Shock Flashcards
LIST THE AETIOLOGIES OF CIRCULATORY SHOCK
1) hypovolaemic due to inadequate venous return
2) cardiogenic, due to inadequate ventricular pump function
3) obstructive, due to vascular obliteration
4) distributive, due to loss of vasoregulatory control
when does tissue hypoperfusion occur and what is the result of it
tissue hypoperfusion is common in all forms of shock, with the possibel exception of hyperdynamic septic shock.
this results in tissue hypoxia and switch from aerobic to anaerobiv metabolism, –> hyperlacticacidaemia and metabolic acidosis.
is high lactic acidosis a marker of tissue hypoperfusion?
not per se, because lactate clearance is often delayed or impaired in shock states. Also, exercise, seizures etc can induce lactic acidosis without cardiovascular insufficiency.
why does sustained circulatory shock results in cellular damage?
ustained circulatory shock results in cellular damage, not from anaerobic metabolism alone, but also from an inability to sustain intermediary metabolism and enzyme production necessary to drive normal mitochondrial performance.
Metabolic failure due to sustained tissue hypoxia may explain why preoptimization and early goal-directed therapy improve outcome, whereas aggressive resuscitation after injury is not effective at reducing mortality from a variety of insults.
Measures of hypoperfusion: what are they and are they effective?
measures of cardiac output, MAP and their changes in response to both shock and its treatment poorly reflect both regional blood flow and microcirculatory blood flow.
Most forms of haemodynamic monitoring measure global parameters like arterial pressure, heart rate, other vascular pressures, and cardiac output.
Potentially, measuringSvo2or the difference between tissuePco2and arterialPco2, referred to as thePco2gap, would allow one to assess effective tissue blood flow since decreases in capillary blood flow initially causes CO2from aerobic metabolism to accumulate.
Hypovolaemia is..?
Hypovolaemia is the cardiovascular state in which the effective circulating blood volume is inadequate to sustain a level of cardiac output necessary for normal function without supplemental sympathetic tone or postural changes to ensure adequate amounts of venous return.
hypovolaemia can occur due to…
It is a relative process and can occur through absolute blood loss, as with haemorrhage and trauma, or fluid and electrolyte loss, as with massive diuresis, diarrhoea, vomiting, or evaporation from large burn surfaces.
the normal reflex responses to hypovolaemia are
increased sympathetic tone, vasoconstriction, and tachycardia. Cardiac output is often sustained by these mechanisms such that heart rate is increased and stroke volume decreased, whereas blood flow distribution is diverted away from the skin, resting muscles, and gut. With tissue hypoperfusion, lactic acidosis develops as a marker of tissue anaerobic metabolism. Thus, hypovolaemia initiates as tachycardia, reduced arterial pulse pressure, and (often) hypertension with a near normal resting cardiac output, followed by signs of organ hypoperfusion (oliguria, confusion) as cardiac output decreases. Systemic hypotension is the final presentation of hypovolaemic shock and—if the clinician waits for this before acting—ischaemic tissue injury is almost always present.
cardiogenic shock: definition, manifestation. differences in acute and chronic heart failure
Cardiac pump dysfunction can be due to either LV or RV failure, or both. LV failure, as described above, is usually manifest by an increased LV end-diastolic pressure, left atrial pressure, and (by extension) pulmonary artery occlusion (‘wedge’) pressure, which must exist to sustain an adequate LV stroke volume. Tachycardia is universal in the patient who is not β-blocked.
The most common cause of isolated LV failure in the critically ill patient is acute myocardial infarction.
