Basic CVS physiology Flashcards
Type of transport used for short distances
Diffusion
Type of transport used for long distances
Convection
Subdivisions of water in the body
TBW: 45 L
Intracellular: 2/3 of TBW
Extracellular: 1/3 of TBW (12L interstitial, 3L plasma)
What portion of the CVS is in series and which is in parallel?
Pulmonary + systemic circulations = in series
Systemic organs = in parallel
Advantages of in parallel circulation
- Systemic organs receive arterial blood of identical composition
- Flow through any systemic organ can be controlled independently
What are 3 blood conditioning organs?
- Lungs: gas exchange
- Kidneys: adjustment of electrolyte composition
- Skin: temperature regulation
Cardiac output standard value
5 L / min
Flow equation
Flow = pressure difference /resistance
Factors determining resistance to blood flow
Radius of tube
Length of tube
Fluid viscosity
R = viscosity x length /pi x r^4
Stroke volume equation
SV = EDV - ESV
Name of the hole through which APs travel from one cardiomyocyte to the next
Gap junction
Effects of NE (SNS) on b-1 adrenergic receptors on cardiomyocytes.
- Increase HR (SA node)
- Increase AP conduction velocity
- Increase force of contraction
- Increase rate of contraction and relaxation
Overall effect: increase pumping
Effects of ACh (PSNS) on muscarinic receptors on cardiomyocytes.
PSNS travels through the vagus nerve to innervate SA node, AV node and atrial muscle.
Effects:
1. Decrease HR
2. Decrease AP conduction velocity
3. Decrease force of contraction
4. Decrease rate of contraction and relaxation
Overall effect: decrease pumping
What is Starling’s law of the heart?
Increase in EDV = increase in SV
5 requirements for effective ventricular pumping action of the heart
- Synchronized contraction of cells at regular intervals
- Valves must be fully open
- Valves must not leak
- Contractions must be forceful
- Ventricles must fill properly during diastole
% of total body blood stored in veins
> 50%. Veins = capacitance vessels
Effect of SNS on arterioles and veins
NE –>alpha-adrenergic receptors for constriction of smooth muscle cells.
Same thing for venules and veins (venoconstriction moves blood out of venous reservoir into the heart, triggering Starling’s law).
*Capillaries are not innervated by the SNS.
Blood composition
40% cells
60% plasma
Hematocrit definition
RBC volume /total blood volume
3 types of blood cells
- Erythrocytes (most abundant, carry O2)
- Leukocytes (immune process)
- Thrombocytes (clotting process)
What is serum?
Fluid obtained from blood sample after blood has clotted (plasma - clotting proteins).
Most abundant plasma protein
Albumin
organism that does not need a CVS
Amoeba (O2 thru diffusion)
Size of cardiomyocyte
100 micrometers (0.1 mm)
Fick’s law of diffusion: what does diffusion depend on?
Flow = area x []gradient x D
- []gradient (c-out - c-in /d)
- area
- diffusion coefficient
What is 1 cc?
cc = cubic centimer
1 cc = 1 mL
Types of vessels (4)
Distribution: aorta + large arteries
Resistance: small arteries and arterioles
Exchange: capillary
Capacitance: veins and venules
Number of aorta, arteries, arterioles, capillaries, venules, veins and vena cava
Aorta: 1
Arteries: 160
Arterioles: 50 million
Capillaries: 10 billion
Venules: 100 million
Veins: 200
Vena cava: 2
Total cross sectional area and flow velocity
Flow = area x velocity
Since cross-sectional area is increasing as we move towards the capillaries and flow is the same, velocity decreases.
4 advantages of a branching network?
- Any cell is very close to a capillary
- High total area of capillary walls
- Low blood flow velocity in capillaries
- High total cross-sectional area
Normal arterial BP
120 /80 (mm Hg)
Normal central venous pressure
5 cm H20
Describe the graph illustrating the mean pressure across the vascular tree related to the resistance
Does the size of the fluctuations between systolic and diastolic pressures decrease as we go down the vascular tree?
Yes, there are virtually no fluctuations past the capillaries
What is hydrostatic pressure?
Pressure exerted by a fluid at equilibrium at a given point within the fluid, due to the force of gravity.
Describe Stephen Hales’ direct method of BP measurement
Tube in horse’s aorta, let the blood go up until the hydrostatic pressure acting downwards = arterial pressure acting upwards
What is perfusion pressure equal to?
Perfusion pressure = arterial pressure - venous pressure, but since venous pressure is much lower than arterial pressure, we say that
Perfusion pressure is equal to arterial pressure.
Other name for laminar flow
Parabolic flow
What is TPR?
Total Peripheral Resistance, which is the resistance against which the aorta has to work.
Find the equation for MAP and its relation to CO and TPR
Since flow = P /R, R = P x Flow.
