Week 5, Lecture 1 Flashcards
which ventricle pumps more blood per minute
left ventricle
The left ventricle pumps more blood per minute than the right ventricle. Although both ventricles pump the same volume of blood over time, the left ventricle is responsible for pumping oxygenated blood to the entire body, which requires a greater force and pressure. In contrast, the right ventricle pumps deoxygenated blood to the lungs, which is a shorter distance and requires less pressure. So, while their output is equal in volume, the left ventricle works harder overall due to the demands of systemic circulation.
what is the flow of blood through the heart
deoxygenated from vena cava –> RA –> tricuspid valve –> RV –> pulmonary valve –> pulmonary circulation (blood to lungs to get oxygen)
oxygenated blood returns through pulmonary veins –> left atrium –> mitral valve –> left ventricle –> aortic valve –> aorta (oxygenated blood to the body)
Deoxygenated Blood Entry: Blood that is low in oxygen returns to the heart from the body through two large veins: the superior vena cava (from the upper body) and the inferior vena cava (from the lower body).
Right Atrium: The deoxygenated blood enters the right atrium, a chamber at the top right side of the heart.
Tricuspid Valve: When the right atrium contracts, blood flows through the tricuspid valve into the right ventricle.
Right Ventricle: The right ventricle pumps the deoxygenated blood through the pulmonary valve into the pulmonary arteries.
Pulmonary Circulation: The pulmonary arteries carry the blood to the lungs, where it picks up oxygen and releases carbon dioxide.
Oxygenated Blood Return: The now oxygen-rich blood returns to the heart through the pulmonary veins.
Left Atrium: The oxygenated blood enters the left atrium.
Mitral Valve: The left atrium contracts, pushing blood through the mitral valve into the left ventricle.
Left Ventricle: The left ventricle, which has the thickest walls to generate high pressure, pumps the oxygenated blood through the aortic valve into the aorta.
Systemic Circulation: The aorta distributes the oxygen-rich blood to the rest of the body.
what are the 2 things that force a cardiomyocyte generates with each systole depends on
- PRELOAD
overlap between actin and myosin during diastole - INOTROPY
amount of calcium available to bind troponin
what is inotropy
AKA contractility
Amount of calcium available to bind to troponin
factors that increase inotropy
HR, SNS, cortisol, TSH
▪ Increased sympathetic nervous system
stimulation
▪ Increased heart rate (“loads” more calcium in the SR during relaxation)
▪ Things that increase SNS effectiveness – thyroid hormone, cortisol, etc.
what is preload
ventricular filling
Preload is the filling pressure of the heart at the end of diastole.
preload vs afterload
Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. Afterload is the force or load against which the heart has to contract to eject the blood.
positive ionotriopic agents (i.e. increase contractility)
certain hormones (e.g., epinephrine) and drugs (e.g., digitalis), can increase the force of contraction, leading to increased sarcomere shortening.
what do positive ionotropic agents do to sarcomere length
increase sarcomere shortening because of increases contraction force
negative ionotropic agents
reduce the force of contraction, which can be associated with reduced sarcomere shortening.
what increases force development
good overlap of actin and myosin
right atrium pressure tracing
A, C, X, V, Y waves
- A Wave – Atrial contraction (atrial systole)
- C Wave – Bulging of tricuspid
- X Wave – Atrial relaxation (atrial diastole)
- V Wave – Passive filling of the atria (ventricular systole)
- Y Wave – Emptying of atria into the ventricles with the opening of AV valves (early diastole).
isovulmetric
there is a change in pressure, but no change in volume
are the valves open or closed if isovolumetric
closed
systole vs diastole
- Systole – when the chamber applies pressure work to blood through contraction
- Diastole – when the chamber no longer applies pressure work to blood through contraction
wiggers diagram good to show that
- The Wiggers diagram is a good way to illustrate that the ventricle cannot:
▪ eject blood into the great artery until its pressure is greater than that in the artery
▪ accept blood from the atria unless its pressure is less than that in the atria - Valves ensure that blood only flows one direction despite the large changes in ventricular pressure
rapid ventricular slowing vs. slower filling
what is rapid ventricular filling because of?
what is rapid ventricular filling aka?
- Rapid ventricular filling is due to the rapid expansion of the ventricle and the drop in volume that ensues
▪ Also known as passive filling, and it is responsible for 80% of ventricular filling at rest
▪ Passive filling takes time – decreased with increased heart rates
what does aorta pressure oscillate between>
around 80-120
Aortic pressure oscillates between systolic and diastolic pressure
what happens when the aortic valve closes? what’s the notch called in between?
- After the aortic valve closes, a secondary wave can be seen
▪ The division between these two waves is known as the dicrotic notch
2 waves with dicrotic notch in between
what is the most accurate marker or aortic valve closeure
dicrotic notch
what is the 2nd wave from in aortic pressure curve
▪ The secondary wave is thought to be formed by the elastic recoil of the aorta against a closed aortic valve
▪ Likely also partially impacted by complex vibrations due to the “weird” shape of the aorta
S3 and S4 sounds in phonocardiogram- are they healthy?
