Shock

DR.SALAH ELDOKANY
M.D.CARDIOLOGY
CARDILOGY CONSULTANT
Meeqat Hospital,Madina,KSA

1. DR.SALAH ELDOKANY M.D.CARDIOLOGY CARDILOGY CONSULTANT Meeqat Hospital,Madina,KSA SHOCK By

2. Learning Objectives On completion of this lecture, the student should be able to; Define and classify shock Describe the pathophysiology of shock Describe the clinical approach to a shocked patient using the ABCDE algorithm Distinguish different types of shock clinically. Describe investigation and management of shock

3. Definition Shock is best defined as “a syndrome characterized by global impairment in tissue perfusion and cellular oxygenation affecting different body systems”. it is different from local organ ischaemia (limb gangrene – myocardial infarction - renal infarction)

4. Classification Traditionally shock is classified into four main groups according to the main mechanism of decompensation: Hypovolaemic shock Cardiogenic shock Obstructive shock Distributive shock

5. HYPOVOLAEMIC SHOCK

6. Causes of hypovolaemic shock: Haemorrhagic: External: bleeding vessel due to stab, haematemesis, melena,...... Internal: rupture spleen, rupture aortic aneurysm. Non haemorrhagic: Plasma loss: as in burn and large raw areas. Fluid loss: excessive vomiting, diahrrea, uncontrolled polyuria.

7. CARDIOGENIC SHOCK

8. Cardiogenic shock It is a shock state in which the primary defect is pump failure . Cardiogenic shock due to left ventricular infarction suggests that more than 40% of the left ventricle is involved.

9. Causes of cardiogenic shock Myocardial infarction (most common cause) Myocardial contusion Myocarditis Acute valvular failure Arrhythmia (severe tachyarrhythmia – severe bradyarrhythmia)

10. OBSTRUCTIVE SHOCK

11. Causes of obstructive shock: Pulmonary embolus Cardiac tamponade Tension pneumothorax

12. Mechanism Obstructive forms of shock are those in which the underlying pathology is a mechanical obstruction to normal cardiac output and a subsequent diminution in systemic perfusion.

13. Cardiac tamponade T he distinction between a pericardial effusion and cardiac tamponade . The pericardium resists sudden stretching, and in acute tamponade the cardiac silhouette may appear normal in size. As a result of the noncompliance of the pericardium, a small amount of fluid (usually less than 200 mL) is all that is necessary to produce tamponade. With chronic distention, however, large volumes of pericardial fluid may accumulate with little to no effect on cardiac physiology. The volume of the effusion alone, therefore, does not dictate the clinical course as much as the acuity of its development. uses of acute pericardial effusion include trauma, ischemic myocardial rupture and aortic dissection Which side? Right (thinner muscle – less pressure) Which chamber? Right atrium (thinner muscles – less pressure) At which phase of cardiac cycle? Diastole (less pressure)

14. Cardiac tamponade Causes of cardiac tamponade: Penetrating chest trauma. Ischemic myocardial rupture. Aortic dissection.

15. Massive pulmonary embolism Cardiac output is restricted either by mechanical obstruction of the pulmonary arterial tree or by pulmonary arterial vasoconstriction induced by the release of secondary mediators.

16. Tension pneumothorax Air enters into the pleural cavity (with ball valve mechanism) Air accumulates with increase in the pleural pressure It causes collapse of the epsilateral lung and mediastinal shift. It causes twist to the great vessels carrying the venous return and the cardiac output. Decreasing the cardiac output to the systemic circulation. Mechanism:

17. DISTRIBUTIVE SHOCK

18. Distributive shock (subtypes): Septic shock. Neurogenic shock. Anaphylactic shock.

19. Septic shock a complex interaction between the pathogen and the host’s immune system The normal physiologic response to localized infection includes activation of host defense mechanisms that result in the influx of activated neutrophils and monocytes , release of inflammatory mediators , local vasodilatation , increased endothelial permeability , and activation of coagulation pathways . These responses occur during septic shock, but on a systemic scale , leading to diffuse endothelial disruption , vascular permeability , vasodilatation , and thrombosis of end-organ capillaries .

