Attach Cardiac Monitor to Patient
2. Insert two large-bore (16-gauge) intravenous (IV) catheters in an upper extremity.
3. Draw blood samples at the time of IV insertion, for
4. Order cross-matched blood if hemorrhage is suspected or if urgent transfusion is anticipated.
In the presence of circulatory collapse, visualization of an enlarged aorta is taken as de facto evidence of leakage or rupture, requiring immediate surgery. Bedside ED US can visualize and measure the abdominal aorta.2,3 Perform bedside US to identify abdominal aortic aneurysm and perform FAST if intra-abdominal hemorrhage is suspected.2,3]
5. Begin rapid infusion of Normal Saline.
a. Initially, give a 1-L bolus over 10–20 minutes pending arrival of blood (adult dose). Remember to exercise caution in patients with congestive heart failure.
b. Reassess the patient after each bolus. Titrate rate of infusion to the blood pressure;
c. Fluid volume should be individualized to each patient. More fluids are needed for profound volume deficits. It is common for patients in septic shock to receive 6 L of crystalloid in the first 24 hours of hospital care. For large fluid volumes, consider using lactated ringer's or plasmalyte to avoid hyperchloremic metabolic acidosis. Adjust for age, weight, and cardiovascular status.
Patients at risk of fluid overload may require intensive monitoring with a pulmonary artery catheter. If the blood pressure fails to respond to initial resuscitation efforts, the rate of fluid administration should be increased.
d. If pulse and blood pressure are in the normal range but there is reason to suspect intravascular volume depletion, obtain orthostatic vital signs. An increase in pulse rate of 30 beats/min after standing for 1 minute (or near-syncope that develops with a lesser increase) represents the loss of a liter of blood or its equivalent (a 20% blood loss for an average adult; roughly 3 L of normal saline).1 The presence of orthostatic tachycardia is useful, but its absence does not exclude severe bleeding. Orthostatic hypotension is a later finding, representing the failure of sympathetic reflex tachycardia to maintain cardiac output. The threshold of 20 points of pulse change may not be applicable to patients on medications such as β-blockers, diabetic patients (who may have autonomic neuropathy), and the elderly (due to the effects of aging on the cardiac conduction system). Tachypnea may indicate a cardiopulmonary process, metabolic acidosis, anxiety, or pain.
6. Insert a urinary catheter to monitor urine output, a sensitive indicator of visceral blood flow.
7. Obtain arterial blood gas to assess the patient's acid–base status and correct if needed
8. Obtain a 12-lead ECG and begin continuous cardiac monitoring.
9. Monitor Scvo2
10. The need for central access should be individually determined. It is also the preferred route for the long-term administration of certain vasopressor therapy.
Restore arterial oxygen saturation to ≥91%. In shock states, consider a transfusion of packed red blood cells to maintain hemoglobin ≥7 to 9 grams/dL.25 If CO can be assessed, it should be increased using volume infusion or inotropic agents in incremental amounts until venous oxygen saturation (mixed venous oxygen saturation [Smvo2] or Scvo2) and lactate are normalized.
Sequential examination of lactate and Smvo2 or Scvo2 is a method to assess adequacy of a patient's resuscitation. Continuous measurement of Smvo2 or Scvo2 can be used in the ED, although recent literature questions the need for this in resuscitation management.20A variety of technologic tools may be used to assess tissue perfusion during resuscitation.30,31,32,33,34,35 These technologies may be available in some EDs, but it is essentially standard of care in intensive care units. Transfer of the patient to the intensive care unit should not be delayed so that monitoring devices can be placed in the ED.15,36
The goal of resuscitation is to use hemodynamic and physiologic values to guide therapy in order to maximize survival and minimize morbidity. No therapeutic end point is universally effective, and only a few have been tested in prospective trials, with mixed results.20,28,29 Hypotension at ED presentation is associated with poor outcomes.37Noninvasive parameters, such as blood pressure, heart rate, and urine output, may underestimate the degree of remaining hypoperfusion and oxygen debt, so the use of additional physiologic end points may be informative.20,28,29,37 A goal-directed approach of MAP >65 mm Hg, central venous pressure of 8 to 12 mm Hg, Scvo2 >70%, and urine output >0.5 mL/kg/h during ED resuscitation of septic shock has been shown to decrease mortality, but which of the metrics accounts for the mortality decrease remains in question.16,19,20,25 Source control, whether with infection, hemorrhage, or other state of shock, is essential in the initial stages of management. If shock or hypotension persists, reassessment at the patient's bedside is essential while considering the important issues in Table 12-8.
