SHOCK

1. SHOCK

2. DEFINITION Shock is a clinical syndrome resulting from gross impairment of tissue perfusion and widespread cellular dysfunction caused by diminution in oxygen delivery.

3. Classification 1.Hypovolemic 2.Cardiogenic 3.Distributive (septic, anaphilactic, neurogenic) 4.Obstructive shock (pulmonary embolism, cardiac tamponade, constrictive pericaditis, tension pneumothorax)

4. HYPOVOLEMIC SHOCKCauses: External or internal hemorrhage (trauma, gastrointestinal, pulmonar, retroperitoneal) Fluid loss or sequestration-grastrointestinal, urinary or cutaneous (dehydration, vomiting, diarrhea, polyuria, burns)

5. Clinical Correlates of Hemorrhage* *ATLS; 2004. Man70kg

6. TREATMENT • Identification source of blood or fluid loss. Stopping Bleeding • Oxigenation and ventilation • Tidal volume 7-10 ml/kg • O2 – oxigen saturation > 94% • RR • sedation • PEEP !!!

7. TREATMENT Venous access must be secured early. Insert two or more large bore IVs (14- to 16-gauge) peripheral IV catheters. Infusion pumps allow infusion of 1 L of crystalloid in 10 to 15 min and 1 unit of packed RBCs in 20 min. Fluid Replacement Choices: Conventional “crystalloids “ Colloid solutions

8. Crystalloids

9. Colloids Additional cost and potential risk of colloids Coagulopathy – Dextran, HES >20 ml/kg Impaired cross-matching – Dextran Allergic reactions

10. Saline versus Albumin Fluid Evaluation (SAFE) Study colloids, although considerably more expensive than crystalloids, are no more effective in restoring blood volume

11. Packed Red Blood Cells Indications: Hb< 100 g/l in patients with signs of tissue hypoxia

12. Cardiogenic Shock  Hemodynamiccriteria: • Sustainedhypotension (systolicbloodpressure < 90 mmHgforatleast 30 minutes) • Reducedcardiacindex (<1.8 l/min/m2 without support or < 2.0-2.2 l/min/m2 with support ); • elevatedpulmonaryarteryocclusionpressure (PAOP> 18 mmHg)

13. Cardiogenic Shock  CAUSES: - myocardial infarction - cardiomyopathy - cardiac contusion - myocarditis - cardiac valve problems - ventriculoseptal defects - overdose of drugs such as beta blockers or calcium channel blockers - arrhyhmya (bradyarrhythmiasor tachyarrhythmias)

14. TREATMENT Emergency revascularization with either PCI or CABGS is recommended in suitable patients with cardiogenic shock due to pump failure after STEMI irrespective of the time delay from MI onset.

15. Percutaneous coronary intervention (coronary angioplasty) cardiologist feeds a deflated balloon from the inguinal femoral artery until they reach the site of blockage in the heart. At the blockage, the balloon is inflated to open the artery, allowing blood to flow. A stent is often placed at the site of blockage to permanently open the artery.

16. CABGS(Coronary artery bypass graft surgery) Urgent GABG is indicated in patients with coronary artery not amenable to PCI.

17. Fibrinolytic therapy is reserved for patients without contraindications who are unsuitable candidates for either PCI or CABGS

18. Cardiogenic Shock TREATMENT Mechanical ventilation should be contemplated Morphine (4 to 8 mg initially, 2 to 8 mg IV every 5 to 15 min if needed) relieves pain and anxiety, reduces excessive sympathetic activity, and decreases oxygen demand, preload, and afterload. Atrial bradyarrhythmias or tachyarrhythmias or ventricular tachyarrhythmias can reduce cardiac output and should be corrected promptly with antiarrhythmic drugs, cardioversion, or pacing .

19. TREATMENT Fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Generally recommended options for  fluid administration are: 250-500 mls of crystalloid infused over 20-30 minutes. When arterial pressure remains inadequate, therapy with vasopressor agents, titrated not only to blood pressure but also to clinical indices of perfusion and mixed venous oxygen saturation, may be required.

20. Vasopressors Norepinephrine is considered first-line drugs for hypotension in this situation. Norepinephrine (0.02 to 1.0 µg/kg/minute) acts primarily as a vasoconstrictor, has a mild inotropic effect, and increases coronary flow.

