1. Cardiology For Phase 1a Maria Digby & Rowena Speak
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2. What we’re going to cover…
1st Half
Physiology
Pharmacology
Anatomy
ECG
2nd Half
Pathophysiology + Clinical Scenarios
More Pharmacology!
Question time
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3. Ventricles Phase 0: depolarisation – Na+ in
Phase 1: partial repolarisation – Na+ channels shut, K+ out
Phase 2: plateau – Ca2+ in through L-type channels
Phase 3: repolarisation – K+ out
Phase 4: resting potential – (-90mV) – Na+/K+ ATPase
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4. SAN
Phase 4 = pacemaker potential – less K+ out, Na+ in through F-type channels, Ca2+ in through T-type channels
Phase 0 = slower depolarisation – Ca2+ in through L-channels NOT Na+ in like depolarisation ventricles!)
Phase 3 = repolarisation – K+ out
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5. Antiarrhythmic drugs: Vaughan Williams classification
Class I: Na+ channel blockers
1a) Quinidine – moderate blocker
1b) Lignocaine – weak blocker
1c) Flecainide – strong blocker
Class II: Beta blockers: block sympathetic stimulation - atenolol
Class III: K+ channel blockers: prolong repolarisation - amiodarone
Class IV: Ca2+ channel blockers: verapramil I IV
Phase 4
Phase 0
Phase 1
Phase 2
Phase 3
0 mV
-80mV II
III
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6. Cardiac cycle AP = aortic pressure LVP = left ventricular pressure
LAP = left atrial pressure
LVEDV = left ventricular end diastolic volume
LVESV = left ventricular end systolic volume
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7. Cardiac cycle: Systole
After ventricular filling, pressure in ventricles > in atria = AV valves close (SOUND 1 = “lub”)
Isovolumetric contraction: ventricles contracts when all valves are shut (this increases pressure in ventricles)
Ventricular ejection: pressure in ventricles > in pulmonary artery/aorta = semilunar valves open and blood flows out of ventricle
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8. Cardiac cycle: Diastole
Diasystole
After ventricular ejection, pressure in pulmonary artery/aorta > than in ventricles = semilunar valves shut (SOUND 2 = “dub”)
Isovolumetric relaxation: ventricles relax when all valves are shut (this decreases the pressure in the ventricles)
Ventricular filling: pressure in ventricles < in atria = AV valves open
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9. Cardiac cycle: “atrial kick”
Ventricular filling is mostly a passive process
But towards the end of diastole, the atria contract causing a small increase in pressure in the ventricles = “atrial kick”
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10. Cardiac cycle: dicrotic notch
When the aortic valve closes, blood rebounds against the valve causing a decrease then a rebound of aortic pressure = dicrotic notch
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11. Equations: learn these!!
SV = EDV - ESV
CO = HR x SV
MAP = DP + 1/3(SP-DP)
BP = CO x TPR
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12. Monitoring MAP: Baroreceptors
Where are the arterial baroreceptors?
a) Carotid sinus + b) Aortic arch
Baroreceptors detect changes in arterial pressure
Afferent nerve (Glossopharyngeal)
CNS (Medullary Cardiovascular Centre)
Efferent nerve
Sympathetic outflow to heart and arterioles
Parasympathetic (Vagus) outflow to heart
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13. CO TPR BP Maintaining MAP (BP = CO x TPR)
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14. Maintaining MAP: 1. Changing CO
CO = HR x SV
Change Heart Rate
Sympathetic nervous stimulation of the heart
Parasympathetic nervous stimulation of the heart (Vagus)
Plasma adrenaline
Change Stroke Volume
Sympathetic nervous stimulation of the heart
Plasma adrenaline
End-diastolic ventricular volume (preload) – FRANK-STARLING MECHANISM
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15. FRANK-STARLING MECHANISM – learn this!
At any given heart rate….
Any ↑ Venous Return….
