M2 L3 Flashcards
(109 cards)
1
Q
What is End Diastolic Volume
A
End Diastolic Volume (EDV) is the amount of blood in a ventricle at the end of diastole, just before the heart contracts.
2
Q
What is stroke volume?
A
how much blood is pumped out with each beat
3
Q
What is End systolic volume?
A
the amount of blood left in a ventricle after it contracts (at the end of systole).
4
Q
What is Isovolumetric
ventricular contraction
A
It’s the phase right after the ventricles start contracting, but before the semilunar valves (aortic and pulmonary) open.
so all valves are closed
5
Q
What is happening at step 2?
* discuss valves
* discuss pressures
A
The left ventricle blood volume is increasing due to passive filing from the atria
- AV valve open, Semilunar closed
- Atrial pressure is higher than ventricular pressure
6
Q
What is happening at steps 3, 6, 7
* discuss diastole and systole
* discuss valves
A
Step 3: SA node fires (atria depolarizes - P wave) –> atrial contraction
Step 6: AP reaches the AV node which causes the nodal delay and allows ventricles to fill with blood from atria which causes their pressure to increase
Step 7: the end diastolic volume is reached (end of ventricular diastole)
- atria = systole, ventricles = diastole
- AV open, semilunar closed
7
Q
What is happening at steps 8, 9, 10, 11
* discuss diastole and systole
* discuss valves
A
Step 8: AP spreads
down to the
Purkinje fibers,
causing ventricular
depolarization and
the QRS wave
Step 9: LV
pressure increases
over atrial
pressure, and AV
valves close.
Step 10: Isovulmetric contraction occurs (working towards building up LV pressure to surpass aortic pressure)
Step 11: LV volume still at EDV level
- atria = diastole, ventricles = systole
- AV valve closed, semilunar closed because aortic pressure still higher than LV
8
Q
What is happening at steps 12, 13, 14, 15, 16
* discuss diastole and systole
* discuss valves
A
Step 12: LV pressure surpasses aortic pressure. semilunar opens
Step 13: LV ejects blood, pressure peaks
Step 14: Blood leaves LV (dec volume)
Step 15: End systolic volume stage
Step 16: beginning of LV depolarization (T wave)
- atria = diastole, ventricles = systole
- AV valve closed, semilunar open
9
Q
What is happening at steps 17, 18, 19
* discuss diastole and systole
* discuss valves
A
Step 17: LV goes through relaxation/diastole
Step 18: aortic semilunar valve closes bc aortic pressure surpasses LV
Step 19: LV still relaxing - pressure still higher than atria = AV valve closed
- atria/ventricle = diastole
- AV valve closed, semilunar closed
10
Q
What is happening at steps 21, 22, 23, 24
* discuss diastole and systole
* discuss valves
A
Step 21/22: Atria passively fills with blood - AV valve open since atria pressure higher than LV pressure
Step 23: rapid filling of LV (from LA which was passively filling with oxygenated blood from the pulmonary veins during LV contraction and ejection)
step 24: reduced filling of LV
11
Q
What is rapid filling of the LV?
A
Immediately after AV valves open, blood rushes quickly into LV DUE TO: a large pressure gradient between atria (high) and ventricles (low)
12
Q
Why is having more time in diastole important?
A
longer diastole supports better filling, better oxygen supply to the heart muscle, and lower stress on the heart.
13
Q
Time of ventricular diastole decreases with
increased heart rate (500 msec to 125 msec)
* Why would that be okay? Think of different rates of
ventricular filling.
A
Most of the ventricular filling happens very quickly during the early phase of diastole, immediately after the mitral and tricuspid valves open (called the early rapid filling phase). This means that even with a shorter diastolic period, the ventricles can still fill sufficiently.
14
Q
What happens when the mitral valve opens?
A
Atrial pressure > LV pressure → Blood flows from left atrium into left ventricle (ventricular filling starts).
step 1
15
Q
What happens during atrial contraction?
A
The atrium contracts, pushing the last bit of blood into the LV → LV reaches End-Diastolic Volume (EDV); slight pressure rise.
step 3
16
Q
What happens when the mitral valve closes?
A
LV pressure > Atrial pressure → Mitral valve closes; end of filling, start of contraction. (step 4)
17
Q
What is isovolumetric contraction?
A
Both valves closed; LV contracts → Pressure rises sharply, but volume stays constant.
step 5
18
Q
What happens when the aortic valve opens?