Acute LV failure is manifest by increased sympathetic tone (tachycardia, hypertension), impaired LV function (increased filling pressure and reduced stroke volume), with minimal RV effects (normal central venous pressure), and increased O2extraction manifest by a lowSvo2. Cardiac output need not be reduced and may in fact be elevated, owing to the release of catecholamines as part of the acute stress response; vascular resistance is increased. By contrast, in chronic heart failure, although sympathetic tone is elevated, the heart rate is rarely over 105/min, and filling pressures are elevated in both ventricles consistent with combined LV failure and fluid retention. Again, cardiac output is not reduced except in severe heart failure states, but a cardinal finding is the inability of the heart to increase output in response to a volume load or metabolic stress (exercise). Furthermore, owing to the increased sympathetic tone, splanchnic and renal blood flows are reduced and can lead to splanchnic or renal ischaemia.
obstructive shock: definition and aetiology
Obstruction in this context means mechanical obstruction of blood flow or ventricular filling. The most common cause of obstructive shock is pulmonary embolism leading to acute RV failure, but isolated RV dysfunction can occur in the setting of an acute inferior wall myocardial infarction, also as a consequence of pulmonary vascular disease (chronic obstructive pulmonary disease, primary pulmonary hypertension).
. When RV dysfunction predominates and is induced by pulmonary parenchymal disease, it is referred to as…. and it manifests with …
rdial infarction, also as a consequence of pulmonary vascular disease (chronic obstructive pulmonary disease, primary pulmonary hypertension). When RV dysfunction predominates and is induced by pulmonary parenchymal disease, it is referred to as cor pulmonale, which is associated with signs of backward failure, elevated RV volume and pressures, systemic venous hypertension, low cardiac output, as well as reduced renal and hepatic blood flow. LV diastolic compliance decreases as the right ventricle dilates due to ventricular interdependence, either from intraventricular septal shift or absolute limitation of biventricular volume due to pericardial restraint. Thus, pulmonary artery occlusion (‘wedge’) pressure is often elevated for a specific LV stroke work, giving the erroneous appearance of impaired LV contractility, but if LVEDV were measured it is possible that no change in LV function would be seen if this were plotted against LV stroke work.
Cardiac tamponade can occur from ….
its cardinal signs?
Cardiac tamponade can occur from either (1) ventricular dilation limiting biventricular filling due to pericardial volume limitation, (2) acute pericardial effusion due to either fluid (inflammation) or blood (haemorrhage), which needs not be great in quantity, and (3) hyperinflation, which can act like pericardial tamponade to limit biventricular filling.
The first two aetiologies are rarely seen, whereas the third commonly occurs.
The cardinal sign of tamponade is diastolic equalization of all pressures, central venous pressure, pulmonary arterial diastolic pressure, and pulmonary artery occlusion (‘wedge’) pressure. Since RV compliance is greater than LV compliance, early on in tamponade there may be selective reduction in RV filling.
distributive shock. definition
Loss of blood flow regulation occurs as the endstage of all forms of circulatory shock, but as the initial presenting process it is common in sepsis, neurogenic shock, and adrenal insufficiency. Sepsis is a systemic process characterized by activation of the intravascular inflammatory mediators and generalized endothelial injury, but it is not clear that tissue ischaemia is an early aspect of this process.
Acute septicaemia is associated with … .
what does the clinical picture look like?
Acute septicaemia is associated with increased sympathetic activity (tachycardia, diaphoresis) and increased capillary leak with loss of intravascular volume. Before fluid resuscitation this combination of processes resembles simple hypovolaemia, with decreased cardiac output, normal to increased peripheral vasomotor tone, and very lowSvo2, reflecting systemic hypoperfusion.
LV function is often depressed, but only in parallel with depression of other organs, and this effect of sepsis is usually masked by the associated hypotension that maintains low LV afterload.
However, most patients with such a clinical presentation receive initial volume expansion therapy such that the clinical picture of sepsis reflects a hyperdynamic state rather than hypovolaemia, which has been referred to as ‘warm shock’ in contrast to all other forms of shock.
