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HYPOTENSION, SHOCK

HYPOTENSION, SHOCK. Kapocsi Judit Semmelweis University 1 st Department of Medicine. REGULATION. SHORT TERM BAROREFLEX LONG TERM COMPLEX SYSTEM CENTRAL MECHANISMS PERIPHERAL MECHANISMS. HYPOTENSION DEFINITION. Mean blood pressure (BP)=COxTPR Normal BP 120/70 + -20 mmHg

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HYPOTENSION, SHOCK

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  1. HYPOTENSION, SHOCK Kapocsi Judit Semmelweis University 1st Department of Medicine

  2. REGULATION SHORT TERM BAROREFLEX LONG TERM COMPLEX SYSTEM CENTRAL MECHANISMS PERIPHERAL MECHANISMS

  3. HYPOTENSION DEFINITION • Mean blood pressure (BP)=COxTPR • Normal BP 120/70+-20 mmHg • Hypotension BP<100/70 mmHg • Syndrome

  4. Hypotension Syndrome • Definition of hypotension based mainly on blood pressure level • BUT!!! • Hypotension represents a complex syndrome in which hemodynamic,neurohumoral and metabolic abnormalities influence the development and progression of blood supply insufficiency of organs

  5. Shock-definition • The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then, if prolonged, to irreversible cellular injury.

  6. Syncope • Sudden transient loss of consciousness, usually due to transient cerebral hypoperfusion Causes: cardiac: arrhythmias peripheral vascular: drugs (increased peripheral vasodilation) vaso-vagal syncope (stress, pain) hypersensitive carotid sinus orthostatic hypotension other: (volume depletion, bleeding, high temperature, petit mal, hypoglicemia)

  7. Shock-classification • Classification: hypovolemic (dehydration, hemorrhage) cardiogenic (ischemic myocardial injury, heart failure) distributive sepsis (endotoxins) anaphylaxis (hyper-acut immune response) extracardiac obstructive (pericardial tamponade, pulmonary emboli)

  8. Shock-pathomechanism • CO or circulating blood volume decrease---tissue perfusion decrease---anaerob metabolic pathway---acidosis---compensatory mechanisms---increased sympathetic tone---exhaustion---more severe tissue damage---cardiovascular insufficiency

  9. Main clinical symptoms • Hypotension • Tachycardia • Tachypnea • Abnormal mental status • Poor peripheral perfusion • Renal insufficiency

  10. Main clinical symptoms • Clinical findings seen in shock are common to all forms • In certain diseases two forms of shock may be present

  11. SHOCK The state in which profound and widespread reduction of effective tissue perfusion leads first to reversible, and then, if prolonged, to irreversible cellular injury. Life-threatening, high mortality situation The key of the successful management is the early recognition Diagnosis in time!

  12. INVESTGATIONAL METHODS • Catheter into the pulmonary artery: measurement of pulmonary artery occlusion pressure („wedge pressure”)- indirect measurement of the end diastolic pressure in the left ventricle, measurement of CO (calculation of systemic vascular resistace index-SVRI) • Mixed venous oxygen count (MVO2) determination

  13. HYPOVOLEMIC SHOCK • Causes: dehydration or hemorrhage • Clinical characteristics: pale, cool skin, flat peripheral veins, collapsed jugular veins, decreased urine output, altered mental status • Hemodynamic status: decreased preload, decreased ventricular diastolic pressure and volume, hypotension (PCWP low, CI low, SVRI:high • MVO2 decreased

  14. CARDIOGENIC SHOCK Causes: • ischemic myocardial injury • acute valvular dysfunction • acut myocarditis • rapid and slow cardiac rhythms • congestive heart failure • hypertrophic cardiomyopathy with obstruction • Traumatic myocardial contusion

  15. Damages in the heart • Acut: myocarditis, valvulitis (left ventricular dysfunction, dilation, relative mitral and/or tricuspid valve vitium, heart failure) • Later: platelet-fibrin thrombi on the valves, fibrosis, calcification Mitral valve stenosis and/or regurgitation Aortic valve regurgitation and/or stenosis

  16. CARDIOGENIC SHOCK • Clinical characteristics: jugular and peripheral veins may be distended, mid-diastolic galopp sound, pulmonary edema • Hemodynamic status: increased ventricular preload (PCWP, CVP, ventricular volume, SVRI increased), CI decreased • MVO2 reduced

