Flashcards in Heart Physics - a pump Deck (62):
What is meant by Cardiac Output?
• Volume of blood pumped per minute by the left ventricle
• Left heart function number
What three factors can independently affect stroke volume?
How can the Heart Rate help control cardiac output?
• Set by pacemaker cells in SA node
• Highly regulated by autonomic nervous system
• Resting HR - 70bpm (untrained, non-athletes)
• Max HR up to 200bpm
• Max HR can be estimated as 220 minus age
• Can compensate more than stroke volume because the range is bigger, so it's the primary method of regulating cardiac output
What are the two basic mechanisms by which the heart can control cardiac output?
• Heart Rate
• Stroke Volume
What is meant by Cardiac Index?
• CO normalized to body size,in terms of m^2 or surface area
• Usually 2.6 - 4.2 L/min/m^2
What is normal Cardiac output, at rest?
• 4-6 L/min
• HR - 70bpm
• SV - 70ml/beat
• CO = 70*70=4,900 mL/min = 4.9L/min
What is meant by stroke volume?
• Volume of blood pumped per beat
Besides using stroke volume, and instead using pressure measurments, how can you determine Cardiac Output?
• Arterial pressure/total peripheral resitance
Venous return ends up being what factor that controls/affects contractility?
• Venous return, if increased, means preload is increased
• Diameter of ventricle increases because volume in ventricle increases
What must be true about Cardiac output and venous return?
• Cardiac output MUST equal venous return (on average)
• Venous return = voulume of blood into right atrium per minute
• Cardiac output must be the same for left and right sides of the heart (on average)
• Edema results if volumes are not closely matched.
In a healthy person, the cardiac outputs of the right and left hearts are equal. What happens if they are not?
• Edema, either peripheral or pulmonary
• Driven by the hydrostatic pressure forces in the capillary beds?
The strength of contraction in the heart is controlled by what two mechanisms?
• Legth dependent intrinsic mechanism - Frank-Starling Law of the Heart
• Length-independent mechanism = ionotropy
○ Most obviously regulated via sympathetic nervous system stimulation
What happens during ventricular diastole?
• at the end of diastole, the left atrium has filled with oxygenated blood from the pulmonary vein
• Contraction, triggered by SA node wil increase atrial pressure and force open the AV valve
• Atrial systole is the "a wave"
• Once the AV valve opens there is rapid villing of the ventricle with blood
What happens in the isovolumetric contraction phase?
• The wave of depolarization reaches ventricle, causing ventricular contraction
• Fluid is incompressible so there is a rapid increase in pressure
• This pressure increases with no valves being open because aortic pressure is above ventricular pressure at first and ventricular pressure rapidly becomes greater than atrial pressure
What happens during the ejection phase?
• As the ventricle continues to contract, the ventricular pressure exceeds that in the aorta and the aortic valve is pushe dopen and blood begins to flow
• Ventricular pressure drops with ventricle relaxation, but ejection continues until pressure of aorta is above ventricular pressure closing the aortic valve
What are the phases of the ventricular contraction cycle?
• Atrial systole and ventricular filling
• Isvolumetric contraction
• Isovolumetric relaxation
• Diastole (at the start of new cycle)
What happens during the isovolumentric relaxation phase?
• Both valves are closed due to pressure differentials but the ventricle is relaxing and pressures are falling
Does the aortic valve close immediately once the aortic pressure exceeds left ventricular pressure?
• No, not immediately. The inertia of blood leaving the ventricle keeps it open just a bit longer before pressure takes over and closes the valve
What two curves bound the pressure and volume changes in the left ventricle?
• Systolic pressure-volume relation
• End diastolic pressure-volume relation
What is the Starling curve?
• The top curve bounding the pressure volume relation
• Made up of ascending limb and descending limb
What is the end diastolic pressure-volume relationship?
