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Flashcards in The cardiovascular system Deck (68):

Purpose of the CV system

Transport system for materials on which the cells of the body absolutely depend: oxygen, CO2, hormones, heat. Maintaining of homeostasis is essential for surviva


Components of CV system

Blood, blood vessels (arterioles, arteries, capillaries, venules, veins), heart -> pump and pipes


Organisation of CV system

Pulmonary (lungs) and systemic (rest of body - parallel) circulations


Structure-function relationship in heart

Network of pipes connected to chambers allowing blood to flow through heart in correct direction and don’t mix de/oxygenated blood thick septum. Left ventricle wall thicker compared to right as higher pressure for left venticule, so needs to be thicker to pump blood to all bod


Origin or heart beat

Intrinsic AP generation from Pacemaker cells starts heart beat. Network allows AP to be conducted around the heart.



Cardiac autorythmic cells display pacemaker activity
Membrane potential slowly depolarises, or drifts between AP until threshold is reached pacemaker potential
Cyclic processes that determine basic heart rate
Absence of nervous stimulation (autonomic control nerve and skeletal muscle cells RMP constant unless cell is stimulated – generates AP spontaneously – no necessary external stimuli)
External influence of autonomic NS to slow/speed up heart rate of SA
Ionic mechanism responsible for the pacemaker potential (Increased Na+ current, decreased K+ current, increased inward Ca2+ current)


Initial slow depolarisation the threshold

Na+ entry through a voltage gated Na+ channel found only in cardiac pacemaker cells
If (funny) channel opens when membrane is hyperpolarised at the end of repolarisation from the previous AP
Net inward Na+ current so membrane potential moves towards threshold (normally voltage gated channels open when membrane depolarise


Progressive reduction in the passive outflow of K+

- Cardiac pacemaker cell K+ permeability does not remain constant between AP (nerve and skeletal muscle, it does)
- K+ channels open at end of preceding AP slow close at negative potential;
- Rate of K+ efflux reduced at the same time the slow inward leak of Na+ occurs
- Net drift towards threshold


Ca2+ entry (2nd half of AP generation)

- If close
- Transient Ca2+ channels open (T-type Ca2+ channels) before membrane reaches threshold
- Brief influx Ca2+ further depolarised membrane, bringing it to threshold
- T-type Ca2+ channels close


Rising phase

- L-type Ca2+ channels open, large Ca2+ influx (nerve, muscle, Na+)


Falling phase

- L-type Ca2+ channels close
- Voltage gated K+ channels open
- End of the AP, slow closure of the L+ channels to next AP generation


AVN delay

0.1s AP slowly transmitted ventricles contract after atria – allows atria to fully contract to pass almost all blood to ventricles, generates AP at a slower frequency to SAN (can take on job of heart contraction sufficient for survival 50/min vs 70.min


Bundle of His

Left and right of bundle branches


Purkinje fibres

spread throughout ventricular myocardium
If AP conduction is blocked between atria and ventricles, then atria beat ~70/min and ventricles assume slower rate of contraction ~30/min determines by Purkinje fibres (idiobentricular pacemakers)
Complete heart block when conducting tissue between atria and ventricles is damaged (heart attack) and becomes non-functional
Ventricular rate of 30/min very sedentary existence; patient becomes comcatosed artificial pacemaker


Ionic basis of cardiac muscle AP

Cardiac AP differs in ionic mechanism and shape from SAN AP
RMP -90mv constant until excited by electrical activity propagated from SAN
AP of cardiac muscle cells show a characteristic plateau
RMP, K+ channel open and leaky (inward rectified K+ channel)
AP brings about cardiac muscle contraction because L-type Ca2+ channels in the T (transverse) tubules initiate a much larger Ca2+ release from SR.
A long refractory period prevents tatnus of cardiac mculclse second AP cannot be triggered until excitale membrane has recovered from preceding AP
250 ms = plateauc pahse; 300 ms cntraction phase - Thus cannot stimulate cardaiac muslce cell until conractuon is nearly iver
No summation or tatni (skeletal)
Protective – cycle filling and emptying for normal function
Inactivation of NA+ cells


