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50 Cards in this Set
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hemodynamic criteria for cardiogenic shock
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Hemodynamic criteria for cardiogenic shock include (1) sustained hypotension [systolic blood pressure (BP) <90 mm Hg], (2) reduced cardiac index (<2.2 L/min per m2), and (3) an elevated (>18 mm Hg) pulmonary artery occlusion pressur
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hemodynamic criteria for cardiogenic shock
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Hemodynamic criteria for cardiogenic shock include (1) sustained hypotension [systolic blood pressure (BP) <90 mm Hg], (2) reduced cardiac index (<2.2 L/min per m2), and (3) an elevated (>18 mm Hg) pulmonary artery occlusion pressur
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hemodynamic criteria for cardiogenic shock
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Hemodynamic criteria for cardiogenic shock include (1) sustained hypotension [systolic blood pressure (BP) <90 mm Hg], (2) reduced cardiac index (<2.2 L/min per m2), and (3) an elevated (>18 mm Hg) pulmonary artery occlusion pressur
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Cardiogenic shock usually results from
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from an acute myocardial infarction (AMI) that affects over 40 percent of the left ventricular myocardium
The overall incidence of cardiogenic shock in AMI is 6 to 8 percent, a rate that remained constant from 1975 to 1997.3,4 Although some patients have cardiogenic shock on initial presentation, the median time from the onset of infarction to the development of shock is 8 h.5 |
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Cardiogenic shock usually results from
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from an acute myocardial infarction (AMI) that affects over 40 percent of the left ventricular myocardium
The overall incidence of cardiogenic shock in AMI is 6 to 8 percent, a rate that remained constant from 1975 to 1997.3,4 Although some patients have cardiogenic shock on initial presentation, the median time from the onset of infarction to the development of shock is 8 h.5 |
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Cardiogenic shock can develop from mechanical complications of an AMI
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myocardial free-wall rupture, acute ventricular septal defect (VSD), or mitral regurgitation from valvular dysfunction or papillary muscle rupture. Less common causes of cardiogenic shock include myocardial depression from conditions such as sepsis or myocarditis, LV outflow obstruction (e.g., aortic stenosis), and severe regurgitation of LV output (acute aortic regurgitation or mitral valve chordae rupture).
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Cardiogenic shock can develop from mechanical complications of an AMI
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myocardial free-wall rupture, acute ventricular septal defect (VSD), or mitral regurgitation from valvular dysfunction or papillary muscle rupture. Less common causes of cardiogenic shock include myocardial depression from conditions such as sepsis or myocarditis, LV outflow obstruction (e.g., aortic stenosis), and severe regurgitation of LV output (acute aortic regurgitation or mitral valve chordae rupture).
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The history should attempt to exclude other causes of shock
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such as sepsis, gastrointestinal hemorrhage, or massive pulmonary embolism; ask about a history of pre-existing valvular disease or injection drug use.
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The history should attempt to exclude other causes of shock
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such as sepsis, gastrointestinal hemorrhage, or massive pulmonary embolism; ask about a history of pre-existing valvular disease or injection drug use.
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Shock is characterized by hypoperfusion and is often, but not always, accompanied by hypotension. Systolic BP is usually below 90 mm Hg, although it can be higher with pre-existing hypertension. A higher BP may reflect compensatory increases in SVR. A pulse pressure less than 20 mm Hg may be evident, due to
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extreme vasoconstriction
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Shock is characterized by hypoperfusion and is often, but not always, accompanied by hypotension. Systolic BP is usually below 90 mm Hg, although it can be higher with pre-existing hypertension. A higher BP may reflect compensatory increases in SVR. A pulse pressure less than 20 mm Hg may be evident, due to
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extreme vasoconstriction
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the lung fields may be clear despite hypotension and jugular venous distention. in what etiology of cardiogenic shock
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However, with RV infarction, the lung fields may be clear despite hypotension and jugular venous distention. Cool, pale extremities with skin mottling indicates poor perfusion.
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the lung fields may be clear despite hypotension and jugular venous distention. in what etiology of cardiogenic shock
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However, with RV infarction, the lung fields may be clear despite hypotension and jugular venous distention. Cool, pale extremities with skin mottling indicates poor perfusion.
