Cardiovascular Physiology Flashcards
why is the cardiovascular system important?
1. transport
- nutrients, gases
- wastes, hormones
2. temperature regulation
organization of the CV system
arteries carry blood away from the heart
arteries become arterioles then capillaries
capillaries is where exchange occurs
capillaries reunite to form venules and then veins
veins carry blood back to the heart
Total blood volume: 4-6 litres
pulmonary circuit - 15% blood volume (between heart and lungs)
systemic circuit - 85% blood volume - arteries 10%; capillaries 5%; veins 70%
heart anatomy
myocardial cells
contractile - myocardial cells (cardiomyocytes)
nodal and conducting - myocardial cells
skeletal - striated (thin/thick)
- cylindrical cells
- mitochondria
- Ca2+ to contract
- motor neuron AP
cardiomyocytes - striated (thin/thick)
- short and narrow, branched cells
- lots of mitochondria
- Ca2+ to contract
- electrically connected
nodal and conducting cells
minimal actin and myosin but self-excitable
- generates action potentials to spread through heart for contraction
- examples: Sinoatrial Node, Atrioventricular (AV) Node, Purkinje Fibres, Bundle of His
excitable cells
depolarization: cell becomes more positive than RMP
repolarization: positive cell returns to RMP
neuron vs nodal cell RMP
neuron vs nodal cell action potential
nodal cell - Ca2+ in (depolarization); K+ out (repolarization)
takes around 0.8 seconds
-40 mV threshold
no hyperpolarization
pacemaker potential (yellow line)
neuron - Na+ in (depolarization); K+ out (repolarization)
takes around 4 milliseconds
-55 mV threshold
hyperpolarization
SA Nodal Action Potential
SA node sends action potentials for each heart beat
threshold = -40 mV
yellow line - pacemaker potential (increase Na+, increase Ca2+, decrease K+)
the conducting system: AP propagation
- Sinoatrial (SA) node (100 AP/min)
- Atrial Muscle
- Atrioventricular (AV) node (action potential SLOW here)
- Bundle of His
- Bundle Branches (L & R)
- Purkinje Fibres (action potential FAST here to push out blood)
- Ventricular Muscle
Electrocardiogram (ECG)
* important: for muscles to contract, you NEED an action potential first
sum of all electrical events in the heart
body fluids conduct electricity well
recorded by surface electrodes
P -> Atrial depolarization
QRS -> Ventricular depolarization
T -> Ventricular repolarization
what can an ECG tell us?
- heart rate
- heart damage (myocardial infarction)
- conduction issues
- rhythm disturbance
- effects of drugs
heart rate
resting ~ 70 beats/min
maximum: 220 - your age in years
parasympathetic innervation: rest & digest (ACh)
ACh binding its receptor will:
- increase K+ permeability
- decrease Na+ permeability
- decrease Ca2+ permeability
- also AV node innervation
sympathetic innervation: fight or flight (NE)
NE (norepinephrine) binding it’s receptor will:
- increase Na+ permeability
- increase Ca2+ permeability
- also AV node and ventricular muscle innervation
cardiac cycle: heartbeat events
things to understand:
- blood moves down a pressure gradient
- the ECG event occurs before heart muscle contraction or relaxation
- when pressure lines cross, something happens to the heart valves (open/close)
- systole = contraction, diastole = relaxation
cardiac cycle: heartbeat phases
phases:
- Atrial Systole
- Isovolumetric Ventricular Systole
- Ventricular Systole
- Isovolumetric Ventricular Diastole
- Late Ventricular Diastole
phase 1: Atrial Systole
phase 1
ECG: P wave before
pressures: increase pressure in Atrial but higher than ventricular pressure
volume: increase ventricular volume, blood gets pumped from atrial to ventricular (80% of blood is already in the ventricular because AV valve is open)
valves: AV open
phase 2: Isovolumetric Ventricular Systole
phase 2
ECG: QRS wave before
pressures: increase in ventricular pressure, exceeds atrial pressure, but lower than aortic pressure
volume: no change
valves: all valves closed
phase 3: ventricular systole
phase 3
ECG:
pressures: increase in ventricular pressure, higher than atrial pressure and aortic pressure
volume: decrease in ventricular volume
valves: aortic valve open
phase 4: isovolumetric ventricular diastole
phase 4
ECG: T wave before
pressures: decrease in ventricular pressure, drops below aortic pressure, but is higher than atrial pressure
volume: no change
valves: all valves closed
phase 5: late ventricular distole
phase 5
ECG: —
pressures: decrease in ventricular pressure, drops below atrial pressure and lower than aortic pressure
volume: increase in ventricular volume, blood enters from atrial to ventricular
valves: AV valve open
repeats again - phase 1: atrial systole
phase 1
ECG: P wave before
pressures: increase in Atrial pressure, but higher than ventricular pressure
volume: increase in ventricular volume
valves: AV valve opens
stroke volume
during one ventricular systole = stroke volume
cardiac output
per minute of ventricular contractions = cardiac output
what controls stroke volume?
