control of the cardiovascular system

Question 1

function of cv system

Answer 1

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

Question 2

heart valves

Answer 2

-Opening and closing of a valve is determined by the pressure gradients across the valve (i.e. it is passive)

Question 3

chordae tendieae and papillary muscles

Answer 3

-Chordae tendinae and papillary muscles stop them opening under pressure – they have no role in valve opening

Question 4

valve insufficiency

Answer 4

causes regurgitation of blood, which can lead to heart failure

Question 5

phase 1 - atrial systole

Answer 5

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

Question 6

phase 2- isovolumetric contractions

Answer 6

• 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

Question 7

phase 3- rapid ejection

Answer 7

-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

Question 8

phase 4- reduced ejection

Answer 8

-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

Question 9

phase 5_ isovulmetric relaxtion

Answer 9

• 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)

Question 10

phase 6- rapid filling

Answer 10

• 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

Question 11

phase 7- reduced filling

Answer 11

• 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

Question 12

electrical conduction co-ordinates contractions

Answer 12

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

Question 13

signals and purkinje fibres

Answer 13

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

Question 14

ECG- ELECTROCARDIOGRAM

Answer 14

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

Question 15

ECG labels

Answer 15

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

Question 16

cardiac muscles

Answer 16

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

Question 17

cardiac muscle cells structure

Answer 17

cardiomyocyte-> sarcomere
z line at sides
thick filament- with circle
thin filament
cross bridge formation generates active tension

Question 18

excitation- contraction coupling in cardiomyocytes

Answer 18

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

Question 19

regulation by adrenoceptors

Answer 19

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+

Question 20

effects of adrenoceptors

Answer 20

Effects are:
Positive inotropy (contractility)
Positive chronotropy (heart rate)
Positive dromotropy (conduction speed)
Positive lusitropy (relaxation)

Question 21

determinants of ventricular function- after load

Answer 21

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

Question 22

determinants of ventricular function- preload

Answer 22

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