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Acute mitral regurgitation can occur from
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Acute mitral regurgitation can occur from chordae tendinea rupture or papillary muscle dysfunction. Chordae tendinea rupture is characterized by a soft holosystolic murmur at the apex radiating to the axilla but is often obscured by rales. With papillary muscle dysfunction, the murmur starts with the first heart sound but terminates before the second. An acute VSD is associated with a new loud holosystolic left parasternal murmur, often with a palpable thrill, that decreases in intensity as the intraventricular pressures equalize.
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Acute mitral regurgitation can occur from
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Acute mitral regurgitation can occur from chordae tendinea rupture or papillary muscle dysfunction. Chordae tendinea rupture is characterized by a soft holosystolic murmur at the apex radiating to the axilla but is often obscured by rales. With papillary muscle dysfunction, the murmur starts with the first heart sound but terminates before the second. An acute VSD is associated with a new loud holosystolic left parasternal murmur, often with a palpable thrill, that decreases in intensity as the intraventricular pressures equalize.
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what ecg findings supports the diagnosis of AMI.
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ST-segment elevation in two or more contiguous ECG leads supports the diagnosis of AMI.
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what ecg findings supports the diagnosis of AMI.
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ST-segment elevation in two or more contiguous ECG leads supports the diagnosis of AMI.
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The level of serum B-type natriuretic peptide (BNP) correlates with
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LV end-diastolic pressure and ventricular stretch. BNP has good direct correlation with pulmonary artery occlusion pressures as measured by a pulmonary artery catheter. BNP also is an excellent predictor of the clinical development of heart failure after AMI.10 Normal serum BNP levels are less than 100 pg/mL.
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The level of serum B-type natriuretic peptide (BNP) correlates with
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LV end-diastolic pressure and ventricular stretch. BNP has good direct correlation with pulmonary artery occlusion pressures as measured by a pulmonary artery catheter. BNP also is an excellent predictor of the clinical development of heart failure after AMI.10 Normal serum BNP levels are less than 100 pg/mL.
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An acute VSD is confirmed by echocardiography or right heart catheterization demonstrating an
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O2 saturation step-up from the right atrium to the RV.
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An acute VSD is confirmed by echocardiography or right heart catheterization demonstrating an
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O2 saturation step-up from the right atrium to the RV.
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In suspected cardiogenic shock wht is the DD
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AMI is always a possibility. Dyspnea in cardiogenic shock is common, so pulmonary embolus, emphysema exacerbation, and pneumonia are considered. Hypertension, peripheral vasoconstriction, and dyspnea suggest acute pulmonary edema. Although diffuse ST-T changes can be seen with acute pericarditis or myocarditis, a nondiagnostic ECG should prompt the consideration of other causes of hypotension. These include aortic dissection, pulmonary embolus, pericardial tamponade, acute valvular insufficiency, hemorrhage, or sepsis. Overdose by a toxin with negative inotropic or chronotropic effects (e.g. β-blocker, calcium channel blocker, or digoxin overdose) should be considered.
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In suspected cardiogenic shock wht is the DD
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AMI is always a possibility. Dyspnea in cardiogenic shock is common, so pulmonary embolus, emphysema exacerbation, and pneumonia are considered. Hypertension, peripheral vasoconstriction, and dyspnea suggest acute pulmonary edema. Although diffuse ST-T changes can be seen with acute pericarditis or myocarditis, a nondiagnostic ECG should prompt the consideration of other causes of hypotension. These include aortic dissection, pulmonary embolus, pericardial tamponade, acute valvular insufficiency, hemorrhage, or sepsis. Overdose by a toxin with negative inotropic or chronotropic effects (e.g. β-blocker, calcium channel blocker, or digoxin overdose) should be considered.
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Endotracheal intubation is often necessary to maintain oxygenation and ventilation. However, the change to positive pressure ventilation may
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further decrease preload and CO and worsen hypotension. The physician should anticipate this occurrence and be prepared to administer a fluid bolus, in the absence of pulmonary congestion, or initiate the appropriate vasopressor or inotrope.
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Endotracheal intubation is often necessary to maintain oxygenation and ventilation. However, the change to positive pressure ventilation may
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further decrease preload and CO and worsen hypotension. The physician should anticipate this occurrence and be prepared to administer a fluid bolus, in the absence of pulmonary congestion, or initiate the appropriate vasopressor or inotrope.
