Phase 1a
Lauren Barker and Chiara Beck
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Aims
• Anatomy
– Surface Anatomy
– Heart Borders
• Physiology
– Muscle Contraction
• Filaments
• Action Potential
– Cardiac Cycle
• Nodes
– Regulation of MAP
• Effectors of CO and TPR
• Baroreceptors and Chemoreceptors
The Peer Teaching Society is not liable for false or misleading information…
Aims
• Anatomy
– Surface Anatomy
– Heart Borders
• Physiology
– Muscle Contraction
• Filaments
• Action Potential
– Cardiac Cycle
• Nodes
– Regulation of MAP
• Effectors of CO and TPR
• Baroreceptors and Chemoreceptors
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Surface Anatomy
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Surface Anatomy
Location: L 3rd IC
space
Auscultation:
Right sternal
edge, 2nd IC
space
Location: L 3rd
CC
Auscultation: L
2nd IC space
Location: R 4th
IC space
Auscultation: R
5th IC space
Location: L 4th
CC
Auscultation:
APEX L 5th IC
space, midclavicular line
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Borders of the Heart
Superior: R 3rd
CC  L 2nd CC
Anterior:
sternocostal
surface
Left: 2nd IC
space, 2/3cm
from midline
 apex
Right: 3rd 
6th CC (2/3cm
from midline)
Inferior: Sternal
6th CC  apex
AKA
diaphragmatic
surface
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Aims
• Anatomy
– Surface Anatomy
– Heart Borders
• Physiology
– Muscle Contraction
• Filaments
• Action Potential
– Cardiac Cycle
• Nodes
– Regulation of MAP
• Effectors of CO and TPR
• Baroreceptors and Chemoreceptors
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Physiology – Cardiac Contraction
• Different to normal
muscle contraction
– Extracellular calcium
ions
– Sustains depolarisation
of cardiac muscle cells
for longer
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Physiology – Sarcoplasmic Reticulum
The sarcoplasmic
reticulum is the
membrane
network that
surrounds the
contractile
proteins.
Consists of
sarcotubular
network at the
centre and the
subsacrolemnal
cisternae.
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Physiology – Contraction
• Sliding of actin over myosin by ATP hydrolysis
through the action of ATP-ase in the head of
the myosin molecule.
• When Ca2+ floods in, it binds to troponin,
therefore moving tropomyosin off actin,
exposing the binding sites.
• The head of the myosin molecule forms
crossbridges that interact with actin.
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Physiology – Contraction
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Physiology – Thick Filaments
• Myosin:
– 2 heavy chains – alpha and beta myosin heads
– 4 light chains
– Perpendicular at rest
– Bends towards the sarcomere centre during
contraction
– Hydrolyses ATP, interacts with actin
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Physiology – Thin Filaments
• Actin:
– Globular protein
– Double stranded helix
– Both form F actin
– Activates myosin ATP, interacts with myosin
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Physiology – Thin Filaments
• Tropomyosin:
– Elongated molecule made of 2 helical peptide
chains
– Regulates interaction!!
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Physiology – Thin Filaments
• Troponin:
– TnI: inhibits actin and myosin binding
– TnC: Ca2+ binding sites
– TnT: binds troponin to tropomyosin
– TnC drives away TnI allowing interaction
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Physiology – Myosin ATP-ase
• ATP binds to the myosin head inducing a small conformational
shift in the actin-binding site which reduces its affinity for
actin causing the myosin head to release the actin filament.
• This causes the myosin head to ‘cock back’ into place. ATP is
then hydrolysed leaving ADP and Pi bound to the myosin.
• Weak interactions with actin cause the myosin to release the
Pi which triggers the ‘power stroke’.
• As myosin attaches, the ADP is released and it binds tightly to
the actin.
Rigor Mortis: lack of ATP, therefore the myosin cannot detach from the actin,
meaning the muscles stay contracted.
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Physiology – Action Potential
•
•
•
•
•
4
resting membrane
potential (diastole)
0
depolarisation
1
transient outward
partial repolarisation
2
plateau
3
repolarisation
Hypocalcaemia?
