Cardio arterial pressure Flashcards
How pre-load, after-load and contractility alter systolic arterial pressure and stoke volume (20 cards)
Cardiac output (ability to eject blood) depends on what four variables?
heart rate, preload, afterload, contractility
What is contractility?
intrinsic ability of the heart to develop pressure/wall stress and to shorten independent of preload and afterload
measure with ejection franction
increase contractility - positive inotropic effect
isometric force?
pressure the heart develops during systole when ejection is prevented (aka when the aorta is cross clamped)
what happens to systolic force and stroke volume and muscle shortening as you increase the preload?
the systolic force produced by the muscle increases and ability to eject blood (stroke volume) increases
if decrease preload - muscle shortening rate is decreased (because Ca sensitivty decreased and steric blocking)
Preload is also called
Left ventricular end diastolic pressure. It is how full you fill the ventricle. End diastolic wall stress
What is the LaPlace relationship?
Wall stress = (ventrcular pressure x ventricular radius) / ventricular wall thickness
S = (Pxr)/2H
What happens when you reduce the diastolic sarcomere length below 2.2 um?
The number of cross bridges that can form to produce force decreases. force is maximal at 2.2 um, when reduce sterically block corss bridge attachment. When get down to 1.65 um Z-disks collide and make restoring force that reduces the net force further.
Also recoil force at start of diastole that promotes Ventricular suction
other mechanism to increase sarcomere length beyond 1.65 um
increased troponin affinity for Ca - accounts for 60% of length changes
Titin
as the muscle sarcomere lengthens, titin pulls the thick colser to the thin and more cross bridges can form and produce force
leftward shift in relationship between force and Ca
Starling Length-Tension curve
2 physiological functions
- assures that ouput of left and right hearts are matched regardless of relative strength of the two ventricles (reduced filling of undamaged ventril to match decreased output of damaged ventricle)
- increase in ability to increase force with increasing filling is needed to overcome Law of Laplace (which requires when the volume of ventricle increses the force needed to produce a pressure is increased)
systolic force (wall stress) increases more the filling of the heart than required by Laplace
what happens when EDV is reduced?
hearts ability to eject blood is inhibitied, sarcomere length decreases
(oppositely if EDV increases, sarcomere length increase and get dyspnea
What measurements can you use to assess if ventricles working properly?
EDP, EDV, atrial EDP
What is after-load?
tension or wall stress developed during ejection, the load against which the heart must eject blood
just after pressure in ventricle exceeds arterial pressure, blood is ejected and sarcomere shortens (rapidly and then slower to a stop)
measure via arterial pressure and systemic vascular resistance
Why does shortening get slower during systole?
1) as the sarcomere length decreases, the force is reduced by overlap of thin and compression of thick
2) SR Ca pump reduces Ca conc and thus number of crossbridges reduce and get relaxation
inverse relationship between velocity of shortening and force
wall stress remains constant
what happens if increase afterload?
blood is ejected later and sarcomere shortens slower (stroke volume decreases)
wall stress remaining constant
V and A pressures increases during rapid ejection
factors affecting after-load
ventricular radius - dilation means afterload increases
systemic vascular resistance - increase blood volume, decrease arterial compliance, increase in a or p valves, afterload increases
wall thickness
adjustments you can make in cardiac function to maintain cardioc ouput when stroke volume decreases because reduced preload?
increase the heart rate
CO = SV x HR
The amount of Ca released into the myoplasm during systole when normal resting condition is…
enough to activate 30% of all the cross bridges
so if you increase Ca relase, you activate more cross bridges
Increased contractility
positive inotropic
increase stroke volme and ventricular pressure during sympathetic stimulation
adrenergic stimulation reduces affnity of troponin for Ca
increase isometric force, increase rate of rise of force during isovolumetric conctraction, increase rate of shortening at start of ejection, increase extent of shortening (SV increases), decrease duration of contraction-relaxation cycle
increases ejection fraction, incrase rate of rise of pressure during isovolumic contraction, increase rate of rapid ejection, increase SV and CO, increase arterial pulse pressure (also happen if increase preload)
What does ischemia do to the heart?
reduced ability to remake phosphate needed and thus reduced ATP and pH, increased intracellular Pi, inhibits Na/K and SR Ca pump, increase intracellular Na and extracellular K
reduced Ca released by SR, so less bound to troponin and corss bridges inhibitied and slow detachment
negative inotropic effects
- decrease max isometric force, decrease rate of rise of force, decrease rate of shortening, decrease extrent of shortening (SV decreases), increase duration of contraction-relaxation cycle
- decrease ejection fraction, decrese rate of rise of pressure, decrease rate of rapid ejection, decreased CO, decreased arterial pulse pressure