A
LV pressure > Aortic pressure → Aortic valve opens; blood starts ejecting
into the aorta.
step 6
19
Q
What is isovolumetric relaxation?
A
Both valves closed; LV relaxes → Pressure drops rapidly, volume stays constant. step 9
20
Q
Name all the steps here
A
- Mitral valve opens
- Blood from atria flow to LV
- Atria contract, push rest of blood to LV
- Mitral valve shuts
- Isovolumetric contraction
- LV pressure > aortic pressure
- Blood from LV ejects into aorta
- LV finishes contraction
- Isovolumetric relaxation
21
Q
What is preload
A
The volume of blood in the ventricles at the end of diastole
(end-diastolic volume)
referred to as the “stretch” on the ventricle
22
Q
What is after load?
A
The resistance (or pressure) the left ventricle must pump against when ejecting blood
“the squeeze”
23
Q
What is cardiac output?
A
The volume of blood pumped by each ventricle per minute.
24
Q
What is the formula for cardiac output?
A
CO = HR x SV
- SV is volume of blood pumped per beat; EDV - ESV
25
What happens if you INCREASE preload (↑ EDV)
↑ Preload → Slightly higher diastolic pressure (bc more blood) + higher systolic pressure
(LV fills more and pumps harder)
26
What happens if you DECREASE preload (↓ EDV)
↓ Preload → Lower diastolic pressure (bc less blood) + lower systolic pressure
(LV fills less and pumps weaker)
27
What happens if you INCREASE afterload (↑ resistance the heart pumps against)
The heart has to work harder to eject blood because the pressure in the aorta (or pulmonary artery) is higher.
↑ Afterload → Higher systolic ventricular pressure, lower stroke volume, higher ESV
28
What happens if you DECREASE afterload (↓ resistance)
The heart faces less resistance when ejecting blood.
↓ Afterload → Lower systolic ventricular pressure, higher stroke volume, lower ESV
29
which NS branch can alter stroke volume
the sympathetic branch
30
What are two pathways that can increase stroke volume?
Extrinsic control
Intrinsic control
31
What is extrinsic control
(control comes from sympathetic NS, not heart)
increase cardiomyocyte
contraction force by altering calcium handling via cAMP → increase blood ejected from heart → decrease ESV
* Increase cAMP
* cAMP inc calcium which inc contractile strength
32
what is the Frank-Starling Mechanism
* Ex?
explains how the heart automatically adjusts its force of contraction based on how much it fills with blood
Ex: the intrinsic relationship
between increasing EDV and
increased SV
The greater the stretch of
cardiomyocytes caused by
increased EDV, the more
tension is generated, resulting in a stronger contraction force and a larger SV (think of a rubber band)
33
Frank-Starling Law of the Heart
What happens to Ca2+ sensitivity during cardiomyote lengthening?
During cardiomyocyte lengthening, Ca2+ sensitivity at the myofilaments increases, which facilitates a more forceful contraction
34
What is intrinsic control?
(control comes from heart)
increase venous return →
increase EDV (preload) → increase cardiomyocyte contraction force bc more blood to push out
○ more blood activates Frank-Starling mechanism
35
how do sympathetic and parasympathetic work to control cardiac output
Sympathetic: Increases both HR and SV → increases cardiac output
Parasympathetic: Decreases HR → decreases cardiac output
36
What causes sarcomere length to increase in the heart?
Increased end-diastolic volume (EDV) stretches the cardiac muscle fibers, lengthening the sarcomeres.
37
How does increased sarcomere length improve contraction strength?
It enhances actin-myosin overlap and increases sensitivity to calcium, improving cross-bridge formation.
38
What is the relationship between EDV and contraction force?
As EDV increases, sarcomere stretch increases, which strengthens the force of contraction (until the optimal length is reached).
39
what type of control is the Frank-Starling mechanism under?
intrinsic
40
What happens if the sarcomere is stretched beyond its optimal length?
Cross-bridge formation becomes less efficient, and contraction force decreases.
41
What does an increase in sarcomere length allow for?
better binding of calcium ions to the muscle
fibers, and results in an increased force of contraction of the heart, or inotropy
42
what is inotropy
the force or strength of heart muscle contraction.
43
What is extrinsic activation triggered by?
ncreased NE/E release and
binding to beta-adrenergic
receptors, leading to increased efficiency in calcium utilization, enhancing sarcomeric-based contraction force
44
How does the frank starling curve change with sympathetic stimulation?