Reduced refractory
period
Tetany: spasms of
the hands, feet,
larynx, and cramps.
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Aims
• Anatomy
– Surface Anatomy
– Heart Borders
• Physiology
– Muscle Contraction
• Filaments
• Action Potential
– Cardiac Cycle
• Nodes
• Cycle
– Regulation of MAP
• Effectors of CO and TPR
• Baroreceptors and Chemoreceptors
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Physiology – Conduction System
• SA node:
• Located near the entrance of the
SVC
• “Pacemaker”
• AV node:
• Located in the bottom of the
right atrium
• Only electrical connection
between the atrium and ventricle
• Slow propogation
• Bundle of His
• Purkinje fibres
• Distributes the impulses
throughout the ventricles
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Physiology – Cardiac Cycle
3 main events:
• LV contraction
• LV relaxation
• LV filling
Preload: load present before LV
contraction has started
Afterload: load after the ventricle starts
to contract
Sounds:
• “Lub” – low pitched, closure of AV
valves, marks onset of systole
• “Dub” – louder, closure of semilunar
valves, marks onset of diastole
The Peer Teaching Society is not liable for false or misleading information…
Aims
• Anatomy
– Surface Anatomy
– Heart Borders
• Physiology
– Muscle Contraction
• Filaments
• Action Potential
– Cardiac Cycle
• Nodes
– Regulation of MAP
• Effectors of CO and TPR
• Baroreceptors and Chemoreceptors
The Peer Teaching Society is not liable for false or misleading information…
Physiology – Regulation of MAP
Average arterial blood
pressure over a total
cardiac cycle
The sum of resistances
to flow offered by all
systemic blood vessels
MAP = CO X TPR
The volume of
blood each
ventricle pumps
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Physiology – Effectors of CO
• Increase in sympathetic innervation to heart 
INCREASE in BP
• vasoconstriction
• increased myocardial contractility
• increase plasma adrenaline
• Affects Heart Rate (HR) and Stroke Volume (SV)
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Physiology – Effectors of TPR
• Vasodilators (decrease in TPR):
• NO
• CO2
• decrease in O2
• Inflammatory mediators
• ANP (hormonal)
• Vasoconstrictors (increase in TPR):
• Sympathetic nerves
• ADH
• Angiotensin II
• Adrenaline
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Physiology – Arterial Baroreceptors
• Stretch-sensitive receptors found in wall of carotid sinus
and aortic arch
• Send neurons to medullary cardiovascular centre in brain
• Key role in short-term regulation eg exercise
• If becomes long term then adopt a new base line pressure
• Main control in long-term BP regulation is blood volume.
• FEEDBACK LOOP
• Sensitivity is affected by sympathetic
stimulation/hypertension
Carotid sinus: glossopharyngeal nerve (CN 9) – more sensitive as going to brain
Aortic arch: vagus nerve (CN 10)
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Physiology – Arterial Baroreceptors
Stimulus
Decreased sympathetic
outflow to kidneys
Increased
renal blood
flow and urine
Increased
sympathetic
outflow to SA node
Increased heart rate
(HR)
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Physiology – Chemoreceptors
• Small highly vascular bodies in the aortic arch and medial
to carotid sinus.
• Stimulated by a fall in O2 and pH/increase in CO2
• Involved in the control of respiration and reflex 
vasoconstriction
• Less important than baroreceptors in the control of
circulation
• CO2 and pH affect peripheral; O2 affects central
• Increase in CO2  vasoconstriction, increase in PR
and BP
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Pathology
•
•
•
•
•
•
Atherosclerosis
Heart failure
Thromboembolism
Shock
Myocardial infarction
Arrhythmias:
– ECG
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Atherosclerosis
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Atherosclerosis
1.
2.
3.
4.
5.
6.
7.
Endothelia injury – increased permeability.
LDL forms fatty streaks.
Monocytes attracted  macrophages.
Take up oxidised LDL to form foam cells.
