Long: CVS
What is postural hypotension?
Also called orthostatic hypotension is a form of low blood pressure as you stand up from sitting or lying. It leads to a head rush.
What are prodromal symptoms?
Early symptoms that indicate to a patient that disease or a fit such as epilepsy are imminent. In epilepsy, prodromal symptoms include specific smells, photosensitivity, speech difficulty etc.
What does this equation mean in terms of how the total peripheral resistance compares to any individual resistance (RT compared to R1 or R2 etc.)?
It means that the TPR is less than any of the individual resistances. TPR = 1/Rt = 1/R1 + 1/R2 + 1/R3...
What does the ECG measure?
It measures the electrical potential of the heart between two electrodes placed on the skin.
What is the importance of Starling's law?
It regulates stroke volume for us and makes sure CO = venous return because a decrease in preload leads to a smaller stroke volume. This balances the outputs of the right and left ventricles.
What do we mean by 'the annulus fibrosis electrically insulates the atria from the ventricles'?
It stops conduction getting down the bundle branches in the septum without the AVN firing.
What is the intrinsic heart rate? What does its value imply about whether parasympathetic or sympathetic innervation usually dominates?
It's the heart rate you'd have if you remove all sympathetic and parasympathetic innervation to the heart. Its value is 100-110bpm. Since resting heart rate < intrinsic heart rate, vagal/parasympathetic input must be dominant at rest
What is a lead?
It's the positioning of the two electrodes when measuring the potential difference of the heart.
What is central venous pressure, CVP?
It's the pressure of the blood returning to the heart and is hence also called the filling pressure/preload
What's total peripheral resistance?
It's the total resistance that the heart has to work against when it's pumping blood. It's largely made up of the resistance brought about by the arterioles.
Does muscle tension occur at the same time as the action potential?
NO, there is a slight delay
Sinus Bradycardia
Normal heart rhythm that is less than 60bpm • Normal rate • Regular, narrow QRS
What do the action potentials of the AVN look like?
Similar to the SAN (so no rapid sodium channels causing depolarisation, it's the calcium channels instead)
What do the action potentials in the atria look like?
Similar to the ventricles
What is an escape rhythm?
When the ventricles of the heart receive no stimulation from either the SAN or the AVN, it can generate a slow escape rhythm. It indicates failure in the electroconductivity in the heart, and can occur in heart blocks.
1st degree AV block
When there is an abnormally long PR interval because there is a slowing of conduction through the AVN • Rate is variable • Regular narrow QRS • P waves present • P:QRS is 1:1 • Long PR interval >200ms
2nd degree AV block Subtype: Mobitz II
When there is normal PR interval but every so often there is a dropped beat (as opposed to Wenckebach where is cyclical). This is usually a problem with the bundle of His • <60bpm • Irregular narrow QRS • P:QRS not 1:1 • Dropped QRS complex every so often
What is cardiac pacing?
When you insert metal wires into the pacemaker areas of the heart with a box that is placed under the chest skin to activate the heart and generate heartbeats
What is radiofrequency ablation?
When you know where re-entry is happening, you can go in with a small needle that burns away this area, stopping re-entry.
How does increasing preload affect stroke volume?
According to Starling's law, the more you stretch a cardiac myocyte, the more force it will generate upon contraction up to a point. Past a critical point the stroke volume starts to decrease
Describe the electrophysiology of the SAN action potential:
1. Phase 4 o Ion channels open that allows a slow inward current of Na+. This depolarises the cell gradually and is why the phase 4 line is on the rise o At around -50mV, a second type of ion channel called transient Ca2+ channels (T-type Ca2+ channel) opens. This helps to further slowly depolarise the cell, bringing the membrane potential closer to the threshold potential. o A little bit later, the long-lasting Ca2+ channel opens (L-type Ca2+ channel), which allows even more calcium in and pushes the membrane potential past threshold potential. Phase 0 o The T-type Ca2+ channels close before the upstroke o The quick upstroke is mainly due to Ca2+ quickly moving into the cell via the L- type Ca2+ channels that opened towards the end of phase 4. o The upstroke is also partially due to the funny current which remains until the end of phase 0 Phase 3 o The L-type Ca2+ channels start to close, meaning depolarisation stops o K+ channels open, allowing K+ out of the cell, which repolarises it Phase 4 o The K+ close once repolarisation has repolarised the cell to -60mV again o This opens inward Na+ channels, which slowly depolarises the cell (funny current)
What are the factors determining stroke volume?
1. Intrinsic factors - preload and afterload 2. Extrinsic factor - contractility (as its controlled by the ANS)
What are the 'lub dub' sounds called and what are they caused by?
