control of the cardiovascular system Flashcards
function of cv system
Transport of nutrients, oxygen, waste products around the body
Thermoregulation (generally core to skin)
Buffers body pH and electrolytes
Transport of hormones (e.g. adrenaline from adrenals)
Assists in response to infection
heart valves
-Opening and closing of a valve is determined by the pressure gradients across the valve (i.e. it is passive)
chordae tendieae and papillary muscles
-Chordae tendinae and papillary muscles stop them opening under pressure – they have no role in valve opening
valve insufficiency
causes regurgitation of blood, which can lead to heart failure
phase 1 - atrial systole
AV valves open, aortic and pulmonary valves closed
SA node initiates P wave on ECG
Active filling to top-up ventricle: ‘a wave’
Contributes 10-40% of LV filling
LVEDP = LV end-diastolic pressure
S4 is due to blood turbulence during atrial contraction
phase 2- isovolumetric contractions
- all valves closed
-QRS complex; LV depolarisation
LV & papillary muscles contract
AV valves close – S1 ‘lubb’ sound
Rapid ↑P with no change in volume
LV geometry becomes spherical
phase 3- rapid ejection
-aortic and pulmonary valves open
-LVP > aortic P → valve opens
P difference only a few mmHg
Max. outflow velocity occurs
Atria continue to fill, but P dips due to atrial relaxation
phase 4- reduced ejection
-aortic and pulmoanry valves open
-T- wave repolarisation
LV muscle starts to relax
Rate of ejection ↓
Atrial pressures gradually rise due to continuous venous return
phase 5_ isovulmetric relaxtion
- all valves closed
- LVP ↓ rapidly
LVP < aortic P → valve closes
S2 short sharp ‘dupp’ sound
Aortic P rebounds (dicrotic notch) and remains high due to elastic recoil and TPR
LVESV = LV min. vol. (~50ml)
phase 6- rapid filling
- AV valves open- aortic and pulmonary valves closed
-LVP < atrial P → AV valves open
LVP ↓ despite filling due to continued relaxation: creates diastolic suction
And rapid, passive filling
S3: due to filling turbulence is heard in young or if EDP high
Atrial P ↓ rapidly
phase 7- reduced filling
- AV valves open, aortic and pulmonary valves closed
Passive filling almost complete
↓ pressure gradient = ↓ filling
LVP ↑ with filling and LV become stiffer (less compliant)
Prolonged phase at rest
electrical conduction co-ordinates contractions
Impulses generated within the sinoatrial node (SAN) spreads over the atria followed by the ventricles via the atrioventricular node (AVN)
AVN slows conduction velocity to create delay between contraction of atria and ventricles
signals and purkinje fibres
Signal propagated via Bundle of His and Purkinje fibres to inner walls
Spreads between myocytes via gap junctions at the intercalated disks
Depolarisation results in contraction
ECG- ELECTROCARDIOGRAM
Detects phasic change in potential difference between electrodes on surface of heart and limbs
The body acts as volume conductor
Recorded on paper or computer
Useful for diagnosis of arrhythmias, myocardial infarction, cardiomyopathy, iatrogenic abnormalities
ECG labels
P wave- atrial depolarisation
QRS complex- ventricular depolarisation
T wave- ventricular re-polarisation
P-R interval- delay through AV node
S-T interval - plateau phase of AP
cardiac muscles
Troponin complex:
TnI – inhibits actin-myosin binding
TnC – conformational change with Ca2+ binding moves TnI from myosin binding site allowing cross-bridge formation = contraction
Myosin head: hydrolyses ATP required for actin and myosin cross bridge formation
cardiac muscle cells structure
cardiomyocyte-> sarcomere
z line at sides
thick filament- with circle
thin filament
cross bridge formation generates active tension
excitation- contraction coupling in cardiomyocytes
Action potential causes membrane depolarisation
Ca2+ enters via L-type calcium channels
Ca2+-induced calcium release from sarcoplasmic reticulum (SR) amplifies signal
Cross-bridge formation at myofilaments
= contraction
Removal of Ca2+ via sodium-calcium exchanger (NCX) and re-uptake into SR
= relaxation
regulation by adrenoceptors
Exist in α and β forms with subtypes of each
Heart contains predominantly β1 on nodal tissue, conducting system and the myocardium
Bind norepinephrine (NE) released by sympathetic nerves but also circulating adrenaline (epinephrine)
Increases intracellular Ca2+
effects of adrenoceptors
Effects are:
Positive inotropy (contractility)
Positive chronotropy (heart rate)
Positive dromotropy (conduction speed)
Positive lusitropy (relaxation)
determinants of ventricular function- after load
The load against which the heart has to work to eject blood
Determined by aortic pressure, aortic compliance, and total peripheral resistance (TPR)
E.g. hypertension or aortic stenosis increase afterload
Failing heart sensitive to afterload since less able to generate higher pressures to open valves and eject blood
determinants of ventricular function- preload
Preload = myocyte stretch prior to contraction
Markers: end-diastolic volume (EDV) or pressure (EDP)
↑ sarcomere length means more overlap between filaments allowing for more cross-bridge formation = ↑ force
Determined by venous return, LV compliance & function
Note: preload generates more force, but the “intrinsic contractility” (inotropy) is not altered
