Critical Care Tutorial

Here are the Shock Key Points from the Critical Care Tutorials

1. Blood Pressure is Cardiac Output multiplied by Peripheral Resistance.

2. Cardiac Output is Heart Rate times Stroke Volume.

3. Hypotension is caused by either inadequate Cardiac Output or inadequate Peripheral Resistance

4. Heart Rate, Stroke Volume and Total Peripheral Resistance exist in dynamic equilibrium: these interactions maintain blood pressure. If one of the three becomes abnormal, the other two compensate. This represents the cardiovascular physiologic reserve.

5. Hypotension is an indication of 1) an abnormality of Heart Rate, Stroke Volume or Peripheral Resistance, & 2) failure of the others to compensate.

6. Shock is acute circulatory failure leading to inadequate tissue perfusion and end organ injury: it classified as being due to malfunction of 1) the Pump (cardiogenic), 2 ) the Tubing (distributive), or 3) the Fluid (hypovolemic).

7. The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be accompanied by a tachycardia.

8. Low Stroke volume is caused by a problem with reception or a problem with ejection.

9. Problems with reception are: inadequate venous return or cardiac inflow obstruction.

10. Fluid loss is caused by either absolute hypovolemia (e.g. blood loss) or relative hypovolemia (“third spacing”).

11. Cardiac inflow obstruction is caused by a pericardial (tamponade) or intrathoracic process (PEEP), or a lesion within the heart itself (mitral stenosis).

12. Problems with ejection include pump failure (ischemia, overload, contusion, inflammation) and outflow obstruction (embolism, aortic stenosis, aortic crossclamps).

13. Shock caused by low peripheral vascular resistance is caused by loss of tonic vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis or sepsis, leading to relative hypovolemia.

14. Vasodilation associated with septic shock occurs due to increased synthesis of nitric oxide, activation of ATP-sensitive potassium channels in vascular smooth muscle, and deficiency of vasopressin.