LO - Cardiovascular

Question 1

Describe the heart as a functional syncytium

Answer 1

At intercalated discs, cardiac muscle cells form tight gap junctions. Allows rapid diffusion of ions, spread of action potentials.
2 Syncytiums: Atrial and Ventricular

Fibrous tissue surrounds the atrioventricular valvular opening…this separates atria from valves, potentials do not travel through this tissue

Question 2

Cardiac Action Potential:

Answer 2

Phase 0: Depolarisation
Voltage-gated Na+ channels open.
Influx of Na+ down electrochemical gradient.
Membrane potential becomes more positive.

Phase 1: Initial Repolarisation
Na+ channels inactivate
Voltage-gated K+ channels open
K+ efflux down electrochemical gradient causes membrane potential to become more negative.

Phase 2: Plateau
K+ permeability decreases about 5 fold
Voltage-gated Ca2+ channels open
Influx of Ca2+ down electrochemical gradient cancels out K+ efflux, so little change in membrane potential

Phase 3: Repolarisation
Ca2+ channels inactivate
K+ efflux remains
Membrane Potential becomes more negative

Phase 4: Resting Membrane Potential
Averages about -90mV

Question 3

“EC-Coupling”

Answer 3

Refers to the mechanism by which the action potential causes the myofibril to contract.

1. When an AP spreads over a cardiac muscle cell, it spreads to the interior of the cell along the transverse Tubule membrane.
2. The AP causes voltage-gated Ca2+ channels to open. Ca2+ enters the cell.
3. This activated ryanodine receptor channels in the sarcoplasmic reticulum, triggering calcium release into the sarcoplasm.
4. Calcium diffuses into the myofibrils and catalyses the reactions that promote actin/myosin filament sliding, therefore contraction.
5. At the end of the plateau, calcium is pumped back into the SR and extracellular fluid.

Transport into SR: via calcium ATPase Pump
Removed from cell via sodium-calcium exchanger.

Question 4

Auto-Rhythmicity of heart

Answer 4

SA node pacemaker

and spread through heart…

Question 5

Regulation of Heart Pumping

Answer 5

TWO MECHANISMS

1. Frank-Starling Mechanism: response to increases in volume of blood in heart. The greater the heart muscle is stretched, the greater the force of contraction, the greater the stroke volume.
   Actin/Myosin filaments at a more optimal degree of overlap for force generation.
2. ANS:
   Sympathetic (increases heart rate, strength of contraction. 30% above)
   Parasympathetic (via vagus nerve, decreases HR)

Question 6

ECG - P wave

Answer 6

caused by electric potentials generated when the atria depolarise before atrial contractions

Question 7

ECG - QRS Complex

Answer 7

ventricular depolarisation

Question 8

ECG - T wave

Answer 8

ventricular repolarisation

Question 9

ECG P-R Interval:

Answer 9

0.16 seconds

time between excitation of the atria and the beginning of electrical excitation of the ventricles

Question 10

ECG S-T Segment:

Answer 10

interval between ventricular depolarisation and repolarisation

Question 11

Venous Pump and why required

Answer 11

Valves in veins that ensure blood flows in the correct direction, toward the heart

When we move our legs, muscle contraction compresses the veins, valves ensure blood is propelled toward heart. Overcomes gravitational force.

Efficient to keep pressure in feet of a walking adult at around 20mmHg rather than 90mmHg.

Question 12

Circulatory Shock - Definition

Answer 12

A generalised inadequate blood flow through the body such that tissue is damaged - especially due to too little oxygen and other nutrients being delivered.

Question 13

Circulatory Shock - Causes

Answer 13

W/ Decreased Cardiac output:

1. cardiac abnormalities that decrease pumping ability: myocardial infarction, severe heart valve dysfunction
2. decreased venous return: diminished blood volume, decreased vascular tone, obstruction in venous return pathway.

W/O Decreased Cardiac output:

1. Increased metabolic rate, normal CO inadequate.
2. Abnormal tissue perfusion - vessels besides those that supply local tissues with nutrition.

Question 14

Main Stages of Circulatory Shock

Answer 14

Non-Progressive: Natural compensatory mechanisms eventually cause full recovery w/o outside therapy

Progressive: W/O therapy gets worse until death

Irreversible: No known therapy is adequate to prevent death

Question 15

Which mechanisms kick in to recover from haemorrhagic shock?

Answer 15

1. Baroreceptor reflexes: sympathetic stimulation to circulation
2. CNS-Ischemic: more powerful sympathetic stimulation, activated if arterial pressure drops below 50mmHg
3. Reverse-Stress-Relaxation of the circulatory system: Vessels constrict around reduced blood volume.
4. Increased release of renin by kidneys and formation of angiotensin II: constricts peripheral arterioles, decreases water/salt loss by kidneys
5. Increased release of Vasopressin: constricts peripheral arterioles and veins & increases water retention by kidneys
6. Nor/epinephrine released by adrenal medullae: constricts peripheral arterioles % increases HR
7. Compensations to restore normal blood volume: increased thirst, salt appetite
   increased water/fluid retention by kidneys

Question 16

MICROCIRCULATION

Answer 16

1. Each NUTRIENT ARTERY entering the organ branches 6-8 times until becoming small enough to be arterioles (10-15 micrometres).
2. ARTERIOLES branch 2-5 times until being small enough (5-9micrometres) at their ends where they supply capillaries with blood. Arterioles are highly muscular so diameter can change.
3. METARTERIOLES (Terminal Arterioles) do not have a continuous muscular coat but smooth muscle fibres encircle the vessels at intermittent points.
4. At the point where each TRUE CAPILLARY originates from the metarteriole a smooth muscle fibre encircles the capillary - the PRECAPILLARY SPHINCTER. This can open and close entry.
5. VENULES are larger than the arterioles and have a much weaker coat, but pressure is less so they can still contract.

Question 17

VASOMOTION - What is it?

Answer 17

Intermittent contraction of the metarterioles and precapillary sphincters causing intermittent blood flow.

Question 18

VASOMOTION - Regulation

Answer 18

Most important known factor is conc. of oxygen in the tissue, when tissue oxygen decreases below normal level, the intermittent periods of capillary blood flow occur more often and last longer.

Question 19

Mechanisms of Blood Flow Control:

Answer 19

ACUTE CONTROL
Achieved by rapid changes in local vasodilation/vasoconstriction of arterioles, metarterioles, precapillary sphincters to maintain appropriate local tissue blood flow.
Increased metabolism leads to increased blood flow.

LONG TERM CONTROL
Controlled, slow changes over days, weeks, months. Changes come about due to change in physical size or number of vessels supplying the local tissue.

Question 20

Theories for blood flow regulation mechanisms

Answer 20

Vasodilator Theory:
The greater the rate of metabolism, the greater the production of vasodilator substances such as histamine, adenosine, CO2, K+.
These substances diffuse to the precapillary sphincters and cause vasodilation.

Oxygen Demand Theory:
Because oxygen is required for muscle contraction, in the case of increased metabolism with reduced O2 availability, vascular muscle relaxes - causes dilation of blood vessels

Question 21

Humoral Control of Blood Flow:

Answer 21

Definition: control by substances secreted or absorbed into the body fluids (e.g. hormones)

Vasoconstrictor agents:
angiotensin II, nor/epinephrine, Vasopressin/ADH

Vasodilator agents: Bradykinin, Histamine