Rising phase of cardiac muscle AP

Membrane potential reversal ~+20 mv - +30mv due to increases in Na+ permeability (activation of voltage-gated Na+ channels) peak potential Na+ permeability decreases. (Na+ channels close) In ventricle, sodium is the driver of AP


Peak potential of cardiac muscle AP

K+ channel open (transient) to allow fast limited efflux to give e a brief small repolarisation


Plateau phase of cardiac muscle AP

Membrane potential maintained close to peak posoite level ~100ms actuation slow L-type Ca2+ channels. K+ channels close (transient/leaky)


Rapid falling phase of cardiac muscle AP

Slow L-type Ca2+ channels
Ordinary voltage gated L+ channels open RMP restored ordinary voltage gates K+ channels close and leaky K+ channels open


Phase 1 - diastole

Relaxed state, no contraction
Blood flows through atria to ventricles (AV open) by pressure gradient (no contraction)
Pressure in veins sufficient to drive blood into heart (Venous return)
Aortic pressure falls as no blood is being pumped in but other end is flowing to organs
Semilunar valves closed – no pass into pulmonary system
Ventricular pressure lower than that in aorta and pulmonary arteries, but rises due to volume of blood inside increasing
End phase 1 atria contract driving more blood into ventricles
Atria relax ventricular systole begins
Atrial pressure rises (constant), causing the


Phase 2 - systole

Ventricles contract
Ventricle pressure exceeds atrial pressure (early in systole) - high volume and contracting
AV valves close
Atrial pressure falls slightly as no longer contracting
Semilunar valves closed ventricular pressure not high enough force open
No blood flowing into out ventricle volume constant-isovolumetric contraction
Sound where AV valves close turbulent blood flow around valves as they close, causing an obstruction in blood flow, forming eddies
By end this phase ventricular pressure great enough force open semilunar valves


Phase 3 - systole

AV closed and semilunar valves open, so blood ejected (ventricular ejection) to pulmonary and systemic circulatory systems
Atrial pressure rises
Aortic pressure falls
Blood ejected into aorta and pulmonary arteries through semilunar valves and ventricular volume falls
Ventricular pressure rises then declines
Falls below aortic pressure, semilunar valves close ending ejection (and systole)
Beginning diastole


Phase 4 - diastole

AV closed and semilunar valves open, so blood ejected (ventricular ejection) to pulmonary and systemic circulatory systems
Atrial pressure rises
Aortic pressure falls
Blood ejected into aorta and pulmonary arteries through semilunar valves and ventricular volume falls
Ventricular pressure rises then declines
Falls below aortic pressure, semilunar valves close ending ejection (and systole)
Beginning diastole


Diastole and systole times

Diastole 0.5 s filling time
Systole 0.3 sec


Aortic pressure

Diastole no blood in aorta, aortic valves closed
Blood leaves aorta down stream systemic circulation
Lose volume lose pressure = minimum diastolic pressure
Systole (Phase 2) aortic pressure continues fall aortic valve open only when ventricular pressure becomes high enough to force it open
Aortic valves open ejection begins aortic pressure rises quickly (phase 3)
Flow blood into aorta faster than leaving)
Systolic pressure - max


Stroke volume

volume blood in ventricles just before ejection minus volume of blood in ventricle just after ejection


Ejection fraction

Ejection fraction (EF) ratio volume ejected in one beat (SV) to volume contained in ventricle immediately prior to ejection (EDV)
Tells us if heart is pumping efficiently - low = muscle weakness. Can improve SV and EJ to increase blood to tissue


Heart sounds

Stethoscope lub soft, low-pitched first sound
Dup louder sharper, higher pitched
lub- Dup, lub-Dup
Heart sounds start systole (phase 2) AV valves close 1st sound lub
Start diastole (phase 4) semilunar valves close dup
Turbulent blood flow as valve narrow not by valves snapping shut



Non-invasive way of monitoring electrical heart activity
Records overall spread of electrical current through the heart as a function of time during the cardiac cycle
Uses electrodes to monitor ab/normal electrical activity, not not mechanical
Combinations of leads give a 3D picture of how electrical activity flows through the heart/body
P wave –atrial contraction
QRS complex -ventricular contraction
T wave – ventricular repolarisation


PR segment

AV nodal delay


ST segment

ventricle completely depolarised (cardiac cells in plateau phase), ventricular activation is complete and are contracting and emptying.


