Phase 1a
Miles BenjaminDaniel Bradbury
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1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
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Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
The Peer Teaching Society is not liable for false or misleading information…
Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
Muscle
• Action potential arrives at sarcomere.
• Opening of Ca2+ channels.
• Influx of calcium ions.
• Initiates muscle contraction.
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• Three types of troponin:• Troponin C – calcium binds to cause a
conformational change in Troponin I.• Troponin T – binds to tropomyosin, forming a
tropomyosin – troponin complex.• Troponin I – inhibtory binds to actin, to hold
the tropomyosin – troponin complexes in place.
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Troponin
• Contraction of involuntary striated muscle.– Controlled by Ca2+
– Increase in concentration causes contraction
• Sliding filament theory
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Cardiac Contraction
• Contraction of the left and right atria.– blood pressure in
atria increases forcing blood into the ventricles.
– begins with the onset of the ‘P’ wave on ECG
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Atrial Systole
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Ventricular Systole• Ventricular systole is the
contraction of the left and right ventricles.
• Blood is forced out of the pulmonary and aortic valves
• “Lubb – Dub”– Lubb is the closure of AV
valves at beginning of ventricular systole.
– Dub is the closure of aortic and pulmonary at end of ventricular systole.
• QRS complex
Diastole• When do coronary arteries perfuse heart
tissue with blood?• Diastole!• In diastole the heart is in an mostly un-
contracted state• As pressure drops in ventricles, AV valves
open. Blood begins filling chambers again.
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Leaving the heart• Cardiac Output
CO = SV x HR• SV = Stroke Volume• HR = Heart Rate• 5+ litres a minute• Are ventricles pumping effectively?
• P wave– Atrial depolarization, SA node towards the AV
node, spreads from the right to left atrium.
• QRS complex– Rapid depolarization of the right and left
ventricles. Larger muscle so larger amplitude.
• T wave– Repolarisation of the ventricles.
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Main waves
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
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Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
• Definition– The average arterial blood pressure over the
entire cardiac cycle
• Formula?
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Mean Arterial Pressure
• Definition– The average arterial blood pressure over the
entire cardiac cycle
• Formula?
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Physiology
MeanArterial
Pressure (MAP)
CardiacOutput
(CO)
TotalPeripheralResistance
(TPR)
= x
• Definition– Volume of blood ejected by each ventricle per
minute
• Formula?
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Cardiac Output
• Definition– Volume of blood ejected by each ventricle per
minute
• Formula?
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Physiology
CardiacOutput
(CO)=
Heart Rate(HR)
xStroke Volume
(SV)
• Definition– Total resistance to flow of blood by all systemic
blood vessels
• Which level of blood vessel offers the most resistance?• Arterioles offer the most resistance to vascular
flow as they can be changed by vasoconstriction or vasodilation
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Physiology
• Controlling TPR– Locally
• Active hyperaemia ↑ demand by organ = vasodilation• Flow autoregulation ↓ supply to organ =
vasoconstriction
– Extrinsic• Autonomic nervous system • Hormones whole host of vasodilators/constrictors
– NO
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Physiology
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
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Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
• Definition- Formation of plaques in the intimal
layer of medium to large sized arteries. HARDENING OF THE ARTERIES
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Atherosclerosis
• PathophysiologyLDL oxidation → macrophages & lymphocytes to absorb oxidised LDL → foam cells. White cells
cannot process oxidised LDLs → inflammation & continuation of cycle. Fatty streak → fibrous plaque → atherosclerotic plaque
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Atherosclerosis
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Atherosclerosis• Risk Factors
– Age– FH– Obesity– Male– Smoking– Diabetes Mellitus – Hyperlipidaemia– Hypertension
• Angina• Claudication• MI• Aneurysm
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Outcomes of Atherosclerosis
• Atherosclerosis of coronary arteries• Pathophysiology
– Increased demand without proportional increase in oxygen supply
• Clincal Features– SOB, Nausea, Fatigue, Chest Pain
• Stable vs. Unstable
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Angina
• Diagnosis– ECG (ST depression), exercise tolerance,
coronary angiogram
• Treatment– Immediate= GTN Spray– Long Term= ????????
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Angina
• Diagnosis– ECG (ST depression), exercise tolerance,
coronary angiogram
• Treatment– Immediate= GTN Spray– Long Term= Statins, Beta Blockers,
Antiplatelets:ACE inhibitors, Calcium Channel blockers
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Atherosclerosis – Angina
• Complete blockage of coronary artery• Clinical Features
– Severe crushing chest pain, Dyspnoea, Nausea, Sweating, Feeling of terror
• Diagnosis– ECG, Bloods, Raised Cardiomyocyte
• Treatment– Antiplatelet, BB,Statins, PCI
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Atherosclerosis – MI
• Ischaemia, usually do to atherosclerosis• Typically presents as elderly person who gets leg
pain when walking• After they rest for a few minutes the pain goes
away and they can start walking again
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Intermittent Claudication
• Localised, permanent dilation of artery• Can be asymptomatic until it ruptures• Ruptured abdominal aneurysm causes sudden
severe abdominal pain – surgical emergency• Aortic dissection – blood between layers of aorta
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Aneurysm
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
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Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
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Thromboembolism
• Deep vein thrombosis• Pulmonary embolism
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
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Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
An acute failure of the CVS to perfuse the tissues
• Hypovolaemic – blood loss
• Anaphylactic – type I hypersensitivity
• Septic – vasodilation caused by bacterial toxins
• Cardiogenic – heart failure
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Shock
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
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Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
• Where the heart is unable to pump enough blood to satisfy the needs of the metabolising tissues.