- autonomic nervous system innervation
- preload on the heart
autonomic effects on stroke volume
parasympathetic: remember, little innervation to cardiac contractile cells
- acetylcholine is the neurotransmitter released
- decrease Ca2+ premeability, so decreases strength of contraction and thus decreases stroke volume (minimally)
sympathetic: innervates ventricular cardiomyocytes
- norepinephrine/epinephrine binds receptors
- increases Ca2+ permeability, so increasesstrength of contraction and thusstroke volume
other heart volumes
end diastolic volume (EDV): amount of blood in the ventricle after atrial systole
stroke volume = EDV - ESV
end systolic volume (ESV): amount of blood in the ventricle after ventricular systole
what controls stroke volume?
- autonomic nervous system innervation
- preload on the heart
changing stroke volume: preload
preload: the “load” on the heart prior to contraction
this load is the end diastolic volume (EDV)
the larger the EDV, the more stretch on the ventricles
larger contraction (bigger stroke volume)
end diastolic volume and period
an increase in EDV = an increase in period
=> increases the stretch of the contractile cells of the ventricles
=> increases the force of contraction of these cells upon systole
=> increases the amount of blood ejected from the heart
=> increases stroke volume
=> increase cardiac output
Frank-Starling’s Law
Frank-Starling Law states: “a increase in EDV will cause an increase in stroke volume”
increase EDV by more venous return
during dynamic exercise
- muscle pump
- sympathetic nervous system
- respiratory pump
result = increase SV => increase CO2
sympathetic nervous system and venous return
remember the SNS affects SA node (HR) and ventricular muscle (SV)
but also innervates blood vessels
- causes a small constriction of veins
- increases venous return
- increases EDV, SV & CO
organization of the CV system
anatomy of a blood vessel
tunica externa
- fibrous connective tissue
tunica media
- smooth muscle
- elastic fibres
tunica interna
- endothelial cells
blood vessels: general properties
structure and tissue content determines the vessel’s function
arteries
distribution vessels
structure:
large diameter
thin walls compared to diameter
lots of elastic => easy to distend
blood characteristics:
very high blood pressure
high blood flow
low resistance, small drop in pressure
purpose:
“shock absorbers”
arterioles
resistance vessels
structure:
small diameter
thick walls compared to diameter
lots of smooth muscle
smooth muscle innervated by SNS
blood characteristics:
large drop in pressure
slower blood velocity
purpose:
controls blood flow (vasoconstriction, vasodilation)
relationship: pressure, blood flow & resistance
- blood flows down a pressure gradient (high to low)
- but resistance decreases flow
blood flow = pressure gradient / resistance
resistance
blood flow = (P1 - P2) x r4
blood flow with resistance
total blood flow doesn’t change with added resistance to an arteriole
capillaries
exchange vessels
structure: one endothelial cell thick very thin walls for diffusion
blood characteristics: low blood pressure, small drop in pressure
very low blood velocity
huge total cross-sectional area for diffusion
purpose: exchange of gases, nutrients, etc
blood velocity & total cross-sectional area
more cross-sectional area = slower flow
slower flow = maximize exchange
capillary structure: exchange vessels
in skin, muscles, lungs, CNS: Not so permeable
in kidneys, intestines, some other tissues: More permeable
exchange by filtration and reabsorption
filtration: movement of fluid out of a capillary
reabsorption: movement of fluid into a capillary
Four Starling Forces
- capillary hydrostatic pressure (Pc)
- interstitial fluid hydrostatic pressure (PIF)
- capillary plasma osmotic pressure (Πc)
- interstitial fluid osmotic pressure (ΠIF)
hydrostatic pressures: Pc & PIF
capillary: due to pressure of blood moving through (15 to 35 mmHg)
interstitial fluid: due to pressure of fluid found here (-3 to +6 mmHg)
proteins influence exchange
movement of fluid due to proteins = osmotic pressures (Π)
osmotic pressures: Πc & ΠIF
- capillary plasma osmotic pressure (Πc)(25 mmHg)
- interstitial fluid osmotic pressure (ΠIF)(1-5 mmHg)
putting the starling forces together
net filtration pressure
Net filtration pressure = Kf [(PC + πIF) - (πC + PIF)]
(OUT) (IN)
Kf = filtration coefficient (larger = leakier capillary)
positive number = filtration