TP segment

Heart muscle completely depolarised, at rest ventricles filling


P-Q (P-R) segment

interval onset P wave and onset QS complex = conduction time through AV node


QT segment

interval onset QRS complex to end of T wave =ventricle contraction (systole)


RR segment

interval timing between QRS peaks = time between heart beats


How to determine HR from ECG

Dived 60s by R-R interval



Speeding up of heart



Slowing down of heart



Abnormal heart rhythm - atrial and ventricular contraction not in sequence


Heart block

Blood not getting through, so QRD complex in normal rhythm, damage fibres in atria from SAN to AVN - P waves


ST elevation

Heart attack - some heart muscles die - myocardial infarction



Uncoordinated chaotic contractions


Cardiac output

Cardiac Output (CO) is volume blood pumped by each ventricle per minute (not the total amount of blood pumped by the heart).
During any period time the volume of blood flowing pulmonary circulation = volume flowing systemic circulation
Therefore, CO each ventricle normally same (although beat-to beat basis, minor variations may occur.)
High pressure for systemic but same CO, each ventricle has the same amount of blood
The two determinants of CO are heart rate (beats per minute) and stoke volume (volume of blood pumped per beat or stroke
Cardiac Output = Heart Rate X Stroke Volume
Therefore, regulation of HR and SV so that CO is maintained even if pressure drops


Influence of autonomic NS on CO

Heart rate determined primarily by autonomic influences on SAN heart innervated ANS
Parasympathetic vagus nerve to atria, SAN, AVN, ventricles sparse brain stem; rest and digest – slow down
Sympathetic cardiac sympathetic nerve to atria, SAN, AVN, ventricles spinal cord fight or flight response – increases HR
NS can change firing rate of SAN to change HR
Also can innovate ventricles contraction rate influences
Antagonistic parasympathetic vs sympathetic work together and integrate signals
At rest, parasympathetic dominates – sympathetic influence on SAN inhibited by parasympathetic to slow down (or at 120bpm) – P delays rise time to TH for firing, K+ channels take longer to close
S increases HR – p still active, shortens time to reach TH K+ channels close a lot faster and AP is generated faster


Hormone effects of autonomic on CO

adrenaline (epinephrine) noradrenaline (norepinephrine) increase HR


SV determined by extent of venous return by sympathetic activity

Intrinsic (mechanism = how venous return affects cardiac contraction strength) control related to extent venous return
Extrinsic control related to the extent of sympathetic stimulation of the heart
= increase in strength of heart contraction and SV


Effects of ANS of HR and structures influencing the heart

Increased end-diastolic volume results in increased SV:
Intrinsic control of SV – heart’s inherent ability to vary SV, depends upon a direct correlation between end-diastolic volume and stroke volume
As more blood returns to heart, the heart pumps out more blood, but heart does not eject all the blood it contains
Mechanism dependent on length-tension relationship of cardiac muscle (like skeletal muscle)


Frank-Starling Law of the Heart

the heart normally pumps out during systole the volume of blood returned to it during diastole: increased venous return results in increased stroke volume


Shift of Frank-Starling curve to left by sympathetic stimulation

for the same end-diastolic volume (A), a larger stroke volume (B to C) is ejected on s stimulation as a result of increased contractility of the heart. Shift to left dependent on the extent of sympathetic stimulation. Improves efficiency of system by improving contractility increasing strength giving a bigger SV


Heart failure, contractility of heart decreases

o Decrease in cardiac contractility
o Sympathetic response -contractility (limited)
o Kidneys conserve salt/water expand blood volume and hence EDV.
o Fibres operate descending limb curve
o Congestive heart failure
o Reduce water salt retention and enhance contractility
o 100% mortality unless transplant
o Heart failure= losing ventricle ability to contract as long as they need – thinning of wall and/or over stretching of the heart
o Cant generate normal SV
o Automatically stimulates s NS shifting curve to left, stimulating failing heart = closer to normal but system is damaged – SV generation ability is improves
o Increase EDV
o Mechanisms conserving water and sodium – expand plasma blood volume = increase in diastolic volume = increase in SV to normal rate
o Should switch off S NS once blood volume expanded but doesn’t in failing heart hypertensive, abnormal activation of S NS
o Curve then falls and SV cannot improve – cross bridges overstretched so none form


