SHOCK

1. SHOCK Nir Hus MD., PhD. Ryder Trauma Center Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

2. Introduction • Shock management is essential in the care of the surgical patient. • Alfred Blalock's classic textbook, Principles of Surgical Care: Shock and Other Problems. • A syndrome not a diagnosis, causes still remain enigmatic. • Glucose and fatty acids are essential units organisms use to make energy: in the presence of oxygen life can sustain itself, in its absence it cannot. • Lactic acid accumulation causes denaturation of proteins, metabolic chaos. • Oxygen delivery is the geometric product of arterial oxygen saturation, hemoglobin concentration, stroke volume, and heart rate. • The most important task in shock intervention is early recognition of the shock syndrome. Second is optimization of above four parameters. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

3. Adrenal Reflex Response • Metabolic derangements of shock come after the clinically recognizable, and neuroendocrine-mediated reflex response. • Reflex response mediators: • ↑ Catecholamines first causes heart rate acceleration. Second, peripheral arterial beds and splanchnic beds empty into the systemic circulation. Third, potassium is shifted to intracellular compartments. May be masked by beta blockers. • ↑ Renin in response hypovolemia causes increase in circulating angiotensins. This contributes substantially to overall splanchnic vasoconstriction. In addition, ADH secretion causes water and sodium retention. Net effect is decreased urine output. • Other hormones secreted somewhat later in response to shock include glucagon, cortisol, and growth hormone. Collectively, they create a state similar to diabetes. Presents as a mild hyperglycemia due to gluconeogenesis and insulin resistance. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

4. Guyton’s Venous Return Curve • When the right atrial pressure is equal to the no-flow pressure in the venous circulation, forward flow into the heart ceases (Pms). • The slope of the curve is the reciprocal of the venous resistance. At all points on the curve, Ohm's law applies: the venous return is equal to the difference between the no-flow and right atrial pressures, divided by the venous resistance. • (B) Effects of changing the Pms on the venous return curve. Because the circulatory system is a closed system, cardiac out put and venous return are equal. • Augmenting the Pms (e.g., by a fluid bolus) shifts the oblique portion of the curve to the right, whereas acute diminution of Pms pressure (e.g., during homorrhage) shifts the oblique portion of the curve to the left. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

5. Contractility: Frank-Starling • The normal relationship between preload and performance is shown on the dotted curve. • Systolic deterioration rotates the curve downward. • Diastolic deterioration shifts it rightward (black curves). • Administration of an inotrope rotates the normal curve up and to the left (counterclockwise; blue curve). Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

6. Cardiac Performance • The venous return curve is superimposed on the familiar Frank-Starling curve that relates a surrogate for left ventricular preload (right atrial pressure) to cardiac output. • Because the circulatory system is closed, venous return must equal cardiac output, and the system's performance is described by the intersection of the two curves. • The curves can be shifted by disease and further shifted by interventions to counteract disease states. • The reason the cardiac function curve extends into the negative range of right atrial pressures is that pleural pressure is normally negative. • The net transmural pressure (the pressure across the wall of the right atrium that will cause blood to flow into the right ventricle) remains positive even when right atrial pressure is marginally negative relative to the atmostphere. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

7. 3 Pathways to Shock (3 P’s) • Once shock is recognized, the surgeon must simultaneously identify and reverse the underlying cause while performing resuscitation. • Perfusate deficiency: ↓ Intravascular volume, ie: hypovolemic shock. • After 10% volume loss, the adrenal neuroendocrine response to shock becomes clinically apparent. • Compensation fails at approximately 30% volume loss, clinically manifested as the onset of systolic and diastolic hypotension. • During hypotension, blood flow redistribution occurs in favor of the brain, at the expense of the heart and the kidneys. A 40% to 50% volume loss exhausts all compensatory mechanisms. • Pump deficiency: primary pump failure and/or inability of the pump to accept the perfusate (obstructive). • Primary failure examples: MI, dysrrhythmias, rupture of papillary muscle rupture • Obstructive examples: tension ptx, tamponade, pulmonary embolism, air embolism • Pipe deficiency: Neurologic distributive problems that allow blood to pool into the periphery and to pass by starving tissues without unloading nutrients. • Central interruption of SNS - spinal cord injury or neuraxial instillation of local anesthetic agents, ie. spinal or epidural anesthesia. • Peripheral interruption of SNS – sepsis. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

8. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

9. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

10. Hypovolemic Shock • Acute hypovolemia shifts the venous return curve down and to the left, reflecting the acute fall in mean systemic pressure (Pms). • The intersection of the normal cardiac function curve with the left-shifted hypovolemic venous return curve causes the decrease in cardiac output (lowermost black dot). • The physiologic “fight-or-flight response” releasing catecholamines from the circulation improves cardiac performance, sliding the cardiac performance curve upward and leftward along the compromised venous return curve (second black dot). • Administration of a pure vascular constrictor such as phenylephrine would improve Pms but worsen venous resistance, leading to a less favorable slope in the venous return curve (lowermost blue dot). • The most effective therapy is restoration of circulating volume. Crystalloid resuscitation further diminishes resistance by dilution of the rheologically active erythrocytes, and therefore shifts the venous return curve up and to the right. • The new cardiac output is even higher than the original cardiac output (uppermost dot) because of these favorable effects on resistance. Also illustrated is a compromised cardiac function curve that can be used to predict the consequences of volume loss in patients with limited cardiac function. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

11. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

12. Cardiogenic Shock • Effects of Dopamine. • Cardiac dysfunction causes the typical change in the cardiac output curve, pivoting it down and to the right (lowermost black dot). • The homeostatic response of the venous circulation—the accumulation of fluid—allows venous pressure to rise, shifting the mean systemic pressure (Pms) to the right while leaving venous resistance (the slope of the venous return curve) unchanged. The new intersection is at the rightmost black dot. • Administration of dopamine increases not only cardiac performance but Pms, leaving venous resistance more or less unchanged. These combined effects result in a new intersection located at the blue dot. • Effects of Dobutamine. • The administration of dobutamine improves cardiac function similar to dopamine. • The predominantly b-adrenergic stimulation of dobutamine causes a fall in venous resistance. There are two consequences. • Pms may fall back to normal • The slope of the venous function curve (the reciprocal of venous resistance) changes, pivoting the curve up and to the right (blue dot preferred over dopamine in cardiogenic shock. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

13. Septic Shock • Early sepsis causes a sudden, marked vasodilation. Mean systemic pressure (Pms) and venous resistance both fall. • As a consequence, the oblique portion of the venous return curve shifts to the left (fall in Pms) and also rotates downward and to the left (increase in venous resistance). • When sepsis is recognized promptly, aggresive volume resuscitation can restore Pms while venous resistance remains constant, creating a resuscitated venous function curve. • Sepsis can cause both an afterload reduction leading to seemingly increased cardiac performance (uppermost blue dot) or severe myocardial dysfunction (lowermost blue dot). • If sepsis is unrecognized and myocardial depression supervenes, cardiac function can be inadequate to sustain life (lowermost dot). Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

14. Obstructive Shock, ie. Tension Ptx • Cardiac function shifts far to the right. • The intersection of the cardiac function curve with the abscissa is equal to the pleural pressure: at right atrial pressures less than pleural pressures, the atrium cannot fill and therefore no blood can be ejected. • Neither endogenous nor exogenous inotropes can shift the cardiac function curve to the left; the intersection with the abscissa is fixed by the pleural pressure. • Inspection of the lowermost venous return curve shows that pleural pressure similarly limits venous return. The composite performance is described by the rightmost dot. • The mean systemic pressure (Pms) is markedly increased owing to blood being squeezed out of the thorax and by endogenous catecholamine release. • Neither volume infusion (the middle venous return curve) nor administration of catecholamines (the left-shifted cardiac function curve) creates much improvement in cardiac output (blue dots). The only effective therapy is immediate relief of the excessive pleural pressure by conversion of the tension pneumothorax to an open pneumothorax (needle decompression). Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

15. Neurogenic Shock • With a spinal injury below T-4, cardiac performance is unchanged, and the major effect is on venous tone. Mean systemic pressure (Pms) falls, with relatively little effect on venous resistance, yielding the performance intersection marked by the middle black dot. • Sympathetic denervation of the heart, characteristic of spinal cord lesions above T-4, leads to compromised cardiac performance and a circulatory equilibrium (lowermost black dot). Volume infusion is required to restore Pms, and the addition of dopamine yields improved venous return and cardiac function curves (blue dot). Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

16. Shock Management - I • Resuscitation from shock must begin immediately on recognition, for restoration of oxygen delivery is the imperative. • The simple ABC approach is effective. Emphasis on neck veins and auscultation during PE. • SaO2 should be kept above 95%. • A pulse should be sought, along with BP, and EKG. • NG for gastric aspiration prevents aspiration. • Immediate crossmatching of blood with a determination of hemoglobin concentration is key. • Rapid infusion with LR (20 mL/kg) should be done within 5 minutes. This will increase preload, diminish venous resistance, and possibly decrease arterial afterload, all of which augment cardiac performance. The bolus can be repeated immediately if the shock is not immediately responsive. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

