The Regulation of Cardiac Output Flashcards
cardiac output
the volume of blood pumped by the ventricle per unit of time (ml/min)
stroke volume
the volume of blood pumped in one cardiac cycle
heart rate
the total number of cycles (beats) per minute
change in pressure
the pressure difference across the network (driving pressure)
total peripheral resistance
- resistance to flow in the vascular regions (arteries and veins)
what factors regulate cardiac output?
- preload
- afterload
- heart rate
- contractility
(divided into coupling factors and cardiac factors)
what are the coupling factors?
- they involve the functional coupling of the heart and blood vessels
- preload
- afterload
what is preload?
the initial stretching of a single cardiac myocyte PRIOR TO CONTRACTION
- the passive stretch of the LV at the end of filling (EDV)
what is afterload?
= the pressure that the chambers of the heart are “working against”
- ventricles must generate enough pressure to open the aortic or pulmonary valves
- is a consequence of the aortic pressure (LV) and/or pulmonary artery pressure (RV)
- factors that impede ejection of blood from the ventricles
cardiac factors
= intrinsic to the heart and are modulated by neural and hormonal stimulation
- heart rate
- contractility
- determined by Ca level in cardiomyocyte cytoplasm
what is heart rate?
the number of APs or cardiac cycles per unit of time
what is contractility?
the intrinsic ability of the heart to contract, independent of preload and afterload
what is inotropy?
= contractility
how is cardiac output controlled by these factors?
what is the pressure-volume loop?
it depicts the changes in ventricular pressure and volume during one cardiac cycle
how can we understand the changes in preload, afterload, and contractility and how it affects the cardiac cycle?
the pressure-volume loop
factors that affect preload include:
- vascular resistance = arteriolar and capillary bed resistance to flow and venous vascular resistance
- venous capacitance = volume of blood stored in the venous circulation
- ventricular filling time
what happens when you increase preload?
how can you measure preload clinically?
determine:
- RA pressure
- RV preload
- central venous pressure
what must be maintained for ventricular contraction?
venous return = cardiac output
what is the Frank Starling relationship?
- based on the length-tension relationship of single cardiac cells
- the volume of blood ejected by the ventricle depends on the volume of the ventricle at the end of diastole
why is it important to understand the frank-starling relationship?
- if the degree of overlap is too low, you cannot generate enough force to contract
- if there is too much overlap, you generate poor contraction
- helps our understanding of the heart function and what could be going wrong clinically
- if the heart is not generating enough force –> increase preload –> increase stretch –> increase to optimum length –> increase contractility
- adaptive mechanism
- if venous return increases –> EDV increases –> SV increases (relationship will remain linear until very high levels of EDV are reached
what factors affect afterload?
- the volume of blood in the arterial circulation
- the pressure in the aorta at the onset of ejection
- the compliance of the aorta
- the size of the aortic valve
what happens when afterload (AoP) increases?
- the pressure against which the ventricle contracts is much greater
- the larger pressure increases the resistance to the ejection of blood (more blood left in ventricle and higher ESV)
what happens with persistent increased afterload?
the heart compensates by increasing the EDV to maintain normal SV
what influences contractility changes?
- contractile proteins –> alter cardiac performance
- intracellular Ca concentration during excitation-contraction coupling
how does sympathetic stimulation alter contractility?
- release of epinephrine and norepinephrine
- isoproterenol (act on beta-1 receptors)
- stimulation
how does positive inotropic drugs alter contractility?
- digitalis (Na-K ATPase blocker)
- increase Ca and increases contractility
how does negative inotropic drugs alter contractility?
- toxins
- general anesthetics
- ACh
- beta adrenergic receptor blockers (propanolol)
- decrease Ca and decrease contractility
what happens when contractility is enhanced?
- the heart is able to increase the force and pressure generated during systole
- leads to ejection of a larger blood volume from the ventricles
- there is a shift in the active tension curve to the left
how does contractility affect the frank-starling relationship?
- positive inotropic drugs enhance contractility
- negative inotropic drugs reduces contractility
- the SV and CO is altered
what happens when there is an increased heart rate?
SV increase
CO increases
similar effect to increasing contractility
how does sympathetic activation alter heart rate? parasympathetic?
- higher rate of AP firing
- decreased rated of AP firing
autonomic influences of cardiac function
about hypertension:
= high blood pressure
- usually asymptomatic until damaging effects occur
how is hypertension diagnosed?
- when BP readings are taken at least 2-3 times at 2 or more separate appts
- abnormally high BP
what is essential hypertension?
- 90-95% of patients
- unknown cause
- spontaneous onset
what is secondary hypertension?
- 5-10% of patients
- caused by an underlying/secondary condition
- like: renal disease, endocrine disorders, or other identifiable causes
what causes hypertension (anatomically)?
- an increase in systemic vascular resistance (SVR) or total peripheral resistance (TPR)
- due to changes in vascular tone (state of constriction) of systemic resistance vessels
- an increase in CO due to changes in HR and SV
categories of hypertension
see more about dealing with it on slide 94
