RELATED ANATOMY
●90% right coronary artery gives the posterior interventricular artery- Right dominant
Coronary circulation
●Heart receives blood supply from two coronary arteries and their branches.
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1.Left coronary artery
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2.Right coronary artery
●Although anastomoses occur between the terminations of the right and left coronary arteries, these are usually inefficient.
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●Thrombosis in one or other of these vessels leads to death of the area of heart muscle supplied (a myocardial infarction).
●Blood supply to the heart is directed from epicardium to endocardium.
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●Large forces and /or pressures are generated within the myocardial tissue during contraction.
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●Intramyocardial forces on coronary vessels - - collapse during systole thus increasing coronary vascular resistance.
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●Left ventricular myocardium - - coronary flow is lower during systole eventhough systemic arterial pressure is highest during systole.
The venous drainage of the heart
●The bulk of the venous drainage of the heart is achieved by veins which accompany the coronary arteries and which open into the right atrium.
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●The rest of the blood drains by means of small veins (venae cordis minimae) directly into the cardiac cavity.
Nerve supply
●The nerve supply of the heart is derived from
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1.the vagus (cardio-inhibitor) and
2.the cervical and upper thoracic sympathetic ganglia(cardio-accelerator) by way of superficial and deep cardiac plexuses- also dilate coronary arteries.
Referred Pain
●Referred pain is pain perceived at a location other than the site of the painful stimulus/ origin. Irritation of a visceral organ frequently produces pain that is felt not at that site but in a somatic structure that may be some distance away.
●Axons of pain fibers conveyed by the sensory sympathetic cardiac nerves reach T1-T5 segments of the spinal cord mostly through dorsal root ganglia of the left side. Since these dorsal root ganglia also receive sensory impulses from medial side of arm , fore arm and upper part of chest pain gets referred to these areas.
Related physiology
Heart sounds
●Vibrations - closure of heart valves
●Cardiac cycle - 2 main heart sounds
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1.1st sound S1- closure of atrioventricular (AV) valves (low pitch)
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2.2nd sound S2 - closure of aortic and pulmonary valves (high pitch)
During expiration pulmonary and aortic valves close at the sametime ; during inspiration aortic valve closes slightly before the pulmonry valve. This is due to low impedance of the pulmonary tree.
3rd and 4th heart sounds not always heard
●3rd sound - ⅓ of diastole - vibrations caused by rapid ventricular filling. May be normal
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●4th sound - immediately before 1st sound. Always pathological (high atrial pressure or stiff ventricle) S1
- Soft at low heart rates(ventricles well filled with blood and cusps of AV valves float up)
- Loud in severe tachycardia (poor filling)
S2
- Physiological splitting of S2 : closure of aortic and pulmonary valves in inspiration produce separate sounds(aortic closes before pulmonary valve)
Cardiac cycle
●Each cardiac cycle : 2 phases
1.Diastole
2.Systole
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●Electrical events followed by mechanical events of the heart
1.Late diastole
2.Atrial systole
3.Isovolumetric ventricular contraction
4.Ventricular ejection
5.Isovolumetric ventricular relaxation
6.Early diastole
Late diastole
●Mitral and tricuspid valves open
●Aortic and pulmonary valves closed
●Rate of filling declines as ventricles fill
●Cusps of valves drift up
●No heart sounds
●About 70% of the ventricular filling occurs passively during diastole
Atrial systole
●Semilunar valves closed
●30% increase in ventricular volume
●Final volume : END DIASTOLIC VOLUME Isovolumetric ventricular contraction
●Event between closing of AV valves and opening of semilunar valves
●Ventricular volume unchanged
●Ventricular pressure builds up Ventricular systole
●Ventricular pressure overcomes the aortic and pulmonary artery pressure
●Ejection rapid and then slow
●AV valves - pulled down by contraction of ventricular muscle - atrial pressure drop
●Late ejection - ventricular pressure falls below aortic pressure, but aortic valve remains open
●STROKE VOLUME - The amount of blood ejected by the ventricles during systole
●Semilunar valves shut at the end of ventricular systole Isovolumetric ventricular relaxation
●Semilunar valves closure to opening of AV valves
●Ventricular pressure declines rapidly
●No change in volume
●Remaining blood : END SYSTOLIC VOLUME Early diastole
●Atrial diastole - filling (AV valves shut) - atrial pressure increases
●Ends when ventricular pressure < atrial pressure and AV valves oprn
●Ventricular filling
Length of Systole and Diastole
●Duration of systole relatively constant
●At high heart rate diastole is shortened to a great degree than systole
●Upto a certain heart rate cardiac output increases- later decrease
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CLINICAL IMPORTANCE ?