* discuss ESV, EDV, and SV
When the sympathetic nervous system is activated, the Frank-Starling curve shifts up and to the left --> due to increased contractility with the same EDV, the heart ejects more blood.
So it increased SV without changing EDV (but obv ESV dec bc ejecting more blood which means SV inc)
45
How can extrinsic and intrinsic control work together?
* Explain with an example using exercise
Intrinsic: More venous return from working muscles → inc EDV → stronger contraction via Frank-Starling mechanism.
Extrinsic: Sympathetic activation → inc contractility (inotropy), inc heart rate (chronotropy) which inc stroke volume (also via β-adrenergic stimulation)
46
How do epinephrine and norepinephrine work to affect SV?
increase stroke volume by making heart muscle cells contract more strongly. They bind to β₁-adrenergic receptors, which raises cAMP levels and activates protein kinase A (PKA). This causes L-type calcium channels to stay open longer during the plateau phase of the action potential, allowing more calcium to enter the cell. More calcium also gets released from the sarcoplasmic reticulum through RyR receptors, and phospholamban is inhibited so SERCA can quickly pump calcium back into storage.
this boosts calcium availability and speeds up calcium cycling, which increases the strength and efficiency of each heartbeat, raising stroke volume.
47
how else does the
sympathetic nervous system work to increase cardiac output?
By increasing heart rate, E/NE acts on increasing pacemaker
activity and increasing Na+ and Ca2+ flux in the cell (time to
depolarization is quicker).
48
Describe why an increase in the end-diastolic volume (pre-load) leads to an increase in Stroke Volume.
Increasing the preload (EDV) stretches the walls of the ventricles which lengthens the cardiomyocytes which would increase the contracility and amount of blood ejected in each heartbeat.
ESV can stay the same, but inc EDV will lead to inc SV due to stronger contraction. This is the Frank-Starling law.
The stretch improves the overlap between actin and myosin filaments and increases the sensitivity of the contractile machinery to calcium, resulting in a stronger contraction.
49
Explain the mechanism for why a stretch in cardiomyocytes leads to a stronger contraction
The stretch improves the overlap between actin and myosin filaments and increases the sensitivity of the contractile machinery to calcium, resulting in a stronger contraction
50
Is a pressure-volume loop an accurate representation of the timing of diastole and systole in the left ventricle?
No, PV loops are not plotted over time. In a healthy resting adult, ventricular diastole is ~60% of the cardiac cycle, ventricular systole is ~40%
51
Label the Pressure-Volume Loop with the terms from the word bank in green. Couple the reading of an ECG to the left ventricular Pressure-Volume Loop, terms are presented
in purple.
52
Why is end diastolic volume where it is
It marks the end of diastole (ventricular filling is complete).
The volume is at its highest (~135 mL in the right diagram).
The pressure is still low, because the ventricle hasn’t started contracting yet. This is the point just before isovolumetric contraction begins.
High volume, low pressure → bottom right on the graph.
53
Why is end systolic volume where it is
It marks the end of systole (ventricular contraction/ejection is done). The volume is at its lowest (~65 mL or so) - what’s left after ejection.
The pressure is still somewhat high, since the heart has just finished contracting but is about to relax.
Low volume, high pressure → top left on the graph.
54
What cardiac diseases can alter preload?
Diseases that increase preload:
* Heart failure (especially right-sided): causes fluid retention and venous congestion.
* Tricuspid or mitral regurgitation: allows blood to flow backward into the atria, increasing volume returning to the ventricles.
* Atrial septal defect: increases blood flow into the right atrium and ventricle.
Diseases that decrease preload:
* Hypovolemia (e.g., from hemorrhage or dehydration): reduces venous return.
* Pericardial tamponade or constrictive pericarditis: restrict ventricular filling.
* Venodilation from drugs (e.g., nitrates): reduces venous return.
55
What types of cardiac disease would lead to an increase in cardiac afterload?
* Hypertension: increased systemic vascular resistance.
* Aortic stenosis: narrowing of the aortic valve increases resistance to left ventricular outflow.
* Coarctation of the aorta: congenital narrowing increases resistance downstream.
* Pulmonary hypertension (for the right ventricle): increases right ventricular afterload.
56
What are arteries?
