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WP1 - Fainting

Wednesday, 6 March 2013


7:28 PM

Learning Targets
Medical Science
• What is the structure of the heart? (review and extend Year 1)
○ Pericardium
 Membrane surrounding and protecting the heart
 Fibrous pericardium
□ Tough connective tissue
□ Attached to the diaphragm and great vessels
□ Prevents the overstretching of the heart
 Serous pericardium
□ Double layer
□ Between a layer of serous fluid
○ Layers
 Epicardium
 Myocardium
□ 95% of heart
□ Cardiac muscle
 Endocardium
□ Thin layer of endothelium
□ Smooth lining
□ Continuous with endothelial lining of blood vessels
○ Chambers of the heart
 4 - left and right atria and ventricles
 Atria
□ Smooth posterior walls
□ Right atrium - rough anterior wall, left atrium both walls are smooth
□ Between the right and left there is an interatrial septum
 Ventricles
□ Contains trabeculae carnae
□ Papillary muscle attach chordae tendinae to the walls
○ Main Vessels
 Superior Vena cava
□ Returns deoxygenated blood from head
□ Opening in the upper back of the right atrium
 Inferior vena cava
□ Larger than the SVC
□ Return deoxygenated blood from the lower half of the body
□ Backwards and upwards
□ Guarded by a semilunar valve
 Aorta
□ Sends oxygenated blood to body
□ From upper left ventricle
 Pulmonary trunk
□ Deoxygenated blood from right ventricle
 Pulmonary veins
□ Transport arterial blood to left atrium
□ There are 4 left, right, superior, inferior
□ No valves

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• What controls heart rate and the muscle pump? (review and extend year 1)
○ Intrinsic mechanism of the heart - Frank-Starling Mechanism
 Amount of blood pump is determined by venous return
 The greater the muscle is stretched by filling the greater the force of contraction
and amount of blood pumped into the aorta
 Stretch of atrial wall results in the increase of heart rate by 10-20%
○ Nervous control of the heart
 Sympathetic
□ Can increase the heart rate from 70 bmp upto 180-200 bpm
□ Can increase the force of contraction by almost double
□ 2-3x the cardiac output
□ Sympathetics keep the resting heart rate up to 30% higher than withough
□ The inhibition of sympathetics can decrease heart rate and cardiac output
by almost 30%
 Parasympathetics
□ Strong stimulation can stop the for a few seconds
□ Then the heart over comes and beats 20-40bmp as long as the
parasympathetic stimulation continues
□ Vagal fibres distributed mainly to atria
 Decreases the heart rate rather than the force of contraction
 Can decrease by 50% or more
 Temperature
□ Increased body temperature increases heart rate
□ Decreased body temperature decreased heart rate

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Decreased body temperature decreased heart rate

• How does the electrical activity of the heart relate to the muscle pump? (cf APs, ionic
changes and excitation-contraction coupling?
○ Ventricular Action Potential
 Phase 4
□ Resting potential
 Phase 0
□ Following the opening of Na+ channel - dramatic influx of positive ions in the
cells
□ Leads to rapid change in the transmembrane potential which moves
from -90mV and +20mV
□ Depolarisation
 Phase 1
□ Na+ channel does not remain open for long as it a voltage fated channel and
closed by the changed transmembrane potential
□ K+ transient outwards channel opens allowing K + out of the cell
□ Transmembrane potential moves towards 0
 Phase 2
□ Change in potential causes L-type Ca2+ to open
□ Ca2+channel remains open longer than Na+ channel
□ Prolonged depolarized state of muscle cell membrane to plateau
□ Rise in intracellular Ca2+ causes contraction of myofibrils within the myocyte
through process of excitation coupling
 Phase 3
□ High concentration of Ca2+ also leads to the opening of several K+ channels
□ As K+ leaves the cell transmembrane gradient becomes increasingly negative
which closes the L-type Ca2+ channels and repolarisation of myocyte
membrane
○ Excitation-Contraction coupling
 Action potentials trigger muscular contraction
 At rest free intracellular Ca2+ is <0.1 µmol/L
□ Not a true reflection of the concentration of Ca2+ ions in the myocyte
 Following opening of L-type Ca2+ channels there is a release of Ca2+ from the
sarcoplasmic reticulum
 After the release from the sarcoplasmic reticulum, free intracellular Ca 2+
concentration can rise thousandfold to around 100µmol/L
□ Binds to troponin complex and activation of the actin-myosin complex which