TPR = MAP/CO, so MAP = CO x TPR
Since CO = SV x HR,
MAP = SV x HR x TPR
Increase in total peripheral resistance = increase in MAP to maintain CO
By putting vessels in series, we are _______ the overall resistance.
Increasing.
R = R1 + R2
By putting vessels in parallel, we are _______ the overall resistance.
Decreasing
Compliance equation, and which vessels are more compliant?
C = delta V /delta P
Change in volume for a given change in pressure.
Veins are more compliant than arteries (offer less resistance).
MAP equation (TO KNOW)
MAP = CO x TPR
MAP = HR x SV x TPR
How to calculate pulse pressure
Systolic pressure - diastolic pressure
How to calculate MAP + approximation
MAP = diastolic + 1/3 pulse pressure
Approx 100 mm Hg
What is the Windkessel effect?
Windkessel = air kettle
Concept of intermittent pump, when is on, transfers pressure energy (either to air or to arterial walls), so that when the pump is off this pressure energy is what drives the flow forwards, so that there is a constant output pressure despite intermittent input pressure.
Two requirements for the Windkessel effect to work
High TPR
High compliance of the arteries so that they can store the energy
3 ways to maintain constant perfusion to an organ
since flow = perfusion pressure (=P arteries) /Resistance,
- Adjust flow to organs according to individual needs (by adjusting resistance)
- Minimize fluctuations in Pa (via neuro-hormonal control)
- Keep flow to organ constant despite fluctuations in Pa
Describe the general characteristics of blood pressure control systems
- A lot of them
- Span over different speeds of actions and different strengths
- Span over various BP measurements
Reflex that is the last to kick in at the lowest BP
CNS ischemic response
First reflex to kick in following change in pressure
Baroreceptors
Where are baroreceptors located?
Carotid sinus
Arch of aorta
General role of baroreceptors
Inform the brain as to what BP is.
High BP = lots of firing of the baroreceptors
Role of baroreceptors when sensing decrease in BP
Activation of SNS and inhibition of PSNS
- Increase HR
- Increase contractility of ventricles
- Increase arteriolar and venous constriction
(When BP increases, there is a negative feedback system)
Term for what happens to the arterial pressure when removing the baroreceptors (experiment)
Labile hypertension
Role of baroreflex is to minimize fluctuations in MAP, NOT to control the sheer value of the MAP.
3 sites of action of the RAAS
- Brain
- Arterioles
- Kidney /adrenal glands
Functioning of the RAAS (organs involved)
- Production of renin by the kidney
- Production of angiotensinogen (long peptide) by liver
- Conversion of angiotensinogen to angiotensin (10-peptides long) I by renin
- Production of angiotensin converting enzyme (ACE) by the lungs
- Conversion of angiotensin I to angiotensin II (8 peptides-long) by ACE
- Angiotensin II acts on arterioles, brain and adrenal glands
Effect of angiotensin II on the arterioles
Vasoconstriction (increase TPR = increase MAP)
Effect of angiotensin II on the brain
Remember: MAP = CO x TPR
- Release of ADH (= vasopressin).
Vasopressin = vasoconstrictor = increase TPR = increase MAP
- ADH = antidiuretic hormone, decreases renal secretion of Na+ and H2O.
- This increases plasma volume, which increases blood volume, which increases venous pressure.
- Increase in venous pressure increases venous return, which increases end-diastolic volume.
- Through the Frank-Sterling mechanism, increase in EDV = increase in SV
- This increases CO, and increase CO = increase MAP
Effect of angiotensin II on the adrenals and kidney
Angiotensin II binds to receptors on the kidney, causing increased aldosterone release, which has anti-diuretic effect (same thing as ADH release from the brain).
4 large classes of anti-hypertensive drugs acting on the RAAS system
- ACE inhibitors
- AT-II receptor blockers
- Aldosterone receptor antagonists
- Renin inhibitors
Describe renal control of blood volume
Output of urine increases LARGELY with a rise in BP to reduce plasma volume, etc etc until MAP is reduced. Very sensitive system.
The gain is infinite due to the RAAS and nervous system (decreased aldosterone, decreased ADH, decreased sympathetic drive to kidneys)
Describe parasympathetic control of HR
PSNS = decreased HR at the SA node
Preganglionic axon comes from medulla oblongata, synapses onto ganglion with ACh onto nicotinic receptors, and then postganglionic axon synapses onto SA node with ACh onto muscarinic receptors.
Rapid onset.
Drug used do block muscarinic receptor on the SA node and effect.
Atropine.
Effect: inhibition of PSNS effects, therefore preventing the decrease in HR. Given to people with sinus bradycardia.
Describe sympathetic control of HR
Preganglionic axons with ACh onto nicotinic emerge from spinal chord. Post-ganglionic axons with NE act onto B-1 adrenergic receptors to increase HR.
