IHD Flashcards

1
Q

Describe normal coronary anatomy and physiology

A

LCA- develops from the left aortic sinus, bifurcates into LAD and LCx

LAD-supplies anterior wall of LV, intraventricular septum and part of the RV
LCx-Supplies the lateral and posterior walls of the LV

RCA-supplies the RA,RV and some LV, develops form the right aortic sinus divides into the posterior descending artery which supplies the inferior wall and marginal artery and the intraventricular septum

Circumflex-supplies lateral and posterior parts of the LV

Coronary veins- after suppling o2 to myocardium, deoxy blood is collected by the coronary veins, great cardiac vein, middle cardiac vein and coroanary sinus emptying into the RA

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2
Q

What is coronary perfusion?

A

pressure gradient that drives blood through arteries
-difference between aortic diastolic pressure and right atrial pressure (pressure in RA)

-occurs/favoured in diastole because during systole the myocardium contracts compressing the coronary arteries, reducing blood flwo

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3
Q

Describe oxygen demand and consumption

A

Coronary arteries supply oxygen form myocardial muscle function (MVO2)

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4
Q

What factors influence o2 demand?

A

-heart rate
preload
-afterload
-contractility
-wall tension( lapace law )
-blood oxygen content

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5
Q

What factors influence O2 supply?

A

-coronary perfusion pressure
-coronary vascular resistance
-external compression
-intrinsic regulators
-local metabolites
-neural innervation
-endothelial factors

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6
Q

Describe the different circulatory regulators affecting the blood flow

A

autoregulation- Vasoconstriction/vasodilation

endothelial regulation- endothelial cells lining blood vessels release substances such as Nitric oxide which is a vasodilator

metabolic regulation-increase in metabolic demand
-neuronal regulation- NS

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7
Q

Describe the factors that supply o2

A

HR- increased HR, increases cardiac output, less time spent in diastole, less filling of the heart- o2 debt

O2 content in the blood, high or low HB levels

vascular tone and endothelial functions regulate blood vessel dilation and constriction

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8
Q

Describe the factors that affect o2 demand

A

metabolic activity- needs more oxygen to supply myocardial cells, so produces more ATP

Increased HR- needs more oxygen to beat at an increased rate

-preload and afterload-if preload increases the heart has to work harder to release blood so it increases o2 demand, increasing the afterload means the heart has to work harder to overcome the pressure to eject blood, more oxygen needed for myocardial cells to respire to produce ATP

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9
Q

Name some factors that lead to the pathophysiology of IHD

A

Atherosclerosis

endothelial dysfunction-reduced ability of blood vessels to dilate appropriately in response to increased demand,reduced nitric oxide leads to vasodilation impairment

-myocardial ischemia- impaied ATP production leads to cellular dysfunction and myocardium swelling and lactic acid build up, electrical changes lead to arrhythmias

angina-myocardial oxygen demand exceeds supply and acute coronary syndrome results in plaque rupture and thrombus formation

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10
Q

Name some symptoms of IHD

A

-Angina- stable or unstable or variant
-Dyspnea
-MI
-HF
-cardiac arrest
-arrhythmias
-radiating pain

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11
Q

Tests used to identify IHD

A

-blood tests
-ECG
-ECHO
-left heart catheritisation

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12
Q

What are serum markers?

A

substances that can be measured in the blood and are used to diagnose, monitor or assess the severity of medical conditions

markers include things such as-proteins, enzymes,antibodies,hormones, metabolites, genetic markers

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13
Q

Describe some cardiac serum markers

A

Troponin ( Tnl and TnT)- protein released when the heart muscle is damaged, elevated levels are diagnostic of acute MI and myocardial injury

Creatine kinase (CK)- CK-MB is isoezyme specific to the heart and can be elevated in an acute MI

BNP-hormone released when there is increased pressure in heart chambers used to diagnose HF

Myoglobin-protein released when muscle tissue is injured such as heart tissue, a sensitive but not specific marker for myocardial injury

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14
Q

What are high levels of troponin?

A

levels rise within 3-6hrs after myocardial injury and stay elevated for 7-10 days (highly specific for Cardiac muscle)

normal range is less than 0.01-0.1 ng/mL

severe-0.1ng/mL
Extreme severe-1.0ng/mL

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15
Q

What are high levels of CK-MB?

A

rises within 4-6 hrs of myocardial injury peaks at 12-24hrs and returns to normal within 48-72 hrs
(less specific to cardiac muscle than troponin can be caused by other muscle injury)

elevated levels more that 5ng/mL

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16
Q

What is a STEMI?

A

-ST elevation myocardical infarction

-acute MI that occurs when there is a complete blockage of a coronary artery leading to heart muscle damage

17
Q

How do we identify a STEMI on an ECG?

