reregulation of cardiac output Flashcards
what is cardiac output regulated by
- preload
- afterload
- HR
- contractility
what is the definition of coupling factors
involve the functional coupling of the heart and blood vessels
what are the two coupling factors and define them
- preload- the initial stretching of a single myocyte prior to contraction
- after load- is the pressure that the chambers of the heart are working against
during afterload, what pressures is the heart working agaisnt
- ventricles must generate enough pressure to open the aortic and pulmonary valves due to the aortic pressure in the left ventricle and oulmonary artery pressure in the right ventrcile
whats the definition for cardiac factors and what are they modulated by
- cardiac factors are intrinsic to the heart and are modulated by neural and hormonal stimulation
what are the two cardiac factors
- heart rate- number of action potentials or cardiac cycles per unit time
- contractility- the intrisic ability of the heart to contract, independent of preload and afterload
what is intropy and what is it determined by
synonymous with contractility and is determined bu calcium levels in cardiomyocyte cytoplasm
what does the pressure volume loop depict
changes in ventricular pressure and volume during one cardiac cyle
the PV loop can demonstarate how changes in _____,_____, and ______ can affect the cardiac cyle
preload, afterload, and contractility
what is preload
stretching force that sets the muscle length just prior to the onset of contraction
what determines preload
the passive stretch of the left ventricle at the end of filling
what volume is is preload determine by
EDV determined by venous return
what factors affect prelaod
- Vascular resistance ( arteriolar, vappilary, venous resistance)
- venous capcitance ( volume of blood in the venous circulation
- ventricular filling time
how can preload be determined clinacally
by measuring
- right ventricylar preload
- right atrial pressure
- central venous pressure
what relationship does each ventricular contraction work to maintain
Venous retturn= CO
what is the frank starling relationshop
- based on the length tention relationship of a single cardiac cell
- the volume of the blood ejected by the ventricle depends on the volume of blood present in the ventricle at teh end of diastole
what happens to EDV and SV when venous return increases
they increases
until when does the linear relationship between EDV and SV volume remain linear
until high levels of EDV are reached
what factors affect afterload
1) the volume of blood in the arterial circulation
2) the pressure in the aorta at the onset of ejection
3) the complaince of the aorta
4) the size of the aortic valve
what happens when the afterload ( aortic pressure) is increased(2)
- The pressure against which theventricle contracts is much greater
- The larger pressure increases the resistance to the ejection of blood so:
* more blood remains in the left
ventricle
* higher end-systolic volume (ESV)
what happens when an increased afterload persists
the heart compensates under these condition
by increasing the EDV to maintain a normal
stroke volume.
what do changes to contractility involve
involve contractile proteins and alter cardiac performance
what do changes in contractility directly correlate to
correlate to intracellular ca concentration during excitation and contraction coupling
how can contractility be increased and decreased
- sympathetic stimulation
> epineph/norepineph - postive ionotropic drugs
> digitalis ( Na/K ATPase blocker) - negative inotropic drugs
what are the negative inotropic drugs
- toxins
- general anesthetics
- Ach
-B-adrenergic blocking drugs (propanalol)
what happens when contractility is enhanced
- The heart is able to increase the force and pressure generated during systole, leading to the ejection of a larger blood volume from the ventricles
- There is a shift in the active tension curve to the left
what do postive and negative ionotropic drugs do to contractility
- postive ionotropic drugs increase contratility
- negative ionotropic drugs reduce contractility
what changes in the frank starling relationship when contractility changes ( and what stays the same)
- changes in contractility lead to alterations in SV and CO when EDV/ atrail pressure are unchanged
what happens to CO when HR increases with a given SV and what is this similar to
CO is also increased similar to the effect of increased contractility
memorize this table
is hypertention symptomatic
no usually asymptomatic until is damaging effects such as stroke, myocardial infarction, renal dysfunction, visual problems
when is hypertension diagnosed
when the BP readings are taken at least two to three times at two or more separate appointments
before diagnosing a patient
- bc BP varies throughout the day
what percentage of people have essential hypertension and what is the cause
90-95% and the cause is unknown
what percetnage of patients does secondary hypertension and what is the cause
5-10%, it is secondary to renal disease, endocrine disorders etc
what is the cause of the increase in arterial blood pressure in hyper tensive pts:
- caused by an increase in systemis vascular resistance or total peripheral resistance due to changes in vascular tone of the systemis resistance levels
- caused by an increase in CO due to changes in HR and SV
what are the normal, elevated, High BP stage 1,stage2 and hypertensice crisis values?