1. Lub = first heart sound, S1 = closure of the atrioventricular valves 2. Dub = second heart sound, S2 = closure of the semi-lunar valves
How can you tell from an ECG if the heartbeat is regular or not - what do you look for?
1. Normal rate 2. Regular, narrow QRS 3. P waves present 4. Length of P wave is equal to length of QRS complex
Describe the electrophysiology of the ventricular myocyte action potential:
1. Phase 4 - the resting membrane potential is largely due to the permeability to K+ 2. Phase 0 - activation of the voltage gated Na+ channels leads to rapid depolarisation of the cell as the Na+ rushes into the cell 3. Phase 1 - the voltage gated sodium channels close and there is a little rush of K+ out of the cell, causing a little spike of repolarisation 4. Phase 2 - the plateau phase is caused by an inward current of Ca2+ through slowly activated calcium channels, which counteracts repolarising currents hence causing a plateau. This Ca2+ current allows the cell to stay depolarised for longer 5. Phase 3 - The calcium channels become inactivated and delayed rectifier K+ channels open, allowing a rapid efflux of potassium
What are the risk factors for developing endocarditis?
1. Poor dental hygiene 2. Dental procedures 3. Valve defects and prosthetic valves 4. Intravenous drug use
How does hypokalaemia affect the ECG?
1. Prolonged PR interval 2. ST depression 3. Shallow T wave 4. U wave appears (prolonged repolarisation of purkinje)
Describe and explain what underlying CV issues can lead to syncope?
1. SAN disease - a disease of the SAN that makes it not do its job properly so you get tachybrady syndrome, where your heart rate can vary greatly. It's usually found in the elderly 2. Carotid sinus syncope - when you feint because of an excessive baroreceptor reflex that leads to hypotension and bradycardia to the point where you loose consciousness. This occur because the carotid sinus is hypersensitive (hypersensitive carotid sinus -> carotid sinus syncope) 3. Complete heart block (see below) 4. Ventricular tachycardia or fibrillation
What is the % of oxygen in the blood of the right atrium?
70%
What is the % of oxygen in the blood of the left atrium?
99%
Supraventricular tachycardia
A cardiac arrhythmia arising from improper electrical activity of the heart. It originates at or above the AVN, often due to re-entry. It can be contrasted with the potentially more dangerous ventricular tachycardias, which are rapid rhythms that originate within the ventricular tissue. SVTs include both atrial tachyarrhythmia (flutter and fibrillation) and nodal arrhythmias. SVTs are most commonly AVNRTs (see below). Can be treated with Valsalva maneuver and adenosine.
What does the ECG look like in someone with Wolff-Parkinson-White syndrome?
A characteristic delta wave and a negative T wave
What is the annulus fibrosis?
A fibrous ring around the heart that electrically insulates the atria from the ventricles
Sinus tachycardia
A normal heartbeat that is elevated, due to normal things like exercise • Normal rate • Regular, narrow QRS • P waves present • Length of P wave is equal to length of QRS complex
What is pre-syncope?
A state of light-headedness, muscle weakness, blurred vision and generally feeling you're about to feint, as opposed to actually feinting (syncope)
What is syncope?
A transient loss of consciousness (TLOC) that is a result of hypoperfusion to the brain due to decrease blood pressure and heart rate. It is characterised by rapid onset, short duration and complete recovery
What are ectopic beats?
An Ectopic beat is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from somewhere other than the SAN. An ectopic beat can be further classified as either a premature ventricular or atrial contraction.
What is an arrhythmia?
An arrhythmia is an irregular heartbeat
What is AV block?
An impairment of the conduction between the atria and the ventricles
What is a palpitation?
An undue awareness of the heartbeat
How does the Valsalva maneuver affect your heart rate?
At first it decreases it because your aortic pressure spikes as you strain and increase intrathoracic pressure. Towards the end of the maneuver your heart rate increases to compensate for the drop in aortic pressure
What is endocarditis?
Bacterial valve infection
Why does the SAN dominate over the AVN in terms of setting the heart rate?
Because it's intrinsic rate at which it will generate action potentials is higher than the AVNs intrinsic rate. If it were up to the AVN alone, we'd have a heart rate of around 40bpm.
How does Starling's law explain postural hypotension?
Because when you stand up, blood transiently pools in your legs due to gravity (before vasoconstriction occurs to counter this). This leads to a decreased CVP -> decreased preload -> decreased CO -> hypotension.
How does holding breath affect HR?
Bradycardia
What is the only electrical connection between the AVN and the ventricles?