The haemodynamic profile of sepsis is one of increased cardiac index, normal pulmonary artery occlusion (‘wedge’) pressure, elevatedSvo2, and a low to normal arterial pressure, consistent with loss of peripheral vasomotor tone.
what can be the causes of the loss of sympathetic tone?
Acute spinal injury, spinal anaesthesia, general anaesthesia, and central nervous system catastrophe all induce a loss of sympathetic tone. The resulting hypotension is often not associated with compensatory tachycardia, hence systemic hypotension can be profound and precipitate cerebral vascular insufficiency and myocardial ischaemia. Since neurogenic shock reduces sympathetic tone, biventricular filling pressures, arterial pressure, and cardiac output all decrease. Treatment consists of reversing the primary process and supporting the circulation with infusion of an α-adrenergic agonist, such as phenylephrine, dopamine, or noradrenaline
Acute adrenal insufficiency can present with hyperpyrexia and circulatory collapse.
Hypovolaemic shock:
what factors influence the development of hypovolaemic shock?
Hypovolemic shock represents more than a simple mechanical response to loss of circulating volume. It is a dynamic process involving competing adaptive (compensatory) and maladaptive responses at each stage of development.
• Although intravascular volume replacement is always a necessary component of resuscitation from hypovolemia or hypovolemic shock, the biologic responses to the insult may progress to the point where such resuscitation is insufficient to reverse the progression of the shock syndrome. Patients who have sustained a greater than 40% loss of blood volume for 2 hours or more may be unable to be effectively resuscitated. □ A series of inflammatory mediator, cardiovascular, and organ responses to shock is initiated, which supersede the importance of the initial insult in driving further injury. • The rate of loss of intravascular volume and the preexisting cardiac reserve is of substantial importance in the development of hypovolemic shock. * Although an acute blood loss of 1 L in a healthy adult may result in mild-tomoderate hypotension with a reduced pulmonary wedge pressure (PWP) and CVP,46 the same loss over a longer time may be well tolerated because of compensatory responses, such as tachycardia, increased myocardial contractility, increased red blood cell 2,3-diphosphoglycerate, and increased fl uid retention. * A similar slow blood loss may lead to substantial hemodynamic compromise, however, in an individual with a limited cardiac reserve even while the PWP and CVP remain elevated.
hypovolaemic shock, its course and compensatory emchanisms
- Acute loss of 10% of the circulating blood volume is well tolerated with tachycardia the only obvious sign.
- CI may be minimally decreased despite a compensatory increase in myocardial contractility.
- SVR typically increases slightly, particularly if sympathetic stimulation augments MAP.
○ Mild-to-moderate hypotension and decreased CI may be present. Orthostasis (with a blood pressure decrease of 10 mm Hg and increased heart rate of 20 to 30 beats per minute) may become apparent. There is a marked elevation in SVR, and serum lactate may begin to increase. With decreases of the circulating volume of 40% or more, marked hypotension with clinical signs of shock is noted.
○ CI and tissue perfusion may decrease to less than half of normal.
○ Lactic acidosis is usually present and predicts a poor outcome.
Cardiogenic shock results from…
Hemodynamically, cardiogenic shock is characterized by
• Cardiogenic shock results from the failure of the heart as a pump
• It is the most common cause of in-hospital mortality in patients with Q wave myocardial infarction. • Hemodynamically, cardiogenic shock is characterized by increased ventricular preload (increased ventricular volumes, PWP, and CVP) (see Table 22-1). • Otherwise, hemodynamic characteristics are similar to those for hypovolemic shock (see Table22-1). ○ In particular, both involve reduced CI, stroke volume index, and ventricular stroke work index with increased SVR. ○ Because of inadequate tissue perfusion, the Sv¯O2 is substantially reduced, and the arteriovenous oxygen content difference is increased. ○ The degree of lactic acidosis may predict mortality.
The pathophysiology of cardiogenic shock secondary to a right ventricular infarction and failure
different than other forms of cardiogenic shock.