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□ Binds to troponin complex and activation of the actin-myosin complex which
results in muscle contraction
 Amount of Ca2+ entering a cell is small but essential in order to
□ Triggering the sarcoplasmic reticulum
□ Maintaining adequate levels of Ca2+ in intracellular stores over time
 Closure of L-type channels leaces a high intracellular concentration of Ca2+ permits
continuing activation of the actin-myosin complex
 For myofibril contraction to cease, free Ca2+ concentration needs to be below 0.1
µmol/L
 Achieved by:
□ Uptake by sarcoplasmic reticulum
 Approximately 80% is taken back by Ca2+/ATPase pumps
 The action of the pumps is regulated by phospholambin (protein)
which increases the rate of Ca2+ resequestration
□ Extrusion of Ca2+ from the cell
 Remaining 20% by either Ca2+/Na+ or Ca2+/ATPase pumps
 Powered by Na2+ gradient which is maintained by Na+/K+ pump - which
is electrogenic
 Na+ ions returned to interstitial fluid while extracellular K+ ions are
pumped back ioto the cell so re-establishing the transmembrane
potential

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• What is the structure and function of cardiac muscle?
○ Intermediate between cardiac and smooth
○ Muscle fibres
 Long cylindrical cells
 One or two centrally located nuclei
 Ends of fibers split into a number of branches
○ Intercalated discs
 Specialised junctions between cardiac muscle cells
 Functions
□ Hold walls together
□ Anchor myofibrils to transmit contract(?)
□ Provide areas of low electrical resistance
○ Sarcoplasmic Reticulum
 Only responds to nerve stimulation
 Action potential down T-tubules into muscle induces depolarisations
 Initiate cross-bridge cycling
○ Key muscle contractile protein

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Professional Practice
• What is syncope OR Why do people faint?
○ Sudden loss of consciousness caused by inadequate cerebral blood flow
○ Presyncope symptoms
 Dizziness
 Feeling of warmth
 Diaphoresis (sweating)
 Light-headedness
 Nausea
 Visual blurring
○ Cardiovascular causes of syncope:
 Vascular
□ Vasovagal neurogenic) syncope
 Most common cause of syncope
 Emotional disturbances
 Recovery is usually within a few seconds - person lies down
 Frequently recurrent, precipitated by:
◊ Hot
◊ Crowded
◊ Alcohol
◊ Fatigue
◊ Severe pain
◊ Hunger
◊ Prolonged standing
◊ Emotional or stressful situations
 Postural (orthostatic)
□ Happens due to a change in position and systolic pressure drops 20mmHg or
more
□ Causes include
 Physical deconditioning
 Patients who have anti-hypertensives, vasodilators or hypovolaemia
 After sympathectomy as the vasopressor reflexes are abolished
 Post-prandial hypotension
□ Drop in systolic blood pressure of 20mmHg within 2 hours of eating
 Micturition Syncope
□ Loss of consciousness usually occurs at night or after voiding urine
 Carotid sinus syncope

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 Carotid sinus syncope
□ Hypersensitivity occurs in men >50
□ Occurs when
 Tight collar
 Looking up
 Turning head
 Obstructive
□ Restriction from the heart to the rest of the circulation between different
chambers
□ Causes:
 Aortic stenosis
 Hypertrophic cardiomyopathy
 Pulmonary stenosis
 Pulmonary hypertension/embolism
 Defective prosthetic valve
□ Arrythmias
 Rapid tachycardia
 Profound bradycardia
 Artificial pacemaker failure
• How do you investigate a patient with syncope who has passed out/fainted?
○ History
 Onset - gradual or sudden
 Character - lose consciousness
 Timing - duration, recovery
 Exacerbating factors - actions, emotional stress
 Previous occurences
 Current treatment
 Differential diagnosis
 Family history
○ Red flags
 Chest pain
 Exertational onset
 Dyspnea
 Lower back pain
 Severe headaches
 Palpitations
 Visual impairment
 Ataxia
 Slurred speech
○ Physical Examination
 Take heart rate and blood pressure while standing, sitting and supine
 Vital signs
 Lung sounds
 Examination of carotid and jugular
 Neurological exam
 Trauma
○ Lab studies to find specific cause
 Serum glucose - hypoglycaemia
 Complete blood count - GI hemorrhage
 Serum electrolytes - hyponatremia
 Cardiac enzyme - myocardiall ischaemia
 Total Creatine Kinase - prolonged seizure
 Unrinalysis - UTIs
○ Imaging
 Chest radiography
 Head CT scanning
 Chest/abdominal CT
 Brain MRI/ Magnetic resonance arteriography

