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Cardio Exam 2 > Lect 5- Ischemic Heart Disease > Flashcards

Lect 5- Ischemic Heart Disease Flashcards

1
Q

Ischemic heart disease definition

A

inadequate supply of blood and oxygen to a portion of the myocardium
occurs when there is an imbalance b/w oxygen supply and demand

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2
Q

what is the most common cause of myocardial ischemia?

A

atherosclerotic disease

atherosclerotic lesions reduce blood flow to the myocardium

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3
Q

what are powerful risk factors for IHD?

A

obesity, insulin resistance, and Type 2 DM

overlap b/w risk factors

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4
Q

major pathophysiological mechanism behind IHD

A

imbalance b/w myocardial oxygen demand (MVO2) and delivery

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5
Q

hypoxia vs ischemia

A

• Ischemia is a broader term vs hypoxia is a more narrow term
○ Ischemia is lack of oxygen as well as nutrients whereas hypoxia is just lack of oxygen
hypoxia exacerbates effects of atherosclerosisPatho of IHD can be affected by factors that affect these three things (MVO2, oxygen-carrying capacity of the blood, and coronary blood flow)

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6
Q

the oxygen-carrying capacity of the blood is determined by:

A

the inspired level of O2, pulmonary function, Hb conc and function

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7
Q

coronary blood flow

A

Major factor which regulates blood flow is resistance of all of these coronary arteries
1.) Large epicardial arteries (R1) 2.) prearteriolar vessels (R2) and 3.) arteriolar and intramyocardial capillary vessels (R3)
In the absence of significant flow (atherosclerotic obstructions), the major determinant of coronary resistance is R2 and R3

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8
Q

Coronary blood flow is controlled by what?

A

Metabolic regulation= exercise, emotional stress, etc

Autoregulation= blood flow is kept at certain range independent to changes in BP (protective mechanism)

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9
Q

Rupture of a plaque

A

fibrous cap is broken → tissue factor that is separated from blood is released → initiates coagulation/ thrombosis → can cause narrowing of blood vessel or complete occlusion or can resolve w/o any clinical sx
○ If you have complete occlusion → MI

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10
Q

other causes of IHD

A

spasm, thrombi, emboli, BP decrease (from blood loss), Aortitis, congenital abnormalities, left ventricular hypertrophy (since O2 demand is higher), severe anemia, abnormal constriction or failure of normal dilation of resistance vessels

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11
Q

where is there coronary atherosclerosis?

A

sites of increased turbulence in coronary flow and branch points in the epicardial arteries

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12
Q

what are the risk factors for coronary atherosclerosis?

A

exactly the same as for atherosclerosis

high LDL, low HDL, smoking, HTN, DM

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13
Q

severity of symptoms in IHD

A

depends on degree and location of stenosis and how fast it develops (chronic process and it takes years to get to the stage where sx are present)

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14
Q

50% stenosis in IHD

A

Usually pts do not have sx if they do regular activities but they might have sx if they do cardio/ exercise

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15
Q

80% stenosis in IHD

A

blood flow AT REST may be reduced

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16
Q

which arteries are particularly hazardous to develop stenosis?

A

left main coronary artery or the proximal left anterior descending

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17
Q

formation of collateral vessels

A

GOOD!
Collateral circulation affects the way the disease is produced
Formed when gradually developing stenosis

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18
Q

effects of ischemia

A

inadequate perfusion; decreased myocardial O2 tension; mechanical, biochemical and electrical disturbances

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19
Q

what are the mechanical effects of ischemia?

A

regional disturbances of ventricular contractility; segmental hypokinesia; segmental akinesia; segmental dyskinesia
all eventually lead to reduced myocardial pump function

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20
Q

effects of acute ischemia

A

transient left ventricle failure and mitral regurgitation (if the papillary muscle apparatus is involved; papillary muscles control the valves in the heart)
Mitral regurgitation= reversed blood flow; blood goes back from left ventricle to left atrium

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21
Q

what effect of transient ischemia would we see in clinic?