B1 agonist - increase HR
B1 antagonist (beta blocker) - decrease HR (used to treat hypertension)
Which branch of the ANS controls ventricular contractility?
Sympathetic!
NE synapses onto beta-1 adrenergic receptors. This is called inotropy.
What is inotropy?
Heart contractility.
Effect of beta-1 adrenergic receptor agonist onto MAP
increase contractility and HR = increased SV and HR = increased MAP.
2 reasons for changing vessel diameter
- Set appropriate flow for each organ
- Maintain MAP
4 things that control radius of blood vessels
- ANS
- Hormones
- Endothelium
- Waste products
Describe sympathetic control of vessel tone
NE acts on alpha-1 adrenergic receptors.
Activation = contraction of smooth muscle.
Describe parasympathetic control of vessel tone in the genitalia
Sexual excitation = increase PSNS input = ACh onto endothelial cells, which leads to vasodilation (decreased TPR) and increased flow.
Describe sympathetic control of adrenal glands
Release ACh onto adrenals (no ganglion, directly onto adrenals).
Adrenals produce 2/3 Epinephrine and 1/3 NE. These are both alpha and beta agonists, so therefore the overall effect is an increase in MAP.
Orthostasis definition
Maintenance of upright standing posture
Describe CVS response to orthostasis.
Upon orthostasis, reflexes will act quickly to maintain MAP.
When standing up, hydrostatic pressure increases. This leads to an accumulation of blood in the legs and a potential loss of plasma volume, which decreases venous return and therefore SV, therefore MAP.
- Despite the immediate drop in SV, CO is preserved thanks to an immediate increase in HR (about 1.5x).
- CO still decreases a bit, but MAP is preserved. This is thanks to the increased TPR, which is also an immediate reflex. This is due to constriction of vessels in unessential organs.
- Venoconstriction by SNS leads to increase venous return.
What action can restore all values that were different from orthostasis? How?
Phasic muscle pump. This increases venous return and the blood goes back in the circulation.
Describe the cardiovascular response to aerobic exercise.
- Cardiac output increases linearly with power. This is largely due to a linear increase in HR (max HR = 220 - age), and not to a linear increase in SV (SV barely changes - decreased diastolic filling time).
- MAP is relatively preserved because the TPR decreases (blood flow is redirected to the skeletal muscles (skeletal muscle vasodilation)).
- Oxygen consumption increases x9 and the difference in O2 between arteries and veins increases x3. The rest is due to increase in CO.
VO2 = CO x a-vO2 diff
Describe regional blood flow in exercise
Increases:
Slight increase to brain
3.5x increase to heart
12x increase to skeletal muscles
4.5x increase to skin (heat loss)
Reductions to non-essential organs: abdominal organs, kidneys, etc.
How does training change CVS response to exercise?
Max CO is increased.
Max HR is unchanged, but baseline HR is lower so it can go higher for a longer period of time.
There is ventricular hypertrophy, leading to increase in SV.
What do each of these letters represent?
a: atrial contraction (following p-wave)
x: atrial relaxation
c: ventricular contraction
x’: further atrial decrease in pressure due to downwards movement of the atrium caused by ventricular contraction
v: atrial filling
y: opening of AV valve and filling of the ventricles
Normal pulmonary circulation pressures?
24/8 (mm Hg)
Ejection fraction formula + normal ranges
EF = stroke volume /EDV
Normal ranges 55% - 70%
Definitions of diastolic and systolic pressures.
Pressures in the aorta.
Systolic: highest aortic pressure at peak ventricular contraction
Diastolic: lowest aortic pressure, occurs at the end of diastole
Formula for MAP
MAP = systolic pressure + 1/3 pulse pressure
4 heart sounds + what they represent + are they normal
S1 = closing of the AV (mitral) valve when ventricular pressure >atrial pressure. Initiates isovolumic contraction phase.
S2 = closing of the semilunar (aortic) valve when aortic pressure >ventricular pressure. Initiates isovolumic relaxation pahse.
S3 = normal or abnormal heart sound heard shortly after beginning of diastole when there is exaggerated diastolic filling.
S4 = abnormal heart sound due to atrial contraction when blood goes against a very stiff and non-compliant ventricle. End of diastole.
3 determinants of stroke volume
Preload
Afterload
Ventricular contractility
What is afterload?
The force against which the ventricles has to act during systole. = pressure in the aorta (MAP).
Allure of the pressure-volume loop as preload varies.
Allure of the pressure-volume loop as afterload varies.
Pressure in the aorta is higher, so ventricles need to overcome a higher pressure in order to open the aortic valve. This leads to a prolonged isovolumic contraction phase.
The ejection curve hits the ESPVR at an earlier moment, so SV decreases.
Clinical situations leading to increased afterload
Hypertension
Aortic valve stenosis
Allure of the pressure-volume loop as contractility varies.
