1. PRINCIPLES of DIAGNOSIS and TREATMENT of SHOCK University of Medicine and Pharmacy, Iasi School of Medicine ANESTHESIA and INTENSIVE CARE Conf. Dr. Ioana Grigoras MEDICINE 4 th year English Program Suport de curs

2. SHOCK syndrome – sum of signs and symptoms induced by multiples causes multiples causes – the same clinical picture common pathophysiological pathway – cause primary pathophysiologogical event (specific for each type of shock) compensatory phenomena decompensatory phenomena death causative event - great degree of severity without treatment causes death shock treatment - the treatment of the cause + the interruption of the pathophysiological events

3. SHOCK DEFINITION clinical syndrome induced by various causes and characterized by the reduction of the effective tissue perfusion pressure and generalized cellular dysfunction. Effective tissue perfusion pressure = tissue perfusion pressure resulting in adequate oxygen tissues delivery which matches tissue oxygen consumption. Systemic disease (affects all the organs and tissues) Variable clinical picture ( depends on: –the severity of perfusion deficit –causative factor –the moment of temporal evolution – preexisting diseases The treatment aims the interruption of the pathophysiological cascade + causative treatment

4. SHOCK Key concept Tissue hypoperfusion inappropiate oxygen delivery Clinical syndrome characterized by the generalized imbalance between tissue oxygen delivery and tissue oxygen consumption resulting in anaerobic metabolism and organ and system dysfunction. –oxygen debt –anaerobic metabolism – metabolic acidosis

5. SHOCK CLASIFICATION (Weil and Shubin) Hypovolemic shock –reduction of effective circulating blood volume (hypovolemia) Cardiogenic shock –reduction of cardiac output induced by primary cardiac causes Extracardiac obstructive shock –reduction of cardiac output induced by extracardiac primary causes Distributive shock –maldistribution of blood flow caused by vasodilation

6. PATHOPHYSIOLOGY Initial event: –  blood circulating volume → hypovolemic shock –  cardiac output → cardiogenic shock –maldistribution of blood flow → septic shock Initial event → compensatory phenomena → decompensatory phenomena → cascade of pathophysiological events which depend on: –natural evolution of the disease→ continuously worsening process –therapeutic intervention→ interruption of the cascade + new problems SIRS cause of shock – sepsis effect of treatment – ischemia-reperfusion phenomena

7. PATHOPHYSIOLOGY hypovolemia  cardiac output can coexist în maldistribution of blood any type of shock flow any type of shock can evolve from one form to another

8. CLINICAL DIAGNOSIS OF SHOCK Clinical picture varies with : –Type of shock –Severity of shock –Causative factor –Preexisting conditions – Previous therapeutic interventions COMMON CLINICAL SIGNS OF SHOCK STATES –Tachycardia –Tachypnea –Arterial hypotension –Altered mental status –Oliguria

9. SHOCK CLINICAL DIFFERENTIAL DIAGNOSIS OF SHOCK STATES: We have to answer two questions : –Is cardiac output decreased or increased? –Is the heart empty or too full? BP = CO x SVR

10. CLINICAL DIFERENTIAL DIAGNOSIS OF SHOCK STATES: We have to answer the question: Is cardiac output decreased or increased ?  cardiac output is increased (hyperdynamic shock): –warm extremities –large pulse wave –good color return to the nail bed – full peripheral veins – reduced diastolic pressure  cardiac output is decreased (hypodynamic shock): –cold extremities –small pulse wave –delayed return of color to the nail bed –collapsed peripheral veins

11. CLINICAL DIFERENTIAL DIAGNOSIS OF SHOCK STATES: We have to answer the question?: Is the heart too full or empty?  Is the heart too full? ­turgescent jugular veins ­dyspnea, pulmonary rales, cyanosis ­ precordial pain ­abnormal heart sounds and cardiac murmmurs ­ECG abnormalities  Is the heart empty? ­collapsed jugular veins ­intense thirst ­pallor ­history or clinical signs of hemorrhagic or non-hemorrhagic losses

12. HEMODYNAMIC EVALUATION OF THE SHOCK STATE Arterial blood pressure Heart rate ECG Pulse oximetry Central venous pressure Cardiac output and PAOP SvO 2 Transthoracic and transesophageal echocardiography

13. HEMODYNAMIC EVALUATION OF THE SHOCK STATE ARTERIAL BLOOD PRESSURE –Noninvasive nonautomatic measurement palpation method auscultation method –Noninvasive automatic measurement Advantages: noninvasive method (without risks) automatic method (saves time, frees personnel for other tasks) measurement at setted time intervals Disadvantage: no accuracy in case of hypotension long lasting measurement – difficult to record sudden variations of blood pressure may cause superior limb edema ( frequent cuff inflation) –Invasive measurement arterial catheter Advantages: real time measurement of blood pressure accurate measurement for both elevated and reduced values of arterial blood pressure allows repeated samples of arterial blood for blood gases analysis allows blood samples for other laboratory analysis (no venous puncture) Disadvantages: risk of complications (ischemia, trombosis, hemorrhage) requires experience( arterial puncture) requires medical equipment