A

angina pectoris= chest pain

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22
Q

what effect of prolonged ischemia would we see in clinic?

A

acute MI
• Prolonged ischemia= severe narrowing/ blockage
• Myocardial infarction= tissue necrosis
○ Irreversible tissue damage/ cells are dying

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23
Q

ECG in IHD

A

Can determine:
if it is reversible vs irreversible process (need to know it before you treat pts)
the duration
the extent of damage
localization
presence of other underlying abnormalities

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24
Q

what will you find on an ECG of a pt with IHD?

A
  • Ischemia= problems with ventricular repolarization
  • ST depression= indicates ischemia (partial thickness)
  • Dramatic ST elevation= entire thickness
25
Q

effects of ischemia

A

electrical instability, which may lead to ventricular arrhythmia’s or ventricular fibrillation

26
Q

diagnosis of IHD

A

many may be asymptomatic
exercise-induced ECG changes
angiography
25% of pts who survive acute MI may not come to medical attention

27
Q

symptoms of IHD

A

• Chronic disease and most of the time asymptomatic (takes many years to develop bad symptoms)
• Complain of pressure, pain, and other forms of chest discomfort
○ Pts not always complaining of pain
• Sometimes angina pectoris is a condition which will eventually lead to MI
○ However, in some pts, the first event to bring them to the hospital is acute MI
• Disease can have a stable course= pt has the same complaints over a long period of time
• Progressive= sx are more often or occurring after less and less exercise
• Death= w/o any sx that can warn the pt that something has gone wrong
chest discomfort due to: angina pectoris, acute MI

28
Q

classification of IHD

A
  1. ) chronic coronary artery disease (CAD)= stable angina
  2. ) acute coronary syndromes (ACSs)= progressive; acute MI, unstable angina, NSTEMI, sudden cardiac death, Prinzmetal’s Variant Angina (special type)
29
Q

reading an ECG

A

• Need to understand that P-wave reflects the initial stimulation and conduction of impulses from atria to ventricles
• QRS= reflects depolarization of ventricles
• Everything after QRS is repolarization
○ ST segment very important for IHD

30
Q

What are the outcomes of a partial occlusion of a blood vessel?

A

• Partial occlusion= can have 2 outcomes
○ Unstable angina pectoris= ischemia but the damage is reversible
○ Acute MI w/o ST elevation= irreversible damage/ necrosis

31
Q

STEMI

A

assoc w/ complete occlusion

32
Q

NSTEMI

A

assoc w/ partial occlusion

33
Q

stable angina pectoris age

A

male over 50 and women over 60 (since until 50 women are protected by estrogen)

34
Q

clinical manifestations of stable angina pectoris

A

chest discomfort (not always pain), crescendo-descresendo, radiates to shoulders, sx relieved by rest or sublingual nitroglycerin, dyspnea, nausea, fatigue, faintness

35
Q

how can you tell if the pt is progressing to unstable angina?

A

ALWAYS ASK

angina occurring with less exertion than in the past, occurring at rest, or awakening the pt from sleep

36
Q

physical examination for IHS

A

search for evidence of atherosclerotic disease at other sites such as carotid arterial bruits (if you put stethoscope on neck, you can hear noise due to narrowing)

37
Q

unstable angina/ NSTEMI definitions

A

angina pectoris or equivalent ischemic discomfort w/ at least 1 of 3 features:
1. occurs at rest, usually for >10 min
2. severe and of new onset (w/in prior 4-6 weeks)
3. occurs with a crescendo pattern
NSTEMI= UA + myocardial necrosis (biomarkers)

38
Q

clinical manifestations of UA/ NSTEMI

A 
chest pain (usually severe enough to be described as frank pain), dyspnea and epigastric discomfort
large ischemia or NSTEMI= diaphoresis, pale, cool skin, tachycardia, basilar rales
39
Q

cardiac markers for UA/NSTEMI

A

CK-MB and troponin
When cells are dying, these cells are released to the circulation
Key to distinguish b/w reversible injury (unstable angina) and MI
direct relationship b/w the degree of troponin elevation and mortality