  17. EXTRACARDIAC OBSTRUCTIVE SHOCK • Causes: pericardial tamponade, constrictive pericarditis, pneumothorax, intrathoracic tumor, pulmonary emboli, acut pulmonary hypertension, aortic dissection • Diastolic filling of right ventricle impaired • Ventricular afterload increased

  18. EXTRACARDIAC OBSTRUCTIVE SHOCK • Clinical characteristics: hypotension, tachycardia, dyspnea, pale or cyanotic skin • Hemodynamic status: is dependent on the site of obstruction, CI and MVO2 are usually low, SVRI high, PCWP normal or low, but in the case of tamponade is high

  19. DISTRIBUTIVE SHOCK • Causes: anaphylaxis, spinal injury, adrenal insufficiency, sepsis • The main characteristics: hypotension because of loss of peripheral resistance, tachycardia, tachypnea, extremities are warm and well perfused • Hemodynamic status: PCWP normal or low, CI high (rarely low), SVRI low

  20. MODS • Multiple organ dysfunction syndrome • Homeostasis can not be maintened without intervention • Microcirculation is the primary target of injury

  21. Primary MODS Well- defined insult • Hypotension • Hypoxemia

  22. HYPOTENSION and/or HYPOXIA

  23. ACUTE RESPIRATORY FAILURE • Primary function of the respiratory system: provide oxygen (O2) to, remove carbon dioxid (CO2) from the tissues • Failure of the respiratory system leads to hypoxemia (decreased PaO2) • Hypoxemia can occur with or without an increase in PaCO2

  24. RESPIRATORY FAILURE Type 1 • Abnormally low PaO2 with low or normal PaCO2 • Caused by lung diseases (eg. ARDS) Type 2 • Abnormally low PaO2 with high PaCO2 • Caused by central nervous system depression or COPD acut exacerbation

  25. ACUT RESPIRATORY DISTRESS SYNDROME (ADRS) Diagnosis • Evaluation of hemodynamic status • Exclusion of left ventricular failure and chronic lung disease • Diffuse pulmonary infiltrate on chest radiography • PaO2<50 mm Hg on Fi O2 >0.60 • Decreased respiratory complience<50 ml/cm H2O (Fi O2=fraction of inspired oxygen)

  26. ACUT RESPIRATORY DISTRESS SYNDROME (ADRS) Diagnosis • PaO2 and Fi O2 ratio is<-200 • Bilateral pulmonary infiltrates on a frontal chest radiograph • PCWP<-18 • Can occur as the result of direct lung injury (aspiration, viral pneumonia), or as a part of MODS

  27. ACUT RESPIRATORY DISTRESS SYNDROME (ADRS) Pathomechanism • Damage of pulmonary capillary endothelium or epithelial mebrane • Increased permeability of alveolar-capillary membrane • Pulmonary edema and intrapulmonary shunting • Hypoxemia and tissue hypoxia Death or survival

  28. Secondary MODS Result of the host response to an insult • Systemic inflammatory response diseases (SIRS) • Chracteristics of SIRS: body temperature>38 0C or<36 0C, heart rate>90 beats/min, respiratory rate>20/min, PaCO2<32 mmHg, white blood cell count>12.000 4/cu mm, <4000 4/cu mm, or> 10% immature (band) form. • When SIRS develops in response to infection, the patient has sepsis syndrome

  29. SEPSIS Caused by bacterial or fungal infection Mediators of inflammatory response • TNF-alpha • Interleukin 1,2 and 6 • Gamma interferon

  30. SEPSIS SYNDROME Clinical manifestations • Fever,chills • Hyperventillation • Hypothermia • Mental status changes • Hypotension • Leukopenia, thrombocytopenia • End-organ failure: lung, kidney, liver, heart, disseminated intravascular coagulation

  31. Treatment • Should be focused toward underlying disease • Supportive therapy for failing organs (blood transfusion, fluid, electrolits, oxygen, mechanical ventillation) • Drug therapy (vasoactive drugs, antibiotics, hormones, antibodies) • Control in the intensive care unit

  32. Vitious circle in the pathomechanism of circulatory shock HYPOTENSION, HYPOXIA IMPAIRED AUTOREGULATION HUMORAL FACTORS EXHAUSTION INCREASING BP METABOLIC ACIDOSIS VASOCONSTRICTION TISSUE HYPOPERFUSION

  33. THANK YOU FOR YOUR ATTENTION

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