14. HEMODYNAMIC EVALUATION OF THE SHOCK STATE HEART RATE –Measurement methods: Manually - frequency of pulse waves (ATTENTION in case of atrial fibrillation) pulse oximetry ECG monitoring

15. HEMODYNAMIC EVALUATION OF THE SHOCK STATE ELECTROCARDIOGRAPHY –Allows: Real time heart rate measurement Detection and diagnosis of cardiac arrhythmias and response to treatment Detection of myocardial ischemia (ECG abnormalities) and the response to treatment

16. HEMODYNAMIC EVALUATION OF THE SHOCK STATE PULSE OXIMETRY –Allows measurement of Sa0 2 in peripheral arterial blood –The principle of measurement : red light absorption is different in oxyhemoglobin and reduced hemoglobin –Equipment with source of red light and sensor –Is applied on the thin peripheral tissues, which permit transillumination: Digital (finger or toe) probes Ear probes Nasal probes –Advantages: Allows continuous non-invasive evaluation of the arterial blood oxygenation Allows heart rate measurement Allows detection of arrhythmias (without diagnosis) Allows evaluation of the pulse wave amplitude Allows gross evaluation of peripheral perfusion –Disadvantages: The measurement unreliable in case of painted nails Frequent artefacts caused by movements Low accuracy of blood oxygenation evaluation Measurement impossible when tissue perfusion pressure is very low

17. HEMODYNAMIC EVALUATION OF THE SHOCK STATE CENTRAL VENOUS PRESSURE – central venous catheter (the tip of catheter in superior vena cava) –catheter introduced through internal jugular, external, subclavian, axilary, brachial vein Methods of measurement: water column method automatic method (transducer) –Advantages: allows monitoring of CVP (venous return); evaluates heart filling (right ventricle) allows monitoring of treatment response –Disadvantages: risks of central venous catheterization (pneumothorax, cervical or mediastinal hematoma, infection, gas embolism) requires special equipment (for automatic measurement) for elevated values of CVP, inaccurate evaluation of right heart filling

18. HEMODYNAMIC MONITORING OF THE SHOCK STATE PULMONARY ARTERY CATHETER –Catheter ~ 1m long introduced through a central vein - the tip of the catheter in one pulmonary artery branch –Catheter introduced through internal jugular or subclavian vein – passes through superior vena cava, right atrium, right ventricle, common pulmonary artery, one principal branch of pulmonary artery, ramifications of pulmonary artery

19. MONITORING

25. PULMONARY ARTERY CATHETER –Hemodynamic data: Measured parameters: –central venous pressure/ right atrium pressure (preload of right ventricle) –pressures in pulmonary artery (systolic, dyastolic and mean) –PAOP – pulmonary artery occlusion pressure (preload of left ventricle) –cardiac output (thermodilution method) –SvO 2 Calculated parameters: –cardiac index, stroke volume –pulmonary vascular resistance (afterload of right ventricle) –systemic vascular resistance (afterload of left ventricle) –oxygen delivery, oxygen consumption, oxygen extraction ratio –Advantages allows measurement and calculation of some hemodynamic parameters – shock diagnosis allows monitoring of treatment response –Disadvantages: Risks of central venous catheterization (pneumothorax, cervical or mediastinal hematoma, infection, gas embolism) + specific complications (pulmonary infarction, cardiac perforation, etc.) requires special equipment (for automatic measurement) difficult interpretation of hemodynamic data

26. HEMODYNAMIC EVALUATION OF THE SHOCK STATE METHODS OF CARDIAC OUTPUT EVALUATION AND MONITORING –Thermodilution method intermittent (Swan-Ganz catheter) continuous ( modified Swan-Ganz catheter ) –Method of arterial pressure curve analysis (“pulse contour” method ) PiCCO system (central venous catheter + special arterial catheter + equipment) LiDCO - Pulse CO system –echocardiography transthoracic transesophageal

27. INTERMITTENT MEASUREMENT OF CARDIAC OUTPUT - thermodilution method -

28. HEMODYNAMIC EVALUATION OF THE SHOCK STATE METHODS OF CARDIAC OUTPUT EVALUATION AND MONITORING – Thermodilution method intermittent (Swan-Ganz catheter) continuous ( modified Swan-Ganz catheter ) –Method of arterial pressure curve analysis (“pulse contour” method ) PiCCO system ( central venous catheter cateter + special arterial cateter + equipment) LiDCO-Pulse CO system –echocardiography transthoracic transesophageal