Causes ↑ End-Diastolic Volume…
Causes ↑ stretch in the cardiac muscle (Preload)…
Causes ↑ forceful contraction…
Which ↑ Stroke Volume and thereby the Cardiac Output
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16. Maintaining MAP: 2. Changing TPR
The arterioles are the principle site of resistance to blood flow
Vasoconstriction
Local: Endothelin-1, internal blood pressure (myogenic response)
Neural: Sympathetic nerves
Hormonal: Adrenaline (on alpha receptors), Angiotensin II, Vasopressin (aka Antidiuretic hormone)
Vasodilation
Local: decrease in Oxygen, increase in CO2/H+, Nitric Oxide, Eicosanoids, Prostacyclin
Neural: Neurons that release Nitric oxide
Hormonal: Adrenaline (on beta 2 receptors), Atrial Natriuretic Peptide
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17. Important point…
There is sympathetic stimulation to both the heart and arterioles
But there is no parasympathetic stimulation to the arterioles, only to the heart
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18. Terms to understand…
Active hyperaemia – vasodilation in response to an increase in metabolic activity
Flow autoregulation – vasodilation in response to decreased pressure
Reactive hyperaemia – when a tissue’s blood supply has been completely occluded, on removal of the occlusion there is a profound, transient increase in blood flow
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19. GO LOOK AT… VANDERS - especially page 399 (12th edition)
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20. Long term regulation of MAP
The Baroreceptor reflex is a short term regulator. They end up adapting to a maintained change in pressure.
The most important long-term regulator of arterial pressure is blood volume – this is regulated by the Renin-Angiotensin-Aldosterone System (RAAS)
ACE inhibitors inhibit RAAS to reduce blood volume
(have a quick look at RAAS – try to understand it but don’t worry about memorising it until Phase 1b!)
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21. RAAS
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22. Haemostasis Platelet plug Clotting cascade
Clotting factors dependent upon Vitamin K: II, VII, IX, X
Haven’t got time to talk about this now – make sure you understand the principles of it
Important for understanding pharmacology of Aspirin, Clopidogrel, Warfarin, Heparin and Fibrinolytics
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23. Anatomy - valves Valve Surface marking Auscultation area Tricuspid
4th intercostal space
-midline
5th intercostal space
-right and left sternal edge
Pulmonary
3rd costal cartilage-sternal junction
-left
2nd intercostal space
-left sternal edge
Mitral
4th intercostal cartilage
-left, midclavicular line
Aortic
3rd intercostal space
-left half of sternum
-right sternal edge
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24. Anatomy - valves
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25. Valve pathology Pathology Cause Murmur Mitral stenosis Rheumatic fever
Mid-diastolic
Mitral regurgitation
Ischaemic heart disease, MI, Rheumatic fever
Pan-systolic
Aortic stenosis
Calcific valve disease, Rheumatic fever
Ejection-systolic
Aortic regurgitation
Rheumatic fever, bicuspid aortic valve
Diastolic
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26. Rheumatic fever Endocarditis Post-Streptococcus pyogenes infection
(Scarlet fever, Strep throat)
Damages heart valves
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27. Anatomy – heart borders
Right: formed by right atrium, runs between 3rd and 6th right costal cartilages approximately 2-3cm from the midline in the adult
Left: formed by left atrial appendage + left ventricle, apex  2nd left intercostal space 2-3cm from midline
Inferior: formed by right atrium and right ventricle + tiny bit of left ventricle
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28. Anatomy – aorta Thoracic Right + left coronary arteries
Brachiocephalic (aka innominate) artery
Left common carotid artery
Left subclavian artery
Passes through diaphragm at T12
Abdominal
Abdominal aortic aneurysm – expansile, pulsatile mass, midline, above umbilicus
Bifurcates at L4
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29. Electrocardiography (ECG) – heart rate
Quick estimation = 10 x no. of QRS complexes on one rhythm strip (check speed of ECG is 25mm/s)
Sinus bradycardia < 60bpm
Sinus tachycardia >100bpm
Normal PR interval = s
Normal QRS complex = s
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30. ECG – AV block 1st degree – PR interval prolonged, >0.20sec
2nd degree:-
Mobitz type I - progressive lengthening of PR interval with each successive complex until a P wave is not conducted
Mobitz type II – PR interval constant, QRS complexes dropped intermittently or in fixed ratio to P wave rate
3rd degree - Complete dissociation of P Waves and QRS complexes
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31. ECG Atrial flutter = saw tooth pattern
Atrial fibrillation = irregularly irregular rhythm
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32. ECG – Ventricular fibrillation: fine and coarse
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33. Useful websites http://www.cvphysiology.com
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34. Pathology/Pathophysiology
Normal arterial structure
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35. Getting old ain’t pleasant
Progressive fibrous thickening of intima
Fibrosis + scarring of muscular or elastic media
Accumulation of mucopolysaccharide-rich ground substance
Fragmentation of elastic laminae
ATHEROSCLEROSIS
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36. Atherosclerosis Prevented? Some predisposing factors?
