Sandbox/00007: Difference between revisions
Line 207: | Line 207: | ||
* '''[[Norepinephrine]]''' | * '''[[Norepinephrine]]''' | ||
:* ''Dosage and Administration'' | :* ''Dosage and Administration'' | ||
::* Mix 1 ampule (4 mg) in 250 mL of [[Intravenous sugar solution|D5W]] or [[Intravenous sugar solution|D5NS]]. | ::* Mix 1 ampule (4 mg) in 250 mL of [[Intravenous sugar solution|D5W]] or [[Intravenous sugar solution|D5NS]]. Avoid dilution in [[normal saline]] alone. | ||
::* [[IV|IV infusion]] 0.5–1.0 μg/min | ::* [[IV|IV infusion]] 0.5–1.0 μg/min; titrate to raise [[blood pressure]] (up to 30–40 μg/min). | ||
::* Do not administer in same IV line as alkaline solutions. | ::* Do not administer in same IV line as alkaline solutions. | ||
:* ''Indications'' | :* ''Indications'' | ||
::* For severe [[cardiogenic shock]] and [[hemodynamic|hemodynamically]] significant hypotension ([[SBP]] <70 mm Hg) with a low systemic vascular resistance. | ::* For severe [[cardiogenic shock]] and [[hemodynamic|hemodynamically]] significant hypotension ([[SBP]] <70 mm Hg) with a low [[systemic vascular resistance]]. | ||
::* This is an agent of last resort for management of ischemic heart disease and shock. | ::* This is an agent of last resort for management of [[ischemic heart disease]] and [[shock]]. | ||
==Don'ts== | ==Don'ts== |
Revision as of 22:26, 18 April 2014
Cardiogenic Shock Resident Survival Guide |
---|
Overview |
Causes |
FIRE |
Diagnosis |
Treatment |
Do's |
Don'ts |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Zaghw, MBChB. [2]
Overview
The clinical definition of cardiogenic shock includes decreased cardiac output with evidence of tissue hypoxia in the presence of adequate intravascular volume.[1]
Causes
Life Threatening Causes
Cardiogenic shock is a life-threatening condition and must be treated as such irrespective of the underlying cause.
Common Causes
- Arrhythmic
- Mechanical
- Acute mitral regurgitation (papillary muscle rupture, chordae tendinae rupture)
- Free wall rupture
- Hypertrophic cardiomyopathy
- Obstruction to left ventricular filling (mitral stenosis, left atrial myxoma)
- Obstruction to left ventricular outflow tract (aortic stenosis, hypertrophic obstructive cardiomyopathy)
- Ventricular septal defect
- Myopathic
- Pharmacologic
Click here for the complete list of causes.
FIRE: Focused Initial Rapid Evaluation
A Focused Initial Rapid Evaluation (FIRE) should be performed to identify patients in need of immediate intervention.
Boxes in the salmon color signify that an urgent management is needed.
Abbreviations: CBC, complete blood count; CI, cardiac index; CK-MB, creatine kinase MB isoform; CVP, central venous pressure; DC, differential count; ICU, intensive care unit; INR, international normalized ratio; LFT, liver function test; MAP, mean arterial pressure; MVO2, mixed venous oxygen saturation; PCWP, pulmonary capillary wedge pressure; PT, prothrombin time; PTT, partial prothrombin time; SaO2, arterial oxygen saturation; SBP, systolic blood pressure; SCVO2, central venous oxygen saturation; SMA-7, sequential multiple analysis-7.
Does the patient have cardinal findings that increase the pretest probability of cardiogenic shock?