Bundle of His
How are atrial myocytes connected?
By intercalated discs that have gap junctions. This forms a syncytium, where one action potential is able to spread to all of the muscle.
AV nodal reentrant tachycardia
Caused by a re-entrant loop in the architecture of the AV node. In this re-entry, you get block of the fast- pathway because its refractory (in its refractory period) so the impulse has to go down the slow. It then travels back up the fast and then down the slow in a re-entry loop. This means the atria and ventricles contract at more or less the same time • Long PR segment as impulse goes down slow pathway • Another P wave found immediately after QRS segment because of re-entrant loop
What is positive chronotropy?
HR +ve chronotropy: HR faster!
What cause hypokalemia?
Hypokalemia is a lack of potassium in the blood, and is caused by low dietary K+, diarrhoea, excessive sweating or urine production and an increased blood pH
What is the physiological advantage of there being a slow conduction velocity through the AVN?
It allows the ventricles to properly fill with blood before an action potential reaches them and they have to contract
A U wave can sometimes appear. What causes it?
It appears due to the prolonged repolarisation of the Purkinje fibres
How is cardiac output related to mean arterial pressure and total peripheral resistance?
If you related the equation ΔP = QR to the entire system, ΔP can be thought of as MAP, Q can be thought of as cardiac output and R can be though of as TPR, which leads to the equation MAP = TPR x CO, which is more commonly written as CO = MAP/TPR
2nd degree AV block Subtype: Mobitz I (Wenckebach)
PR interval gets longer and longer until after 3 or 4 beats the atria depolarise (P wave) but the ventricles don't (QRS complex). The PR interval is longest just before the dropped beat and shortest just after the dropped beat. • Rate is <60bpm • Irregular narrow QRS • P:QRS is not 1:1 • PR gets bigger and bigger until dropped beat
What equation describes how resistance varies with radius?
Poiseulle's law, which states that R = 8vL/πr4, where L is the length of the vessel, v is the viscosity of the fluid and R is the resistance. We need to know that R α 1/r4. So if the radius shrinks by half, then the resistance will increase by (24 = 16) a factor of 16!
What is preload?
Preload is the stretch on the myocytes prior to contraction, and is set by the filling pressure/central venous return. The larger the central venous pressure, the more the cardiac myocytes will fill before contraction, the more they stretch, the more the preload.
What cells in the heart conduct the action potentials?
Purkinje Fibres (wide diameters for rapid conduction)
What is re-entry?
Re-entrant arrhythmias occur when an electrical impulse recurrently travels in a tight circle within the heart, rather than moving from one end of the heart to the other and then stopping
What is the physiological pacemaker?
SAN
What 2 structures in the heart are capable of generating their own action potentials?
SAN and AVN, because they have 'excitable' cells
How does the electrophysiology of the AVN change when the heart rate has to get higher?
The Na+ channels open slightly more, allowing sodium in at a slightly faster rate (i.e. funny current/pacemaker potential gets greater). This means the T- type and then L-type Ca2+ channels open earlier and so depolarisation occurs sooner after the end of the last action potential. On the graph, this means the phase 4 line steeper, but does not affect the slopes of the phase 0 or 3 much.
What cells in the heart generate the action potentials?
The cells in the SAN and AVN. They are modified myocytes with few contractile filaments, and so do not contract.
What is the main factor in arterioles that determines resistance?
The diameter of the vessel
Which current do we have to thank for the SANs automaticity/excitability?
The funny current (slow inwards current of Na+), which is also called the pacemaker potential.
3rd degree/complete block
The impulse generated in the SAN does not reach the ventricles in any heartbeat. The ventricles depolarise and contract thanks to the escape rhythm. Atrial depolarisation is unrelated to ventricular depolarisation • <60bpm • Regular broad QRS • P wave and QRS wave is unrelated, and often rate of P waves > rate of QRS complexes
CO must be equal to venous return and RV CO must equal LV CO. What happens during left-sided heart failure?
The left side of the heart is failing to pump out enough blood so RV output > LV output. This leads to a 'backlog' of blood in the pulmonary system -> oedema due to the increased hydrostatic pressure
What percentage of total blood volume is found in the following regions of the CV system?
Veins: 70% arterial: 10% capillaries: 5% Heart and lungs: 15%
What is vasovagal syncope?
The most common cause of feinting. When you feint due to overstimulation of the vagus nerve (!!!PARASYMPATHETICS) on the heart, leading to hypotension and bradycardia -> decreased perfusion in the brain -> feinting. The causes are vast but include: o Arousal or stimulants such as tickling o Sudden onset of extreme emotions o Trauma such as hitting your funny bone o The sight of blood or other stressful stimuli
What is heart rate?
