Flashcards in Cardio Deck (166)
Why are arterioles, and to a lesser extent, arteries called resistance vessels?
They act as muscular sphincters to provide vascular resistance and redirect flow as required. This is the main regulator of blood pressure
What is a name for capillaries, venous sinusoids and small vessels?
What is the distribution of blood normally?
65% in peripheral veins
20% in heart and lungs
10% in peripheral arteries
What can change blood distribution?
Exercise, where blood is diverted to skeletal muscle and heart
What is the tunica intima?
The innermost layer of vessels.
Endothelium which lines the entire vascular system
What is the tunica media?
Middle layer of vessels (absent in capillaries)
Thickest layer in arteries
Comprised of muscle tissue, elastic fibres and collagen
What is the tunica adventitia?
Comprised of connective tissues, nerves, vessel capillaries
What are the three types of capillaries?
Continuous - continuous cytoplasm, continuous basal lamina, bidirectional transport via transcytosis - in the brain, thyroid, bone and lung
Fenestrated - discontinuous cytoplasm, fenestrations may have a diaphragm, unidirectional filtration, continuous basal lamina. - villi, kidneys
Discontinuous - discontinuous cytoplasm, bidirectional filtration, discontinuous basal lamina. - spleen
What are the layers of the heart
Endocardium - innermost
Myocardium - heart muscle
Visceral later - inner serous layer
Parietal layer - outer serous layer
What are the borders of the heart?
Upper left 2nd intercostal space
Lower right 2nd intercostal space
6th right costal cartilage
5th left intercostal space
T4/5 - T8/9
What is diastole
When the ventricles are relaxed. At the end of diastole, both atria contract. The volume of blood in the ventricles after this is the end diastolic volume
What is systole
When ventricles contact. Blood is also entering atria
What is isovolumetric contraction? And what happens after?
Between the closing of the AV valves and the opening of the aortic and pulmonic valves. Ventricular pressure increases as contraction doesn't push out any blood
Then comes rapid ejection phase
As ventricular depolarisation occurs (t wave), pressure in ventricles reduce and force of ejection drops. This is reduced ejection phase as blood is pulled out by the movement of blood
What is stroke volume
Amount of blood pumped out of each ventricle per beat. Around 75ml but may double in exercise
What is cardiac output?
Stroke volume x heart rate
Around 5L at rest but up to 25L during exercise
What can affect cardiac output?
Preload - the stretch on the heart muscle due to the end diastolic volume - this increases sarcomere length and therefore an increase in contractile force, increasing stroke volume
Afterload - the load that the ventricles must pump blood against. If peripheral vascular resistance increases, cardiac output will decrease initially but then return to normal as Frank starling law takes place. Increased end diastolic volume due to increased resistance --> greater stretch of sarcomeres --> greater stroke volume increased
Functionality of the heart - encompasses heart rate and contractility which is modulated by the SNS and PSNS
Why is cardiac muscle termed myogenic?
Because cells in the sinoatrial node generate their own regular, spontaneous action potentials
Which ions cause the depolarisation in heart cells?
What are the three phases in the sinoatrial nodal action potentials?
At the end of depolarisation, the membrane potential is around -60mv. Ion channels open which allow a slow inward flow of Na called funny currents. This depolarises the cell, and at around -50mv, T-type calcium channels open, causing phase 4
Phase 4 - spontaneous depolarisation that occurs during diastole and triggers the action potential once the membrane potential reaches threshold ~ -40mv
At -40mv L-type calcium channels open
Phase 0 - T-type calcium channels and funny current channels close.
Phase 3 - K channels open and flows outwards, depolarising the cell and L-type calcium channels close. Keep flowing out until the cell is at around -60mv again and the cycle is spontaneously repeated
Explain the action potentials in non-pacemaker cells in the heart
Have a true resting membrane potential - phase 4
When rapidly depolarised to threshold of around -70mv there is rapid depolarisation (phase 0) causes by sodium channels
Phase 1 is the initial repolarisation by opening of transient K channels
This repolarisation is delayed by the large inward slow Ca at the same time which is long lasting. This causes a plateau which distinguishes cardiac action potentials from skeletal muscle or nerves
Phase 3 is when calcium channels close and repolarisation happens quickly again
What are cardiomyocytes joined together with?
Intercalated discs made of:
- fascia adherens which are anchoring sites for actin and allow for transmission of force
- desmosomes which stop separation of myocytes via intermediate filaments
- gap junctions which allow for the passage of action potentials cell to cell via connexons
What is excitation-contraction coupling?
The process where an action potential triggers a myocyte to contract
When the myocyte is depolarised by an action potential, calcium ions enter (phase 2) through L-type channels located on the sarcolemma. This calcium triggers calcium to be released form the sarcoplasmic reticulum through ryanodine receptors. This is called calcium induced calcium release.
This free calcium binds to troponin C. This induced a conformational change which exposes a site on actin that is able to bind to the myosin ATPase on the myosin head. This results in ATP hydrolysis that supplies energy for a conformational change in the actin-myosin complex.
They slide past each other and contract the sarcomere.
At the end of phase 2, calcium concentration decreases leading to troponin 1 once again inhibiting the actin binding site and ATP binds to myosin head. The sarcomere returns to initial length
What is the order in which parts of the heart contract?
SAN --> atria --> AVN --> annulus fibrosis --> ventricles (bundle of His and Purkinje fibres)
What is the annulus fibrosis?
Non conducting band between atria and ventricles
How long is a large square on the ECG?
0.2 seconds and 0.5mV
What are the parts of the ECG
P - depolarisation of the atria
Q- left to right depolarisation of the interventricular septum
R- depolarisation of main mass of ventricles
S- depolarisation of last part of ventricles at base
T - repolarisation of ventricles
Why isn't the repolarisation of the atria and other things seen on the ECG?
Why is the T wave positive?
Although it is repolarisation, the wave progresses from the base towards the apex. The change in polarity and direction cancel each other out. In pathological conditions where the action potential is prolonged, or the conduction from apex to base is slow, the T wave may be inverted
Which vessels provide the most resistance?
Arterioles as they have the thickest walls in relation to their lumen