A

-ST elevation is > 1mm in limb leads and >2mm in precordial leads

-Inferior wall infarction - leads II,III AVF show ST elevation ( suggest RCA obstruction)

-Anterior wall infarction- leads V1-V4 show ST elevation (suggests LAD obstruction)

-Lateral wall infarction- Leads I, aVL, V5, V6 show ST elevation (suggests LCA obstruction)

-posterior wall infarction - ST depression in anterior leads ( V1-3) and tall R waves

(inverted T waves, Pathological Q waves)

18
Q

Define NSTEMI

A

-non ST elevation myocardial infarction

-does not cause ST segment elevation on ECG. Associated with partial blockage of coronary artery leading to myocardial ischemia and damage to heart muscle

19
Q

How do we identify a NSTEMI on an ECG?

A

-ST depression in contiguous leads, >1mm and may be horizontal or downsloping

-T wave inversion

20
Q

NSTEMI changes based on location?

A

-inferior wall(RCA or LCA)
-ST depression/ T wave inversions in leads II, III, aVF

-Anterior wall ( left anterior descending artery)
ST depression/T wave inversion in leads V1-4

-Lateral wall (LCA)
ST depree/ T wave inversion in leads I, aVL,V5, V6

21
Q

What is a T wave inversion?

A

-downward deflection of T wave

-occurs in the leads that correspond to the region of the heart affected by ischemia or injury

22
Q

Define pathological Q waves

A

-abnormal deep and wide Q waves on and ECG indicating MI or permanent heart muscle damage

-Q waves suggest the heart muscle has been necrosed due to prolonged ischemia

23
Q

What is the criteria for pathological Q waves?

A

duration- greater than 0.04s
depth-more than 25% of the height of the following R wave in the same lead
Shape- deep negative deflection

24
Q

decribe ECG changes pre and post infarction

A

pre-infarction​

within minutes – tall / hyperacute T waves​

within minutes / hours – ST elevation​

within hours – loss of R wave height; appearance of Q waves; T wave inversion​

within a week or more –ST returns to normal​

months afterwards – T wave returns to normal​

25
Q

how do we diagnose an MI?

A

-history
-ECG
-raised cardiac enzymes
-structural wall abnormalities

26
Q

name some complications of an MI

A

Arrhythmias​

Cardiogenic shock​

LVF/ RVF​

Cardiac rupture (VSD, Papillary/free wall rupture)​

Mitral regurgitation​

Aneurysm​

Pericarditis (Dressler’s syndrome)​

Thromboembolism​

Depression​

27
Q

Define LVEF

A

-measurement used to assess the pumping efficency of the LV - expressed as a proportion of blood pumped out of the LV with each heartbeat relative to the total amount of blood in the ventricle before contraction

-normal range 50-70%

28
Q

What is left heart catheterization?

A

-medical procedure to assess the function of the left side of the heart particularly the LV, LA nad coronary artreies to diagnose CAD.

-procedure unvolves inserting a catheter through blood vessels and injecting contrast dye to visualise heart chambers and arteries

29
Q

What treatments are used for a STEMI?

A

-reperfusion therapy
-percutaneous coronary intervention- angioplasty
-Fibrinolysis-thrombolytic therapy
-CABG
-medication such as antiplatelet, anticoagulants, thrombolytics, beta blockers,statins

30
Q

What is an angioplasty?

A

catheter with a baloon is inserted in the blocked artery and the baloon is inflated to open up the blockage- a stent is placed to keep the artery open and prevent reocclusion

31
Q

What is fibrinolysis/ thrombolytic therapy?

A

medications such as tPA, streptokinase or reteplase used to dissolve the blood clot causing the blockage

32
Q

What is a CABG?

A

surgically rerouting blood around blocked coronary artery using a graft from another body part

33
Q

What treatments are used for a NSTEMI?

A

-antiplatelet, anticoagulant,beta blockers,ACE inhinitors, statins
-reperfusion therapy

34
Q

Name 2 different stents used in PCI

A

Bare metal stents
drug eluting stents

35
Q

What are drug eluting stents?

A

coated with a polymer that slowly releases medication ( immunosuppresant or antiproliferant) this drug helps prevent overgrowth of tissue within the stent reducing the risk of restenosis

-pros-Reduced restenosis, better for patients with complex lesions
-cons-risk of late stent thrombosis, longer duration of dual antiplatelet therapy

36
Q

What are bare metal stents?

A

-metal mesh tubes inserted into the artery to keep open after balloon angioplasty.

-Pros-lower cost, shorter duration of antiplatlet therapy
-cons-high risk of restenosis, more likely to require repeat procedures

37
Q

Prognosis of MI

A

Timing of revascularization​

Size of MI​

Extent of LV dysfunction​

Extent of CAD​

Recurrent ischaemia​