Download Peer Teaching Cardio

Phase 1A
Andrew Hu + Elaine Pang
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Aims and Objectives
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The tiniest amount of heart anatomy
Activation and Contraction
Cardiac Cycle
Control of MAP
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Anatomy
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Anatomy
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Sino-atrial node
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Called the pacemaker
P-wave
Located in the right atrium
Transmits across both atria
Transmission goes to AV node
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Atrioventricular node
• Specialised myocytes
• Base of the right atrium
• Transmit impulse deliberately
slowly (0.1s)
• Purely there to allow for atrial
contraction
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Atrioventricular node
• Impulse then travels down the
IVS
– Initially as AV bundle (His)
– Splits into RBB and LBB
• Splits into the Purkinje fibres at
base of ventricles
• Spreads upwards and outwards
– Contract from base
– 20-40 bpm
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Actin and Myosin
Troponin C – calcium
binds to cause
conformational change
in Troponin I
Troponin T – Binds to
tropomyosin forming a
tropomyosin troponin
complex
Troponin I – binds to
actin, to hold the
tropomyosin – troponin
complexes in place
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Contraction
1. Excitation
2. L Type Ca channels in T tubules open causing
influx of Ca
3. Ca binds to sarcoplasmic opening lateral sacs
releasing more Ca
4. Ca binds to TnC moving tropomyosin
5. Allows energized myelin to bind to actin
6. Repolarization and Ca reuptaken
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Myocyte Contraction
Energised cross-bridge binds to actin
Cross-bridge moves
ATP binds to myosin → cross bridge detaches
Hydrolysis of ATP → cross-bridge becomes
energised
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Events of the Cardiac Cycle
VENTRICULAR FILLING (DIASTOLE)
• Passive filling of the ventricles – Ventricular volume and pressure increases
• AV valves are open
• Semi lunar valves are closed
ISOVULUMETRIC CONTRACTION (SYSTOLE)
• Ventricular pressure> Atrial pressure
• Causing the AV valves to close
EJECTION (SYSTOLE)
• Ventricular pressure> Atrial pressure
• Causing the semi lunar valves to open.
ISOVOLUMETRIC RELAXATION (DIASTOLE)
• Both semi lunar and AV valves are closed
• When ventricular pressure < atrial pressure, AV valves open
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http://www.beltina.
org/pics/cardiac_cy
cle.gif
Heart Sounds
• Four heart sounds.
• Usually only the first two can be heard –
‘LUBB DUBB’
• 1st heart sound = due to the closure of the AV valves
• 2nd heart sound = due to the closure of the semi lunar valves
• 3rd heart sound = due to the sudden rapid flow of blood into
the ventricles during diastole
• 4th heart sound = due to the flow of blood into the ventricles
due to atrial contraction
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ECG Representation
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Mean Arterial Pressure
MAP = the average arterial blood pressure over
an entire cardiac cycle
Mean
Arterial
Pressure
(MAP)
=
Cardiac
Output
(CO)
x
Total
Peripheral
Resistance
(TPR)
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Cardiac Output
CO = the volume of blood each ventricle pumps
Therefore, CO = the volume of blood flowing
through either the systemic (or pulmonary)
circuit per minute
Cardiac
Output
(CO)
=
Heart
Rate
(HR)
x
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Stroke
Volume
(SV)
Total Peripheral Resistance
TPR = the sum of the resistances to flow offered
by all the systemic blood vessels
The arterioles are the principle site of resistance
to vascular flow (their radii can be changed by
vascular smooth muscle contraction/relaxation)
Therefore, TPR is essentially the same as the
Total Arteriolar Resistance
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So, to summarise…
Heart
Rate
(HR)
Stroke
Volume
(SV)
Total
Peripheral
Resistance
(TPR)
Cardiac
Output
(CO)
Mean
Arterial
Pressure
(MAP)
Sensors of MAP
Arterial baroreceptors
• Stretch-sensitive
receptors
• Blood vessel wall stretch
→ pressure within blood
vessel
• Located in the carotid
sinus and aortic arch
• Send neurons to the
Medullary Cardiovascular
Centre
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Arterial Baroreceptor Reflex
↑ MAP
↓ MAP
↑ Arterial Baroreceptor Firing
↓ Arterial Baroreceptor Firing
Medullary Cardiovascular Centre
Medullary Cardiovascular Centre
↓ MAP
↑ MAP
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Effectors of MAP
Heart
Rate
(HR)
Stroke
Volume
(SV)
Total
Peripheral
Resistance
(TPR)
Cardiac
Output
(CO)
Mean
Arterial
Pressure
(MAP)
Effectors of CO
Heart Rate (HR)
• Activity of sympathetic
nerves to heart
• Activity of parasympathetic
nerves to heart
• Plasma adrenaline
Stroke Volume (SV)
• Activity of sympathetic
nerves to heart
• Plasma adrenaline
• End-diastolic ventricular
volume (preload)
– Dependent on venous
pressure
Effectors of TPR
Vasoconstrictors (↑ TPR)
• Local
– Endothelin-1
• Neural
– Sympathetic nerves
• Hormonal
– Adrenaline
– Anti-Diuretic Hormone
– Angiotensin II
Vasodilators (↓ TPR)
• Local
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–
–
↓ O2 (hyperaemia)
CO2
NO
Inflammatory mediators
• Neural
– Neurons that release NO
• Hormonal
– Atrial Natriuretic Peptide
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