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37. Atherosclerosis Effects medium and large arteries Risk factors: Aging
Male
Hypertension
Smoking
Diabetes mellitus
Hyperlipidemia
Increase LDL
Decreased HDL
Having a factor 7 genetics
Lifestyle
Exercise
Obesity
Diet
Stress and personality
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38. Drugs – ‘all’s well that ends well’ ;)
Calcium channel blockers “ipine”s eg: amlodipine
ACE Inhibitors “il”s eg: ramipril
Angiotensin Receptor Blockers “sartans” eg: candesartan
Diuretics “ide”s eg: loop – furosemide, thiazide – bendoflumethiazide and K sparing - Amiloride
Beta blockers “olol”s eg: atenolol
Statins “statin”eg: simvastatin
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39. Clopidogrel - is an oral, thienopyridine class antiplatelet agent
Anticoagulants “rin” eg: warfarin and heparin
NSAIDS “profen” eg: ibuprofen, aspirin *so doesn’t work for everything
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41. Angina Pectoralis Caused by chronic heart disease
Atherosclerosis in the coronary artery
Means less O2 to heart muscle
Crushing chest pain
No troponin
No new changes on ECG
Stable or unstable?
Stable
- Caused by activity / stress (watching Barnsley)
- relieved by GTN/rest
Unstable
- NOT relieved by GTN /rest
- Can occur at rest
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42. MI
What is an MI? How does it occur? How does it present? How is it prevented?
ST elevation myocardial infarction
Non-ST elevation myocardial infarction 
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43. MI - STEMI Crushing chest pain
Feeling of “impending doom” in Barnsley – “gonna miss Barnsley play at weekend” ;)
Nausea
Sweating
SOB
Clammy skin
Raised Troponin level
ST elevation on ECG
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44. MI - STEMI STEMI Ambulance MONA A and E β blocker (atenolol)
Thrombolytics (tPA or streptokinase)
ACE inhibitor (lisinopril)
Clopidogrel
Back at home
Warfarin
Aspirin
β Blocker (metoprolol)
ACE inhibitor
Statin (simvastatin)
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45. MI - NSTEMI
Infarct
Feeling again same “impending doom” - Barnsley be relegated?
