Neil A. Shah
Lecture by Alain Broccard, M.D.
Definition: An inability to adequately satisfy the oxygen demands of the tissue.
- Oxygen delivery is determined by three variables: Hb, O2 sat and cardiac output.
- Hb – If it is acutely low you cannot carry oxygen to your tissues (RBCs)
- O2 sat – if your hemoglobin is not wed to oxygen it has no oxygen to deliver (respiration)
- Cardiac output – Stroke volume x Heart Rate
- Stroke volume affected by 3 variables
- Preload – what is put into the heart to pump out
- Preload = venous return
- Determined by 3 things:
- Mean capillary pressure – main determinant. This is the pressure in your total vasculature if you were to stop the heart. It is determined by the amount of blood (total blood volume) and the volume of the venous compartment (is it a big or small tube). If you put the same volume in a small bag the pressure would be higher, if you put the same volume in a large bag the pressure would be lower.
- Right atrial pressure – if you've got something pushing back against the venous side then you can't fill the RA very well. Venous resistance – usually negligible.
- Afterload – the resistance the heart must overcome to push any blood forward
- Afterload problems causing shock are rare but include PE (giant clot you're trying to push against – like a cork in your CO) and a big valvular clot.
- Contractility – how hard the heart beats
- CO is the amount of O2 leaving the heart NOT the amount making it to target organs
- Tissue perfusion
- Tissue perfusion is determined by two variables: the Oxygen delivery (as above) and the mean arterial pressure (is it getting to the end organs).
- CO can be excellent with crappy perfusion
- For example – if you made an aorto-caval fistula your heart would be making great CO, you'd be oxygenating your blood well but you wouldn't be perfusing your end organs.
- Poor tissue perfusion is due to either inadequate oxygen delivery or decreased perfusion pressure. Put another way, you essentially address oxygen delivery with measures to increase CO, but if that doesn't increase tissue perfusion you probably need to add pressors to increase perfusion pressure.
- Clinical assessment of shock
- Change in BP from baseline (20% or 40 mmHg drop)
- Altered mental status
- Decreased urine output
- Clinical features
Cap refill/ Pulse Pressure
Neck Veins / Lung crackles
Long / Weak
Inc. or NL
Long / Weak
Down / Neg
Down / Neg
- Since the brain and kidney are oxygen dependant and sensitive to changes in input they are very good for clinical assessment of tissue perfusion. Altered mental status and oliguria/anuria are good clinical markers of tissue hypoperfusion.
- Swan-Ganz catheter data by shock type
Mixed venous O2
Nl or Up
Nl or Up
Nl or Inc.
Nl or Up
- Mixed venous O2
- Defined as O2 in pulmonary arteries
- Determined by two things:
- Input oxygen to tissue
- Extraction of oxygen by tissue
- Normal value is ~70%
- Why is it normal or increased in distributive shock?
- In distributive shock the cells themselves are sick, usually from cytokine poisoning, and they are abnormally using oxygen.
- There may also be shunting in the microcirculation leading to less O2 being used.
- Lab values
- Lactate can be a helpful indicator of tissue hypoperfusion especially a trend.
- Treatment of shock
- Five big things
- Get access
- Give fluid – the only contraindication would be LV failure where you risk increasing pulmonary edema.
- Give oxygen
- Consider intubation
- Does the patient have difficulty guarding their airway due to AMS?
- Also, is the work of breathing using oxygen that otherwise would be benefiting target tissues?
- Normally you use ~5% of your CO to supply muscles driving respiration.
- Severe tachypnea can lead to up to 50% of CO being wasted on the work of breathing.
- Ventilation takes away the work of breathing from the CO demand thus leaving more for other organs.
- Is the shock due to medical or surgical problems?
- For example bleeding can be medical (pt with INR of 12) or surgical (pt with GSW that lac'd the femoral artery). Both will have hypovolemic shock from their hemorrhage but both will require different initial treatment.
- Don't get scared. Keep these simple things in mind:
- Variables you can change: heart rate, preload, afterload, BP and contractility.
- Giving volume (normal saline) will change preload.
- Increasing blood pressure (MAP) will improve organ perfusion and this is done with pressors.
Beta 1 (+ chronotropy (HR) and + inotropy (contractility)
Beta 2 (vasodilation)
Most arrhythmogenic; metabolized to NE
Almost never wrong to use this.
More arrhythmogenic than NE, but still good.
Not helping heart. Not used alone.
Don't use alone.
- If the chart doesn't work here is the order: Dopamine, norepinephrine, epinephrine, phenylephrine, dobutamine.
- Notes: Dopamine - most arrhythmogenic, metabolized to NE; NE - almost never wrong to use this; Epi - more arrhythmogenic than NE, but still good
- Often used with dobutamine
- Can be used with epi/norepi to get more vasoconstriction so you can back off on the beta effects of these two meds.
- If pt has a fixed CO, like in a PE, you can kill the patient with this agent alone. Why? Well, they can only pump so much b/c there is a big occlusion that's decreasing the volume that the LV gets to see and pump to the body. If you dilate the vasculature you've just killed your MAP and now your end organs aren't going to see any of that small CO that your heart is making.
- Very useful if:
- You've increased volume.
- You've increased BP
- You're still not getting good end organ perfusion.
- Here the B2 effects can cause vasodilation @ the target organs à better tissue perfusion.
- Example clinical scenario – putting it all together
- Septic patient comes in with BP 75/50 and a CVP of 3.
- Shock type?
- Distributive. This patient has big time dilation secondary to cytokines and they're third spacing all kinds of fluid. Their effective circulating volume, the volume available to carry oxygen and be pumped by the heart and go to end organs, is low.
- Step 1
- Give fluid. You dump in 4L of NS.
- CVP increases to 12 (normal 8-12) and BP comes up to 85/50.
- Pt still AMS and anuric.
- Step 2
- Try to increase MAP to increase end organ perfusion
- Give norepi (tighten down the arteries which should increase the BP)
- CVP to 10, MAP to 65 (better), mixed venous O2 50% (not bad)
- Lactate still 3 (ULN = 2.1)
- Check the HCT and Hb is 12 – no need to transfuse.
- Step 3
- You've given volume (inc. preload), the heart is working just fine in terms of contractility and heart rate and you have a fair MAP. Unfortunately you're still not perfusing end organs well. What can you do?
- Give dobutamine. The vasodilation effects will help perfuse end organs and you're not dealing with a situation where the pt has a fixed CO.
- Patient looks better.