Contractility: how much pressure can the ventricular wall generate upon a certain stretch (volume).
Higher contractility: shift upward and leftward of the ESPVR.
Therefore, the end-systolic volume decreases, which leads to increased SV and no change in preload.
Chronotropic meaning
Effect on the heart rate.
Positive chronotropic = increased HR
Inotropic meaning
Effect on the contractility of the muscle.
Positive inotropic = increased contractility.
Most widely used tool for measurement of cardiac function
Echocardiography
Doppler echocardiography = info about blood flow velocity and direction
What are some less used imaging techniques for measurement of cardiac function?
Cardiac angiography
Radionuclide ventriculography
Cardiac MRI
Relationship between cardiac output and a-vO2 difference
CO = VO2 /(a-v O2 difference)
What is the thermodilution method?
Method of CO measurement.
Saline of known temp is injected through a catheter at right atrium.
Measurement of change in temperature at the pulmonary artery, which is proportional to CO.
Colder = less CO
Interpretation of results of thermodilution method
Greater CO = colder for less time
Less CO = less cold for more time
2 venous compartments
- Peripheral: large (60% blood in body)
- Central: small, intrathoracic (venae cavae and RA)
Properties of peripheral venous compartment
Highest anatomical amount of blood, highest compliance and very low resistance.
What is anatomical volume?
Amount of fluid required to fill a compartment without exerting external pressure on its walls.
Interpret a compliance of 110 mL / mmHg
110 mL of fluid are required to exert 1 mm Hg pressure.
Mean systemic filling pressure meaning
= MSFP.
Pressure in the circuit that results from the difference between anatomical volume and the normal blood volume (reminder that anatomical volume does not exert pressure, and any extra volume exerts presure).
Typical value for the entire circuit = 7 mm Hg.
Variables affecting the P(msf)
- Circulating blood volume
- Compliance of peripheral venous system
What is venous return?
Rate at which blood enters the central venous compartment.
What impacts venous return flow?
Flow = delta P /resistance
Inlet pressure = mean systemic filling pressure
Outlet pressure = central venous pressure
Describe the venous return curve
Venous return (Y) depending on Right atrial pressure (X), which is the same thing as central venous pressure.
Venous return (flow) decreases as RAP (outlet pressure) increases. Resistance = slope of the curve
How can CVP be roughly estimated?
By observing the height of a patient’s internal jugular vein pulsations.
High vein = high RAP
More precise = putting catheter in the heart to measure pressure in the RA.
2 causes for low CVP
High CO curve
Low VR curve
2 causes for high CVP
Low CO curve
High VR curve
How to measure the left atrial pressure
Swan-Ganz catheter, placed in a vein, then goes through the right ventricle and wedges itself into the pulmonary artery.
Then, we inflate the cuff in the pulmonary artery. That stops the blood flow. We can measure the pressure after the catheter, which is = to BP in the LA.
3 roles of cardiac electrical system
- Produce rhythmic cardiac contraction at rate appropriate for body’s needs
- Ensure synchronous contraction of each chamber of the heart.
- Prevent excessively rapid or slow rates.
What is the fastest intrinsic pacemaker?
The SA node
Role of the AV node
Conducting the SA node impulse slowly to allow for optimal ventricular filling (high refractory period)
Role of His-Purkinje system
“Super highways”
Ensure synchronous contraction of the ventricles.
Describe 4 phases of action potential at the cellular level (fast-response AP)
Phase 0: Rapid increase in Na+ current causing rapid depolarization of cardiac muscle cells. Equilibrium potential of Na+ is 60 mV.
Phase 2: Rapid Ca2+ influx through L-type calcium channels, balanced with K+ efflux.
Phase 3: Ca2+ channels close gradually and there is a return to baseline. Efflux of K+.
Phase 4: Resting phase (between -80 and -90 mV). Determined by the permeability of membrane to K+ channels.
What causes the refractory period in fast-response APs?
The delayed reopening of Na+ channels, which only reactivate when the cell reaches an AP of -60mV. Action potential duration is the driver for refractoriness.
Relative ion concentrations outside vs inside of cell for Na+, Ca2+ and K+ and equilibrium potentials for each.
Na+: higher []outisde than inside. EP = +60 mV.
Ca2+: higher []outside than inside. EP = +40 mV.
K+: higher []inside than outside. EP = -85 mV.
Which types of cells have fast channels and which have slow channels?
The cells in the atria and in the ventricles, along with the His-Purkine system, have fast channels.
The SA node and AV node have slow channels.
What cells are spontaneously automatic in the heart?
His-Purkinje system, AV and SA nodes.
Difference between slow and fast-response channels
Slow channel: higher resting potential. The upstroke is entirely mediated by Ca2+ (no Na+). Refractoriness is determined by Ca2+ channel recovery. Activation is slower.