Adhesion of platelets to endothelium.
Release cytokines and GF.
Migration of smooth muscle cells from media
to intima  stabilize growing region.
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Complications
• Plaque rupture: fibrous plaque ruptures
exposing cholesterol etc.
• Strong clotting reaction in blood.
•
•
•
•
Angina
Intermittent claudication
MI
Stroke
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Heart Failure
• Definition: heart is unable to pump enough blood to
satisfy needs of metabolizing tissues.
• Breathlessness
• Tiredness
• Fatigue
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Heart Failure
• CAUSES:
– Myocardial dysfunction
– Volume overload
– Obstruction to outflow
– Compromised ventricular filling
– Altered rhythm
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Right Heart Failure
• Symptoms:
– Swollen ankles
– Fatigue
– Anorexia
• Signs:
–
–
–
–
Raised jugular venous pressure
Hepatomegaly
Pitting oedema
Ascitis
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Left Heart Failure
• Symptoms:
– Fatigue
– Breathlessness
– Dyspnoea, orthopnoea, paroxysmal nocturnal
dyspnoea.
• Signs:
–
–
–
–
Cardiomegaly
Added heart sounds
Tachycardia
Crackles in lung bases
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Congestive Heart Failure
• Mixture of both left and right.
• Almost always right secondary to severe left
heart failure.
• Cor Pulmonale?
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Thromboembolism
• Thrombus: blood clot forming inside vessel wall.
• Thromboembolism: obstruction of a blood vessel by
a dislodged blood clot.
• Embolus: detached, travelling, intravascular mass:
Examples: cholesterol, fat, air (gas) and tissue
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Thromboembolism
Stasis
Vessel Wall
Blood
Constituent
s
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Thromboembolism
Arterial Venous
Characteristics
High pressure
Platelet rich
Low pressure
Fibrin rich
Examples
MI
Stroke
Treatment
Antiplatelets
DVT
Pulmonary
Embolism
Anticoagulants
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Shock
• Definition: failure of cardiovascular system to
adequately perfuse tissues.
• Hypovolaemic shock
• Distributive shock:
– Septic
– Anaphylactic
• Cardiogenic shock
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Shock
• Symptoms:
–
–
–
–
–
Faintness
Dizziness
Sweating
Pallor
Reduced level of consciousness
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Shock
• Signs:
–
–
–
–
–
–
Pale, cold, clammy skin
Rapid, weak pulse
Tachycardia, decreased stroke volume
Rapid, shallow breathing
Impaired urine output
Confusion
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Hypovolaemic Shock
• Fall in circulating blood volume: blood or fluid.
• Loss of blood:
–
–
–
–
Trauma
Acute GI bleed
Haemorrhage
Operations
• Loss of fluid:
–
–
–
–
–
Severe burns
Dehydration
Pancreatitis
Vomiting
Diarrhoea
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Hypovolaemic Shock
• Class I-III: increasing in severity:
– Pulse increases
– Respiratory rate increases
– Urine output decreases
– Mental status declines
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Cardiogenic Shock
• ‘Pump Failure’
• Interruption of cardiac function.
• Heart unable to maintain circulation.
–
–
–
–
–
–
MI
Cardiac tamponade
Myocarditis
Pulmonary embolism
Valve failure – endocarditis
Fluid overload – poor left ventricular function
• Obstructive shock?
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Septic Shock
• Sepsis: systemic inflammatory response
associated with an infection.
• Septic shock: sepsis complicated by persistent
inappropriate hypotension.
• Unresponsive to fluid resuscitation.
• Treatment with vasoconstrictors.
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Anaphylactic Shock
•
•
•
•
•
•
Hypersensitivity reaction.
Massive release of histamine.
Peripheral vasodilatation – hypotension.
Vascular permeability – loss of plasma.
Bronchial muscle contraction – dyspnoea.
Oral, laryngeal and pharyngeal oedema.
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Myocardial Infarction
• Definition: necrosis of heart muscle due to
impaired oxygen supply.
• Usually occlusion of coronary artery by
unstable atherosclerotic plaque.
