A 58 year old man is admitted to the Intensive Care Unit, intubated and ventilated. Haemodynamic monitors have been inserted and the following haemodynamic measurements have been recorded:

Mean arterial pressure                        53 mmHg

Central venous pressure                      15 mmHg

Cardiac output                                   6.8 L/min

Cardiac index                                       3.8 L/min/m2

21.1. Describe this circulatory disturbance.

21.2. Give five possible clinical scenarios consistent with the above circulatory dusturbance.

21.3. A review of the notes reveals that this man has a positive blood culture with Staph. aureus. Outline three mechanisms  that lead to vasodilation in sepsis?

21.4. Briefly outline what initial agent you will use to treat the circulatory disturbance and how would you initially titrate the dose of the agent

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College Answer

21.1. Describe this circulatory disturbance.
Hyperdynamic circulation with moderate hypotension (Increased cardiac output and hypotension suggests low SVR). More information needed before labelling this as ‘shock’. If they mention vasodilated state that is also acceptable.
If they mention the word shock, that is incorrect .

21.2. Give five possible clinical scenarios consistent with the above circulatory dusturbance.

°     Septic shock
°     Non-septic inflammatory states
°     Pancreatitis
°     Burns
°     Post cardio-pulmonary bypass
°     Vasculitis
°     Thyrotoxicosis
°     Induced hypotension – nitroprusside, GTN
°     A-V fistula – trauma, Pagets etc
°     B1 deficiency
°     Severe liver disease
°     Severe anaemia
°     Spinal shock
°     Other
°     Anaphylaxis – data inconclusive
°     Poisonings – CO, CN

21.3. A review of the notes reveals that this man has a positive blood culture with Staph. aureus. Outline three mechanisms  that lead to vasodilation in sepsis?

°     Reduced Ca2+ entry into vascular SM myocyte due to membrane hyperpolarisation following K+ efflux via activated ATP-sensitive K+ channels.
°     Activation of inducible NO synthase, increasing NO production (cyclic GMP)
°     Relative deficiency of endogenous vasopressin
°     Relative adrenocortical insufficiency

21.4. Briefly outline what initial agent you will use to treat the circulatory disturbance and how would you initially titrate the dose of the agent

Lots of ways of doing this and any sensible answer is acceptable. Some units titrate mcg/kg/min, others will for example put 6 mg in 100 ml such that 1 ml/hr = 1 mcg/min

Candidate must comment on the need to confirm adequate volume before winding up the noradrenaline (or at least simultaneous Norad and volume replacement). Lots of ways to assess volume.

One reasonable titration scheme is:
°     Starting dose 0.1 mcg/kg/min
°     Usual dose range 0.05 to 0.5 mcg/kg.min
°     Titrated to MAP > 65 mm Hg
°     Higher MAP if pre-existing hypertension

Discussion

Noradrenaline in resuscitation of septic shock and the calculation of SVR are all discussed in a related chapter in the Required Reading section.

21.1 - This looks like a hyperdynamic circulation with decreased peripheral resistance. You can even calculate SVRI using the usual equation:

SVRI = ([MAP-RAP] × 79.9) / CI

Thus, the SVRI is ([59-15] × 79.9 )/ 3.8

= 925 dynes×sec/cm5/M2

That is pretty low - the normal range is 1800-2400.

21.2 Why would the peripheral resistance be so low?

  • Septic shock
  • Anaphyactic shock
  • Neurogenic (spinal) shock
  • Vasodilation due to SIRS following a global hypoxic/ischaemic injury
  • SIRS due to cardiopulmonry bypass
  • Vasodilation due to pharmacological agents (eg. nitrates)
  • Vasodilation due to severe liver disease

21.3 Mechanisms of vasodilation in sepsis:

21.4 is asking about noradrenaline. A good specific answer would provide doses. In order to sound professional, one should talk in terms of μg/kg/min. Thus, the patient could be started at 0.1μg/kg/min, which for a 100kg person ends up being about 10ml/hr of a standard dilution (6mg in 100ml). One would then titrate this dose up or down, depending on the individial response.

References

References

Ince, Can. "The microcirculation is the motor of sepsis." Critical Care 9.Suppl 4 (2005): S13.

 

Landry, Donald W., et al. "Vasopressin deficiency contributes to the vasodilation of septic shock." Circulation 95.5 (1997): 1122-1125.

 

Parrillo, Joseph E. "Pathogenetic mechanisms of septic shock." New England Journal of Medicine 328.20 (1993): 1471-1477.

 

Titheradge, Michael A. "Nitric oxide in septic shock."  Biochimica et Biophysica Acta (BBA)-Bioenergetics 1411.2 (1999): 437-455.

 

Landry, D. W., and J. A. Oliver. "The ATP-sensitive K+ channel mediates hypotension in endotoxemia and hypoxic lactic acidosis in dog." Journal of Clinical Investigation 89.6 (1992): 2071.

 

Van Amersfoort, Edwin S., Theo JC Van Berkel, and Johan Kuiper. "Receptors, mediators, and mechanisms involved in bacterial sepsis and septic shock."Clinical microbiology reviews 16.3 (2003): 379-414.

 

Breil, I., et al. "Effects of bradykinin, histamine and serotonin on pulmonary vascular resistance and permeability." Acta physiologica scandinavica 159.3 (1997): 189-198.

 

Hanasawa, K., and M. Kodama. "[Sepsis and organ failure--its pathogenesis and treatment]." Nihon Geka Gakkai zasshi 99.8 (1998): 523-527.

 

Landry, Donald W., et al. "Vasopressin deficiency contributes to the vasodilation of septic shock." Circulation 95.5 (1997): 1122-1125.

 

Marik, Paul E., and Gary P. Zaloga. "Adrenal insufficiency during septic shock*." Critical care medicine 31.1 (2003): 141-145.

 

McGillivray-Anderson, Karen M., and J. E. Faber. "Effect of acidosis on contraction of microvascular smooth muscle by alpha 1-and alpha 2-adrenoceptors. Implications for neural and metabolic regulation." Circulation research 66.6 (1990): 1643-1657.