* what lined by?
elastic/muscular vessels that deliver blood from the heart to organs
lined by a thick layer of smooth muscle cells
57
What are arterioles? What do they do
small blood vessels that branch out from arteries and lead into capillaries
control blood pressure through
vasodilation/vasoconstriction that controls how much blood enters the capillary beds of various tissues. directly affects BP
58
What are capillaries
site of gas exchange
59
What are venules?
small vessels that transfer blood from capillaries to veins
60
What are veins
blood vessels that return blood to the heart
61
What is flow rate?
volume of blood passing through a vessel per unit of time
62
Flow rate formula?
F = ΔP/R
F = flow rate of blood through a vessel
ΔP = pressure gradient
R = resistance of blood vessels
63
What is the pressure gradient?
the difference in pressure between the beginning and end of a vessel
64
How does blood flow (in terms of pressure)
Blood flows from an area of higher pressure to an area of lower pressure down a pressure gradient
65
What happens with greater pressure gradient?
* ex?
The greater the ΔP, the greater the flow rate through the vessel
Exercise (your heart pumps harder → higher pressure gradient → more blood to muscles)
66
Relationship of Flow to Pressure Gradient?
if ΔP in Vessel 2 is twice that of Vessel 1, the flow is also twice as much in Vessel 2.
* even if the pressures going in/out are bigger numbers, if u do the math and its the same ΔP, the the flow is the same
67
What is resistance?
the hindrance to blood flow
through a vessel
68
What things can affect resistance?
* Blood viscosity – friction between molecules of a fluid during flow
* Vessel length – the longer the vessel, the greater the resistance to flow (vasodilation)
* Vessel radius – the smaller the radius, the greater the resistance (vasoconstriction)
69
What is a determinant of resistance to flow?
vessel radius
70
Explain: R (or resistance) is
proportional to 1/r4
Resistance is inversely proportional to the fourth power of the radius.
So:
* If the radius doubles, resistance drops by a factor of 16 (inc flow)
* If the radius is halved, resistance increases by a factor of 16 (dec flow)
71
What do arteries serve as?
low-resistance, rapid-transit
passageways that act as pressure reservoirs due to elastic fibers, driving blood flow when ventricles are in diastole
72
what is Systolic Pressure:
Peak pressure exerted by ejected blood against
vessel walls during cardiac systole
73
What is diastolic pressure
The minimum pressure in arteries when blood is draining off into vessels downstream
74
What is pulse pressure?
The difference between systolic and diastolic pressures
75
What is the MAP?
Mean Arterial Pressure (MAP): The average driving pressure
throughout the cardiac cycle
76
Formula for MAP?
diastolic pressure + 1/3 (pulse pressure)
ex: At 120/80: MAP = 80 + (1/3) 40 = 93 mmHg
77
What is MAP monitored and regulated by?
Baroreceptors (blood pressure reflexes)
78
Two baroreceptor locations?
1) Cardiac Sinus
2) Aortic arch
79
How do baroreceptors work?
When blood pressure rises, these receptors detect the increased stretch of the blood vessel walls.
They send signals to the brainstem (specifically the medulla oblongata), which responds
80
What do baroreceptors do if pressure is too high?
activate parasympathetic
They send increased signals to the medulla to:
* Decreasing heart rate (bradycardia)
* Dilating blood vessels (vasodilation)
* Reducing the strength of heart contractions
81
What do baroreceptors do if pressure is too low?
They send fewer signals to the brain and it causes:
* Increasing heart rate (tachycardia)
* Constriction of blood vessels (vasoconstriction)
* Increasing heart contraction strength
82
What is The Baroreceptor-Autonomic Nervous System (ANS) Reflex
a negative feedback loop that uses signals from baroreceptors to adjust blood pressure through the autonomic nervous system.
83
What does the Baroreceptor-Autonomic Nervous System (ANS) Reflex do with low blood pressure?
Baroreceptors detect reduced stretch in arteries --> decrease firing to medulla --> medulla activate sympathetic
Sympathetic nervous system
activates the release of
NE/E to increase the activation
of smooth muscle cells
(through binding to adrenergic
receptors), resulting in the
vasoconstriction of arteries (INC RESISTANCE = INC BP)
84
What are blood reservoirs?
* ex?
parts of the circulatory system that can store large volumes of blood and release it when needed to help maintain adequate circulation and blood pressure
ex: veins
85
What is concentric hypertrophy?
Concentric hypertrophy occurs when the heart muscle (especially the left ventricle) thickens and the chamber size remains the same or decreases.
86
What happens to the EDV during concentric
hypertrophy?
