learning on easy education on CME Shock .pptx

Briefly on shock and stages

1. APPROACH TO SHOCK Presented by : Farahin

2. Outlines Definition of Shock Pathophysiology of shock Classification of Shock Hypovolemic Shock Cardiogenic Shock Obstructive Shock Distributive Shock

3. Definition of Shock Life threatening emergency Reversible in appropriately recognized and treated Inadequate perfusion of tissue , such that the oxygen and blood volume delivery fails to meet the cellular metabolic and consumption need.

4. Pathophysiology: Cellular Insufficient delivery of oxygen and glucose Cells switch from aerobic to anaerobic metabolism If perfusion is not restored in a timely fashion, cell death ensues

5. Pathophysiology: Microvascular Tissue ischemia  activation of the immune and coagulation systems Hypoxia and acidosis activate complement and neutrophils  generation of O2 free radicals and cytokine release This leads to injury of the capillary of endothelial cells Damaged endothelium loses its integrity and becomes ‘leaky’. This allows fluid to leaks out and tissue edema ensues

6. Pathophysiology: Systemic Cardiovascular ↓ preload and afterload  compensatory baroreceptor response  ↑ sympathetic activity, release of catecholamines This results in tachycardia and vasoconstriction (except in septic) Respiratory As there is metabolic acidosis and ↑ sympathetic response  ↑ in RR  ↑ excretion of CO2 This produce a compensatory respiratory alkalosis Renal ↓ perfusion pressure  ↓ glomerular filtration  ↓ urine output  stimulates renin- angiotensin- aldosterone axis This leads to further vasoconstriction and ↑ water and sodium reabsorption in the kidney Endocrine Due to preload, ADH secreted by by pituitary resulting in vasoconstriction and ↑ resorption of water from kidney. Adrenal cortex will release cortisol and contributes to sodium and water reabsorption and sensitizing the cells to catecholamines

7. STAGES OF SHOCK

8. HISTORY May be difficult or impossible due to altered mental status Prior medication and history may help Possibility of trauma in unconscious patient without witness PHYSICAL EXAMINATION Physical examination of patient in shock must be done thoroughly ABCDE approach helps to efficiently evaluate patient while balancing management priorities

9. ED EVALUATION Vital signs are important indicators of the patient’s physiologic status

10. DIAGNOSTIC STUDIES

11. Classification of Shock ◦ TYPES OF SHOCK HYPOVOLAEMIC ( Intravascular volume loss) Haemorrhagic (Trauma) Non-haemorrhagic (DKA/AGE/Dengue fever) CARDIOGENIC (Ineffective pumping due to heart damage) Myocardial infarction Arrhythmias Mechanical Cardiomyopathy DISTRIBUTIVE (Abnormal blood flow in the small vessels caused by generalized peripheral dilatation due to inflammatory causes) Septic shock Anaphylactic shock Neurogenic shock OBSTRUCTIVE (Blood flow to and from the heart is blocked due to obstructive presure ) Pulmonary embolism Cardiac tamponade Tension pneumothorax

12. HYPOVOLAEMIC SHOCK

13. HYPOVOLAEMIC SHOCK The most common form of shock and to some degree is a component of all other forms of shock. Can be divided into two: Hemorrhagic Non- hemorrhagic

14. HISTORY History of trauma, recent surgery, evidence of bleeding, vomiting, diarrhea or GI illness point to fluid loss PHYSICAL EXAMINATION Cold peripheries, low pulse volume, prolonged CRT. Pallor in setting of bleeding INVESTIGATION FBC – Haemoglobin and haematocrit Electrolytes – Potassium, Calcium Acid/base – Lactate, acidosis/alkalosis Renal function – BUN: creatinine ratio > 20 Coagulation study – Prolonged due to coagulopathy Imaging – CXR, FAST scan, CT scan, Angiography TREATMENT

15. CARDIOGENIC SHOCK

16. 2. CARDIOGENIC SHOCK Result from failure of the cardiac “pump” to forward delivery of blood and, therefore, oxygen to the tissues, leading to shock. Pressure in one or both ventricles may elevate due to inefficiencies in the right or left side of the heart. When pressure elevate on the left side, pulmonary oedema may occur causing right heart dysfunction and leads to systemic congestion. In response to reduction in cardiac output, systemic vascular resistance increase in response to catetholamine stimulation and angiotensin II.

