WEEK 6 Flashcards
Standard limb leads
SSL I = right arm to left arm
SSL II = right arm to left leg
SSL III = left arm to left leg
State the normal ranges and know what events in the heart the P wave, QRS complex and T wave correspond to as well as PR interval and QT interval
P WAVE = Atrial depolarisation
QRS COMPLEX = Depolarisation of ventricles ~0.08 seconds
T WAVE = Ventricular repolarisation
PR INTERVAL = Time from atrial depolarisation to ventricular depolarisation (mainly due to transmission through the AV node) 0.12-0.2 seconds
QT INTERVAL = Time for ventricles to depolarise and repolarise ~0.42 seconds at 60bpm
Illustrate the sequence of changes in pressure and volume in the chambers of the heart
throughout the cardiac cycle.
- Inatrial systole:
- Atrioventricular valves open so blood can enter ventricles
- Atrial pressure increases as the atria contract.
- Ventricular pressure increases slightly (and in proportion to the atria) as blood from the atria enters the ventricles.
- Ventricular pressure rises to a pressure greater than the atrial pressure causing the atrioventricular valve to shut. This produces thefirst heart sound (S1).
- Inventricular systole (isovolumetric contraction):
- Atrioventricular valves shut and semilunar valves open: blood leaves the heart through the great arteries RATHER THAN re-entering the atria
- Ventricular pressure increases as the ventricles contract.
- Both the mitral and aortic valves are shut so the volume of the ventricle stays the same whilst the ventricle contracts, therefore this stage is called an isovolumetric contraction.
- Ventricular pressure increases to a point where it becomes equal to the arterial pressure, causing the aortic valve to open.
- Inventricular systole (ejection phase):
- Ventricular pressure continues to rise as the ventricles continue to contract until it reaches a peak.
- During this phase, blood is ejected from the heart (hence why it is called the ejection phase).
- Arterial pressure increases as blood enters the aorta from the ventricles and the aorta contracts to pump blood around the body.
- Ventricular and arterial pressures decrease after reaching a peak as blood is leaving them.
- Ventricular pressure falls lower than arterial pressure, at which point the aortic valve will close. This produces thesecond heart sound (S2).
- Indiastole:
- Both aortic and mitral valves are shut, so the volume of the ventricles is constant whilst they relax. Therefore, this stage is called an isovolumetric relaxation.
- When the ventricular pressure falls below the atrial pressure, the mitral valve will open.
- Atrial and ventricular pressure initially drops slightly, but as the blood enters the atria, pressures start to rise again due to diastolic filling.
CONTRACT = SYSTOLE
RELAX = DIASTOLE
Describe the importance of these factors in the control of cardiac output.
⬆️HR causes small ⬆️ CO and ⬇️ SV
WHY??
- The shortened cardiac interval cuts into the rapid filling phase
- The reduced end diastolic volume reduces preload
- So according to Starling’s law, stroke volume is reduced
What offsets the effects of increased heart rate?
HR increases
- Via decreased vagal tone
- Increased sympathetic tone
Contractility increases
- Via increased sympathetic tone
- Alters inotropic state and shortens systole
Venous return increases
- Via venoconstriction and skeletal/respiratory pumps
- Maintains preload
Total peripheral resistance falls
- Due to arteriolar dilation in muscle, skin and heart
- Reduces afterload
Identify other inputs to the medullary cardiovascular centres.
- Cardiopulmonary baroreceptors
- Sensing central blood volume
- Central chemoreceptors
- Sensing arterial pCO2 and pO2
- Chemoreceptors in muscle
- Sensing metabolite concentrations
- Joint receptors
- Sensing joint movement
- Higher centres
- Hypothalamus and cerebral cortex
Describe the components and function of the arterial baroreceptor reflex.
