1
Q
What is Pulmonary Circulation?
A
Low Pressure circulation to the lungs
2
Q
What is Systemic Circulation?
A
High Pressure circulation to send oxygenated blood to tissues
3
Q
What is Cardiac Output?
A
Volume of blood pumped per minute by each ventricle
Cardiac Output = Heart Rate x Stroke Volume
4
Q
What is Diastole?
A
Period of Relaxation
5
Q
What is Systole?
A
Period of Contraction
6
Q
What is Stroke Volume?
A
Volume of blood ejected by the left ventricle in each cardiac cycle (EDV-ESV)
7
Q
What is End-Diastolic Volume (EDV)?
A
Volume of blood left in the ventricle at the end of ventricular relaxation
8
Q
What is End-Systolic Volume (ESV)?
A
Volume of blood left in the ventricle at the end of Ventricular contraction
9
Q
What is Ejection Fraction?
A
Ratio of SV:EDV
10
Q
What is the Cardiac Cycle?
A
The time from the start of one heart beat to the start of the next heart beat–> one complete cycle of the heart
11
Q
What are the 5 Phases of the Cardiac Cycle?
A
- Late Diastole
- Isovolumetric Contraction
- Ventricular Ejection
- Isovolumetric Relaxation
- Early Diastole
12
Q
What happens in Late Diastole?
A
- Ventricular Filling
2. Atrial Contraction (when the ventricle is 75% full)
13
Q
What happens to Atrial and Ventricular Pressure during Late Diastole?
A
They both increase in Atrial Contraction
14
Q
Which Heart valves are open and closed in Late Diastole?
A
AV valves are open, Pulmonary valves are closed
15
Q
What happens in Isovolumetric Contraction?
A
- All Valves are closed
- Ventricle starts contracting
- Rapid increase in ventricular pressure
- Slight increase in atrial pressure due ventricle pushing against AV valves
- When Left Ventricular Pressure exceeds Aortic Pressure (80mmHg), aortic valve opens
16
Q
What happens in Ventricular Ejection?
A
- AV Valves are closed, Pulmonary and Aortic Valves are open
- Ejection is most rapid during the early part (first 1/3)
- Expels Stroke Volume (70mL), leaving 50mL of blood in the heart
- Aortic Pressure rises to about 120mmHg
17
Q
What happens in Isovolumetric Relaxation?
A
- All valves are closed
- Blood left in the heart is ESV
- Ventricle relaxes and Ventricular Pressures falls until the AV valves open and begins filling the ventricle again
18
Q
What happens in Early Diastole?
A
- Ventricular Filling
- The Atria is filled and the AV valves open
- Atrial Pressure rises due to filling of atrium
- Ventricular pressure starts to slowly rise
- Aortic pressure slowly decreases to around 80mmHg
- Ventricles are about 75% full before Atrial Contraction occurs again
19
Q
What are the different cells in the heart?
A
- Pacemaker cells
- Specialised Conducting Fibres
- Myocardial Cells
20
Q
Where is the Action Potential in the heart generated?
A
Sino-atrial (SA Node)
21
Q
What is the resting membrane potential of the pacemaker cell?
A
-55mV
22
Q
What is the Threshold Potential of the Pacemaker Cell?
A
-40mV
23
Q
Describe what happens in an Action Potential of a Pacemaker Cell?
A
- Pacemaker cell spontaneously depolarises to threshold due to “funny” channels allowing Na+ into the cell
- At threshold, Slow L-type Ca2+ channels open–> Action Potential occurs due to influx of Calcium, not Sodium
- After roughly 200msec–> Repolarisation, Ca2+ channels close, K+ channels open
- Hyperpolarisation–> K+ channels close, triggers “funny” channels to open again
24
Q
Describe the Action Potential of A Ventricular Myocardial Cell
A
Phase 0: Rapid Depolarisation–> Opening for fast, voltage-gated Na+ channels due to impulse from nearby cells
Phase 1: Na+ channels close, Slow, L-Type Ca2+ channels open
Phase 2: Plateau Phase of Action Potential–> Weak inward flow of Ca2+, balanced by slow outward flow of K+ driven by concentration gradient (refractory period)
Phase 3: Repolarisation–> Ca2+ channels close and Voltage-gated K+ Channels open
Phase 4: Rest Period–> K+ channels close and excess Na+ is removed by Na+/K+ pump
25
Why must there be a refractory period in the Action Potential of a Ventricular Myocardial Cell?
