051 053 Cardiodynamics and cardiac output in normal and altered function Flashcards
HR and SV are not independent of each other. In what ways might changing HR alter SV?
As heart rate increases, the filling time and thus end-diastolic volume will decrease. Stroke volume will then be reduced through the frank-starling relationship.
How might a change in SV alter heart rate?
As stroke volume decreases, the blood pressure will decrease. This is will be detected by baroceptors. The baroreceptors will suppress its effect, causing increased sympathetic drive and decreased parasympathetic drive, which causes a higher heart rate by the SA node.
What is the relationship between venous return and cardiac output in a healthy heart?
Increasing venous return will increase cardiac output by increasing stroke volume. But increasing cardiac output does not necessarily increase venous return as the capacitance of the circulation can absorb an increase in cardiac output.
What is the force of myocardial contraction determined by intrinsically?
Length of myocardial fibres and contractility
What is inotropy and chronotrophy?
Inotropy is the force of contraction. Chronotrophy is the rate of contraction.
What is the ventricular preload?
Passive tension in the ventricular wall at the end of diastole.
What determines ventricular preload?
Central venous pressure, venous return, cardiac filling time.
What does the term ventricular afterload mean?
This is the pressure against of which the heart must work to eject blood. (i.e. aortic pressure)
What determines ventricular afterload?
Systemic blood pressure, total peripheral resistance.
What is the effect of increasing afterload on muscle fibres and ventricular stroke volume?
There is reduced shortening of the muscle fibres and decreased stroke volume.
What occurs when there is an increased arterial blood pressure on stroke volume?
It increases afterload, which causes SV to decrease.
How does the cardiovascular function adjust to compensate for blood loss?
During blood loss, there is a decreased central venous pressure, cardiac filling, and hence end diastolic volume. This causes a decrease in stroke volume from the right ventricle, and a corresponding decrease in cardiac output and mean arterial blood pressure. This is detected by the kidneys and vessels. Baroreceptors will detect the drop in blood pressure and increase sympathetic drive to cause venoconstriction. Kidneys will stimulate the renin-angiotensin-aldesterone process, which cause more fluid retention to raise pressure. As a result there will be higher heart rate, increased inotropic state. Capacitance vessels will also reduce capacity of venous system and thus increase return.
What is the frank-starling relationship?
Total energy liberated by the heart is determined by the diastolic volume and therefore by muscle fibre length at beginning of contraction.
Can hypervolemia be compensated?
To a certain extent by fluid retention and sympathetic activation.
What are different ways used to measure cardiac output?
Oesophageal dopple monitor (measuring speed of blood cells using ultrasound), Pulmonary artery catheter measuring pressure and temperature drops, Echo cardiography (structure), Lithium Dye dilution (measuring concentration changes), pulse contour anaylsis.