The number of beats per minute
What is the absolute refractory period, how is it made longer and why is it advantageous?
The period of time where another action potential cannot be generated. This time is made longer by the slowly activated Ca2+ channels, which increases the time the cells are depolarised. This long refractory period is advantageous because it means the heart cannot have tetanic contraction. Tetanic contraction would make the heart not work because if its constantly contracted no blood would flow anywhere as the heart would never have time to fill and empty.
What is respiratory sinus arrhythmia (RSA)? Why does this occur?
The phenomenon whereby your heart rate increases when you inhale, and decreases when you exhale. During the process of RSA, inhalation temporarily suppresses vagal activity, causing an immediate increase in heart rate. Exhalation then decreases heart rate as it causes vagal activity to resume.
What is afterload?
The pressure against which the heart has to pump, which is set by the mean arterial pressure. A higher MAP = increased afterload
What is end diastolic pressure (EDP)?
The pressure exerted on the walls of the ventricles due to the EDV. A higher EDP leads to more cardiac myocyte stretching.
Atrial fibrillation
The regular impulses produced by the SAN are overwhelmed by rapid electrical discharges produced in the atria and adjacent parts of the pulmonary veins. This results in a total loss of rhythm. • Rate is variable • Irregular narrow QRS • No P waves
Atrial flutter
The result of a re-entrant rhythm that can easily degenerate into atrial fibrillation. There is a rhythm, but it's abnormal • Rate variable • Regular, narrow QRS • Sawtooth atrial activity (so lots of P waves)
What test can be used to diagnose why syncope is happening?
The tilt test, where you are strapped into a table that you lay on flat. After 15 minutes, its turned upright quickly, and the doctor monitors you heart on an ECG amongst other things to try and diagnose why its happening
What is the cardiac output?
The volume ejected by the heart per minute
What is ventricular end diastolic volume (EDV)?
The volume of blood in the ventricle at the end of diastole, before the start of systole
What are the two types of flow patterns through vessels?
Turbulent and laminar
What are the fast and slow pathways of the AVN?
Two ways in which impulses can travel to the AVN. Issues arise when one of them is blocked
Ventricular fibrillation
Ventricular fibrillation is a condition in which there is uncoordinated contraction of the cardiac muscle of the ventricles in the heart, making them quiver at up to 500bpm rather than contract properly, leading to loss of cardiac output • Rate 150 - 500bpm • Chaotic deflections of varying amplitudes • No identifiable P, QRS or T waves
Ventricular tachycardia
Ventricular tachycardia is a type of tachycardia that arises from improper electrical activity of the heart that starts in the ventricles • Rate >120bpm • Regular broad QRS • P waves variable but usually absent
How are these feeling different to vertigo?
Vertigo can have similar feelings but is coupled with the unique feeling that you or the room you are in is spinning
What is the stroke volume?
Volume of blood ejected per beat
Junctional bradycardia
When the SAN doesn't work and the heartbeat is reliant on the AVN intrinsic heart rate, which as mentioned before is low (hence the bradycardia). • <60bpm • No P wave • Regular, narrow QRS
What is valve regurgitation?
When the valves don't close properly and so blood flows back
What syndrome do you get if you have another pathway down?
Wolff-Parkinson- White syndrome, where you get a bindle of Kent too!
Describe the different types of vessels in the body?
arteries: Windkessel effect (elastic reservoir) -> It keeps the systemic blood pressure up during diastole.
What is positive dromotropy?
conduction SPEED through AVN. +ve dromotropy: +rate of conduction at AVN
What is positive inotropy?
contractile STRENGTH +ve inotropy: incr heart force of contraction
What are the 3 layers of the heart?
endocardium, myocardium, epicardium
How does pressure and velocity of the blood compare to the total cross-sectional area of the type of vessel?
o As cross sectional area increases (arteries -> capillaries), the pressure drops, as does the flow rate o As it increases again (capillaries -> veins), the flow rate increase again but the pressure stays low
Describe what the peaks represent in a typical lead II ECG.
o P wave - atrial depolarisation o PR interval - the time between the end of atrial depolarisation and the start of ventricular depolarisation. ! This represents the conduction velocity in the AVN (i.e. a positive dromotropic agent would shorten the PR segment) ! o QRS complex - ventricular depolarisation o T wave - ventricular repolarisation
The ventricles are filled by:
o The atria contracting and pushing blood into the ventricles (active 30%) o The relaxing of the ventricles which 'sucks' blood into it before it contracts (passive 70%)
