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CV > Angina and ischemia > Flashcards

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
Q

Stable angina Tx

A

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
Q

Unstable angina/NSTEMI Tx

A

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
Q

STEMI tx

A

administer same as stable angina IMMEDIATELY

fibrinolytics

Primary PCI: immediate angioplasty and usually stenting

28
Q

Percutaneou coronary intervention/PC transluminal coronary angioplasty

A

Under fluoscopy
balloon-tipped catheter inserted through peripheral artery
inflate in CA
1/3 patients redevelop symptoms within 6 months

29
Q

Coronary stents

A

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
Q

Drug-eluting stents

A

antiproliferative medication released over 2-4 weeks

31
Q

Coronary artery bypass graft

A

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
Q

Nitrate

A

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
Q

b-blockers

A

indications: CAD
CI: obstructive airway disease, LV dysfunction, marker bradycardia/heart block, insulin-treated patients
SE: fatigue, sexual dysfunction

34
Q

Ca channel blockers

A

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
Q

Lipid lowering agents

A

Statins, niacin, fibric acid derivatives, cholesterol intestinal absorption inhibitors, bile acid binding agents
HMG-CoA synthase inhibitors (reduce cholesterol synthesis)

36
Q

ASA

A

Irreversible COX inhibition –> inhibit synthesis of thromboxane A2
Indications: CAD
CIs: gastric bleeding, allergies

37
Q

Heparin

A

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
Q

Fibrinolytics

A

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

CV (16 decks)

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