Angina and ischemia Flashcards

1
Q

Coronary perfusion gradient

A

aortic root pressure - LV pressure

perfused during diastole

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2
Q

Laplace’s equation

A

wall stress = r x p / (2h)

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3
Q

Left main CA

A

originate from left coronary sinus
travels between LA and pulmonary trunk to reach the AV groove, divides into
- LAD
- circumflex

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4
Q

LAD artery

A

anterior interventricular groove
diagonal branches: anterior surface of LV
septal branches: anterior 2/3 of the interventricular septum and the apical portion of the anterior papillary muscle

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5
Q

Circumflex CA

A

left AV groove and passes around the left border of the heart to reach the posterior surface
obtuse marginal branches: supplies lateral & posterior wall of the LV

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6
Q

Right main CA

A

originate from right coronary sinus
right AV groove, passing posterior to btw RA and RV
Marginal branches: RV, including SA and AV nodes
Right posterior descending: distal part of the right main CA, travels from the inferoposterior aspect of the heart to the apex, inferior & posterior walls of both ventricles and posterior 1/3 of interventricular septum

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7
Q

Conductance vessels

A

epicardial &myocardial penetrating
large in diameter
compressed by contracting cardiac muscle during diastole

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8
Q

Resistance vessels

A

Arterioles and capillaries
smaller in diameter
surrounded by smooth muscle, can change diameter in response to stimuli (NO, adenosine)
precapillary sphincters can vary flow through coronary capillaries

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9
Q

Coronary sinus

A

coronary veins accompany the coronary arteries and converge into here
posterior surface of the heart in the AV groove
empties into RA

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10
Q

Stable angina

A
usually due to atherosclerosis of CA
chest pain on exertion
arteries must be >75% occluded
adenosine released locally in response to ischemia (dilates BV, chest pain)
relieved by rest
ST depression
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11
Q

Unstable angina

A

at rest or minimal exertion
artery may be >90% occluded
loss of predictability of anginal attacks
does not respond to NO
ST depression, T wave inversion/depression

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12
Q

Atypical angina

A

do not have chest pain
instead have other symptoms - weakness, faintness, sweating, nausea
more commonly seen in diabetic patients
same pathophysiology as stable angina

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13
Q

MI

A

death of myocardial tissue secondary to ischemia

begin after 15-20 minutes of severe ischemia

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14
Q

First 12 hours of MI - histo & gross

A

 Micro
• EM changes in myocytes and their membranes within the first 15-20 min
• Wavy fibers – intracellular edema
• Coagulation necrosis – hypereosinophilic myocytes
• Contraction band necrosis – compaction of Z-lines of sarcomeres
 Macro
• If no reperfusion of infracted area then pallor due to extrusion of erythrocytes from capillary bead
• If reperfused then hemorrhagic from blood vessel bursting

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15
Q

Vulnerable plaque

A

thin fibrous cap + large soft lipid cholesterol pool underneath
- prone to rupture
usual cause for sudden-onset MI

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16
Q

Progression of MI

A

Subendocardial –> epicardial
subendo more susceptible to ischemia
greater degree of systolic fiber shortening in subendo (high oxygen demand), more flow
greater dependence on diastolic coronary flow
poor collateral development
flow to the endocardium may be reduced by : CAD, LVH, HF with increased LVEDP

17
Q

Determinants of infarct size

A
severity/duration of ischemia
size of area at risk (CAD)
Collateral 
Ischemic conditioning - e.g. hypertrophy
Reperfusion (spontaneous lysis, therapy)
Myocardial oxygen demand and supply
18
Q

Stage of inflammation (12 hours - 5 days) post-MI

A

 Micro
• Influx of PMNs
o If no reperfusion, then they collect at the borders of the infarct
o If reperfusion, then they are distributed diffusely
• Macrophages are seen after about 5 days
• Myocyte nuclei start to disappear and myocytes become attenuated and separated
o Phagocytosis of myocytes occur
 Macro
• Yellow centre with hyperemic border (not reperfused)
• Prominent hemorrhage (reperfused)

19
Q

Granulation tissue formation (1-3 weeks post-MI)

A

 Micro
• Residual macrophages, revascularization, fibroblasts and early collagen formation
 Macro
• Infarct turning from yellow to gray

20
Q

Scar formation (2-8 weeks post-MI0

A

 Micro
• Decrease in inflammatory cells with increasing collagen deposition and prominent capillary vessels
 Macro
• Infarct changing from gray to white as collagenization becomes complete