s3 can be heathy, s4 bad
- S3–oftenfoundinhealthy young adults and children
▪ New emergence is usually pathological in adults (often indicator of myocardial ischemia)
▪ Blood enters a non- compliant or “not-fully- relaxed” ventricle during rapid filling - “Kentucky”(eeisS3)
- S4 – usually pathologic
▪ Ventricle “straining” as the atria contract and “force” blood into a non-compliant ventricle - “Tennessee”(TennisS4)
how does right and left heart differ
right heart has lower ventricle pressure and pulmonary artery pressure is way less than aorta on left side
atrium is relatively similar
- Note the lower pressures that develop in the right ventricle and pulmonary arteries
- Pulmonary artery pressure is ~ 25/7 mm Hg
- Slightly lower atrial pressures in the right vs. left
RV vs LV pressures
RV= 25/4
LV= 120/8
bottom number= end diastolic pressure
RA vs LA for ventricular filling (as atrial contraction ends)
RA= 4
LA= 8
aorta vs pulmonary artery
aorta- 120/80
PA= 25/10
end diastolic volume and end systolic volume
- End diastolic volume (EDV) – the volume in the ventricle at the end of diastole
- End systolic volume (ESV) – the volume in the ventricle at the end of systole
wiggers diagram approximate volume of end systolic and end diastolic volumes
EDV= 120
ESV= 50
what is stroke volume? formula?
the volume ejected with each heartbeat
▪ SV = EDV – ESV
what is cardiac output?
formula?
the volume ejected by each systole X heart rate
▪ CO = SV X HR
ejection fraction? formula?
is the proportion of EDV that is ejected each beat
▪ EF = SV/EDV = (EDV – ESV)/EDV
what corresponds to preload
EDV (end diastolic volume) [[the volume in the ventricle at the end of diastole]]
what is the optimal preload
greater force of contraction due to optimal overlap of actin and myosin in sarcomeres
what are the 3 things that stroke volume is impacted by
- preload
- contractility (ionotropy)
- afterload
what is ionotropy/ contractility dependent on
dependent on calcium handling within the cardiomyocyte – intrinsic ability
what is afterload
the pressure that the heart must overcome to eject blood into the great arteries.
what facctors increase afterload (how much pressure to overcome to eject blood into great arteries)
aorticstenosis,elevatedblood pressure
what is one of the major factors that determines delivery of oxygen and nutreints to tissues
cardiac output
and vascular tone in tissue receiving blood
what is measured as an “estimate” of heart function in heart failure?
ejection fraction (proportion of EDV ejected each beat)
what is the pressure volume loop of the ventricle helpful to measure
▪ Total workload of the heart (ventricle)
▪ Contractility
▪ Compliance of the heart itself
▪ Basic hemodynamic parameters
* EDV * ESV * SV
what is the systolic pressure curve vs diastolic pressure curve in the ventricular pressure volume loop
- Systolic pressure curve – with a given volume, pressure generated during systole is recorded
- Diastolic pressure curve – The pressure is recorded during diastole for the specified volume
pressure volume loop diagram with definitions SLIDE 27
xx
what is the majority of work done by the ventricle? minority?
pressure-volume work
The minority of cardiac work is due to actually ejecting blood from the ventricle into the artery (kinetic energy)
what happens if you increase afterload (the pressure the heart must overcome to eject blood into the great arteries)
decrease SV and ejection fraction
decrease stroke volume (volume ejected with each heart beat) and ejection fraction (the proportion of EDV ejected each beat)
increases myocardial oxygen demand more than ionotropy –> hypertension is energetically expensive
what is afterload technically determined by
tension
technically determined NOT by the systolic blood pressure, but by the tension that the ventricle needs to develop to open the aortic valve
Laplace law and afterload
Laplace law for wall stress
increase pressure or radius then wall tension increases
increase thickeness then wall tension decreases
what happens when you increase preload (the filling pressure of the heart at the end of diastole.)
increase stroke volume (more blood to send out)
what happens to stroke volume if decreases contractility/ ionotropy
lower stroke volume as inotropy decreases
▪ As it decreases, then the amount left at the end of systole also decreases…
* Representing a decrease in ejection fraction
what is a normal ejection fraction
> 50%
increased venous return…
increased venous return→increased preload→ increased stroke volume… but also a slight increase in afterload as the wall tension increases (increase in pressure)
increased afterload…
afterload increases→decreased stroke volume→ increased preload→a new “steady state” with slightly elevated preload but a greater increase in afterload
inotropy increases…
inotropy increases→increased stroke volume→ decreased volume left after systole→a slightly lower preload
effect on cardiac output:
▪ Catecholamines?
▪ Parasympathetic stimulation?
▪ Stretching of the ventricles?
▪ Isolated increases in heart rate (chronotropic and inotropic)?
▪ Increases or decreases in central blood volume?
▪ Increases or decreases in systolic blood pressure?
increases
decrease
increase
increase
increase BV = increase
increase systolic BP = increase
what is the treppe effect
accumulation of calcium in the SR as HR increases
- Notenoughtimeto “remove” calcium from the cell across the plasmalemma
SNS impacts
increase cardiac output
increase heart rate
increase force contraction
what is the most determinant of cardiac ouput
preload and venous return to the heart
▪ As the heart delivers more blood to peripheral tissues, then venous return increases
▪ Force of contraction will also increase as preload increases
▪ This will eventually be limited by the increase in afterload that
occurs as blood pressure rises
cardiac output in each ventricle?
- Cardiac output must be equal between the left and right ventricles for multiple reasons:
▪ Proper tissue perfusion & oxygen delivery
▪ Preventing pulmonary congestion and systemic hypoperfusion
ventricle relations
- PRELOAD OF ONE VENTRICLE DEPENDS ON THE CARDIAC OUTPUT OF THE OTHER.
*******add the formulas of equations