29. CONTINUOUS MEASUREMENT OF CARDIAC OUTPUT -thermodilution method-

30. HEMODYNAMIC EVALUATION OF THE SHOCK STATE METHODS OF CARDIAC OUTPUT EVALUATION AND MONITORING – Thermodilution method intermittent (Swan-Ganz catheter) continuous ( modified Swan-Ganz catheter ) –Method of arterial pressure curve analysis (“pulse contour” method ) PiCCO system ( central venous catheter cateter + special arterial cateter + equipment) LiDCO-Pulse CO system –echocardiography transthoracic transesophageal

31. ECHOCARDIOGRAPHY

32. HEMODYNAMIC EVALUATION OF THE SHOCK STATE ECHOCARDIOGRAPHY: noninvasive method of hemodynamic monitoring –estimates the left ventricle telediastolic volume –estimates the left ventricle ejection fraction –measures cardiac output –estimates the abnormalities of myocardial kinetics (areas of hipo - or akinesis) –estimates valvular dynamics –estimates pericardial liquid

33. HEMODYNAMIC MONITORING OF THE SHOCK STATE OXYGEN SATURATION OF MIXED VENOUS BLOOD (SvO 2 ): measured in right atrium blood SvO 2 allows measurement of oxygen consumption VO 2 allows measurement of oxygen arterio-venous difference Da-vO 2 allows measurement of oxygen extraction ER O 2 allows monitoring of treatment response

34. HEMODYNAMIC PARAMETERS IN DIFFERENT TYPES OF SHOCK HRBPCOCVPPAOPSVRDa-vO 2 SvO 2 Hypovolemic shock ↑  ↑↑  Cardiogenic shock ↑  ↑↑↑↑  Septic shock ↑  ↑ N  N N  ↑

35. Hemodynamic parameters in different types of shock ABBREVIATION: HR – heart rate BP – arterial blood pressure CO – cardiac output CVP –central venous pressure PAOP – pulmonary artery occlusion pressure SVR – systemic vascular resistance Da-v O 2 – oxygen arterial-venous difference SvO 2 – mixed venous blood oxygen saturation

36. MONITORING OF THE PATIENT WITH SHOCK STATE Respiratory monitoring Respiratory rate per minute Respiratory pattern Pulse oximetry Cardiovascular monitoring Neurological monitoring State of consciousness Temperature monitoring Measurement of peripheral/core temperature Diuresis monitoring Hourly monitoring of diuresis Monitoring of arterial gases Blood gas analysis

37. HEMODYNAMIC MONITORING OF PATIENT WITH SHOCK STATE Blood pressure Heart rate ECG Pulse oximetry Central venous pressure Cardiac output and pulmonary artery occlusion pressure Oxygen saturation in mixed venous blood Transthoracic and tranesophageal echocardiography

38. INITIAL LABORATORY INVESTIGATIONS OF THE PATIENT WITH SHOCK STATE shock → systemic disease→ multisystemic evaluation –blood group and compatibility test –plasma and urinary electrolytes –plasma and urinary creatinine and urea nitrogen –liver function test, amylases –haemoglobin, hematocrit, blood white cells count and formula –platelets and coagulation tests –blood gas analysis –ECG –chest radiography + others explorations indicated by possible causes

39. INITIAL TREATMENT OF SHOCK STATES aggressive and early introduction of treatment correction of tissue perfusion improvement/correction of organic dysfunction System approach: ABC

40. INITIAL TREATMENT OF SHOCK STATES A şi B (airway and breathing): – clinical evaluation (respiratory rate and respiratory pattern) laboratory investigations (pulse oximetry, blood gas analysis) Detection of hypoxemia –Oxygenotherapy is rapidly started at first contact with the patient –Indications of endo-tracheal intubation (ETT) and ventilatory support : hypoxemia (  PaO 2 ) ventilatory failure (  PaO 2 + ↑ PaCO 2 ) signs of respiratory fatigue : tachypnea >30 respirations/minute abdomino-thoracic balance utilization of accesory respiratory muscles altered consciousness (  protection of respiratory airways reflexes) for the reduction of respiratory muscles oxygen consumption ETT + ventilatory support+ PEEP → correction of hypoxemia

41. INITIAL TREATMENT OF SHOCK STATES C (circulation): Circulatory resuscitation means more than normalization of arterial blood pressure GOALS: normalization of volemia volume repletion therapy normalization of cardiac output inotropic therapy normalization of tissue perfusion vasomotor therapy (vasopressor/vasodilatator therapy)

42. INITIAL TREATMENT OF SHOCK STATES PRACTICAL APPROACH: –oxygentherapy / endo-tracheal intubation and ventilatory support –peripheral venous access (în hypovolemia – multiple venous access) –blood samples for laboratory analysis –ECG monitoring –non-invasive arterial blood pressure measurement –arterial catheter – urinary catheter – naso-gastric tube – central venous catheter –core/peripheral temperature monitoring –Swan-Ganz catheter/ echocardiography (if necessary)