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Myocardial Infarction
• SYMPTOMS:
– Chest pain
– Radiates to neck and arm
– Shortness of breath
– Sense of anxiety
– Profuse sweating
– Nausea
– Vomiting
– Light-headed
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Myocardial Infarction
• Consequences:
– Arrhythmia
– Heart failure
– Pericarditis
– Rupture:
• Muscle
• Walls
• Valves
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Coronary Arteries
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Coronary Arteries
Left Coronary Artery
Right Coronary Artery
• Left posterior aortic sinus.
• Behind pulmonary trunk.
• Circumflex: left AV groove.
• LAD: diagonal arteries.
• Right anterior aortic sinus.
• Right AV groove.
• Posteriorly in sulcus on diaphragmatic
base.
• Posterior descending artery in IV groove.
• Left atrium
• Most of left ventricle
• Part of right ventricle
• Most of IV septum
• SA node (40%)
• AV node (10%)
• Right atrium
• Most of right ventricle.
• AV septum.
• SA node (60%)
• AV node (90%)
Widow Maker?
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ECG
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Arrhythmias
• Definition: abnormality of cardiac rhythm.
– Sudden death
– Syncope
– Dizziness
– Palpitations
– No symptoms
• Bradycardia: <60bpm
• Tachycardia: >100bpm
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Atrial Fibrillation
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Heart Block
• First degree:
– Delayed AV conduction.
– Prolonged PR interval: >0.22s
• Second degree:
– Some atrial impulses fail to reach ventricles.
– Some P waves followed by QRS complex.
• Third degree:
–
–
–
–
Complete heart block.
All atrial activity fails to reach ventricles.
No association between atrial and ventricular activity.
P waves and QRS complex occur independently.
• Bundle branch block: loss of synchronized ventricles.
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Cardiovascular Therapeutics - Antiplatelets
ASPIRIN
• NSAID
• Decreased prostaglandin
synthesis
• Decreased platelet
aggregation
• Causes gastric ulceration
• Causes bleeding
• Need to know
Clopidogrel/prasugrel AND
GP IIb/IIIa antagonists
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Cardiovascular Therapeutics - Thrombolytics
STREPTOKINASE
• Plasminogen  plasmin
• Plasmin destroys
clots/thrombus
• 1% risk of stroke
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Cardiovascular Therapeutics Anticoagulants
WARFARIN
• Anticoagulant
• Inhibits vitamin K
dependant synthesis of
coagulation factors II, XII, IX,
X
• Takes time to work (2-3
days)
• Bleeding
• Need to learn LMW
heparin/fondaparinux
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Cardiovascular Therapeutics – Hypertension
Drugs
ACE INHIBITORS
• - pril
• Act on the RAA system
• eg Ramipril
ß – BLOCKERS
• Beta-1 receptors in myocardium
• Lowers heart rate, CO, LV contractility, oxygen demand =
lower BP
• Beta-2 receptors in smooth muscle, therefore
contraindicative in asthmatics
• Need to know calcium channel blockers, loop/thiazide
diuretics, aldosterone antagonists, nitrates, digoxin,
angiotensin receptor blockers, etc
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Cardiovascular Therapeutics – Cholesterol
Lowering Drugs
STATIN
• Used to prevent hyperlipidaemia
• Reduces the formation of atherosclerotic plaques
• - statin
• eg simvastatin
Drug that can be used for pulmonary hypertension if all else fails?
Viagra – vasodilator, relaxes arterial wall therefore reducing resistance and
pressure
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Topics we didn’t cover
• Blood disorders (RBC + WBC)
• Haematology (blood groups)
• Cardiovascular genetics
• Detailed cardiovascular histology
• Don’t forget veins!
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Tips
• Histology – PDF
• Revise from lectures!!!
– Recommended reading?
• Past papers!!!
• Formative assessments
• Arteries and nerves!
– If all else fails – recurrent laryngeal.
• Public health, stats, screening!
• Definitions!!
• Handwrittentutorials.com
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