Objectives
- Differentiate between different categories of shock and their hemodynamic profiles
- Recognize commonly used vasopressors and indications for their use
Teaching Instructions
Plan to spend at least 30 minutes preparing for this talk by using the Interactive Board for Learning/Preparing. After you feel comfortable with the content you can present this talk in one of two ways.
- Project the Interactive Board for Presentation OR
- Reproduce a drawing of the differential diagnosis figure and timeline on a whiteboard.
This talk is meant to be translated onto a chalkboard or white board and typically takes ~ 25 – 30 min. Prior to the start of the talk, set up your chalkboard (board set-up). Click on the teaching instructions in each section for additional teaching instructions. These teaching scripts also contain additional background information that may be helpful in preparing to teach about shock. New text with each step of the chalk talk is noted in green.
You may choose to only teach about the pathophysiology and types of shock (~ 15 min) or only about vasopressors (~15 min). There are 3 practice cases at the end which take ~ 5 min each that are optional.
Printouts
Interactive Boards
For Learning
Use for self-directed learning and for preparing to present
Coming soon…
For Teaching
Use for Presenting – there is less text and fewer pop-ups
Practice Cases
CASE 1
45 yo M with ischemic cardiomyopathy (EF 40%) admitted with pneumonia and hypotension. He is febrile to 39.2C, RR 26, SpO2 90% on 5L NC, BP 87/32 (MAP 50). On exam, he has warm extremities, JVP ~ 10 cm, trace BLE edema.
Labs show a Cr of 2.2 (baseline of 1), WBC 18k, lactate 3.2. ECG shows NSR without new signs of ischemia. BNP 500 (baseline range 200-600s).
What type of shock is this?
He is presenting in septic shock (warm extremities, wide pulse pressure, signs of infection). It can be difficult to discern whether there is a component of cardiogenic shock in someone with underlying cardiac dysfunction. A mixed venous O2 saturation (SvO2) can help determine if there is a cardiogenic component. Normal SvO2 is 65-75%. SvO2 is ↓ in cardiogenicshock. In septic shock, SvO2 is typically ↑ (though it may be ↓ in early sepsis).
**Learning Point** SvO2, measured from a central line placed at the cavoatrial junction, is a surrogate for ScvO2 (mixed central venous O2 saturation), which is measured from a pulmonary artery cathether. Interpret SvO2 results with caution. Its value is affected by CO, SaO2, and hemoglobin. It can be falsely low in patients with low SpO2’s and anemia.
How would you manage this patient’s shock?
While IVF resuscitation is an important part of the treatment of septic shock, because he is already mildly hypervolemic and hypoxic, consider very gentle volume resuscitation (e.g. 500 mL IVF). Start NE at 0.1 mcg/kg/min and titrate to MAP > 65. Vasopressin can be added to NE if he is requiring escalating doses. Consider adding dobutamine if he is persistently hypotensive despite volume and vasopressor support.
CASE 2
45 yo man with dilated cardiomyopathy (EF 20%) admitted with hypoxia and altered mental status. On exam, he is afebrile, RR 26, BP 72/45 (MAP 54), SpO2 90% on 5L NC. On exam, he is cold and clammy, JVP 12 cm, 2+ BLE edema. Initial labs (BMP, CBC) are only notable for Cr of 2.2 (baseline 1). An ECG shows sinus tachycardia without ischemic changes. Troponin is minmally elevated at 0.05. BNP > 1500 (baseline 200-500). CXR shows cephalization, Kerley B lines and bilateral pleural effusions.
What type of shock is this? How would you further evaluate him?
This is most likely cardiogenic shock given a history of cardiomyopathy, signs of volume overload on exam. An SvO2 and TTE, while not necessary, may be helpful to confirm the diagnosis. His SvO2 was 42%, suggestive of cardiogenic shock (even in the setting of his hypoxemia). TTE showed an EF of 15-20%, elevated right atrial pressures of 15 cm, but no new WMA.
How would you manage his shock?
He should be started on dobutamine. Though this does cause a mild ↓ SVR, this may paradoxically improve his BP. A drop in SVR lowers afterload and can improve CO.
Don’t give IVF to patients in cardiogenic shock. Their cardiac myocytes are already stretched to a point where they have fallen off the Starling curve, impacting contractility. Diuresis in these situations (when BPs allow) will improve contractility. Sometimes patients requiring some support with NE to safely allow for diuresis.
Case 3
45 yo M with cirrhosis presents with 1 day of hematochezia and orthostasis. On exam, he is afebrile, RR 18, HR 140s, BP 72/45 (MAP 54), SpO2 92% on RA. On exam, he has dry mucus membranes, cold and clammy extremities, JVP is not appreciable. Initial labs (BMP, CBC) are only notable for Cr of 2.2 (baseline 1), plts 110k, hct 24% (baseline 38%), INR 2.4 (at baseline).
What type of shock is this?
How would you manage his shock?
He should have 2 large bore peripheral IVs or an introducer placed for rapid resuscitation. He should receive RBCs (given active bleeding, would not wait for hct to drop below 21%), FFP (to correct INR to < 2), and IVF. Given concerns for possible rapid upper GI bleeding, he should be started on octreotide (for portal hypertensive causes of bleeding) and pantoprazole. GI should be consulted for urgent endoscopy.
Take Home Points
- There are four broad categories of shock: hypovolemic, cardiogenic, obstructive and distributive.
- Inotropes, such as dobutamine, should be used for cardiogenic and obstructive shock to increase cardiac contractility.
- Norepinephrine is the vasopressor of choice for septic shock.
References
Kumar A, et al. Circulatory shock. In: Parillo JE & Dellinger P, eds. Critical Care Medicine: Principles of Diagnosis and Management in the Adult, 4th Edition. Philadelphia, PA. Elsevier Saunders. p. 299-324.e9.
Overgaard CB & Dzavik V. Inotropes and Vasopressors: Review of Physology and Clinical Use in Cardiovascular Disease. Circulation. 2008; 118: 1047-1056.
Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Med. 2017, 43(3): 304-377.