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The conducting system of the heart
●This consists of specialized cardiac muscle found in the sinuatrial node and in the atrioventricular node and bundle
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●The heart-beat is initiated in the sinuatrial node (the ‘pacemaker of the heart’)
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●From there the cardiac impulse spreads throughout the atrial musculature to reach the atrioventricular node
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●The impulse is then conducted to the ventricles by way of the specialized tissue of the atrioventricular bundle (of His)
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This bundle divides into its right and left branches which run immediately beneath the endocardium to activate all parts of the ventricular musculature Cardiac output
●Output of each ventricle / unit time(min)
●Stroke volume – amount of blood pumped by each ventricle per beat
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●Cardiac output = stroke volume * heart rate( 70ml* 72)
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●Typically 5.0- 5.5 litres /minuteRegulation of stroke volume
Stroke volume = End diastolic volume - End systolic volume
●Depends on
- Preload
- Afterload
- Contractility (inotrophy)
Usually all three mechanisms act together - interdependent
Blood pressure
●Blood pressure = cardiac output / total peripheral resistance
Heart failure ●Inability of the heart to maintain a sufficient cardiac output to meet tissue needs
Related pathology
Atherosclerosis
●Definition of atheroma
- Atheroma consists of patchy intimal thickening of arterial walls due to deposition of lipids, proliferation of smooth muscle cells and formation of fibrous tissue
Complications of the atheromatous plaque
(acute plaque change)
●Fissuring of plaque
●Ulceration of plaque
●Superimposed thrombosis
●Embolization
●Aneurysm formation
●Haemorrhage into the plaque
●Calcification
Factors which contribute to coronary atheroma
1.Hypertension
2.Diabetes mellitus
3.Cigarette smoking
4.Increased LDL cholesterol
5.Genetic / familial factors
Pathogenesis of myocardial ischaemia
This depends on two factors:
1.The extent and severity of fixed chronic anatomic disease (atherosclerotic coronary narrowing)
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2.The extent and severity of dynamic plaque changes (acute plaque change, thrombosis, vasospasm)
Myocardial infarction
●Development of an area of myocardial necrosis caused by local ischaemia
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●Pathogenesis is related to occlusive coronary artery thrombosis on a disrupted atherosclerotic plaque
Location of an infarct
Determined by
●Site of vascular occlusion
●Anatomy of the coronary circulation
●Degree of collateral circulation
Laboratory evaluation of myocardial infarction
Cardiac biomarkers
●CK-MB
- Starts rising in 2-4 hours, peaks at 12-24 hours and disappears by 48hours
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●Cardiac Troponin T and I
- Reliable marker for myocardial necrosis
- More specific than CK-MB
- Starts rising in 6-8 hours, peaks at 12-24 hours and remains elevated for 7-10 days
Related hematology
Related pharmacology
Terminology
●Anticoagulants : An agent which suppress, delay or nullify blood coagulation
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●Antiplatelets : Agents that reduce the tendency of platets in the blood to clump and cause clotting
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●Fibrinolysis(Thrombolytics) : Agents which dissolve dangerous clots in blood vessels, improve blood flow, and prevent damage to tissues and organs
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●Antifibrinolytics(Antithrombolytics) : Agents which inhibit or decrease the breakdown of fobrin.
Thrombolytic agents
1.Streptokinase
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2.Tissue plasminogen activators (tPAs)
- Alteplase
- Tenecteplase
- Reteplase Streptokinase (SK)
●No enzymatic activity
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●It binds to human plasminogen and forms an active one-to-one complex with plasminogen
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●This enzymatically active complex converts uncomplexed plasminogen to the active enzyme plasmin which breaks down fibrin
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●The SK-plasminogen complex also catalyses fibrinogen and clotting factors V and Vll
Streptokinase (SK) Limitation
●Its action is blocked by antibodies, which appear about 4 days after initial dose.