17. HISTORY Classically presents with crushing substernal pain, upper extremity, back, epigastric or jaw pain. Atypical chest pain in women and patients with neuropathic changes in heart innervation ( eg diabetic) PHYSICAL EXAMINATION New or changing murmur in valvular disruption Signs of elevated filling pressure  increase JVP in right heart failure, bibasal crepitation on auscultation of the lung in left heart failure Cool and mottled extremities Vital signs: INVESTIGATION TREATMENT  HR – ↑/normal/↓  BP – normal or ↓  RR – ↑  SpO2 – ↓ ECG Cardiac enzymes – troponin, CK,CKMB CXR Echocardiography Optimization of intravascular volume with caution Medication administration – dual anti platelet when necessary Vasopressor support to MAP 65mmHg – noradrenaline and dopamine Fibrinolytic therapy and/pr percutaneous coronary intervention (PCI) Admission to coronary care unit

18. DRUGS RECEPTOR EFFECT DOSE DILUTION IONOTROPES ADRENALINE ɑ 1 and ß receptors Low dose : Beta effects predominate Increasing CO and Vasodilatation Higher dose : Alpha 1 effects predominate Increasing Systemic vascular resistance Also causes splanchnic vasoconstriction, hyperglycemia, increased myocardial O 2 consumption and lactate production   2-10mcg/min 1-2mcg/kg/min   3mg/3cc dilute in 50cc NS   DOPAMINE ɑ 1, ß1, ß2 & dopamine receptors   Low dose : Dopamine effects predominate Increased splanchnic and renal perfusion Higher dose : Alpha 1 and Beta 1 effects predominate Results in vasoconstriction and increased CO 5-20mcg/kg/min   1amp : 5cc : 200mg dilute in 45mls NSD5   DOBUTAMINE ß1 and ß2 receptors   Beta 1 : Increased HR and force of contraction Beta 2 : Peripheral Vasodilatation Useful in low CO state ( Eg : Post MI) Frequently use with Noradrenaline (Peripheral vasoconstriction to maintain Systemic vascular resistance) Run at 2.5-25mcg/kg/min   250-500mg in 50cc NS   VASOPRESSOR NORADRENALINE ɑ 1 receptors   Causes peripheral vasoconstriction Excessive use can increase afterload and reduce CO, reduce renal perfusion, reduce splanchnic blood flows, and impair peripheral perfusion   Run at 0.05-1mcg/kg/min   4mg in 50cc D5% (single strength) 8mg in 50cc D5% (double strength)  

19. OBSTRUCTIVE SHOCK

20. 3. OBSTRUCTIVE SHOCK Impediment to the flow of blood in the cardiopulmonary circuit

21. DISTRIBUTIVE SHOCK

22. 4. Distributive Shock This shock describes the pattern of cardiovascular responses characterising a variety of conditions. This include: Septic shock. Anaphylaxis shock. Spinal cord injury. Characteristic of distributive shock  Vasodilation Anaphylaxis  Vasodilatation due to histamine release. Spinal cord injury  There is failure of sympathetic outflow and adequate vascular tone. Septic shock  Less clear but it is related to the release of bacterial products (endotoxin) and the activation of the immune systems.

23. Septic Shock: The Evolving Changes: 2016 Update: Sepsis 3.0 In sepsis 2.0, SIRS criteria was still used for sepsis and SOFA criteria was predominantly used for severe sepsis. Due to new evidences of poor specificity of SIRS score, the Sepsis Task Force again updated the definition in 2016. Under this new definition, the term “severe sepsis” is redundant. Septic shock was defined as the subset of sepsis with profound circulatory, cellular, and metabolic dysregulation, and associated with a much higher mortality of 40%, compared with the 10% mortality observed with sepsis. The use of qSOFA (Quick Sequential Organ Failure Assessment Screening Tool).

24. qSOFA Score The SOFA score is cumbersome to calculate and requires laboratory values that are not readily available especially outside ICU setting. The qSOFA score was introduced and its use is suggested for non ICU patient. Studies have shown that predicted mortality was similar to those patients identified using the full SOFA score.

25. Septic Shock: Clinical Manifestation

26. Septic Shock: General Management Establishment of Diagnosis FBC, RP, LFT, UFEME, blood cultures and urine cultures. Imaging: CXR (pneumonia), CT abdomen (diverticulitis, abscess). Role of serial procalcitonin  if taken early can guide to abx cessation. Antibiotics and Source Control Early initiation of abx preferably within 1 hours with blood cultures taken prior to that Initiate broad spectrum (according to local guidelines and considering comorbidities) that cover both gram +ve and –ve organisms. If suspecting intraabdominal sepsis, anaerobic coverage is indicated. In patients with immunodeficiencies, consider covering with antifungal. Always keep in mind regarding localised source  infected pressure ulcer or erythematous vascular catheter site. Management may include removal of invasive devices (eg, dialysis catheters, infected orthopedic hardware, or pacemakers) or surgical evacuation of abscess.