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Endotracheal intubation is often necessary to maintain oxygenation and ventilation. However, the change to positive pressure ventilation may
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further decrease preload and CO and worsen hypotension. The physician should anticipate this occurrence and be prepared to administer a fluid bolus, in the absence of pulmonary congestion, or initiate the appropriate vasopressor or inotrope.
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In the prescence of an AMI what should be given unless contraindicated
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aspirin and full-dose heparin should be given unless there is an absolute contraindication.4 If there is adequate BP, chest pain may be relieved by careful use of intravenous nitroglycerin or morphine. β-blockers and angiotensin-converting enzyme inhibitors should be withheld until the patient's condition is stable. Similarly, other vasodilators cannot be used in most cases when hypotension is present.
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In the prescence of an AMI what should be given unless contraindicated
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aspirin and full-dose heparin should be given unless there is an absolute contraindication.4 If there is adequate BP, chest pain may be relieved by careful use of intravenous nitroglycerin or morphine. β-blockers and angiotensin-converting enzyme inhibitors should be withheld until the patient's condition is stable. Similarly, other vasodilators cannot be used in most cases when hypotension is present.
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initial therapy for the hypotension assocaiated with cardiogenic shock
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Initial therapy must be guided by clinical findings. Because some patients with cardiogenic shock develop hypotension without pulmonary congestion, a small fluid challenge (NS 100 to 250 mL) may be appropriate. If there is pulmonary congestion, this volume infusion should be omitted. If there is no improvement in perfusion with the fluid bolus, or there is hypotension with pulmonary congestion, inotropes are considered.
Inotropes do not change outcome but can temporize while ED personnel arrange interventions to restore coronary artery perfusion and LV function.13,14 Inotrope selection depends on the suspected etiology of hypotension. If hemodynamics stabilize after inotropes are started, therapy for pulmonary congestion may be started (i.e., diuretics) while arranging admission to the intensive care unit. |
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initial therapy for the hypotension assocaiated with cardiogenic shock
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Initial therapy must be guided by clinical findings. Because some patients with cardiogenic shock develop hypotension without pulmonary congestion, a small fluid challenge (NS 100 to 250 mL) may be appropriate. If there is pulmonary congestion, this volume infusion should be omitted. If there is no improvement in perfusion with the fluid bolus, or there is hypotension with pulmonary congestion, inotropes are considered.
Inotropes do not change outcome but can temporize while ED personnel arrange interventions to restore coronary artery perfusion and LV function.13,14 Inotrope selection depends on the suspected etiology of hypotension. If hemodynamics stabilize after inotropes are started, therapy for pulmonary congestion may be started (i.e., diuretics) while arranging admission to the intensive care unit. |
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initial therapy for the hypotension assocaiated with cardiogenic shock
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Initial therapy must be guided by clinical findings. Because some patients with cardiogenic shock develop hypotension without pulmonary congestion, a small fluid challenge (NS 100 to 250 mL) may be appropriate. If there is pulmonary congestion, this volume infusion should be omitted. If there is no improvement in perfusion with the fluid bolus, or there is hypotension with pulmonary congestion, inotropes are considered.