Arterial baroreceptor reflex is a short term response to sudden changes in blood pressure
WHEN BLOOD PRESSURE INCREASES
- Baroreceptors release action potentials at a higher than normal rate to NTS (in brain stem)
- NTS activates parasympathetic system and inhibits the sympathetic system (causing vasodilation of blood vessels)
- Decreases heart rate by releasing ACh which acts on pacemaker cells of SA nodes
WHEN BLOOD PRESSURE DECREASES
- Baroreceptors fire at a lower than normal rate to NTS (in brain stem)
- NTS inhibits parasympathetic NS and activates sympathetic NS
- Sympathetic NS releases norepinephrine which increases heart rate
Describe the effect of the Valsalva manoeuvre on the cardiovascular system
= FORCED EXPIRATION AGAINST A CLOSED GLOTTIS
- increased thoracic pressure is transmitted through to aorta
- Increased thoracic pressure reduces the filling pressure from the veins, therefore decrease in VR, EDV, SV, CO, MAPThe reduced MAP is detected by baroreceptors which initiate a reflex increase in CO and TPR
- At end of the manoeuvre, the decrease in thoracic pressure is transmitted through to the aorta
- VR is resorted so SV increases, but reflex effects have not worn offEVENTUALLY BACK TO NORMAL
List the sequence events occurring during excitation-contraction coupling in cardiac muscle
- An action potential depolarizes the cardiac muscle cell membrane.
- Depolarization opens voltage-gated calcium channels in the T-tubules.
- Calcium enters the cell and triggers the release of more calcium from the sarcoplasmic reticulum.
- Calcium binds to troponin, causing a conformational change that moves tropomyosin away from the myosin-binding sites on actin.
- Myosin cross-bridges bind to actin and pull the thin filaments toward the center of the sarcomere, causing muscle contraction.
- Calcium is pumped back into the sarcoplasmic reticulum and out of the cell, causing muscle relaxation.
Compare basis of the action in pacemaker and non-pacemaker tissue
PACEMAKER TISSUE, such as the sinoatrial node (SA node), have the unique ability to spontaneously generate action potentials, which sets the rhythm of the heart. This automaticity is due to the slow, spontaneous depolarization known as the pacemaker potential.
NON-PACEMAKER TISSUE such as the atrial and ventricular muscles, do not spontaneously generate action potentials. They instead rely on the signals initiated by the pacemaker cells. These cells have a stable resting potential and require a stimulus to initiate an action potential.
In terms of action potential shape, pacemaker cells have a less negative resting membrane potential and their action potentials lack a plateau phase, unlike non-pacemaker cells.
Describe the initiation and spread of electrical activity throughout the heart
- The SA node sends an electrical signal that travels through the right and left atria, causing them to contract and pump blood into the ventricles.
- The signal then reaches the AV node, where it is slightly delayed to allow the ventricles to fill with blood.
- From the AV node, the signal travels down the bundle of His, which divides into right and left bundle branches running through the ventricles.
- These branches further divide into Purkinje fibers, which distribute the signal to the ventricular myocardium.
This network ensures that the signal spreads quickly and efficiently.
Explain the significance of Starling forces and the lymphatic system in relation to oedema. (what does starling forces determine? What does this result in?)
Starling forces determine BULK FLOW which results in loss of ~3L of fluid per day which the lymphatic system drains
Define active hyperaemia, pressure autoregulation and reactive hyperaemia.
ACTIVE (METABOLIC) HYPERAEMIA
Trigger is an increase in local metabolism
PRESSURE (FLOW) AUTOREGULATION
Trigger is a decrease in perfusion pressure
REACTIVE HYPERAEMIA
Trigger is occlusion of blood
Identify the various neural, hormonal and local factors affecting arteriolar tone.
NEURAL FACTORS
SYMPATHETIC NERVES
- Release noradrenaline
- Binds to α1 receptors
- Causes arteriolar constriction
- Therefore ↓ flow through that tissue and tends to ↑ TPR and ↑ MAP
PARASYMPATHETIC NERVES
- Usually no effect
- Genitalia and salivary glands are the exception (↑ flow)
HORMONAL FACTORS
ADRENALINE
- Released from adrenal medulla
- Binds to α1 receptors
- Causes arteriolar constriction
- Therefore ↓ flow through that tissue and tends to ↑ TPR and ↑ MAP
LOCAL FACTORS
Local (intrinsic) mechanisms
concerned with meeting the selfish needs of each individual tissue
1. Active (metabolic) hyperaemia
2. Pressure (flow) autoregulation
3. Reactive hyperaemia
Central (extrinsic) mechanisms
- concerned with ensuring that the total peripheral resistance (and therefore Mean Arteriol Pressure) of the whole body stays in the right ball park
CAUSED BY SMOOTH MUSCLE SURROUNDING THE ARTERIOLES