• EDPVR, the lower curve bounding the pressure-volume relationship
• Plotting left ventricular pressure as a funciton of LV volume
• Only DURING the filling of the heart BEFORE contraction
• Determined by passive elastic propertices of the ventricle
○ Kinda like compliance, but the inverse because compliance is deltaV/deltaP and the EDPVR is P on y axis
• Characterised by a shallow slope in normal physiological range, meaning the normal ventricle is compliant
What does increased afterload do?
• Increases pressure the ventricle has to get to to eject blood
What is meant by 'afterload'?
• (analogy) Small weight PLUS large weidght lifted off table
○ Muscle contracts with force equal to both
• For the ventricle, the pressure developed during a contraction (end systolic volume) depends on the afterload
○ Apporximately the aortic pressure, strictly defined as wall stress during contraction
What is the Systolic pressure volume relationship?
• Upper curve bounding the pressure-volume relationship
• The relationship between pressure and volume in the ventricle at the peak of isometric contraction (before ejection phase)
• It also represents the maximum pressure that can be develped by the ventricle for a given set of circumstances
• Much steeper than EDPVR, pressure increases a lot even at low volume
• SPVR includes the passive properties of the heart
○ Inclues diastolic pressure-volume relationship
What is the definition of afterload?
• Load against which a muscle contracts
○ For left ventricle, afterload is pretty much approximated by the aortic pressure
What is the definition of preload?
• The length to which a muscle is stretched before shortening
○ In the ventricle, preload is pretty much the end diastolic volume
What does EDPVR represent?
• EDPVR represents the preload on the heart
What might pathology that results in lower compliance of the left ventricle do to the EDPVR?
• Probably will steepen it over physiological volumes
• Takes less volume change to increase pressure
What does it mean that the EDPVR slope is shallow in normal physiological range?
• EDPVR = end diastolic pressure-volume relationship
• Shallow slope as normal heart is compliant and pressure doesn't change too much as volume increases, until super high levels where the stretch has reached it's end
What is active tension?
• Active tension = difference in force between peak systolic pressure and end diastolic pressure curves
○ Difference between the SPVR and EDPVR curves
• Tension developed by the contraction itself, independent
What is the Bainbridge reflex?
• A function of the sinoatrial node
• Stretched node means increased heart rate
○ This reduces filling and increases ejection
• There are intrinsic SA node mechanisms in play but the major regulatory mechanisms are by sympathetic tone
What are the three (general) molecular mechanisms for starlings law?
• Cardiac titin isoform is very stiff, resisting stretch
• Calcium sensitivy of myofilaments increases as sarcomeres are stretched
○ Same intracelluar Ca produces a greater force of contraction
• Closer lattice spacing
○ Stretched sarcomeres have altered spacing between actin and myosin which results in more force generated per crossbridge
If the right ventricular stroke volume is 60.1 mL/beat and the left ventricular stroke volume is 60mL/beat, what does that mean and what would happen?
• There would be more fluid moving from pulmonary circulation than is going into systemic circulation. If this continued you'd have a problem with back-up
• In one hour you would have 360mL increase in volume in the left heart
• Starlings mechanism will usually compensate and increase rate/amount out
What are the three ways to state Starling's Law?
• Heart responds to an increase in EDV by increasing force of contraction
• Healthy heart always functions on the ascending limb of the ventricular fucntion curve
• What goes in, must come out
○ Cardiac output MUST equal venous returna dn cardiac output from left and right ventricles must match (average)
What is the frank-starling law of the heart?
• Intrinsic mechansim by which the heart adapts to changes in preload (in the normal physiological range)
• When you get beyond Starling's law or violate it, that leads/corresponds to Heart Failure
What is the starling curve?
• The difference between the SPVR and EDPVR for a ventricle
• Also called a ventricular function curve
• Analogous to sarcomere length-tension curves
• There is no single starling curve, but rather families that represent different inotropic states of the heart
The EDPVR represents the distance between what points on the PV loop curve?
• Points A to C look a ton like the EDPVR
How does the PV loop curve help you determine stroke work?
• The area inside the whole box is the stroke work
• Energy in joules per beat
How do you calculate the Ejection fraction?