Nausea
Sweating
SOB
Clammy skin
Raised Troponin
No new ECG changes
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46. MI - NSTEMI NSTEMI Ambulance MONA M= Morphine O = Oxygen N = Nitrates
A = Aspirin
A and E
β blocker (atenolol)
LMW heparin
GPIIb/IIIa antagonist (tirofiban)
Nitrates
Clopidogrel
Back at home
Warfarin
Aspirin
β Blocker (metoprolol)
ACE inhibitor
Statin
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47. Heart Failure
Heart failure = pathophysiological state in which the heart is unable to pump sufficient blood to meet the needs of the metabolising tissues or can only do so with elevated filling pressures
R, L or Congestive
Systolic / diastolic /Both
Excessive salt and water retention
Low cardiac output and raised peripheral resistance
Others – idiopathic, CTD – SLE, RA, myocarditis, HIV, substance abuse and peripartum cardiomyopathy
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48. Ischaemic heart disease – 34% Dilated cardiomyopathy – 32%
Causes:-
Ischaemic heart disease – 34%
Dilated cardiomyopathy – 32%
Primary valvular disease and congenital heart disease – 12%
Hypertensive heart disease – 11%
Other -5%
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49. Physiological Clinical
A state where the heart is unable to pump enough blood to satisfy the needs of the metabolising tissues
Clinical
A symptomatic condition where breathlessness, tiredness and fatigue are associated with a cardiac abnormality that reduces cardiac output
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50. Key concepts - Pathophysiology
Initial insult
Fall in cardiac output
↑Preload to maintain ventricular performance
↑Afterload limits ventricular performance
Maladaptive hormonal responses
Progressive left ventricular remodelling
Progressive decline in cardiac performance
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51. Left heart failure Symptoms: fatigue, exertional breathlessness,
orthopnoea
paroxysmal nocturnal dyspnoea
Signs: (occur late)
cardiomegaly,
added heart sounds,
tachycardia,
crackles in lung bases
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52. Right heart failure Symptoms: -swollen ankles, fatigue, anorexia
Signs: (occur early)
-raised jugular venous pressure
-hepatomegaly
-pitting oedema
-ascites
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53. Congestive A mixture of both left and right heart failure!
Almost always right heart failure secondary to severe left heart failure…
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54. Tetralogy of Fallot
Congenital defect – most common form of cyanotic congenital heart disease
Causes:-
Low O2 levels in the blood leading to cyanosis
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56. Ventricular septal defect Narrowing of the pulmonary outflow tract
Classic form includes 4 defects of the heart and its major blood vessels
Ventricular septal defect
Narrowing of the pulmonary outflow tract
Overriding aorta - shifted over to the RV and ventricular septal defect (usually just from LV)
Right ventricular hypertrophy
Hole between right and left ventricles
The valve and artery that connect the heart with the lungs
Artery that carries O2 rich blood to the body
Thickening of RV wall
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57. Factors that increase risk
Alcoholism in mother
Diabetes
Mother who is over 40 years old
Poor nutrition during pregnancy
Rubella or other viral illnesses during pregnancy
Children more likely to have Downs syndrome
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58. Symptoms Cyanosed (blue skin) Clubbing of fingers Difficulty feeding
Failure to gain wt
Passing out
Poor development
Squatting during episodes of cyanosis
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59. MRI (usually after surgery) Treatment
Signs and tests
Chest Xray
Complete blood count
ECHO
MRI (usually after surgery)
Treatment
Surgery to repair tetralogy of Fallot is done when the infant is very young
Outcome – 90% survive to adulthood and live an active, healthy and productive life
Do have to have regular cardiology appointments
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60. Problem solving time
50 year old man presents with “crushing chest pain”, he was rushed in to AandE from the local Barnsley vs Owls, smoker for 35 years, the chest pain radiates to his jaw. He feels sweaty, nauseous and vomited.
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61. MI Angina Tetralogy of Fallot Right heart failure Football fever
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62. 80 year old retired postman complains of severe onset central chest pain which comes on when he is walking his cat Jess. He sometimes gets it when sitting reading the sports section of the Barnsley Chronicle.
Any ideas?
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63. Unstable Angina pectoralis Palpitations Intermittent claudication
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64. She used to smoke until 2 years ago and is a telesales rep
A 50 year old lady diabetic (type 2) complains of pain when walking in her calves and is relieved by rest.
She used to smoke until 2 years ago and is a telesales rep
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65. Intermittent Claudication DVT (deep vein thrombosis) Pulled a muscle
Cramp
Intermittent Claudication
DVT (deep vein thrombosis)
Pulled a muscle
Been stabbed in the leg in the past
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66. Thank you for your attention