Ventricular wall thickens, but chamber stays same size.
Less room inside chamber to hold blood, so EDV decreases.
87
What happens to the ESV during concentric
hypertrophy?
In concentric hypertrophy, heart thickens to generate more force (in response to like inc pressure in arteries)
Heart is stiffer bc of the thicker muscle and cant fill as well (Dec EDV)
If the heart cant fill as much, it has less blood to pump out - Dec SV
HOWEVER even tho SV is smaller, the heart became stronger and cant contracted
88
What is ejection fraction?
a measurement of the percentage of blood that is pumped out of the heart's left ventricle during each heartbeat
describes how well the heart is pumping blood - helpful to differentiate between HFpEF and HFrEF
89
What is Heart Failure with Preserved Ejection Fraction
HFpEF is a type of heart failure where the heart pumps normally (normal EF), but the ventricle is stiff and cannot fill properly during diastole.
* diastolic heart failure
90
Why would a concentric heart phenotype not alter cardiac function? (in terms of ejection fraction)
Concentric hypertrophy thickens the heart muscle, but the heart can still pump blood effectively because the muscle contracts more forcefully. This means ejection fraction (EF) stays normal, and the heart's pumping ability remains strong. Even though the heart's chamber is smaller, the stronger muscle helps push out enough blood.
91
What is eccentric hypertrophy?
* what can it lead to
heart muscle (myocardium) enlarges and the ventricular chamber dilates (stretches out) to accommodate more blood
can lead to a type of heart failure known as Heart Failure with Reduced Ejection Fraction.
92
what is Heart Failure with Reduced Ejection Fraction
the heart's pumping ability is weakened, and it can no longer pump blood effectively. This is due to a decrease in the ejection fraction
* systolic heart failure
93
What happens to the EDV during eccentric hypertrophy?
heart experiencing enlarging with walls becoming thinner to compensate.
EVD increases because the hearts chambers become larger to accommodate more blood --> inc filling
94
What happens to the ESV during eccentric hypertrophy?
heart experiencing enlarging with walls becoming thinner to compensate.
ESV may inc or stay. it may compensate by inc contractility or it may become weaker with weaker muscles and not pump out as effectively and cause more blood to remain in ventricle (inc ESV --> dec SV)
95
What is the equation for finding ejection fraction?
EF = SV/EDV x 100%
96
Why does stroke volume decrease when afterload increases significantly?
The heart must generate more force to overcome resistance, which slows down sarcomere shortening, reducing stroke volume.
97
What happens to sarcomere shortening and stroke volume when afterload decreases?
Sarcomere shortening increases, which enhances stroke volume.
98
99
How is platelet activation/blood clotting related to atherosclerosis?
Mainly through inflammation
100
What does a rightward shift in the PV loop mean
means the heart’s volumes are increasing - both EDV and ESV
The ventricle is dilated or weakened, so it fills more (↑ EDV) but can’t pump effectively (↑ ESV).
101
what is atherosclerosis
Atherosclerosis is a chronic disease where plaque builds up inside the arteries, leading to narrowing, hardening, and reduced elasticity of the blood vessels.
102
what causes atherosclerosis?
coronary artery disease
103
What is Diffuse Intimal Thickening (DIT)?
: A general thickening of the artery wall, considered a pre-atherosclerotic change that may begin at birth.
104
What is Pathological Intimal Thickening (PIT)?
A stage in atherosclerosis marked by the formation of lipid pools in the arterial intima, beneath vascular smooth muscle cells (vSMCs) and extracellular matrix (ECM).
105
What defines a fibroatheroma in atherosclerosis?
A plaque with a necrotic lipid core and a surrounding extracellular matrix (ECM)/fibrous cap formed by vSMCs.
106
What are the two major complications of fibroatheromas?
Plaque rupture and plaque erosion, both of which can trigger thrombosis.
107
Why is ECM important in plaque stability?
provides structural support. Loss of ECM weakens the fibrous cap, making it prone to rupture.
108
What is plaque rupture
laque rupture is when the fibrous cap of an atherosclerotic plaque tears or breaks open, exposing the lipid-rich necrotic core to the bloodstream.
This is a medical emergency because it can trigger a blood clot (thrombus) that can block the artery.
109
What is plaque erosion
Plaque erosion is a type of atherosclerotic complication where the endothelial layer (inner lining of the artery) becomes dysfunctional or is lost, exposing the underlying ECM - but without rupturing the fibrous cap.
