Function of the Heart

   Figure 1: The Cardiac Troponin-Actin-Myosin Complex

Figure 2: The LV Pressure and Volume curves over time (left) as well as the LV Pressure/Volume Loop     


                            Figure 3: Starling Curves                                         Figure 4: LV Diastolic Curve                                             Figure 5: Putting the Two Together

Interpreting the CVP waveform

Figure 6: The CVP Waveform

The normal CVP waveform (Figure 6) consists of various waves: 


    1) a wave: due to atrial contraction at the end of diastole

    2) c wave: due to the tricuspid valve bulging into the RA during isovolumic contraction

    3) x descent: due to atrial relaxation as the ventricle contracts

    4) v wave: due to filling of the atrium during systole

    5) y descent: due to emptying of the atria into the ventricle during diastole 

Various pathological processes can alter the CVP waveform:

    1) canon a waves:  large a waves seen with AV dissociation (ie JET) as the atrium contracts against a closed tricuspid valve

    2) loss of a waves: occurs in atrial fibrillation as there is no longer a significant atrial contraction

    3) prominent CV wave: occurs with tricuspid regurgitation; as the ventricle contracts, the regurgitation causes an increase in the C and V waves

Figure 7: Pressure, Volume EKG, Heart Sounds over the Cardiac Cycle

Treatment of Hemodynamic Dysfunction

Fundamentally, Ohm's Law states: Voltage= Current X Resistance. This can be applied to hemodynamics in that: Change in pressure = Flow X Resistance.

Hence, for systemic hemodynamics: 

Systemic blood pressure = CO X Systemic Vascular Resistance (SVR)


For any state of hypotension, it is either an issue with cardiac output and/or systemic vascular resistance. Typically, the body will compensate for the perturbation by increasing the other component.

For example: 

1) Decreased cardiac output (ie cardiogenic shock, hypovolemia, bradyarrythmia, etc), the body compensates for low CO by increasing SVR to try and maintain BP. Hence, the patient looks clamped down with poor peripheral perfusion and capillary refill. This is COLD SHOCK. You want to augment cardiac output in this situation (via fluid for increased preload, inotropy for poor contractility, chronotropy for bradyarrhythmias, etc) and perhaps even reduce SVR (decrease afterload) on the stressed heart. The patient is already vasoconstricted and so vasopressor agents that further SVR are less useful in this circumstance (and perhaps even harmful). 

2) Decreased SVR (ie anaphylaxis, distributive shock), the body compensates for low SVR by increasing CO. Hence, the patient is hyperdynamic, has flash capillary refill and bounding pulses. This is WARM SHOCK. You want to use agents (ie norepinephrine) that will increase SVR. The patient is likely already hyperdynamic so inotropic (B1) agents are less useful in this circumstance. 

Figure 8: Common Vasoactives and Their Effects