○ Although some degree of right ventricular involvement is seen in half of inferior myocardial infarctions, only the largest 10% to 20% result in right ventricular failure and cardiogenic shock.68 These infarctions usually involve part of the left ventricular wall as well. Isolated infarctions of the right ventricle are rare.
○ Because therapy of this form of shock requires fluid resuscitation and inotropes (rather than vasopressors), differentiation from other causes of cardiogenic shock is crucial.
○ Conditions compromising right ventricular function, such as cardiac tamponade, restrictive cardiomyopathy, constrictive pericarditis, and pulmonary embolus, also are included in the differential diagnosis.
○ Each of these conditions may manifest with some of the typical clinical and hemodynamic findings of right ventricular infarction, including Kussmaul’s sign and pulsus paradoxus with elevation and equalization of CVP, right ventricular systolic pressure, pulmonary artery diastolic pressure, and PWP.
• Prognosis in this form of cardiogenic shock is distinctly better than that of cardiogenic shock resulting from left ventricular infarction; however, an inferior infarction with right ventricular injury has a substantially worse prognosis than such an infarction without significant right sided involvement.
Obstructive Shock
causes
Extracardiac obstructive shock results from an obstruction to flow in the cardiovascular circuit (see Box 22-2 and Fig. 22-1).
• Pericardial tamponade and constrictive pericarditis directly impair diastolic filling of the right ventricle.
• Tension pneumothorax and intrathoracic tumors indirectly impair right ventricular filling by obstructing venous return.
• Massive pulmonary emboli (two or more lobar arteries with >50% of the vascular bed occluded), nonembolic acute pulmonary hypertension, large systemic emboli (e.g., saddle embolus), and aortic dissection may result in shock owing to increased ventricular afterload.
Obstructive Shock
The characteristic hemodynamic and metabolic patterns are,??
• The characteristic hemodynamic and metabolic patterns are, in most ways, similar to other low output shock states (see Table 22-1).
○ CI, stroke volume index, and stroke work indices are usually decreased.
○ Because tissue perfusion is decreased, the Sv¯O2 is low, the arteriovenous oxygen content difference is increased, and serum lactate frequently is elevated.
○ Other hemodynamic parameters depend on the site of the obstruction. Tension pneumothorax and mediastinal tumors may obstruct the great thoracic veins resulting in a hemodynamic pattern (decreased CI and elevated SVR) similar to hypovolemia (although distended jugular and peripheral veins may be seen). Cardiac tamponade typically causes increased and equalized right and left heart ventricular diastolic pressures, pulmonary artery diastolic pressure, CVP, and PWP.
• In constrictive pericarditis, right and left ventricular diastolic pressures are elevated and within 5 mm Hg of each other.
• Mean right and left atrial pressures may or may not be equal as well.
• Massive pulmonary embolus results in right ventricular failure with elevated pulmonary artery and right heart pressures while PWP remains normal.
• A systemic saddle embolus or aortic occlusion secondary to dissection causes peripheral hypotension and signs of left ventricular failure, including elevated PWP. Clinical signs similarly depend on the site of the obstruction.
Distributive Shock
is caused by and haemodynamically characterised by…
• The defining feature of distributive shock is loss of peripheral resistance.
• Septic shock is the most common form and has the greatest impact on intensive care unit (ICU) morbidity and mortality.
• Hemodynamically, distributive shock is characterized by an overall decrease in SVR (see Table 22-1).
○ Resistance in any specific organ bed or tissue may be decreased, increased, or unchanged, however.
○ Initially, CI may be depressed, and ventricular filling pressures may be decreased.
○ After fluid resuscitation, when filling pressures are normalized or increased, CI is usually elevated.
○ As a result of hypotension, left and right ventricular stroke work indices are normally decreased.
○ Sv¯O2 is increased above normal.
○ Concomitantly, arteriovenous oxygen content difference is narrowed despite the fact that oxygen demand is usually increased (particularly in sepsis).