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 Brain MRI/ Magnetic resonance arteriography
 Ventilation - perfusion
 Echo cardiography
○ Other tests
 Electrocardiography
 Halter monitor/ loop even recorder
 Head up tilt table test
 Electroencephalography
 Stress test
 Cardiac stress test
 Carotid sinus massage
• What drugs affect the function of the heart and how? (general classes B-Blockers, Ca-
channel blockers, stimulants (legal and illegal)
○ Beta blockers
 Beta agonists
□ Adrenaline
□ Beta 1 - dobutamine
□ Beta 2 - salbutamol
□ Terbutaline
 Tachycardia side effect
 Beta antagonists
□ Blocks noradrenaline competitively
□ Used in treatment of cardiac problems (hypertension, arrythmias)
□ Metoprolol, atenolol
○ Calcium channel blockers
 Block cellular entry of calcium
 Therapeutically important blockers act on L-type channels
 L-type agonists exist in 3 classes
□ Phenylalkylamines (veranapril)
 Primarily affects the heart
 Antidysrhythmic effect
□ Dihydropyridines (nifedopine)
 Affects smooth muscle more than the heart
 Profound vasodilation
□ Benzothiazepines (Diltiazem)
 Intermediate effect
○ Pseudoephedrine
 Mimics actiob if sympathetic nervous system
 Acts indirectly on alpha adrenergic receptors
 Results in vasoconstriction
 Uses
□ Decreases blood flow to the nose - decreaseing inflammation and secretion
○ Ecstasy (MDMA)
 Mimics amphetamines
 Amphetamines
□ Related noradrenaline
□ Able to be transmitted in to nerve terminals
□ Displaced noradrenaline escapes into the cytosol stimulating post-synaptic
receptors
○ Caffeine
 Enhances vagal stimulation in low doses
 High doses increase heart rate and cardiac output
 Overstimulation leads to tachycardia and cardiac irregularities
 In high doses it is a vasoconstrictor
 In low doses it is a vasodilator
○ Alcohol
 Depression of vasomotor neurons in medulla
□ Rapid heat loss

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□ Rapid heat loss
 Decreased ADH which leads to dehydration
 Overall CNS depression
○ Adenosine
 Effects:
□ Breathing
□ Cardiac Muscle
□ Afferent nerves
□ Platelets
□ Cardiac conducting tissue
 Administered via IV causes and AV node block
 Alpha 1 receptor is responsible
□ Binds to conducted receptors
□ Transiently slows SA nodal stimulation and decreases AV nodal conduction
• What is an ECG and how is it interpreted?
○ ECG - electrocardiogram
○ Recording of the electrical activity of the heart
○ Usually 12 lead which means that there are 12 different views of the heart
 Normal leads are
□ Right Arm
□ Right Leg - only as a ground to stop AC interference
□ Left Arm
□ Left leg
□ aVR
□ aVF
□ aVL
□ Leads I-VI are on the chest
○ Interpreting ECGs
 Rate
□ Count the number of big spaces between successive R-waves and divide into
300
□ Or count the number of little squares between successive R-waves and
divide into 1500
□ Normal is between 50 to 100
 <50 is bradycardia
 >100 is tachycardia
 Rhythm
□ Regular or irregular
□ Consistent ireegularity or completely irregular
 P-waves
□ Represents the depolarisation of the atria
□ Presence is important
 Duration: less than 2 1/2 little squares or 0.1 seconds
 Amplitude: less than 2 1/2 squares or 0.1 seconds
 Duration of P-R total : 3-5 squares or 0.12-0.25 seconds
 QRS complex
□ Represents depolarisation of centricles
 If there is an initial first downwards deflection it is a Q-wave
 First upwards is called an R-wave
 Any deflection below the baseline after an R wave is an S-wave
□ Duration is <0.1s
□ Amplitude is the Cornell criteria
 S-T segment
□ Between QRS complex and T-wave
□ Begins at the J-point
 Isoelectric with a slight upwards slope
 T-wave
□ Ventricular repolarisation

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□ Ventricular repolarisation
□ Generally 1/8<T-wave<2/3 size of preceding R-wave
□ Axis within 45 degrees of the QRS complex
• What is the emergency management of syncope? (revise coma position from Sem 1 year 1)
○ Treatment
 Assist to ground to prevent injury
 If responsive, leave casualty lying flat
 If unresponsive, immediately place into position and observe DR S ABCD
 Loosen tight clothing at waist/neck
 Do not give anything to eat or drink
 Advise casualty to seek medical assistance

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