21. Inotropic therapy If tissue perfusion remains inadequate despite norepinephrine, inotropic therapy should be initiated. Dobutamine (2.5 to 20 µg/kg/minute), a selective β1-adrenergic receptor agonist, can improve myocardial contractility and increase cardiac output, and it is the initial agent of choice in patients with a low-output syndrome and systolic blood pressures greater than 90 mm Hg. In patients with SBP < 80 mmHg - dopamine or epinephrine

22. Milrinone (phosphodiesterase-3 inhibitor) • increases intracellular cAMP in a non-adrenergic mediated mechanism and provides inotropic, vasodilatory (especially pulmonary) with less chronotropy and arrhythmogenicity when compared to catecholamines.

23. Levosimendan • (a calcium sensitizer  reducing calcium-binding coefficient of troponin C, augmenting contractility without  requirement for increase in intracellular calcium  concentrations) is an inotrope that does not increase  myocardial oxygen demand.

24. Intra-aortic balloon pump An IABP should be used for MI patients when cardiogenic shock is not quickly reversed with pharmacologic therapy.It is efficient as a stabilizing measure before angiography and prompt revascularization

26. ACUTE PULMONARY EMBOLISM

28. CLINICAL PRESENTATION

29. Chest x-ray findings • 14% Normal • 68% Atelectasis or parenchymal density • 48% Pleural Effusion • 35% Pleural based opacity • 24% Elevated diaphragm • 15% Prominent central pulmonary artery • 7% Westermark’s sign • 7% Cardiomegaly • 5% Pulmonary edema

30. EKG features Sinus tachycardia Complete or incomplete RBBB Right ventricular strain pattern Dominant R wave in V1 Right atrial enlargement (P pulmonale) SI QIII TIII  pattern  Atrial tachyarrhythmias - AF, flutter, atrial tachycardia Non-specific ST segment and T wave changes, including ST elevation and depression.

32. ARTERIAL BLOOD GASES Hypoxaemia Hypocapnia Respiratory alcalosis

33. D-dimer - a degradation product of crosslinkedfibrin - are elevated in plasma in the presence of an acute clotbecause of simultaneous activation of coagulation and fibrinolysis - normal D-dimer level renders acute PE unlikely - can therefore be used to exclude PE

34. Ventilation–perfusion scintigraphy • The basic principle of the test is basedon an intravenous injection of technetium (Tc)-99 m labelledalbumin particles, which block a small fractionof pulmonary capillaries and thereby enable scintigraphic assessmentof lung perfusion at the tissue level.

35. Ventilation–perfusion scintigraphy (xenon (Xe)-133gas can be used The purpose of the additional ventilationscan is to increase specificity by the identification of hypoventilationas a non-embolic cause of hypoperfusion due to reactive vasoconstriction

36. Ventilation–perfusion scintigraphy

37. Echocardiography - Right ventricular dilatation, tricuspid insufficiency - mayhelp in the differential diagnosis of the cause of shock, bydetecting cardiac tamponade, acute valvular dysfunction, acutemyocardial infarction or hypovolaemia.

38. Computed tomography It allows adequatevisualization of the pulmonary arteries up to at least the segmentallevel - specificity of 96%

39. Pulmonary angiography • The diagnostic criteriafor acute PE consist of direct evidence of a thrombus, either a fillingdefect or amputation of a pulmonary arterial branch • is invasive and not devoid of hazards

40. TREATMENTHaemodynamicand respiratory support • Isoproterenol, Norepinephrine

41. TREATMENTUNFRACTIONATED HEPARIN 80-U/kg as a bolus injection, followed by infusion at a rate of 18-U/kg/h Subsequent doses of UH should be adjusted using an aPTT, and maintain aPTT prolongation between 1.5 and 2.3 times control

42. VITAMIN K ANTAGONISTS Should be initiated as soon as possible • Anticoagulation with UH should be continued for at least 5 days • Parenteral anticoagulation should be stopped when INR lies between 2 and 3 • Warfarin starting dose 5-7 mg

43. Thrombolysis • is the first-line treatmentin patients with high-risk PE presenting with cardiogenic shockand/or persistent arterial hypotension • RtPA, streptokinase, urokinase

44. Pulmonary embolectomy • Is reserved for patientswith PE who may necessitate cardiopulmonary resuscitation • patients with contraindications or inadequateresponse to thrombolysis • in those with patent foramen ovaleand intracardiac thrombi

45. SEPTIC SHOCK

47. Sepsis is life-threatening organ dysfunction due to a dysregulated host response to infection.

48. CRITERIA FOR SEPSIS Organ dysfunction can be identified as an acute change in total qSOFAscore ≥2 points consequent to the infection.

49. qSOFAscore • Altered mental status GCS<15 • Respiratory rate ≥ breaths per min • Systolic BP ≤ 100 mm Hg

50. Septic shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities substantially increase mortality.