Cardio arterial pressure

Question 1

Cardiac output (ability to eject blood) depends on what four variables?

Answer 1

heart rate, preload, afterload, contractility

Question 2

What is contractility?

Answer 2

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

Question 3

isometric force?

Answer 3

pressure the heart develops during systole when ejection is prevented (aka when the aorta is cross clamped)

Question 4

what happens to systolic force and stroke volume and muscle shortening as you increase the preload?

Answer 4

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)

Question 5

Preload is also called

Answer 5

Left ventricular end diastolic pressure. It is how full you fill the ventricle. End diastolic wall stress

Question 6

What is the LaPlace relationship?

Answer 6

Wall stress = (ventrcular pressure x ventricular radius) / ventricular wall thickness

S = (Pxr)/2H

Question 7

What happens when you reduce the diastolic sarcomere length below 2.2 um?

Answer 7

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

Question 8

other mechanism to increase sarcomere length beyond 1.65 um

Answer 8

increased troponin affinity for Ca - accounts for 60% of length changes

Question 9

Titin

Answer 9

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

Question 10

Starling Length-Tension curve

2 physiological functions

Answer 10

1. 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)
2. 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

Question 11

what happens when EDV is reduced?

Answer 11

hearts ability to eject blood is inhibitied, sarcomere length decreases

(oppositely if EDV increases, sarcomere length increase and get dyspnea

Question 12

What measurements can you use to assess if ventricles working properly?

Answer 12

EDP, EDV, atrial EDP

Question 13

What is after-load?

Answer 13

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

Question 14

Why does shortening get slower during systole?

Answer 14

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

Question 15

what happens if increase afterload?

Answer 15

blood is ejected later and sarcomere shortens slower (stroke volume decreases)

wall stress remaining constant

V and A pressures increases during rapid ejection

Question 16

factors affecting after-load

Answer 16

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

Question 17

adjustments you can make in cardiac function to maintain cardioc ouput when stroke volume decreases because reduced preload?

Answer 17

increase the heart rate

CO = SV x HR

Question 18

The amount of Ca released into the myoplasm during systole when normal resting condition is…

Answer 18

enough to activate 30% of all the cross bridges

so if you increase Ca relase, you activate more cross bridges

Question 19

Increased contractility

Answer 19

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)

Question 20

What does ischemia do to the heart?

Answer 20

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