Cardiovascular Flashcards
Hemodynamics
resistance, flow and pressure
Plasma is ?% of blood
55%
Circulation distributes (6) around the system
ions, water and CO2
heat
hormones
O2 and CO2
Blood circulation regulates (5)
pH Osmolarity Body water Temperature Metabolism
Systemic and Pulmonary circuit are a …. circuit
Series
Get oxygen, deliver oxygen, repeat
Systemic circuit is arranged in a …… circuit
Parallel
Gives all organs their own blood flow
Approx stroke volume (mL)
70mL
60-80mL at rest
What is the stroke volume?
The amount of blood pumped out of each ventricle per beat
What is cardiac output?
The amount of blood pumped out of the heart per minute
Approx resting heart rate
70bpm
Approx cardiac output
5-6L/min
Equation for CO
CO = HR x SV
Blood flows from high to low pressure or low to high?
High to low
higher in the arteries than veins to keep pressure gradient and unidirectional flow
What does friction in the blood vessels cause?
Resistance to blood flow
Loss of energy from pumping
Drop in blood pressure
Blood flow determinants and equation
CHANGE IN PRESSURE from one part of the vessel to another (establish pressure gradient)
RESISTANCE to flow - from length, viscosity or radius of tube
F = (change in)P/R
Poiseuille’s Law
Tells us the 3 factors that govern resistance
- Length of tube
- Viscosity of liquid
- Radius of tube (most impact in blood vessel resistance)
when we double the radius, the resistance increases by a factor of?
16
r^4 =1
2r^4 = 16
Where is most of the blood volume located?
Veins (40%)
How is cross sectional area and velocity of blood flow related
Smaller CSA = faster flow (e.g arteries)
Bigger CSA = slower flow (e.g. capillaries)
Speed and CSA like going from a river to the oean
What determines blood pressure gradient through vessels?
Highest pressure in arteries
Pulsitility needs to dampen before it reaches the capillaries
Primary function of aorta and large arteries
Receives highest pressure of blood and begins damping
- elastic and has to deal with high pulsitile pressure
Primary function of arteries and arterioles
resistance vessels which control the volume of flow through the circulation
- lots of smooth muscle to control radius and direction of blood flow
Primary function of capillaries
exchange of metabolites and O2
Primary function of venules and veins
return conduits, primary reservoir/capacitance of blood
Veins have a a smaller lumen (T/F)
False - larger lumen and thinner walls - adventitia is thickest layer
Arteries have a high elastic content (T/F)
True to deal with pulsitile pressure
Thickest layer in arteries
Smooth muscle and connective tissue (muscularis)
Right AV valve is bi or tricuspid?
tricuspid
Left AV valve is bi or tricuspid?
bicuspid
Layers of heart wall (in to out)
endocardium, myocardium, epicardium, pericardium
Contractile myocardial cells interact with each other via
intercalated discs, gap junctions and desmosomes
An ECG positive wave means that the current is moving towards or away from the lead?
A depolarisation moving toward the lead or a re-polarisation moving away from the lead
An ECG negative wave means that the current is moving towards or away from the lead?
A depolarisation moving away from the lead
The QRS complex represents:
ventricular depolarisation
What is the nodal tissue??
The electrical cells - 1% (small round cells with little or no contractile tissue)
Specialised for the generation and conduction of action potentials
What fraction of contractile cardiac cells contract per beat?
ALL of them!! just stronger or weaker sometimes
Speed of AP generation at SA node
100-110 beats/min
slowed by parasympathetic nerve
Speed of AP generation at AV node
0.05m/s
5cm/s
AP conduction speed through atrial and ventricular myocardium
0.5m/s
Permeability to K+ is lower or higher in nodal cells compared to myocardial cells?
LOWER
Nodal cells let less permeable to K+ leading to an unstable and higher RMP of about -55 (compared to -70mV)
What are funny currents?
funny currents are the spontaneous initiation of action of the funny channels in nodal cells
How does a funny current occur?
funny channels open and allows slow influx of Na+, depolarising the cell from -60mV to -40mV
At -40 the Ca2+ channels open and allow influx of Ca2+ up to +10mV when K+ channels open letting out K+ and re-polarising the cell back to 60mV
Pacemaker potential
The slow depolarisation of the nodal cell from slow influx of Ca2+ between -60 and -40mV
Contractile cell AP process
RMP = 90mV
Positive ions from neighbouring cell leak into the cell and depolarise it up to threshold of -70mV and then fast influx Na+ channels and slow influx Ca2+ channels open and lead to a fast depolarisation up to 0mV
Some K+ leaks out but is balanced by slow Ca2+ influx,
Why can the heart not do tetanus/sustained contraction
longer absolute and relative refractory periods preventing re-excitation of the heart muscle
What are systole and diastole
contraction and relaxation
What happens in arrhythmias and atrial fibrillation?