21
Q

Complications of MI

A

Death: 50% due to ventricular arrhythmia
Arrhythmia; major determinant of post-discharge mortality, ischemic tissue at border zone
Ventricular dysfunction
Cardiogenic shock: infarction >40%
Recurrent infarction: 2-10 days post-MI
Infarct expansion
Myocardial rupture: first few days or 2nd week after MI, at the border
RV infarction: associated with transmural inferior LV MI
Pericarditis: requires transmural infarct
Mural thrombus
Ventricular aneurysm: transmural MI, >2 CAD

22
Q

NSTEMI

A

subendocardial tissue ischemia + necrosis
ST depression, T wave inversion/depression
test for troponin I or T or CK MB in blood

23
Q

STEMI

A

full occlusion
transmural tissue necrosis
ST elevation

24
Q

Common causes of chest pain

A

Cariac: angina, acute MI, pericarditis
Vascular: aortic dissection, PE, Pulmonary HTN
Pulmonary: pleuritis/pneumonia, tracheobronchitis, spontaneous pneumothorax
GI: reflux, peptic ulcer, gallbladder disease, pancreatitis
MSK: costochondritis, cervical disc disease, trauma/strain
Infectious: Herpes zoster
Psychological: panic disorder

25
Stable angina Tx
Pharmaco: sublingual nitro organic nitrates, b-blockers, Ca blockers Prevention of MI: aspirin, lipid-regulation, ACEi Invasive: revascularization: PCI, coronary stents, drug-eluting stents, bypass graft
26
Unstable angina/NSTEMI Tx
Additional to stable angina: heparin use invasive techniques earlier in patients with high-risk features (ST deviation, elevated Trop-I, multiple CV risk factors)
27
STEMI tx
administer same as stable angina IMMEDIATELY fibrinolytics Primary PCI: immediate angioplasty and usually stenting
28
Percutaneou coronary intervention/PC transluminal coronary angioplasty
Under fluoscopy balloon-tipped catheter inserted through peripheral artery inflate in CA 1/3 patients redevelop symptoms within 6 months
29
Coronary stents
Thrombogenic --> give oral antiplatelets larger luminal diameter than PTI, decreased restenosis rate, reduced need for repeated angioplasties risk of restenosis due to neointimal proliferation
30
Drug-eluting stents
antiproliferative medication released over 2-4 weeks
31
Coronary artery bypass graft
requies a bypassable lesion >50% stenosis in left main coronary artery or 2-3 vessel disease with diabetes preferable to angioplasty when there is significant disease of >2 vessels
32
Nitrate
Stimulates release of NO (venodilates, reduce return and dilate CA) Indications: symptomatic acute ischemia CI: preload-dependent patients: aortic stenosis, RV dysfunction, viagra users SE: lightheadedness, headache, palpitations
33
b-blockers
indications: CAD CI: obstructive airway disease, LV dysfunction, marker bradycardia/heart block, insulin-treated patients SE: fatigue, sexual dysfunction
34
Ca channel blockers
non-DHPs: verapamil and diltiazem antagonize V-gated L-type Ca channels reduce inotropy and slow HR, minor vasodilatory Indications: ischemia persistent despite b-blocker/nitrate therapies, or for those with CI to b-blockers CI: LV systolic dysfunction
35
Lipid lowering agents
Statins, niacin, fibric acid derivatives, cholesterol intestinal absorption inhibitors, bile acid binding agents HMG-CoA synthase inhibitors (reduce cholesterol synthesis)
36
ASA
Irreversible COX inhibition --> inhibit synthesis of thromboxane A2 Indications: CAD CIs: gastric bleeding, allergies
37
Heparin
bind and increase potency of antithrombin III inhibit coagulation factor Xa Indications: standard therapy for UA and NSTEMI adjunctive after fibrinolysis or PCI in STEMI
38
Fibrinolytics
alteplase tPA, reteplase rPA, tenecteplase TNK-tPA stimulate natural fibrinolytic system; transform inactive precursor plasminogen into active protease plasmins --> lyses fibrin clots Indications: fibrinolytic therapy in STEMI (ONLY STEMI) CI: underlying bleeding disorders, active peptic ulcer disease, recent stroke, recovering from recent surgery, pregnancy, intracranial tumour/AVM, suspected aortic dissection or pericarditis