Inotropes do not change outcome but can temporize while ED personnel arrange interventions to restore coronary artery perfusion and LV function.13,14 Inotrope selection depends on the suspected etiology of hypotension. If hemodynamics stabilize after inotropes are started, therapy for pulmonary congestion may be started (i.e., diuretics) while arranging admission to the intensive care unit. |
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Pure vasoconstrictors, such as phenylephrine, are generally contraindicated, because
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they increase cardiac afterload without augmenting cardiac contractility
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Pure vasoconstrictors, such as phenylephrine, are generally contraindicated, because
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they increase cardiac afterload without augmenting cardiac contractility
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In acute mitral regurgitation, hemodynamic support can be initiated with
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In acute mitral regurgitation, hemodynamic support can be initiated with dobutamine and nitroprusside. This treatment supports contractility and provides afterload reduction, respectively, and promotes forward systemic blood flow. The IABP is also beneficial for temporary support.4 Acute VSD is treated with dobutamine, nitroprusside, and an IABP.4 Confirmatory evidence for these emergent conditions with two-dimensional echocardiography should be sought, concomitant with emergency consultation from the cardiac surgical team
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In acute mitral regurgitation, hemodynamic support can be initiated with
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In acute mitral regurgitation, hemodynamic support can be initiated with dobutamine and nitroprusside. This treatment supports contractility and provides afterload reduction, respectively, and promotes forward systemic blood flow. The IABP is also beneficial for temporary support.4 Acute VSD is treated with dobutamine, nitroprusside, and an IABP.4 Confirmatory evidence for these emergent conditions with two-dimensional echocardiography should be sought, concomitant with emergency consultation from the cardiac surgical team
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In acute mitral regurgitation, hemodynamic support can be initiated with
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In acute mitral regurgitation, hemodynamic support can be initiated with dobutamine and nitroprusside. This treatment supports contractility and provides afterload reduction, respectively, and promotes forward systemic blood flow. The IABP is also beneficial for temporary support.4 Acute VSD is treated with dobutamine, nitroprusside, and an IABP.4 Confirmatory evidence for these emergent conditions with two-dimensional echocardiography should be sought, concomitant with emergency consultation from the cardiac surgical team
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The IAPB provides
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hemodynamic support by decreasing afterload (which lowers myocardial oxygen consumption) and increasing diastolic BP (which augments coronary perfusion) and should be considered in patients presenting with cardiogenic shock.4,15,16 Recent data suggest that IABP improves survival after thrombolytic therapy by augmenting diastolic perfusion pressure and unloading the LV.17-19 The IABP does not improve survival without successful revascularization or surgical correction of an acute mechanical catastrophe.18
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The IAPB provides
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hemodynamic support by decreasing afterload (which lowers myocardial oxygen consumption) and increasing diastolic BP (which augments coronary perfusion) and should be considered in patients presenting with cardiogenic shock.4,15,16 Recent data suggest that IABP improves survival after thrombolytic therapy by augmenting diastolic perfusion pressure and unloading the LV.17-19 The IABP does not improve survival without successful revascularization or surgical correction of an acute mechanical catastrophe.18
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In cardiogenic shock, early revascularization with percutaneous coronary intervention or coronary artery bypass graft is the most important life-saving intervention.4,17,18,20 The greatest short-term benefit is reported in
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patients younger than 75 years, those with previous MI, and those treated within 6 h of symptom onset.
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In cardiogenic shock, early revascularization with percutaneous coronary intervention or coronary artery bypass graft is the most important life-saving intervention.4,17,18,20 The greatest short-term benefit is reported in
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patients younger than 75 years, those with previous MI, and those treated within 6 h of symptom onset.
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Dopamine, a first-line agent for cardiogenic shock, has dose- dependent effects i.e.
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t infusion rates slower than 2.5 ug/kg per min, dopaminergic stimulation dilates renal, cardiac, and splanchnic vessels. At rates between 2.5 and 5 ug/kg per min, β1-adrenergic effects predominate, with increased heart rate and cardiac contractility. At rates between 5 and 10 ug/kg per min, α- and β1-adrenergic effects occur. At rates faster than 10 ug/kg per min, α-adrenergic tone progressively increases with increased BP and systemic vascular resistance. Dosing usually begins at 3 to 5 ug/kg per min and is titrated up to 20 to 50 ug/kg per min to maintain BP (Table 33-4). Complications include arrhythmias, extremity gangrene, and tachycardia at high doses (which increases myocardial oxygen demand and may extend ischemia). Consequently, the lowest possible dose of dopamine should be used.
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Dopamine, a first-line agent for cardiogenic shock, has dose- dependent effects i.e.
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t infusion rates slower than 2.5 ug/kg per min, dopaminergic stimulation dilates renal, cardiac, and splanchnic vessels. At rates between 2.5 and 5 ug/kg per min, β1-adrenergic effects predominate, with increased heart rate and cardiac contractility. At rates between 5 and 10 ug/kg per min, α- and β1-adrenergic effects occur. At rates faster than 10 ug/kg per min, α-adrenergic tone progressively increases with increased BP and systemic vascular resistance. Dosing usually begins at 3 to 5 ug/kg per min and is titrated up to 20 to 50 ug/kg per min to maintain BP (Table 33-4). Complications include arrhythmias, extremity gangrene, and tachycardia at high doses (which increases myocardial oxygen demand and may extend ischemia). Consequently, the lowest possible dose of dopamine should be used.
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Dopamine, a first-line agent for cardiogenic shock, has dose- dependent effects i.e.