Heart is shaky, SA node is no longer in control, uncoordinated contractions and the heart cant move blood properly, blood moving slower can cause stroke, treated with blood thinners (like aspirin and warfarin)
What happens in ventricular fibrillation and defibrillation?
Is more life-threatening, ventricles pump without filling and if the rhythm is not rapidly reestablished (by defibrillation) then circulation stops and brain death occurs
- almost no cardiac output
- defib depolarises all the cells at the same time and hopes that they all repolarise together and the SA node can take over again
How full are the ventricles before the atria contract? (in%)
80-90%
Intrinsic Control of the heart
local controls originating entirely within the system
preload, afterload and contractility
Extrinsic Control of the heart
Hormonal, endocrine and nervous input
Stroke volume is? (definition and volume)
Explain SV = EDV - ESV
The amount of blood pumped out of the heart per contraction
65-70mL (60% of the blood in the ventricle)
End diastolic volume - End systolic volume, which is the volume before contraction - after
What is preload?
The amount of stretch/ filling of the heart before contraction
Determined by the EDV and EDP: volume and pressure of ventricle before contraction
Frank - Starling mechanism
“More fill - more empty”
If ventricular volume increases, the heart responds by doing more work producing a larger stroke volume
Length - tension relationship
Short muscle - high overlap, generate small amount of contraction
Stretched muscle - fibres cant overlap enough
Afterload
The tension the fibres must generate before they can shorten
The pressure that the ventricles must overcome to force open the semilunar valves
Afterload can increase from hypertension
Catecholamine effect on the heart
Released from adrenal medulla and sympathetic nerves cause contraction and relaxation to occur more quickly
Generate more force more quickly
Ejection Fraction equation
EJ = SV/EDV in mL
about 50 - 70%
Intrinsic mechanisms that control HR
Increase in right atrial pressure effects SA node
Increase in core temp by 1 degree increases HR by 10bpm
Effect of epinephrine on HR
Increase HR and SV
Law of Laplace
Muscle tension (which develops a ventricular pressure) depends on the radius of ventricle and thickness of ventricle wall
In law of laplace, what does a decrease in muscle wall thickness lead to?
increase in tension that needs to be generated (due to compliance of a thin wall compared to a thick wall)
What is the poiseuille relationship?
Laminar flow of a fluid is proportionally related to the radius, and the resistance
Pulse pressure is:
and is determined by:
the difference between systolic and diastolic pressure (120-80 = 40mmHg)
Determined by: SV, speed of ejection, arterial compliance
arteriosclerosis
stiffening of the arteries (decrease in compliance)
Equation for blood flow:
Q = change in Pressure x Resistance
Which vessel type is important for adjusting TPR to maintain MABP?
arterioles
myogenic Regulation
stretching of the blood vessels, reaction is to constrict to prevent potential damage and maintain BP down the line
Sympathetic vasoconstricter nerves are controlled by and work how?
the brainstem, innervates most arterioles and veins and continue as varicosities which release dense-cored vesicles, containing noradrenaline and ATP
a- adrenoreceptors
cause vasocontriction
Activated by noradrenaline, adrenaline and ATP
tonically active
Reduced sympathetic activity results in: (vessels and actions)
vasodilation
Increased HR
Reduced sympathetic activity leads to: (vessels and actions)
vasoconstriction
Increased TPR
happens with blood loss
Vasodilater nerve neurotransmitter chemicals (3)
ACh - acetylcholine
VIP - vasoactive intestinal peptide
NO - nitric oxide
increased plasma epinephrine on arteioles
Increase vasoconstriction and dilation (skin) of the arterioles
increased plasma nor epinephrine on arteioles
Increase vasoconstriction of the arterioles
B2- adrenoreceptors
Causes vasodilation
Acted on by epinephrine/adrenaline
Vasoconstrictors
Adrenaline Noradrenaline ATP Angiotensin II Vasopressin (ADH) Endothelin O2
Vasodilators
Adrenaline (skin B-receptors))
ACh, VIP and NO, PGI2, EDHF
Atrial Natriuretic Peptide (ANP)
Metabolites (CO2, lactate, H+, adenosine)
Myogenic autoregulation
Myogenic/autoregulation when resistance vessels detect and respond directly to and in/decrease in pressure by vasodilation or constriction
When pressure decreases, the vessels dilate to decrease TPR and increase flow
- goal is to keep flow relatively the same
