Cardiac function and monitoring
In surgery, we occasionally need to deal with patients who are very sick and in the intensive care unit. Although most centres rely on anaesthetist in the management of the cardiac and respiration, it is good to have a basic understanding.
Important points and concept
Cardiac output: volume of blood pumped by the ventricle per minute
CO = Heart rate (HR) X Stroke volume (SV)
SV = volume of blood ejected by the ventricle per heartbeat ~ 70ml of blood with each beat
Factors influence the SV to include preload, afterload and muscle contraction.
Let’s have a look at the factors more closely.
Heart rate (HR) and rhythm
Any changes in the rate and rhythm will cause a disturbance within the cardiac output. Bradycardia, for instance, will cause increase myocardial oxygen demand and may lead to ischaemia and infarction. In arrhythmias such as atrial fibrillation (AF), the loss of atrial filling will compromise the ventricular pumping.
Definition: end-diastolic volume of the left ventricle
The determinants include:
- Circulating blood volume – more volume increases preload
- Venous tone – venoconstriction increases preload
- Afterload – any increment will cause reduction of ejection which leads a higher residual volume
- Atrial contraction
- Intrathoracic pressure – important especially in mechanical ventilation
Frank-Starling law: The force of ventricular contraction is related to myocardial fibre length. Hence higher preload increases the cardiac output. However, the heart may decompensate if excessive preload is overwhelming the ventricle’s pumping action.
Definition: tension or stress the ventricle must develop for ejection
Law of Laplace: tension is proportional to the pressure and radius divided by wall thickness
Tension ~ (pressure x radius) / (wall thickness x2)
- increases with larger pressure or becomes dilated
- interdependent with preload
- does not affect the SV in normal heart but may worsen a failing ventricle
The relationship between volume and pressure.
Compliance = volume/ pressure
This concept is applied to the heart and diastolic function.
- less compliance ventricle has a higher ventricular diastolic pressure despite a same end-diastolic volume.
Definition: The intrinsic ability of cardiac muscle cells to shorten to a stimulus.
This shortens muscle leads to ejection of blood and increase contractility leads to a higher SV. Any changes in inotropy reduce ejection fraction.
The autonomic nervous system that is responsible for the inotropic control.
- cathecolamines – increases contractility and increase heart rate. Mediated by adrenergic beta receptor (contractility and rate) and alpha receptors (increase vascular resistance)
- inotropic medications (dopamine, dobutamine, adrenaline)
More info here