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t infusion rates slower than 2.5 ug/kg per min, dopaminergic stimulation dilates renal, cardiac, and splanchnic vessels. At rates between 2.5 and 5 ug/kg per min, β1-adrenergic effects predominate, with increased heart rate and cardiac contractility. At rates between 5 and 10 ug/kg per min, α- and β1-adrenergic effects occur. At rates faster than 10 ug/kg per min, α-adrenergic tone progressively increases with increased BP and systemic vascular resistance. Dosing usually begins at 3 to 5 ug/kg per min and is titrated up to 20 to 50 ug/kg per min to maintain BP (Table 33-4). Complications include arrhythmias, extremity gangrene, and tachycardia at high doses (which increases myocardial oxygen demand and may extend ischemia). Consequently, the lowest possible dose of dopamine should be used.
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Dobutamine usually is used for
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signs of poor perfusion when systolic BP is higher than 90 mm Hg. Primarily a selective β1-adrenergic agonist, it also has mild α1- and β2-adrenergic effects. This sympathomimetic agent improves myocardial contractility and augments diastolic coronary blood flow without inducing excessive tachycardia. The net effect is increased CO, lowered SVR, and reduced LV filling pressure, with little BP change. Dobutamine is started at 2 to 5 ug/kg per min, and it is titrated up to 20 ug/kg per min according to clinical and hemodynamic responses. Complications include arrhythmias, nausea, and headache. If there is an inadequate response to this agent alone, dopamine may be added to support blood pressure.
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Dobutamine usually is used for
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signs of poor perfusion when systolic BP is higher than 90 mm Hg. Primarily a selective β1-adrenergic agonist, it also has mild α1- and β2-adrenergic effects. This sympathomimetic agent improves myocardial contractility and augments diastolic coronary blood flow without inducing excessive tachycardia. The net effect is increased CO, lowered SVR, and reduced LV filling pressure, with little BP change. Dobutamine is started at 2 to 5 ug/kg per min, and it is titrated up to 20 ug/kg per min according to clinical and hemodynamic responses. Complications include arrhythmias, nausea, and headache. If there is an inadequate response to this agent alone, dopamine may be added to support blood pressure.
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Dobutamine usually is used for
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signs of poor perfusion when systolic BP is higher than 90 mm Hg. Primarily a selective β1-adrenergic agonist, it also has mild α1- and β2-adrenergic effects. This sympathomimetic agent improves myocardial contractility and augments diastolic coronary blood flow without inducing excessive tachycardia. The net effect is increased CO, lowered SVR, and reduced LV filling pressure, with little BP change. Dobutamine is started at 2 to 5 ug/kg per min, and it is titrated up to 20 ug/kg per min according to clinical and hemodynamic responses. Complications include arrhythmias, nausea, and headache. If there is an inadequate response to this agent alone, dopamine may be added to support blood pressure.
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used when there is inadequate response to other pressors.
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Norepinephrine is used when there is inadequate response to other pressors. Primarily an α1-agonist, norepinephrine infusion is started at 2 ug per min and titrated according to response. Complications are similar to those with high-dose dopamine.
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used when there is inadequate response to other pressors.
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Norepinephrine is used when there is inadequate response to other pressors. Primarily an α1-agonist, norepinephrine infusion is started at 2 ug per min and titrated according to response. Complications are similar to those with high-dose dopamine.
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Milrinone is a
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phosphodiesterase inhibitor that increases cyclic adenosine monophosphate, increases contractility and CO, and causes peripheral vasodilation. The drop in SVR may require additional therapy with vasopressors to maintain BP, so milrinone use in cardiogenic shock is best guided by hemodynamic measurements from a pulmonary artery catheter. Milrinone is administered with a loading dose of 50 ug/kg IV over 10 min, followed by a maintenance infusion of 0.5 ug/kg per min.
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Milrinone is a
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phosphodiesterase inhibitor that increases cyclic adenosine monophosphate, increases contractility and CO, and causes peripheral vasodilation. The drop in SVR may require additional therapy with vasopressors to maintain BP, so milrinone use in cardiogenic shock is best guided by hemodynamic measurements from a pulmonary artery catheter. Milrinone is administered with a loading dose of 50 ug/kg IV over 10 min, followed by a maintenance infusion of 0.5 ug/kg per min.
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