Physiology

Question 1

what causes the rising phase of AP in pacemaker cells?

Answer 1

Long lasting (L-type) Ca++ channels resulting in Ca++ influx

Question 2

what causes the falling phase of AP in pacemaker cells?

Answer 2

Inactivation of L type Ca++ channels and activation of K++ channels resulting in k++ efflux

Question 3

what is cell to cell current flow via?

Answer 3

gap junctions

Question 4

why is there an AV nodal delay?

Answer 4

to allow atrial systole to precede ventricular systole

Question 5

phase 0-4 of AP in cardiac myocytes

Answer 5

0- fast Na+ inflex
1- closure of Na+ channels and transient K+ efflux
2- mainly Ca++ influx
3- closure of Ca++ channels and K+ efflux
4- resting membrane potential

Question 6

what is the plateau phase due to?

Answer 6

Influx of Ca++ through L-type channels

Question 7

resting potential of cardiac myocytes?

Answer 7

-90mV

Question 8

what part of the heart does the vagus nerve supply?

Answer 8

SA node and AV node

Question 9

consequence of vagal stimulation in the heart

Answer 9

increased AV nodal delay to slow HR

Question 10

parasympathetic receptor and neurotransmitter

Answer 10

Muscarinic M2 receptors and acetylcholine

Question 11

effect of vagal stimulation on pacemaker cells?

Answer 11

• Takes longer to reach threshold
• Slope of pacemaker potential decreases
• Frequency of AP decrease
• Negative chronotropic effect

Question 12

what part of the heart do cardiac nerves supply?

Answer 12

AV node, SA node and myocardium

Question 13

effect of sympathetic stimulation on the heart

Answer 13

increased HR, increased force of contraction and decreased AV nodal delay

Question 14

neurotransmitter and receptors for cardiac nerve supply

Answer 14

noradrenaline and Bi adenoreceptors

Question 15

effect of noradrenaline on pacemaker cells

Answer 15

• Slope of pacemaker potential increases
• Pacemaker potential reaches threshold quicker
• Frequency of AP increases
Positive chronotropic effect

Question 16

arrangement of cardiac muscle

Answer 16

striated, regular arrangement of contractile protein

Question 17

what is required to turn on cross bridge formation between myosin and actin

Answer 17

Ca++ from the sarcoplasmic reticulum released in the presence of extra-cellular Ca++

Question 18

what is the refractory period?

Answer 18

A period following an AP in which it is not possible to produce another AP. The long refractory period prevents generation of tetanic contraction

Question 19

what is stroke volume?

Answer 19

The volume of blood ejected by each ventricle per heart beat

SV = (End diastolic volume) – (End systolic volume)

Question 20

what determines the end diastolic volume?

Answer 20

the diastolic stretch of myocardial fibres

Question 21

France-Starling Hypothesis

Answer 21

the more the ventricle is filled with blood during diastole (EDV), the greater the volume of ejected blood will be during the resulting contraction (SV)

Question 22

what does stretch increase the affinity of?

Answer 22

Troponin for Ca++

Question 23

what is skeletal muscles optimal fibre length?

Answer 23

resting muscle length

Question 24

what is cardiac muscle optimal fibre length?

Answer 24

Stretched muscle length

Question 25

what is after load?

Answer 25

the pressure into which the heart is pumping

Question 26

consequence of prolonged increased after load?

Answer 26

ventricular hypertrophy

Question 27

postive inotropic effect

Answer 27

increased force of contraction

Question 28

positive chronotropic effect

Answer 28

increased rate of contraction

Question 29

what is the Cardiac output?

Answer 29

The volume of blood pumped by each ventricle per minute

Question 30

what are the four events of the cardiac cycle?

Answer 30

1. Passive filling Pressure in atria and ventricles are close to zero. AV valves are open so blood fills ventricles. Ventricles become 80% full. 2. Atrial Contraction P wave shows atria depolarisation. Atria contracts between P-wave and QRS. Atrial contraction complete EDV (130ml) 3. Isovolumetric ventricular contraction Ventricular contraction starts at QRS. Ventricular pressure rises. When V pressure > A pressure, AV valves shut. First heart sound (LUB). Aortic valve is still shut too so the blood is TRAPPED IN THE VENTRICLES 4. Ventricular Ejection When V pressure > aorta/PA pressure, valves open, and aortic pressure rises. T waves in ECG signal ventricular repolarisation. Ventricles relax and V pressure falls. When V pressure < Aortic/pulmonary pressure, aortic/pulmonary valves shut (DUB) 2nd heart sound 5. Isovolumetric ventricular relaxation Signalled by closure of aortic/pulmonary valves. Ventricle is a closed box again as the AV valve is shut. When ventricular pressure < atrial presure, AV valves open (silent) and a new cycle starts here

Question 31

two calculations for MAP

Answer 31

``` MAP = [(2xDBP) + (SBP)]/3 MAP = DBP + 1/3 PP ```

Question 32

normal ranges for MAP

Answer 32

Normal range is 70-105 mm HG

Question 33

MAP equation

Answer 33

``` MAP = SVR x CO MAP = SVR x HR x SV ```

Question 34

what are the major resistance vessels?

Answer 34

arterioles

Question 35

resistance to flow equation

Answer 35

R directly proportional to n (blood viscosity) and length of blood vessel R is directly proportional to radius of blood vessel to the power 4

Question 36

what are some humeral agents that can cause vasodilation? intrinsic control

Answer 36

- Serotonin - Thromboxane A2 - Leukotrienes - Endothelin

Question 37

causes of vasodilation by relaxation of arteriolar smooth muscles?

Answer 37

- Decreased local PO2 - Increased local PCO2 - Increased local H+ - Increased extracellular K+ - Increased osmolarity of ECF - Adenosine release from phosphate - Histamine - Bradykinin - Nitric Oxide