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Circulatory shock Vasopressors

Circulatory shock Vasopressors. Shock: definition. Shock is the physiologic state characterized by significant reduction of systemic tissue perfusion, resulting in decreased tissue oxygen delivery. This creates an imbalance between oxygen delivery and oxygen consumption.

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Circulatory shock Vasopressors

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  1. Circulatory shockVasopressors

  2. Shock: definition • Shock is the physiologic state characterized by significant reduction of systemic tissue perfusion, resulting in decreased tissue oxygen delivery. • This creates an imbalance between oxygen delivery and oxygen consumption. • Prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes at the cellular level, which can progress to the systemic level

  3. Shock: Stages • Preshock = warm or compensated shock: rapid compensation for diminished tissue perfusion by various homeostatic mechanisms (↑HR, peripheral vasoconstriction, ↑or↓ in BP) • Shock: the compensatory mechanisms become overwhelmed and signs and symptoms of organ dysfunction appear (↑HR, dyspnea, oliguria, acidosis). • End-organ dysfunction: progressive end-organ dysfunction leads to irreversible organ damage and patient death.

  4. Pathogenesis • Impairment in tissue perfusion and vasomotor paralysis that could become irreversible • Mechanisms for the vasodilatation 1. Opening of ATP-Sensitive Potassium Channels→ hyperpolarization of Vascular Smooth Muscle→↓Ca entry →persistent vasodilation 2. Increased Synthesis of Nitric Oxide 3. Generation of free radicals 4. Deficiency of Vasopressin due to exhaustion of hypophyseal stores and rapid degradation of vasopressin in plasma

  5. Classification of Circulatory Shock HYPOVOLEMIC • Hemorrhagic • Trauma • Gastrointestinal • Retroperitoneal • Fluid depletion (nonhemorrhagic) • External fluid loss - Dehydration - Vomiting - Diarrhea - Polyuria

  6. Classification of Circulatory Shock CARDIOGENIC • Myopathic (myocardial infarction, nonischemic cardiomyopathy, septic or pharmacologic myocardial depression) • Mechanical (valvular failure, hypertropic cardiomyopathy ventricular septal defect) • Arrhythmic

  7. Classification of Circulatory Shock EXTRACARDIAC OBSTRUCTIVE • Impaired Diastolic Filling Direct venous obstruction (obstructive tumor) Increased intrathoracic pressure(tension pneumothorax, status asthmaticus) Decreased cardiac compliance (constrictive pericarditis, cardiac tamponade) • Impaired Systolic Contraction Right ventricle ( massive PE, acute PAH) Left Ventricle ( aortic dissection)

  8. Classification of Circulatory Shock DISTRIBUTIVE • Septic (bacterial, fungal, viral, rickettsial) • Toxic shock syndrome • Anaphylactic, anaphylactoid • Neurogenic (spinal shock) • Endocrinologic( Adrenal crisis, thyroid storm) • Toxic (nitroprusside, bretylium)

  9. Shock: Clinical presentation • Cardinal findings - hypotension - oliguria - cool and clammy skin - abnormal mental status - metabolic acidosis • Suggestive findings suggest a particular type of shock

  10. Shock: Evaluation • History: including medications, allergies, procedures, comorbidities, immunocompromised state • Physical examination: JVP, left S3, S4, gallop, new murmurs, arrhythmia, rub, pulsus paradoxus,peripheral edema, fever, rigors, infection focus, abdominal tenderness, GI bleeding, neurological exam, rashes • Laboratory data: Blood work (CBC, Chem, LFT, Amylase/lipase, coags, lactate, ABG), EKG, imaging (Chest/abdominal Xray, CT, Echo), toxicology

  11. Pulmonary artery catheter

  12. A Clinical Approach to Shock Diagnosis and Management Immediate Goals in Shock Hemodynamic supportMAP > 60mmHg PAOP = 12 - 18 mmHg Cardiac Index > 2.2 L/min/m2Maintain oxygen deliveryHemoglobin > 9 g/dL Arterial saturation > 92% Supplemental oxygen and mechanical ventilationReversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L) Maintain urine output Reverse encephalopathy Improving renal, liver function tests

  13. Shock: Management

  14. Shock: Management • Fluids ▪Crystalloids, isotonic (NS) ▪20 mL/kg fluid challenge in hypovolemic or septic shock with re-challenges of 5 - 10 mL/kg ▪100 - 200 mL challenges in cardiogenic shock

  15. Vasopressors • induce vasoconstriction and elevate mean arterial pressure • few controlled clinical trials have directly compared these or documented improved outcomes • adrenergic receptors relevant to vasopressor activity ▪ ά-1in vascular walls, induces vasoconstriction. Also in the heart and can ↑ the duration of contraction but no ↑ chronotropy ▪β-1in the heart, mediate ↑ in inotropy and chronotropy with minimal vasoconstriction ▪β-2in blood vessels induce vasodilation ▪dopa in renal, splanchnic, coronary, and cerebral vascular beds; stimulation leads to vasodilation. A second subtype causes vasoconstriction by inducing norepinephrine release (high doses of medication)

  16. Dopamine • Precursor of norepinephrine and epinephrine • Increases MAP and CO due to increase in SV and to a lesser extent to a HR. Increases CI • Increases oxygen delivery but effects on oxygen consumption mixed (microcirculatory flow) • Dose dependent effects <5 mcg/kg/min→dopa receptors →vasodilation in renal and mesenteric beds 5-10 mcg/kg/min →β1 receptors →increase in cardiac contractility and heart rate >10 mcg/kg/min →ά1 receptors→vasoconstriction and increase in BP

  17. Norepinephrine • Potent ά-adrenergic agent with less pronounced β-agonist effect • Increases MAP by vasoconstriction, 10-15% increase in CO and SV • More potent than Dopamine • Dose range: start with 0.5-1 mcg/min, increase up to 30 mcg/min • Improves tissue oxygenation • Effect on renal hemodynamics- !adequate volume resuscitation prior to norepi start • Effect on splanchnic blood flow - mixed results

  18. Phenylephrine • Selective ά-1 adrenergic agonist, increases BP by vasoconstriction. • Rapid onset of action, short duration, primary vascular effect • Concerns for potential reduction in CO • Dose range: start with 40-60 mcg/min and increase to 100-180 mcg/min until BP stable. • Second line agent • Consider in tachyarrhythmias limiting therapy with other vasopressors.

  19. Vasopressin • Peptide hormone, synthesized in the hypothalamus, stored in pituitary gland. Released in response to decreased intravascular volume, increased osmolarity • Constricts vascular smooth muscle via V1 receptors • Increases vessel responsiveness to catecholamines • Low steady dose vasopressin 0.01-0.04 Units/min • Vasopressin (0.03 Units/min) + Norepinephrine safe • No effect on mortality

  20. Vasopressors: complications of use • Hypoperfusion • Dysrhythmias • Myocardial ischemia • Local effects • Hyperglycemia NO STUDY HAS DEMONSTRATED A SURVIVAL BENEFIT DUE TO ONE VASOPRESSOR COMPARED TO ANOTHER

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