To allow the ventricle to fully contract and relax before the next action potential--> prevents \summation and tetanus in the heart
26
Describe the Conduction Pathway in the heart
SA node--> Internodal Pathways--> AV node--> Bundle of His--> Purkinje Fibres
27
What is the function of the AV node?
1. It is the only means by which excitation can reach the ventricles
2. Delays the impulse by about 100msec--> allows the atria to contract before the ventricles
28
How do we control cardiac output?
We control Heart Rate and Stroke Volume
29
What neurotransmitter does the Sympathetic Nervous System release and where do they act in the heart?
Noradrenaline--> Act on ß1 Adrenoreceptors
30
What is the action of Noradrenaline on the SA Node?
Stimulates Adenylate Cyclase--> Increase cAMP--> cAMP binds to "funny" channels, making them more permeable--> Pacemaker cells will be quicker to depolarise to threshold--> more action potentials--> Increase Heart Rate
31
What is the action of Noradrenaline on the Atria and Ventricles?
Stimulates Adenylate Cyclase--> Increase cAMP--> cAMP increases permeability of calcium--> Greater amounts of calcium in the myocardial cell--> Greater force of contraction--> Increased Stroke Volume
32
What neurotransmitter does the Parasympathetic Nervous System release and where do they act on the heart?
Acetylcholine--> M2 Muscarinic Receptors
33
What is the action of acetylcholine on the SA Node?
Inhibits Adenylate Cyclase--> Decrease cAMP--> Pacemaker cells take longer to depolarise to threshold--? less action potentials--> Decrease Heart Rate
34
What is the action of acetylcholine on the Atria?
Decrease the force of contraction of the atria
35
What is the action of acetylcholine on the ventricles?
Does not inhibit the contraction of the ventricles directly--> the stroke volume is decreased because less blood is pumped into the ventricles from the atria
36
What is Ventricular Escape?
It's when the Ventricle beats at its own slow rate to prevent the heart from completely stopping (when the Atria stops contracting)
37
What is Blood Pressure?
Cardiac Output x Total Peripheral Resistance
38
What is the Baroreflex?
Reflex stimulated by Baroreceptors in response to changes in blood pressure
39
What are Baroreceptors?
They are stretch receptors--> They respond to stretch in the blood vessel wall
40
Where are the Baroreceptors located?
1. Aortic Arch (signals via the vagus nerve)
| 2. Carotid Sinus (signals via Hering's Nerve and the Glossopharyngeal Nerve)
41
What is the Baroreflex in response to an increase in blood pressure?
Increase in Blood Pressure --> Increase Arterial Wall stretch--> Increase Baroreceptor firing--> Vasodilation, decrease heart rate and stroke volume--> Lowers Blood Pressure to normal
42
What is the Baroreflex in response to a decrease in Blood Pressure?
Decrease in Blood Pressure--> Decrease in Arterial Wall Stretch--> Decrease Baroreceptor Firing--> Vasoconstriction, increase Heart Rate and Stroke Volume--> Increase Blood Pressure to normal
43
What is the effect of increased blood tissue demands on cardiac output?
If tissue demands increase--> blood vessels vasodilate to increase blood flow--> TPR decrease and Cardiac Output Increase
44
What is the effect of decreased blood tissue demands on cardiac output?
If tissue demands decrease--> blood vessels vasoconstrict to decrease blood flow--> TPR increase and Cardiac Output decrease
45
What causes pathologically high cardiac output?
Peripheral Vasodilation (decreased TPR)
46
What causes pathologically low cardiac output?
Cardiac damage or low venous return
47
What are the effects of exercise on the cardiovascular system of a fit young adult?
1. Heart Rate increase to 300% resting (200bpm)
2. Stroke Volume Increase to 175% resting (125mL)
3. Cardiac Output increases to 500% resting (25L)
48
What are the effects of exercise on the cardiovascular system of a top athlete?