20. Neurogenic shock Spinal cord injury above the upper thoracic level results in autonomic dysfunction consequent hypotension, bradycardia and warm, dry skin. Mechanism:

21. Neurogenic shock Complete transection of spinal cord. Spinal cord contusion. Causes:

22. Anaphylactic shock Massive histamine release from mast cells after activation by antigen-bound immunoglobulin E (IgE), as well as increased synthesis and release of prostaglandins. These leads to massive vasodilation with decrease in systemic vascular resistance with subsequent hypotension and shock. Mechanism:

23. Pathophysiology of shock At the cellular level: Switch from aerobic to anaerobic metabolism Accumulation of lactate, hydrogen ions and inorganic phosphates Precipitating energy crisis in the cell Loss of cellular integrity Cellular swelling Oxidative stress Lipid peroxidation Mitochondrial dysfunction

24. Clinical findings which might suggest presence of shock: Tachycardia (heart rate > 120 beats/minute) Hypotension (SBP < 90 mmHg) Tachypnea (Respiratory rate > 25 breaths per minute) Altered mental status Delayed capillary refill time. Pale cold extremities Oliguria (<0.5 ml/kg/hr) Classical manifestations of shock:

25. Conduct clinical examination using the Airway, Breathing, Circulation, Disability and Exposure (ABCDE) algorithm. Correct any problem in each component before you switch to the next one. Emergency clinical approach

26. Clinical signs include: Noisy breathing (snoring, grunting) or stridor Absence of protective cough and gag reflexes Drooling, with inability to clear oropharyngeal secretions Management: Manoeuvres: head tilt – chin lift , mandibular thrust. Aiding tools: oropharyngeal airway, nasopharyngeal airway, endotracheal tube. Surgical airway: cricothyrodotomy – tracheostomy. Do not forget your gift O 2 Airway assessment

27. Signs of respiratory distress include: Increased respiratory rate Diaphoresis Use of accessory muscles Intercostal indrawing Cyanosis (late and unreliable sign) Examine the chest – watch for signs of tension pneumothorax Management: You can support breathing by bag – mask ventilation. If tension pneumothorax  needle thoracotomy . Do not forget your gift to the patient pulse oxymeter Breathing assessment:

28. Signs that may be present in a case of shock: Cold extremities Delayed capillary refill Tachycardia Hypotension Weak pulse peripherally and centrally Neck veins (congested or empty) Ascultate the heart (distant heart sound, murmurs, normal). Visible source of blood loss. Do not forget your gifts to the patient: Insert 2 wide pore cannulas – take your blood sample. Attach ECG monitor. Circulation assessment:

29. Management: Give fluid to any shocked patient (500 – 1000 ml) over 10 to 20 minutes. If you suspected a cardiogenic shock, give less fluid You can use vasopressor e.g. Norepinephrine and dopamine. You can use inotrope e.g. Dobutamine and dopamine. Circulation assessment:

30. Level of consciousness using Glascow Coma Score (GCS) Assess the pupillary size bilaterally. Do not forget your gift : check random blood sugar Disability assessment:

31. Full expose patient is a must to make complete examination of the body. So your gift here is to cover your patient again . Exposure:

32. Now you have time to make the other steps of conventional medicine: Complete history taking. Complete examination (from head to heel). Ask for investigations. After emergency algorism (ABCDE)

33. Hypovolaemic shock: Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, pale cold sweaty skin. Empty neck veins – decreased central venous pressure (CVP). Normal heart sounds. Normal breath sounds. Emergency measures: ABCDE Specific investigations: Confirmation of the source of blood loss e.g. upper GIT endoscopy for haematemesis, lower GIT endoscopy for haematochazia, chest X ray for suspected haemothorax, ultrasonography for suspected rupture spleen,… Specific treatment: Replace the lost fluid (fluid, plasma, blood). Secure the source of bleeding (conservative, endoscopic, interventional radiology or surgery)

34. Cardiogenic shock: Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, pale cold sweaty skin. Congested neck veins – high CVP. Murmur (??) Failure crepitations (fine crepitations) if severe left ventricular dysfunction. Emergency measures: ABCDE – be cautious in fluid therapy – consider vasopressor and/or inotropes. Specific investigations: ECG (myocardial infarction – arrhythmia). Echocardiography (to assess EF or valvular lesions). Cardiac enzymes and macromolecules ( troponin , creatine kinase ,…..) Chest X ray (cardiac size and pulmonary congestion).