40
Q

Prinzmetal’s Variant Angina

A

syndrome of severe ischemic pain that occurs at rest but not usually w/ exertion and is assoc with transient ST-segment elevation
due to focal spasm of an epicardial coronary artery
pathogenesis is unclear

41
Q

STEMI

A

myocardial cell death due to prolonged and severe ischemia (b/w 2-4 hours of ischemia)
ST-elevation
Assoc with complete occlusion by thrombus

42
Q

coronary plaques prone to disruption

A

Thin fibrous cap

Thick fibrous cap and thin lipid core= safe; not likely to rupture

43
Q

coronary emboli vs coronary thrombus

A

Coronary emboli= thrombotic material is formed somewhere else in the body and travels to the coronary arteries to occlude them
thrombi are formed at the site of vascular injury in the coronary artery

44
Q

risk factors for STEMI

A

multiple: UA (can progress to clinically obvious MI), hypercoagulability, collagen vascular diseases, cocaine abuse, intracardiac thrombi, coronary emboli

45
Q

clinical manifestations of STEMI

A

pain is deep and visceral; (heavy squeezing, and crushing), occurs at rest (more severe and last longer), weakness, sweating, nausea, vomiting, anxiety

46
Q

physical findings of STEMI

A

substernal chest pain persisting for >30 min and diaphoresis, tachycardia and/or hypotension (anterior MI), bradycardia and/or hypotension (inferior MI), pericardial friction rub, temp elevation

47
Q

diagnosis of STEMI

A

ECG, biomarkers, imaging, non-specific indicators of tissue necrosis and inflammation

48
Q

biomarkers for STEMI

A

cardiac-specific troponin, cardiac-specific troponin-1, CK, CKMB (MB isoenzyme)
released when there is tissue damage

49
Q

what chemical is used as a dye in autopsies to see a fresh MI better?

A

triphenyltetrazolium chloride

50
Q

progression of myocardial necrosis

A
  • Occlusion of coronary artery less than 2 hours= tissue can be helped
  • Occlusion for more than 2 hours= entire area can be necrotic
  • Longer occlusion= larger area of tissue damage
51
Q

stages and histology of MI

A

LOOK AT SLIDE

52
Q

reperfusion

A

RESCUE!=Critical to restore circulation!

however sometimes there are complications to reperfusion

53
Q

preconditioning

A

situation in which repetitive ischemia is preparing myocardium to survive long periods of ischemia

54
Q

consequences of myocardial ischemia followed by reperfusion

A
  • If the blood flow is restored w/in 20 min, the entire area will be healthy/ no necrosis
  • Longer ischemia; reperfusion w/in 2-4 hours= some damaged tissue but some tissue will be healthy after some time
  • Permanent ischemia/ no restoration of blood flow, entire area will be necrotic
55
Q

complications of myocardial ischemia

A

acute left ventricular failure, pulmonary edema, shock, arrhythmias, myocardial rupture, hemopericardium (hemorrhage in myocardial cavity), pericarditis (Dressler Syndrome)

56
Q

acute ischemic injury

A
  • Global cerebral ischemia= Usually assoc w/ systemic reasons (cardiac arrest, shock, severe hypotension)
  • Focal cerebral ischemia= Only the portion of brain is affect
57
Q

global cerebral ischemia

A

mild cases= transient post-ischemic confusional state

severe cases= persistent vegetative state; “Respirator brain”

58
Q

focal cerebral ischemia

A

If sustained, leads to infarction

  • Thrombotic occlusion due to atherosclerosis
  • Embolism
  • Vasculitis
59
Q

2 types of brain infarction

A
  1. ) hemorrhagic= with blood

2. ) non-hemorrhagic (pale, anemic)= due to ischemia

Cardio Exam 2 (7 decks)

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