Questions to Answer if There Is Persistent Shock or Hypotension
Equipment and monitoring Is the patient appropriately monitored? Is there an equipment malfunction, such as dampening of the arterial line or disconnection from the transducer? Is the IV tubing into which the vasopressors are running connected appropriately? Are the vasopressor infusion pumps working? Are the vasopressors mixed adequately and in the correct dose? Patient assessment Do mentation and clinical appearance match the degree of hypotension? Is the patient adequately volume resuscitated? Does the patient have a pneumothorax after placement of central venous access? Has the patient been adequately assessed for an occult penetrating injury (a bullet hole or stab wound)? Is there hidden bleeding from a ruptured spleen, large-vessel aneurysm, or ectopic pregnancy? Does the patient have adrenal insufficiency? The incidence of adrenal dysfunction can be as high as 30% in this subset of patients. Is the patient allergic to the medication just given or taken before arrival? Is there cardiac tamponade in the dialysis patient or cancer patient? Is there associated acute myocardial infarction, aortic dissection, or pulmonary embolus? |
Vasopressors are used when there has been an inadequate response to volume resuscitation or if there are contraindications to volume infusion.
Vasopressors are most effective when the vascular space is "full".
Patients with chronic hypertension may be at greater risk of renal injury at lower blood pressures; These patients need to be with a higher MAP calculated from their currrent high systolic and diastolic pressures.
In others, there appears to be no mortality benefit in raising MAP above the 65 to 70 mm Hg range.
Vasopressor agents have variable effects on the α-adrenergic, β-adrenergic, vasopressin, and dopaminergic receptors.
Although vasopressors improve perfusion pressure in the large vessels, they may decrease capillary blood flow in certain tissue beds, especially the GI tract and peripheral vasculature.
If multiple vasopressors are used, they should be simplified as soon as the best therapeutic agent is identified.
In addition to a vasopressor, an inotrope may be needed to directly increase CO by increasing contractility and stroke volume.
All vasopressors increase myocardial oxygen demand; most should be titrated to desired effect
Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output |
---|---|---|---|---|---|
2.0–20.0 micrograms/kg/min | β1, some β2 and α1 in large dosages | ++++ | + | ++ | Increases |
Side effects and comments | Inotrope only; Causes tachydysrhythmias, occasional GI distress, hypotension in volume-depleted patients; has less peripheral vasoconstriction than dopamine; can cause fewer arrhythmias than isoproterenol |
Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output |
---|---|---|---|---|---|
0.5–20 micrograms/kg/min | α, β, and dopaminergic | ++ at 2.5–5 micrograms/kg/min | ++ at 5–20 micrograms/kg/min | + at 0.5–2.0 micrograms/kg/min | Usually increases |
Side effects and comments | Tachydysrhythmias; a cerebral, mesenteric, coronary, and renal vasodilator at low doses; Surviving Sepsis Campaign second line, lot of overlap with α/β/dopaminergic receptors and dose; can be given through a peripheral IV |
Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output |
---|---|---|---|---|---|
2–10 micrograms/min | α and β | ++++ at 0.5–8 micrograms/kg/min | ++++ at >8 micrograms/kg/min | +++ | Increases |
Side effects and comments | Causes tachydysrhythmia, leukocytosis; increases myocardial oxygen consumption; may increase lactate; no real maximum dose |
Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output |
---|---|---|---|---|---|
0.01–0.05 micrograms/kg/min | β1 and some β2 | ++++ | 0 | ++++ | Increases |
Side effects and comments | Inotrope; causes tachydysrhythmia, facial flushing, hypotension in hypovolemic patients; increases myocardial oxygen consumption; never use alone in shock |
Drug | Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output |
---|---|---|---|---|---|---|
0.5–50 micrograms/min | Primarily α1, some β1 | ++ | ++++ | 0 | Slightly increases | |
Side effects and comments | Useful when loss of venous tone predominates; first-line agent for most situations; should be given through a central line |
Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output | |
---|---|---|---|---|---|---|
10–200 micrograms/min | Pure α | 0 | ++++ | 0 | Decreases | |
Side effects and comments | Reflex bradycardia, headache, restlessness, excitability, rarely arrhythmias; can be used on patients in shock with tachycardia or supraventricular arrhythmias; not good comparatively for septic shock |
Drug | Dose | Action | Cardiac Contractility | Vasoconstriction | Vasodilation | Cardiac Output |
---|---|---|---|---|---|---|
0.01–0.04 units/min | Directly stimulates V1 receptor on smooth muscle | 0 | ++++ | 0 | 0 | |
Side effects and comments | Primarily vasoconstriction; usually started at max dose and not titrated |
Note: 0 = no effect; + = mild effect; ++ = moderate effect; +++ = marked effect; ++++ = very marked effect.
Determine oxygen delivery (Do2).
(DO2) is the volume of oxygen delivered to the systemic vascular bed per minute and is the product of cardiac output (CO) and arterial oxygen concentration (CaO2): DO2 = CO x CaO2.
Oxygen uptake is the amount of oxygen that diffuses from capillaries to mitochondria.
cardiac rhythm monitoring
Adequate central venous pressure
Adequate mean arterial pressure
Adequate central venous oxyhemoglobin saturation
A comprehensive assessment of the adequacy of perfusion is useful to guide resuscitation, rather than merely aiming for an arbitrary mean arterial pressure.