky capillaries). • Leads to a decreased venous return and hence a decreased cardiac output. • This causes a drop in BP, particularly diastolic (increased pulse pressure) • Pulmonary hypertension and myocardial depression may also occur.

31. SIRSis defined by….? • 2 or more of... • Systemic Inflammatory Response Syndrome • TWO or more of:- Temperature greater than 38.5 degrees celsius OR below 35 degrees celsius • - Tachycardia with a pulse greater than 90bpm • - Tachypnoea with a respiratory rate greater than 20 breaths per minute at rest • - Abnormal white blood cell count that is either greater than 12x 109/L or less than 4 x 109/L • Also know what are: • Sepsis, Severe Sepsis, Septic Shock,

32. Septic Shock 2 phases.. What are they? And what happens? • Early/ warm shock • O2 delivery adequate, but consumption low. Sv O2high. • Vasodilated warm peripheries, low venous pressure.  • Bounding or collapsing pulse. • Less tachycardia than hypovolemic shock • Pyrexia or rigors • Late/ cold shock.  • Same as hypovolemic shock.- Circulation, brain, kidney, respiritory, neuroendocrine. And Myocardial depression.

33. SEPSIS SIX Give 3 ( High flow Oxygen + IV fluids + IV Antibiotics) Take 2 ( Blood Cultures + FBC/serum Lactate) Monitor 1 ( urine output) • 1: Take blood cultures • 2: Measure FBC and serum lactate levels • 3: Vasopressors and IV fluid resuscitation • 4: Measure urine output • 5: Broad spectrum empericalintravenous antibiotics (Usually ceftriaxone, a form of cephalosporin) • 6: High flow oxygen • Administer if sepsis is SUSPECTED. Treat as septic until proven otherwise. • Multi organ failure and mortality rates are very high

34. Anaphylactic Shock • IgE mediated – type I hypersensitivity • Allergen stimulates IgE to bind mast cells which then degranulate and release histamine. • Vasodilation and increased capillary permeability. • Initially flushed then in the later stages the pateint becomes cyanosed • Myocardial depression / angioneuroticoedema / Stridor/ Bronchospasm

35. Differences between anaphylaxis and anaphylactical • Sensitisation – required/not required • INSERT

36. Anaphylactic Shock • - within 30 mins exposure • - Cutaneous: erthema, urticaria, oedema, pallor, cyanosis. • - Cardio: tachycardia, hypotension • -Respiratory: Rhinitis, bronchospasm, pulmonary oedema, angioedema • - GIT: vomiting, diarrhoea, cramps • Adrenaline and oxygen. Fluids if needed, steroids and antihistamines for support.

37. Septic • General: • Oxygenation • Fluid replacement  • Inotropes & vasoconstrictors  • EARLY specific measures: • bacterial cultures • antibiotics and surgical drainage (remove source) • Anaphylactic • Oxygen • Adrenaline • Fluids • CPR • Steriods & anti histamines • Hypovoleamic • Oxygenation • Replacement of circulating volume • Diagnosis & treatment of cause of fluid losses Management of all types of shock • Cardiogenic • Thrombolysis • Angiography • supportive measures • Old - Oxygenation - High flow O2 - CPAP/ mask • People- Pharmacological - opioid analgesia/ diuretics/ drugs acting on vasomotor tone and contractility • Fear – Filling - IV fluids guided by CVP, PCWP, TOE • Me - Mechanical suppor - Intra aortic balloon pump - increase myocardial o2 and • Mechanical • PE • full resuscitation • anticoagulation • thrombolysis  • surgery • Cardiac tamponade • Sub- xiphoid pericardiocentesis- Sugicalexploration • Pneumothorax • Immediate decompression with needle, then chest drain with underwaterseal • General measures • A - airway • B - breathing • C - Clear airway obstruction