Baroreceptor reflex

Maintain stable CO/arterial pressure
Baroreceptors - sensory non encapsulated nerve endings located in adventitial layer arteries: aortic arch/carotid sinus – no endothelium layer over the



CO falls, SV falls, HR initially constant and TPR constant but pressure falls as lost CO and volume
Detected by baroreceptors no longer stretched and lack of signal to brain – PS/S NS is trigger to increase HR – SV. Activation of S NS arteries in extremities constrict to maintain BP and more venous return to heart – impact on SV as well as S NS on SV
In HR an SV = increase in CO = raise in arterial pressure
Not back to normal as blood volume lost and pressure to normal would switch off baroreceptors but haven’t replaced lost blood so everything would fall again just below TH – keep CV variability until able to replace blood volume – pressure rise and back to norma



Serve as rapid transit passageways to organs and acts as pressure reservoirs
Large diameters = low resistance
Elastic and fibrous tissue withstands high pressure
Hold volume of CO - pressure reservoir
Low compliance (stretchy)
Driving force for flow during diastole is provided by elastic properties of arterial walls
Systole = greater volume into arteries
Diastole stretched walls passively recoil, exerting pressure on blood, using blood into downstream vessels and ensuring flo



Major resistance vessels due to small radius
Big variation in pressure - fluctuates
Make wider = reduce amount of sympathetic NS influences
Have capacity to alter diameter due to little elastic tissue, thick SM, Sympathetic innervation, hormones, stretch, vasoconstriction and vasodilatio



Exchange of materials between blood and tissues cells, branch extensively to bring blood within reach of essential every cell
Diffusion min distance, max area
Simple endothelium - 1 layer but tight gap junctions so only fluid is removed
Flow rate identical through all levels and = CO



Walls 1/2 thickness of arteries - ~0.5mm
BP low
SM, elastic and fibrous connective tissue
One way valves to blood and heart
Valves in peripheral veins, none in central veins
Volume reservoirs
High compliance
Small change in pressure -> large degree of stretch
Contain more blood than arteries
Valves top back flow due to low pressur


Blood flow

Force exerted by blood against a vessel wall - depends on volume of blood within vessel and its compliance.


Mean arterial pressure (MAP)

Driving force for blood flow
MAP = DP +1/3(SP-DP) ~93mmHg


Flow rate through a vessel

Directionally proportional to pressure gradient and inversely proportional to vascular resistance
Change in P/R


Resistance in vessels

Means pressure drops as blood flows through vessles


Resistance to blood flow

Directly proportional to viscosity of blood and vessel length
Inversely proportional to vessel radius


Fluid flow across capillaries

Stallings forces
Bulk flow - difference in hydrostatic and colloid osmotic pressures between plasma and interstitial fluid
Ultrafiltration at artery end of capillary - water out
Reabsorption at venous end - water in
More is filtered than reabsorbed - excess goes into lymph system and reabsorbed later.
Net change in pressure = outward pressure - inward pressure


Dicrotic notch

pressure falls after max pressure then semilunar valves close slight increase in pressure before falling again


Pulse Pressure (PP)

difference between systolic pressure (SP) and diastolic pressure (DP)
PP = SP - DP


Mean arterial pressure (MAP)

average pressure occurring in aorta during one cardiac cycle
MAP = DP + 1/3 (SP-DP)



vessel wall stretching and relaxing to accommodate blood flow


End diastolic volume (EDV)

Volume of blood in the ventricle at end of diastole
represents the maximum ventricular volume attained during the cardiac cycle, which is reached just before start of ejection.


End-systolic volume (ESV)

Volume of blood in the ventricle at the end of systole, called end-systolic volume (ESV), represents the minimum ventricular volume, which is attained just after ejection.