1. Heart Rate increase to maximum of 200bpm
2. Stroke Volume increases beyond 125mL to 175mL
3. Cardiac Output increases to a maximum of 35L or more
49
In the Frank-Starling Mechanism of the Heart, What is Preload?
The End-Diastolic Volume
50
In the Frank-Starling Mechanism of the Heart, What is after load?
The arterial/total peripheral resistance the ventricle must pump against to eject blood
51
What is the effect on increased Preload on the heart?
An increased preload will lead to increased force of contraction and increased stroke volume because the Cardiac Output must equal Venous Return
52
What is the effect of Afterload in the heart?
Increased Afterload--> Decreased Stroke Volume--> Increased ESV--> Increased EDV--> Increase Force of Contraction--> SV increase back to normal
53
What are the Atrial Reflexes to maintain cardiac output?
1. Baroreflex
2. Sympathetic drive to kidney--> amount of filtration affects blood volume
3. Sympathetic drive to kidney--> RAAS conservation of water affects blood volume
4. Vasopressin Secretion--> Conservation of water is affected
5. Atrial Natriuetic Peptide--> Increases the loss of sodium and water
54
What is the P Wave of the ECG?
Atrial Depolarisation
55
What is the PR-Interval of the ECG
Atrial depolarisation and contraction
56
What is the QRS Complex of the ECG?
Ventricular Depolarisation and Atrial Repolarisation
57
What is the QT interval of the ECG?
Single cycle of Ventricular Depolarisation and Repolarisation
58
What is the ST Interval of the ECG?
Ventricular Contraction
59
What is the T Wave of the ECG
Ventricular Repolarisation
60
What is the TP interval of the ECG
Ventricular Relaxation and Filling
61
How's the ECG Recorded?
From the skin--> The current flows from depolarised to non-depolarised
62
What happens to the ECG when a patient has SA Block?
No P Wave
63
What happens to the ECG when a patient has 1st degree AV Block?
Prolonged PR Interval (0.2s)
64
What happens to the ECG when a patient has 2nd Degree AV Block?
Prolonged PR Interval, missed beats and P:QRS rhythm of 2:1 or 3:2
65
What happens to the ECG when a patient has 3rd Degree AV Block?
Complete block, P and QRS waves are dissociated and have own rhythms
66
What is Stokes-Adam Syndrome?
When a patient has Intermittent complete AV block followed by ventricular escape
67
What causes an Increased Voltage in the QRS complex?
Increased Muscle Mass
68
What causes a decreased voltage in the QRS Complex?
Decreased Muscle mass or damaged muscle (e.g. Myocardial Infarction)
69
What causes Prolonged QRS Complex?
Slow conduction in the ventricles
70
What causes an elevated ST segment?
Acute Myocardial Infarction
71
What is Sinus Rhythm?
Normal SA node rate (HR) of 60-100bpm
72
What is Sinus Tachycardia?
Increased Heart Rate due to Sympathetic Nervous System, Increased Temperature, Cardiac Toxicity
73
What is Sinus Bradycardia?
Decreased Heart Rate at rest sue to overactive Vagus
74
What is Sinus Arrhythmias?
In deep breathing, Increased heart Rate with Inspiration and Decreased Heart Rate with Expiration
75
What are Ectopic Beats?
Premature contractions due to abnormal impulses from abnormal pacemaker sites within the heart outside the SA Node
76
What Starling Forces affect Capillary Filtration?
Outwards: Capillary Blood Pressure, Plasma Protein Colloid Osmotic Pressure
Inwards: Interstitial Fluid Pressure, Interstitial Fluid Colloid Osmotic Pressure
77
What Factors determine Venous return?
1. Pressure gradient to Heart
2. Skeletal Muscle Pump
3. Negative Interthoracic Pressure During Inspiration
4 Venoconstriction
78
What causes Inverted T Wave in the ECG?
Slow conduction through fibres--> Fibres that depolarise first also depolarise first
79
What are causes Premature Ventricular Contractions?
1. Prolonged QRS
2. Increased QRS Voltage
3. Inverted T Wave
4. Anomalous Pathways between Atria and Ventricles
CVR
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