35. Cardiogenic shock: Specific treatment: Be cautious in fluid therapy. Use inotrope ( dobutamine, dopamine in inotropic dose). Intraaortic balloon counter pulsation. Revascularization if myocardial infarction (thrombolytic or coronary intervention). If valvular lesion, valve surgery may be needed. If tachyarrhythmia, consider DC shock and antiarrhythmics ( cordarone , lignocaine ). If bradyarrhythmia, consider atropine and artificial pacemaker (temporary or permanent).

36. Obstructive shock (tension pneumothorax): Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, pale cold sweaty skin. Congested neck veins – high central venous pressure (CVP). Normal heart sounds but displaced. Decreased air entry and tympanic note on percussion on affected side – tracheal shift to the contralateral side. Emergency measures: ABCDE – consider needle decompression during B assessment Specific investigations: Confirmation after release by chest X ray or CT chest. Specific treatment: After needle decompression, we can insert intercostal tube with under water seal.

37. Obstructive shock (cardiac tamponade): Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, pale cold sweaty skin. Congested neck veins – high central venous pressure (CVP). Distant heart sounds. Emergency measures: ABCDE – pericardiocentesis during C assessment . Specific investigations: Echocardiography is diagnostic (diastolic collapse of right atrium and ventricle). Specific treatment: Pericardiocentesis (echocardiography guided, fluoroscopy guided or blind). Surgical intervention if needed (penetrating injury, aortic dissection).

38. Obstructive shock (massive pulmonary embolism): Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, pale cold sweaty skin. Congested neck veins – high central venous pressure (CVP). Some wheezes on lung fields (histamine release). Reversed and splitted second heart sound. Signs of DVT in any limb. Emergency measures: ABCDE. Specific investigations: Echocardiography may be helpful (right heart dilatation and increased pulmonary artery pressure) CT pulmonary angiography (most diagnostic). D- dimer . Doppler on venous system of limb.

39. Obstructive shock (massive pulmonary embolism): Specific treatment: Thrombolytic therapy (streptokinase – urokinase – tissue plasminogen activator). Embolectomy .

40. Distributive shock (septic shock): Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, warm skin (early) – cold skin (later). Empty neck veins – decreased central venous pressure (CVP). Normal heart sounds. Normal breath sounds. Manifestation of infection process: fever, purulent sputum, abscess. Keep in mind how to diagnose (SIRS, sepsis, severe sepsis, sepsis induced hypotension and septic shock)

41. Distributive shock (septic shock): Emergency measures: ABCDE Specific investigations: Serum lactate, C- reactive protein, ESR, blood culture, culture from suspected source of sepsis. Specific treatment: Keep in mind early goal directed therapy: Maintain cvp (8-12 mm Hg) (using fluid) Keep mean ABP ≥ 65 mm Hg (using vasopressor). Keep haematocrit ≥ 30% (using packed RBC transfusion). Keep central venous oxygen saturation ≥ 70% (using dobutamine) Keep urine output ≥ 0.5 ml/kg/h. Antibiotic (broad spectrum then culture based). Corticosteroid (hydrocortisone) in resistant shock. Source control (drainage).

42. Distributive shock (Neurogenic shock): Classical manifestations of shock: hypotension, bradycardia , weak thready pulse, bradypnea or apnea (if high spinal cord affection), altered mental status, oliguria, warm skin . Empty neck veins – decreased central venous pressure (CVP). Normal heart sounds. Normal breath sounds. Manifestation spine injury: pain, tenderness, quadriplegia. Emergency measures: ABCDE – avoid head tilt chin lift. Specific investigations: CT or MRI spine and cord. Specific treatment: Consider vasopressor ( sympathomimetic ) e.g. norepinephrine, dopamine. Consider atropine.

43. Distributive shock (anaphylactic shock): Classical manifestations of shock: hypotension, tachycardia, weak thready pulse, tachypnea, altered mental status, oliguria, warm skin. Empty neck veins – decreased central venous pressure (CVP). Normal heart sounds. Normal breath sounds – wheezy chest (if with bronchspasm). Other manifestations of hypersensitivity: urtecaria, lip oedema, tongue oedema. Emergency measures: ABCDE. Specific treatment: Antihistaminic. Corticosteroids. Vasopressor (adrenaline).

44. THANK YOU