§ The basis of these phenomena may be that although total body perfusion (CI) is increased, perfusion is ineffective in that either it does not reach the necessary tissues or the tissues cannot use the substrates presented. As a reflection of this inadequate “effective” tissue perfusion, lactic acidosis may ensue.
○ In contrast to the other forms of shock, clinical characteristics of resuscitated distributive shock include warm, well-perfused extremities, a decreased diastolic blood pressure, and an increased pulse pressure.
○ Nonspecific signs of shock include tachycardia, tachypnea, decreased urine output, and altered mentation.
what may explain some of the typical metabolic findings of sepsis and septic shock??
- Loss of vascular autoregulatory control may explain some of the typical metabolic findings of sepsis and septic shock. An early theory postulated the existence of microanatomic shunts between the arterial and venous circulations. During sepsis, these shunts were said to result in decreased SVR and increased Sv¯O2.
- Although microanatomic shunting has been noted in localized areas of inflammation, however, systemic evidence of this phenomenon in sepsis and septic shock is lacking.
- “Functional” shunting as a result of defects of microcirculatory regulation in sepsis also has been suggested.
• Relative vasoconstriction would result in tissue hypoxia and lactate production owing to anaerobic metabolism.
• Observations that some capillary beds may be occluded by platelet microaggregates, leukocytes, fi brin deposits, and endothelial damage support this theory.
○ Additional support comes from studies that show evidence of oxygen supply–dependent oxygen consumption in sepsis.• A third theory suggests that circulating mediators cause an intracellular metabolic defect involving substrate use, which results in bioenergetic failure (decreased high-energy phosphate production) and lactate production.
Increased Sv¯O2 could be explained by perfusion, which is increased in excess of tissue oxygen use capability.
The most common trigger for systemic activation of the inflammatory cascade is
• The trigger for systemic activation of the inflammatory cascade is gram-negative bacilli in 50% to 75% of cases of septic shock.
more features of distributive shock
• More than any other form of shock, distributive, particularly septic, shock involves substantial elements of the hemodynamic characteristics of other shock categories (see Fig. 22-1 and Table 22-1).
• As noted, all forms of distributive shock involve decreased mean peripheral vascular resistance.
• Before fluid resuscitation, distributive shock also involves a relative hypovolemic component.
○ The first element of this relative hypovolemia is an increase of the vascular capacitance owing to venodilation.
○ This phenomenon has been directly supported in animal models of sepsis and is reinforced by the fact that clinical hypodynamic septic shock (low cardiac output) usually can be converted to hyperdynamic shock (high cardiac output) with adequate fluid resuscitation.
• Relaxation of vascular smooth muscle is attributed to many of the mediators known to circulate during sepsis.
○ These same mediators also contribute to the second cause of hypovolemia in sepsis, third spacing of fluid to the interstitium owing to loss of endothelial integrity.
○ In addition, numerous studies have shown that human septic shock is characterized by myocardial depression (biventricular dilation and decreased ejection fraction). Circulating substances such as TNF-α, IL-1, PAF, leukotrienes, and, most recently, IL-6 have been implicated in this process.
physiology of arterial pressure
Although cardiac output may be expressed as a function of MAP and vascular resistance (CO = [MAP − CVP]/SVR), cardiac output is not directly dependent on MAP in most physiologic states. Instead, blood pressure typically depends on cardiac output and vascular resistance. Blood pressure does provide a mechanism, however, to sense cardiac output and global perfusion perturbations indirectly for autoregulatory purposes. The ability of all organ vascular beds to support normal blood fl ow depends on maintenance of blood pressure within the defi ned range for that organ (Fig. 22-2).