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●Atleast one year must be elapsed, before it is used again
Recombinant tPAs
●They are not antigenic, can be used in patients likely to have antibodies to streptokinase
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●Claimed to be “clot- selective” than streptokinase as they are more active on fibrin-bound plasminogen than plasma plasminogen
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●It's superior to streptokinase in dissolving older clots
Anticoagulants
●Oral anticoagulants
- Warfarin
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●Parenteral anticoagulants
- Subcutaneous low molecular weight heparin (Enoxaparin)
- Unfractionated heparin IV
●Beta blockers
- Competitive inhibitors of catecholamines at beta-adrenoceptor sites
- Inhibit sympathetic stimulation of heart and smooth muscle
- Reduces heart rate and Contractility via Beta 1receptor blockade
- Ex: cardio selective - Atenolol Metoprolol
- Non-selective - Propranolol
●Calcium Channel Blockers
- Prevent opening of voltage-gated calcium channels
- Bind to alpha 1 subunit of cardiac and smooth muscle L-type calcium channels
- Vasodilator effect on resistance vessels thus reduces afterload
- Coronary artery dilatation
- Negative chronotrophic
- Negative inotrophic effects
●Potassium channel activators
- Activates K ATP channel
- NO donor effects
- Arterial and venodilator
- Ex:Nicorandil
●Selective pacemaker current inhibitor
- Reduces spontaneous beating rate of the sinus node by slowing the diastolic depolarization slope of action potential
- Selective and prolonged reduction in heart rate, both at rest and during exercise
- Ex: Ivabradine
Lipid lowering drugs
●Statins
- Inhibits HMG CoA reductase (rate limiting step in cholesterol synthesis)
- This increases LDL receptors (up-regulation) in the liver and increases clearance of LDL from the circulation
- Ex: Simvastatin, Atorvastatin, Lovastatin
Questions and answers
1.T/F
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A.The conducting system is supplied by the left coronary artery in most of the normal healthy people
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B.Anastomosis between coronary arteries is sufficient to maintain coronary blood supply in acute thrombosis in interventricular arteries
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C.SA node is supplied by left coronary artery in majority
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D.Circumflex artery is a branch of right coronary artery
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E.Blood supply to the endocardium is directed from epicardium
1.A. F- right coronary artery supply except for part of left bundle branch
B. F- effective end arteries
C. F-60%bby right coronary
D. F-right coronary
E. T
02. The second heart sound corresponds in time with
A.Closure of pulmonary and aortic valves
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B.Trigger QRS complex of ECG
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C.Increase in atrial pressure
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D.Increase in ventricular pressure
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E.V wave of JVP
02. A. T
B. F- 1st heart sound QRS complex. 2nd in T wave. QRS complex triggered by ventricular depolarization
C. T- rises after ventricular systole
D. F- falls after ventricular systole
E. T- rapid atrial filling in early diastole
03. Recognised risk factors for coronary atherosclerosis
A.Cigarette smoking
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B.Cirrhosis of the liver
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C.Systolic hypertension
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D.Diabetes mellitus
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E.Hyper-homocysteinaemia
03. A. T
B. F
C. T
D. T
E. T
O4. Regarding myocardial infarction
A.Pallor clearly seen after 24hours in a post mortem
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B.Coagulative necrosis occurs
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C.VSD occurs due to excessive granulation
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D.CK-MB peaks in 48hours
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E.Troponin T rises in both myocardial ischaemia and infarction
04. A. F- 2-3 days. 12hours reddish purple due to stagnant blood
B. T
C. F- occurs 3-7 days after infarct, lysis of connective tissue and inadequate collagen deposition
D. F- 24hours
E. F- only after necrosis of myocardium in infarction
05. T/F
A.Warfarin acts well by oral therapy
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B.Warfarin treatment monitored by INR
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C.Aspirin’s action is brought about by binding with a regulator on the membrane of platets
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D.Antibodies to streptokinase appear about 4 days after the treatment
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E.Streptokinase is fibrin selective
05. A. T
B. T- because it blocks extrinsic pathway
C. F- irreversibly inhibits COX 1. Clopidogrel bonds to ADP receptor
D. T
E. F- tPA is fibrin selective