• Breathlessness, tiredness and fatigue are associated with a cardiac abnormality that reduces cardiac output.
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Heart Failure
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Left Heart Failure• Fatigue and weakness• Exertional breathlessness• Orthopnoea • paroxysmal nocturnal
dyspnoea• Cough / pulmonary
oedema – crackles in ;lung bases.
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Right Heart Failure• Swollen ankles• Fatigue• Raised jugular venous
pressure• Abdominal
swelling/hepatomegaly• Pitting oedema• Ascites• Could be cor pulmonale –
query PE, COPD etc.
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Congestive Heart Failure• Both!• Very often a case of
right heart failure due to severe left failure.
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
The Peer Teaching Society is not liable for false or misleading information…
Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
• Abnormal electrical activity in the heart.• Too fast?• Too slow?• Uncoordinated?
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Arrhythmias
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Bradycardia• Slow heart rate (< 60bpm)• Sinus node disease, AV block, MI, beta blockers.• non-cardiac
– e.g.raised ICP – hypothermia – hypothyroidism
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Bradycardia• AV Block• First degree – delayed conductance, prolongation of PR
interval.• Second degree – when one or more impulses fail to reach
ventricles.– Mobitz 1: progressive lengthening of PR interval each successive
complex until a P wave is not conducted.– Mobitz 2: PR interval constant, QRS complexes dropped intermittently
or in fixed ratio to P wave rate.
• Third degree – No conductance from atria to ventricles. Complete dissociation of P Waves and QRS complexes. Rate 30-40 / min
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Tachycardia•Sinus tachycardia. Rate > 100/min•Causes
–Exercise–Thyrotoxicosis–Catecholamine stimulation (emotion)–Fever–Anaemia–Cardiac failure–Hypovolaemia
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Supra Ventricular Tachycardia•Symptoms include palpitations - sudden onset
–sudden offset or gradually tails away–few seconds to hours/days
•Precipitating factors–Tea, coffee, tobacco, alcohol, exercise, –emotional upset
•Rate 120-260/min
•P-waves may or may not be present
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Atrial Fibrilation•Irregularly irregular rhythm
•Atrium discharge at very high rates 300-500/min
•Ventricular rate slower and irregular
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Atrial FibrilationCauses: Cardiac
- Idiopathic - Rheumatic heart disease - Ischaemic heart disease - Cardiomyopathy - WPW syndrome
Non-cardiac- Alcohol - Carcinoma of bronchus
- Pneumonia - PE
Treatments include aspirin/warfarin (for anticoag) and then drugs to alter rate (beta blockers). Pacemakers, implantable defibs?
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Atrial Flutter• Macro re-entry circuit
within right atrium• On ECG there is a saw
tooth pattern – atrial rate 300/min
– ventricular rate
commonly 150/min• Treatment
– anticoagulants as for AF
– Drugs– rate control difficult – DC cardioversion – ablation
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Ventricular Tachycardia• Broad and complex• Can well tolerated.• Risk factor for
hypotension.• Wide QRS with shift to
left.• Deep S wave.• Treat with drugs
(lidocaine) and DC cardioversion.
• Implantable defib?
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Ventricular Fibrilation• Uncoordinated contraction of ventricles.• Quiver rather than contract.• Usually lead to cardiac arrest > cardiogenic
shock.• Treatement
– Immediate life support– 999– Defibrilation– PCI
1. Physiology– Mechanical activity of heart– Regulation of Mean Arterial Pressure (MAP)
2. Pathology– Atherosclerosis– Thromboembolism– Shock– Heart Failure– Arrhythmias
The Peer Teaching Society is not liable for false or misleading information…
Outline
3. Clinical Problems– Chest Pain– Leg Pain– Murmurs
The Peer Teaching Society is not liable for false or misleading information…
Leg Pain• 74 year old man• Diabetes Mellitus and Hypertension• Heavy Smoker• Sharp pain in his calves when walking• Has to stop walking to relieve pain
• Characterised by cramp-like pain in the legs on exercise
• Muscles deprived of oxygen → lactate production → pain
• Occurs after a certain distance and settles on rest after a certain time
• Caused by atherosclerosis of one or more of the arteries supplying the lower limb
• Same risk factors as for MI
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Intermittent Claudication
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Chest Pain• A 61 year old man presents complaining of increasing SOB on exertion
and tiredness. Previous MI 9 weeks ago. You diagnose heart failure.
What is the pathophysiological definition of ‘heart failure’? (4)How does left heart failure lead to pulmonary oedema? (6)3 reasons why people with heart failure experience a progressive decline in cardiac function (3x2)Another symptom for left ventricular failure besides shortness of breath and fatigue? (2)
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