Vital organs, such as the brain and heart in particular, are able to autoregulate blood fl w over a wide range of blood pressures. Failure to maintain the minimal MAP and perfusion pressure required for autoregulation during hypodynamic circulatory shock indicates a severe reduction in cardiac outpu
Preload depends on …
Preload depends on circulating volume, venous tone, atrial contraction, and intrathoracic pressure among other factors.149,152 Atrial contraction is particularly important in patients with impaired ventricular function. Although accounting for only 5% to 10% of cardiac output in healthy humans, synchronized atrial contraction contributes 40% to 50% of the cardiac output in patients with severe left ventricular dysfunction.152 Increased intrathoracic pressure or increased venous capacitance affect preload by reducing venous return.
Afterload is … and is increased in
Afterload refers to the total resistance to ejection of blood from the ventricle during contraction. Increasing afterload results in decreased extent and velocity of myocardial contraction.
Afterload is increased in pathologic conditions such as aortic stenosis, systemic embolism, and hypertension.
the effects of PEEP ventilation on haemodynamics
Increased intrathoracic pressure owing to mechanical ventilation and positive end-expiratory pressure decrease left ventricular afterload, while increasing right ventricular afterload.
Effects of PEEP on systemic haemodynamics Application of PEEP increases intrathoracic pressure diminishing venous return to the right heart and increasing the right ventricular afterload. These haemodynamic consequences depend on previous ventricular loading conditions and function, and respiratory system compliance. An adequate circulating blood volume is required before application of PEEP to prevent this depression of right ventricular output. Application of PEEP decreases left ventricular stroke volume, while heart rate does not change significantly. # The reduction in stroke volume is mainly due to a decrease in left ventricular preload. This effect may be explained by different mechanisms: decreased venous return to the right heart; increased right ventricular afterload; decreased ventricular compliance; and decreased ventricular contractility.
differences of the effects of PEEP on haemodynamics in normal and chronically failing hearts
In patients with normal cardiac function, the main consequence of increased intrathoracic pressure is the reduction of venous return; in patients with poor left ventricular function or congestive heart failure, the increase in intra-thoracic pressure reduces the left ventricular transmural pressure leading to a reduction in left ventricular afterload and improving left ventricular function. In these patients, cardiac output is relatively insensitive to reduction in venous return because diastolic volume is elevated.
CPAP effecs on haemodynamics
CPAP increases intrathoracic pressure, which may reduce venous return and preload to the heart.
However, this may also be beneficial in offloading the left atrium/ventricle in cardiogenic pulmonary oedema associated with acute left ventricular failure.
Conversely, in patients with relative intravascular depletion, the application of CPAP may cause a further reduction in ventricular preload, stroke volume, cardiac output and blood pressure.
CPAP effects on cerebral perfusion
The application of PEEP may affect the cerebral circulation by haemodynamic and CO2-mediated mechanisms.
The haemodynamic mechanism may alter cerebral circulation both on the arterial side, reducing arterial pressure, and on the venous side, reducing cerebral venous drainage.
According to the concept of the vasodilatory cascade, the decrease in arterial pressure caused by PEEP may diminish cerebral blood flow in patients whose cerebral auto-regulation is impaired, while may cause a compensatory vaso-dilation if auto-regulation is preserved.
In the latter case, vasodilation will lead to an increase in cerebral blood volume and intracranial pressure (ICP), given a reduced intracranial compliance. However, application of PEEP does not induce a significant reduction in arterial and cerebral perfusion pressure if euvolaemia is ensured.
CPAP effects on renal and hepatic perfusion
PEEP decreases splanchnic blood flow and may compromise hepatic perfusion and portal venous drainage. This effect may be explained by a reduction in cardiac output, coupled with elevation of central venous pressure (CVP) and an increased outflow resistance due to a direct compressive effect of the diaphragm on the liver. The resulting passive hepatic congestion can cause moderate elevation of bilirubin and hepatic enzymes. PEEP may also interfere with renal function, even when cardiac output is preserved, by reducing renal blood flow depending on the volaemic state and the amount of applied pressure.