negative number = reabsorption
calculate net filtration pressure
capillary hydrostatic pressure (PC) = 35 mmHg
capillary plasma osmotic pressure (ΠC) = 25 mmHg
interstitial fluid hydrostatic pressure (PIF) = 3 mmHg
interstitial fluid osmotic pressure (ΠIF) = 2 mmHg
Net filtration pressure = Kf [(PC + ΠIF) - (ΠC + PIF)]
= 1[(35 + 2) - (25 + 3)]
= 1[(37) - (28)]
= +9 mmHg
veins
capacitance vessels
structure: valves
large diameter
very thin walls compared to diameter
some elastic fibers and smooth muscle => SNS innervates smooth muscle
blood characteristics: very low blood pressure
medium blood velocity
purpose:“blood reserve”
regulating blood flow
increase blood supply to active tissues and decrease it to inactive tissues
increase or decrease heat loss from the body by redistributing blood
maintain blood supply to vital organs - heart and brain - at all times
main blood pressure (mean arterial pressure)
vasocontrict & vasodilate
vasoconstrict (less flow)
vasodilate (more flow)
mechanisms used to regulate blood flow
- local (intrinsic) tissue environment (temp, gases, pressure)
- humoral (extrinsic) substances in blood
- neural (extrinsic) nervous system
local (intrinsic)
tissue environment (temp, gases, pressure)
autoregulatory mechanisms
1. Myogenic theory muscle stretch
2. Metabolic theory metabolic needs
myogenic theory
sudden increase in blood pressure Blood Flow = (P1 - P2) x r4
=> stretches walls of arterioles
=> smooth muscle in arteriole walls contract (reflex)
=> vasoconstriction
=> decreases blood flow and pressure after contraction
*this protects the capillaries and maintains normal blood flow
metabolic theory
change metabolism, change metabolites and tissue conditions
- increase in CO2
- decrease in O2
- increase in [H+] (increase in acidity = lower pH)
- adenosine from adenosine triphosphate (ATP) breakdown
- temperature
these conditions causes arterioles to vasodilate to increase flow = vasodilator metabolites
hyperventilation
breathing very quickly means there is less carbon dioxide in blood and reduces blood flow
decrease in CO2
increase in pH
vasoconstriction and less blood flow
humoral (extrinsic)
substances in blood
Vasoconstrictors
- Epinephrine
- an amine, released upon SNS activation
- binds to alpha adrenergic receptors, increase blood pressure on most blood vessels - Angiotensin II
- a peptide hormone
- made during low blood pressure - Antidiurtic Hormone (ADH)
- a peptide hormone
- released during low blood pressure
Vasodilators
- Epinephrine
- an amine, released upon SNS activation
- binds to beta2 adrenergic receptors, decrease blood pressure in skeletal muscle & heart - Atrial natriuretic peptide
- a peptide hormone
- released during high blood pressure - Kinins and Histamine
- inflammatory mediators
- binds to smooth muscle receptors
neural (extrinsic)
nervous system
Autonomic Nervous System
1. sympathetic nervous system
- innervates SA & AV node, ventricular muscle
- innervates smooth muscle in veins (venous return => increases EDV)
- innervates smooth muscle in arterioles
2. parasympathetic nervous system
- innervates SA & AV node
- no blood vessel innervation
- but indirect effects because no SNS activation
cardiac output and blood pressure
clinically: Mean Arterial Pressure = diastolic pressure + 1/3 (systolic - diastolic pressure)
recap: Blood Flow = pressure/ resistance
cardiac output (CO) = mean arterial pressure (MAP) / total peripheral resistance (TPR)
rearrange: MAP = CO x TPR
CO = HR x SV
adjusting Mean Arterial Pressure (MAP): Baroreceptor Reflex
Negative Feedback Loop
SET POINT (Mean Arterial Pressure)
=> CONTROL CENTRE (CV centre in medulla)
=> EFFECTOR activate SNS or PSNS (Heart and blood vessels)
=> CONTROLLED VARIABLE (Mean Arterial Pressure)
=> SENSORS (Baroreceptors (mechanoreceptors))
=> back to CONTROL CENTRE (Action Potential)
baroreceptors
located in walls of aortic arch, carotid sinuses
are stretch sensitive sensors = mechanoreceptors
monitor blood pressure
send action potential back to CV centre in medulla of brainstem
what happens when MAP is too high?
stretches aorta and carotid sinuses and activates baroreceptors
=> action potential sent to CV centre
=> CV centre compares signals to set point
=> shuts off SNS and activates PSNS
=> decrease Cardiac Output (decrease Heart Rate and Stroke Volume) and causes vasodilation (decrease Total Peripheral Resistance)
=> decreases Mean Arterial Pressure (MAP)