17. Shock Management - II • UO is the first proxy for the adequacy of organ perfusion, it should be measured every 30 minutes by an indwelling bladder (Foley) catheter. • pH on ABG is best tool for assessment of shock reversal, since the pH falls into the acid range as a consequence of anaerobic metabolism with obligatory accumulation of lactic acid. After adequate resuscitation anion gap acidosis should normalize. • Perfusion of abdominal viscera can be used as an intermediate surrogate to extrapolate perfusion to the brain. The adequacy of mucosal perfusion can be assessed by tonometry. • If there is uncertainty about the magnitude of the cardiac output, it should be measured by thermodilution or aortic flow. CI of 2.5 L/min/m2 of body surface area is the minimum required to deliver sufficient oxygen. • Decreases in either hemoglobin concentration or oxygen saturation require compensatory proportionate increments in cardiac output to maintain oxygen delivery at a minimum value of 500 mL/min/m2. • Calcium should be administered to bring the ionized calcium into the normal range. • Base excess should be determined and sufficient bicarbonate to bring the plasma pH up to 7.2. • Temperature should be measured, and patients warmed if temperatures are less than 33° to 34°C . Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

18. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

19. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

20. Dopamine • Dopamine differs from the other pressors by having accumulating effects with increasing doses. • The receptors occupied first are dopaminergic receptors on the kidney and in splanchnic beds that regionally augment blood flow. Urine output can rise rapidly. • Before those receptors are saturated, however, dopamine begins to occupy b receptors. Vasodilation predominates owing to the combined effects on dopaminergic and b receptors, and as a consequence the heart rate increases. • As the dose is increased (but before the b receptors are saturated), the a receptors become occupied. Vasoconstriction dominates and the heart rate may slow somewhat. The relationship between infusion rate and receptor occupancy is patient specific. Dopamine must therefore be titrated to desired effect. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

21. Other Sympathomimetics… • They are most effective in a slightly acid milieu (pH 7.2 to 7.4). • Hemodynamic effect depends on receptor number and occupancy, and coupling of the receptor to second messengers: all sympathomimetic amines appear to act through one or more internal cell signaling systems. • Receptor number and second messenger coupling appear to be especially important for dobutamine because tachyphylaxis can render the drug ineffective after just a few days' administration. Troubleshoot by rotating with amrinone/milrinone. • Dobutamine acts through a G protein to activate adenyl cyclase and thereby increase the concentration of the second messenger, cyclic adenosine monophosphate (cAMP). • Amrinone augments the concentration of cAMP by inhibiting the degrading enzyme, phosphodiesterase. • Resuscitation from shock is occasionally thwarted by unrecognized endocrinopathies, including hypothyroidism and adrenal cortical insufficiency. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

22. Mechanical Adjuncts • Mechanical adjuncts to the management of shock are reserved for patients with true pump failure. • The adjuncts include intraaortic balloon counterpulsation and ventricular assist devices. All are bridges to definitive therapy. • Intraaortic balloon counterpulsation increases coronary blood flow through critical stenoses by augmenting afterload during diastole. Direct effects on cardiac output are thought to be minimal. • Left and right ventricular assist devices unload the heart directly and can therefore be used when the myocardium itself has failed, not merely its blood supply. • The mechanical adjuncts usually require systemic anticoagulation, which may be relatively contraindicated in patients with recent surgery. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

23. Risks of Resuscitation • Secondary injuries attributable to reperfusion and inflammation associated with resuscitation occur, but are complex, and incompletely understood. • The conclusion that emerges from biologic studies is that the network of mediators and the many affected cells is complex and that mechanisms limiting inflammation are effective as long as the inflammation itself is limited. • The safest course appears to include rapid identification and definitive control of inflammatory stimuli before the network of mediators and affected cells is activated. • The clinical imperative is to find the cause of the shock, to rectify the cause of the shock, and to do so as rapidly as practical. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital

24. Swan-Ganz Catheterization • It is a nontherapeutic device with indications in flux. • Its usefulness depends heavily on the skill of the operator and the expertise of the interpreter. It appears to be overused… • Findings and recommendations after 1996 multicenter study: • Management guided by the PAC may be beneficial for patients with acute myocardial infarction complicated by progressive hypotension or cardiogenic shock. • May be useful in the management of patients with shock unresponsive to fluid resuscitation and use of pressors. • May be useful in patients with septic shock who have not responded to initial aggressive fluid resuscitation and low dose inotropic/vasoconstrictor therapy. • The value of the PAC in other forms of shock is indeterminate, but in any case its use should follow routine management with fluids and pressors guided by central venous and systemic arterial pressure monitoring. • Failure to respond to routine management or uncertainty concerning the response are adequate reasons to use a PAC with its attendant risks. Nir Hus MD., PhD. Ryder Trauma Center Jackson Memorial Hospital