• EF = SV/EDV
• First figure out the SV by EDV - ESV
How do you determine the stroke volume from the PV loop curve?
• SV = stroke volume = amount of blood pumped per beat
• EDV = end diastolic volume = point C
• ESV = end systolic volume = point A
• SV = EDV - ESV = pointC - pointA
How do you caclulate pulse pressure?
• Systolic pressure - diastolic pressure
How can you determine the blood pressure from the PV loop diagram?
• Peak systolic pressure is point E
• End diastolic pressure is point D
• E/D is blood pressure
What factors affect preload?
• Blood volume
○ IV fluid, hemorrhage
• Filling pressure
○ Venous blood pressure, postural changes
• Filling time
○ Reduced at elevated heart rates
• Resistance to filling
○ Right atrial pressure, AV valve stenosis
• Resistance to emptying = afterload
○ Hypertension, pulmonic or aortic stenosis
• Reduced inotropy
• Ventricular compliance
If you hold afterload and inotropy constant, what does increasing the preload do?
• Same as increasing EDV or end diastolic volume
• The immediate effect is an increase in stroke volume via starling's law
○ More contractile force because sarcomere length is increased
• The ventricle compensates for increased venous pressure by having a greater ejection fraction to maintain the same ESV
What does dilated cardiomyopathy due to compliance?
• Interestingly, this INCREASES compliance, and there is a larger EDV for a given pressure
In terms of EDV, what does decreased compliance mean?
• Lower EDV at any given pressure
In hypertrophy, what happens to ventricular compliance?
• Compliance is reduced in hypertrophy
• The EDPVR curve is steeper
• It takes less volume to make the pressure higher
How does changing ventricular compliance affect preload?
• Compliance = change in volume/change in pressure
• On PV plots or PV loop curves, compliance is th ereciprocal of the slope of the EDPVR
• Steeper EDPVR - less compliant
What is afterload?
• The load against which the heart must contract to eject blood
What happens when you hold preload and afterload constant and increase inotropy?
• A new Starling curve, meaning greater systolic pressures are achieved for any given volume
• End result is less ESV, greater EF, same EDV
What normal daily activity relies on inotropy and why?
• Exercise. You need to maintain a high stroke volume even at a high heart rate
• If you didn't change the nature of the contraction, the high heart rate would mean less filling, less ejection
What is happening to inotropy in systolic heart failure and why?
• Reduced inotropy via changes in gene expression and loss of myocytes
What heart pathology results in reduced inotrpy via changes in gene expression and loss of myocytes?
• Systolic heart failure
What is inotropy regulated by?
• Nervous and humoral agents
• Most notably by sympathetic stimulation
What "curve" is generated when inotropy is changed?
• Inotropy changes generate new Starling Curves
○ Systolic ventricular function curves
What is inotropy?
• Inotropy reflects the strength of contraction at any given preload and afterload
○ Independent of fiber length
Is inotropy part of the Frank-Starling response?
• NOPE. They are independent from one another
• Inotropy reflects the strength of contraction at any given preload and afterload
○ Independent of fiber length
If the ESV is increased immediately after increasing afterload, how does the heart eventually compensate?
• The increased ESV means increased EDV, which is preload
• The Starling law will take effect, and the heart will increase the EF to end up at the "set" ESV
What is the summary of the immediate effects of holding all factors constant and increasing afterload?
• EDV unchanged
• EF decreased
• ESV increased
• SV decreased
If you hold preload and inotropy constanct, and increase afterload, what will happen on the next beat?
• With preload increased, the heart responded according the Starling law and compensated by increasing force and ejecting more
• With AFTERLOAD increased, there is more force that must be generated to open the aortic
• The end result is a smaller stroke volume
• Force-velocity relationship shows that shortening velocity is reduced when afterload is increased
○ Systole can be thought of as a fixed time, a fixed event
○ Ventricle develops less pressure, ejection velocity
In dilated cardiomyopathy, will there be more afterload or less?
• More. There is greater wall stress as radius has increased and wall thickness decreased
• Law of LaPlace