❑ Evidence of hypoperfusion
| |||||||||||||||||||||||
YES | NO | ||||||||||||||||||||||
Cardiogenic shock suspected | |||||||||||||||||||||||
Immediate management (click for details)
❑ Intubation with mechanical ventilation ❑ ± Normal saline IV bolus 100–200 mL ❑ ± Norepinephrine IV infusion 0.1–2.0 μg/kg/min ❑ ± Morphine 2–4 mg IV push slowly (in 1–5 min) ❑ Hold antihypertensive medications ❑ Cardiology consultation | |||||||||||||||||||||||
Workup
❑ Lactate | |||||||||||||||||||||||
Immediate goals
❑ SaO2 >90%–92% ❑ CVP 8–12 mm Hg ❑ MAP >60 mm Hg ❑ PCWP 14–18 mm Hg ❑ CI >2.2 L/min/m2 ❑ MVO2 >60% ❑ SCVO2 >70% ❑ Hemoglobin >7–9 g/dL ❑ Lactate <2.2 mM/L ❑ Urine output >0.5 mL/kg/h ❑ ± Correct arrhythmia ❑ ± Correct electrolyte disturbance | |||||||||||||||||||||||
Complete Diagnostic Approach
Treatment
Do's
Diagnostic criteria
- Sustained hypotension (SBP <90 mm Hg or MAP 30 mm Hg below baseline in preexisting hypertension for at least 30 minutes)
- Evidence of tissue hypoperfusion (such as oliguria, cyanosis, cool extremities, and altered mental status)
- Presence of myocardial dysfunction after exclusion or correction of non-myocardial factors contributing to tissue hypoperfusion (such as hypovolemia, hypoxia, and acidosis)
- Sustained hypotension (SBP <90 mm Hg or MAP 30 mm Hg below baseline in preexisting hypertension for at least 30 minutes)
- Depressed cardiac index (<1.8 L/min/m2 of BSA without support or <2.0–2.2 L/min/m2 of BSA with support) in the presence of an elevated wedge pressure (>15 mm Hg).
Immediate management
- Ventilatory support is crucial for maintenance of adequate oxygenation and usually requires intubation with mechanical ventilation.
- IV bolus normal saline should be waived in the presence of pulmonary edema.
- Dosage and Administration
- Mix 1 ampule (4 mg) in 250 mL of D5W or D5NS. Avoid dilution in normal saline alone.
- IV infusion 0.5–1.0 μg/min; titrate to raise blood pressure (up to 30–40 μg/min).
- Do not administer in same IV line as alkaline solutions.
- Indications
- For severe cardiogenic shock and hemodynamically significant hypotension (SBP <70 mm Hg) with a low systemic vascular resistance.
- This is an agent of last resort for management of ischemic heart disease and shock.
Don'ts
- Do not test orthostatic hypotension in hypotensive patients.
- Do not rely solely on SpO2 readings from pulse oximeter. SaO2 from blood gas analysis provides more precise status of oxygenation.
- Do not administer low-dose dopamine (<5 μg/kg/min) to preserve renal function in patients with shock.
References
- ↑ 1.0 1.1 1.2 Califf, RM.; Bengtson, JR. (1994). "Cardiogenic shock". N Engl J Med. 330 (24): 1724–30. doi:10.1056/NEJM199406163302406. PMID 8190135. Unknown parameter
|month=
ignored (help) - ↑ Hollenberg, SM.; Kavinsky, CJ.; Parrillo, JE. (1999). "Cardiogenic shock". Ann Intern Med. 131 (1): 47–59. PMID 10391815. Unknown parameter
|month=
ignored (help) - ↑ 3.0 3.1 Goldberg, RJ.; Gore, JM.; Alpert, JS.; Osganian, V.; de Groot, J.; Bade, J.; Chen, Z.; Frid, D.; Dalen, JE. (1991). "Cardiogenic shock after acute myocardial infarction. Incidence and mortality from a community-wide perspective, 1975 to 1988". N Engl J Med. 325 (16): 1117–22. doi:10.1056/NEJM199110173251601. PMID 1891019. Unknown parameter
|month=
ignored (help) - ↑ Forrester, JS.; Diamond, G.; Chatterjee, K.; Swan, HJ. (1976). "Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts)". N Engl J Med. 295 (24): 1356–62. doi:10.1056/NEJM197612092952406. PMID 790191. Unknown parameter
|month=
ignored (help) - ↑ Forrester, JS.; Diamond, G.; Chatterjee, K.; Swan, HJ. (1976). "Medical therapy of acute myocardial infarction by application of hemodynamic subsets (second of two parts)". N Engl J Med. 295 (25): 1404–13. doi:10.1056/NEJM197612162952505. PMID 790194. Unknown parameter
|month=
ignored (help) - ↑ Reynolds, HR.; Hochman, JS. (2008). "Cardiogenic shock: current concepts and improving outcomes". Circulation. 117 (5): 686–97. doi:10.1161/CIRCULATIONAHA.106.613596. PMID 18250279. Unknown parameter
|month=
ignored (help)