27. Septic Shock: Management Fluid Resuscitation Studies have shown that reducing the duration of hypotension in sepsis is associated with decreased mortality in septic shock. Most of the guidelines suggest an initial fluid bolus of 30 mL/kg. Studies have shown that excess volume administration is associated with worsened mortality, which may be due to associated pulmonary edema requiring prolonged mechanical ventilation and worsened kidney injury. Responsiveness can be best assessed with bedside usg/echocardiography, pulse-pressure variations.

28. Septic Shock: Management Target blood pressure Many guidelines recommend a target MAP of at least 65. The only large randomized trial of 2 blood pressure targets in patients with septic shock attempted to compare the effect of lower MAP target (65–70) compared with higher target (80–85) and did not demonstrate a mortality benefit of one versus the other. Vasopressor Historically, dopamine was recommended as theinitial blood pressure agent of choice in septic shock. However, randomized trials comparing the use of dopamine versus norepinephrine as an initial agent showed higher incidences of tachyarrhythmia and worsened mortality with dopamine compared with norepinephrine. Hence, the current recommendationnis that norepinephrine be used as a first- line agent. Epinephrine has been compared with norepinephrine as an initial agent and did not reveal a mortality difference; however, epinephrine was associated with greater tachycardia and lactic acidosis.

29. ANAPHYLACTIC SHOCK

30. Anaphylactic Shock Common identified causes of anaphylaxis: food (e.g. nuts) - the most common cause in children drugs venom (e.g. wasp sting) Allergic reaction  immune system overreacts to a harmless substance known as an allergen. Anaphylaxis Allergic reaction involve more than one systems (SKIN + CVS/GIT/CNS) Anaphylactic Shock Anaphylaxis + Shock Immediate hypersensitivity reaction (Type I), mediated by interaction of IgE on mast call and basophils triggers release of histamine, leukotrienes, and other mediators that cause diffuse smooth muscle contraction ( eg , resulting in bronchoconstriction, vomiting, or diarrhea ) and vasodilation with plasma leakage ( eg , resulting in urticaria or angioedema). Primary Mediatiors : Histamine, serotonin, eosinophil Secondary Mediators: Bradykinin, prostaglandins

31. Early signs of impending anaphylaxis Nasal itching/ stuffiness Stridor/ hoarseness SOB/ tachypnea Nausea/vomiting/ diarrhea Tingling of face (esp mouth), upper chest, palames, soles Severe anaphylaxis Angioedema of tongue, soft palate, larynx Tachycardia, hypotension, altered mental status, dizziness, wheezing → Cardiac arrest

32. Allergic Reaction : IV Hydrocortisone 200mg / 4mg/kg (Paeds) IV Piriton 10mg / 0.1mg/kg (Paeds) Anaphylaxis : IM Adrenaline 0.5mg (Paeds : 10mcg/kg) repeat every 5 minutes as needed IV Hydrocortisone 200mg (Paeds 4mg/kg) IV Piriton 10mg (Paeds 0.1mg/kg) Neb Salbutamol (Wheezing/rhonci) Anaphylactic Shock : ABCDE IV Adrenaline 0.1mg (1:10000) slow bolus over 5-10mins (Paeds 0.01mg/kg) -1 amp =1mg/ 1:1000, dilute 1 amp in 10cc NS , give 1cc= 0.1mg IVI Adrenaline 3mg in 50cc NS run at 3mls/Hour IM/ s/c Adrenaline: 0.5mg (1:1000) Adult / Paeds 0.01mg/kg IVD 1-2L Bolus IV Hydrocortisone 200mg IV Piriton 10mg

33. Anaphylactic Shock Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication . Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the anterolateral aspect of the middle third of the thigh. Adrenaline Hydrocortisone Chlorpheniramine < 6months 150 micrograms (0.15 ml 1 in 1000) 25 mg 250 micrograms/kg 6 months- 6 years 150 micrograms (0.15 ml 1 in 1000) 50 mg 2.5 mg 6- 12 years 300 micrograms (0.3 ml 1 in 1000) 100 mg 5 mg > 12 years 500 micrograms (0.5 ml 1 in 1000) 200 mg 10 mg

34. Anaphylactic Shock Management following stabilization: Patients who have had emergency treatment for anaphylaxis should be observed for 6–12 hours from the onset of symptoms, as it is known that biphasic reactions can occur in up to 20% of patients. Sometimes it can be difficult to establish whether a patient had a true episode of anaphylaxis. Serum tryptase levels are sometimes taken in such patients as they remain elevated for up to 12 hours following an acute episode of anaphylaxis.