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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the most common cause of myocardial ischemia?

A

atherosclerotic disease

atherosclerotic lesions reduce blood flow to the myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are powerful risk factors for IHD?

A

obesity, insulin resistance, and Type 2 DM

overlap b/w risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

major pathophysiological mechanism behind IHD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where is there coronary atherosclerosis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the risk factors for coronary atherosclerosis?

A

exactly the same as for atherosclerosis

high LDL, low HDL, smoking, HTN, DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

80% stenosis in IHD

A

blood flow AT REST may be reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which arteries are particularly hazardous to develop stenosis?

A

left main coronary artery or the proximal left anterior descending

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

formation of collateral vessels

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effects of ischemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what effect of transient ischemia would we see in clinic?

A

angina pectoris= chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
effects of ischemia
electrical instability, which may lead to ventricular arrhythmia's or ventricular fibrillation
26
diagnosis of IHD
many may be asymptomatic exercise-induced ECG changes angiography 25% of pts who survive acute MI may not come to medical attention
27
symptoms of IHD
• 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
classification of IHD
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
reading an ECG
• 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
What are the outcomes of a partial occlusion of a blood vessel?
• 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
STEMI
assoc w/ complete occlusion
32
NSTEMI
assoc w/ partial occlusion
33
stable angina pectoris age
male over 50 and women over 60 (since until 50 women are protected by estrogen)
34
clinical manifestations of stable angina pectoris
chest discomfort (not always pain), crescendo-descresendo, radiates to shoulders, sx relieved by rest or sublingual nitroglycerin, dyspnea, nausea, fatigue, faintness
35
how can you tell if the pt is progressing to unstable angina?
ALWAYS ASK | angina occurring with less exertion than in the past, occurring at rest, or awakening the pt from sleep
36
physical examination for IHS
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
unstable angina/ NSTEMI definitions
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
clinical manifestations of UA/ NSTEMI
``` 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
cardiac markers for UA/NSTEMI
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
Prinzmetal's Variant Angina
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
STEMI
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
coronary plaques prone to disruption
Thin fibrous cap | Thick fibrous cap and thin lipid core= safe; not likely to rupture
43
coronary emboli vs coronary thrombus
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
risk factors for STEMI
multiple: UA (can progress to clinically obvious MI), hypercoagulability, collagen vascular diseases, cocaine abuse, intracardiac thrombi, coronary emboli
45
clinical manifestations of STEMI
pain is deep and visceral; (heavy squeezing, and crushing), occurs at rest (more severe and last longer), weakness, sweating, nausea, vomiting, anxiety
46
physical findings of STEMI
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
diagnosis of STEMI
ECG, biomarkers, imaging, non-specific indicators of tissue necrosis and inflammation
48
biomarkers for STEMI
cardiac-specific troponin, cardiac-specific troponin-1, CK, CKMB (MB isoenzyme) released when there is tissue damage
49
what chemical is used as a dye in autopsies to see a fresh MI better?
triphenyltetrazolium chloride
50
progression of myocardial necrosis
* 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
stages and histology of MI
LOOK AT SLIDE
52
reperfusion
RESCUE!=Critical to restore circulation! | however sometimes there are complications to reperfusion
53
preconditioning
situation in which repetitive ischemia is preparing myocardium to survive long periods of ischemia
54
consequences of myocardial ischemia followed by reperfusion
* 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
complications of myocardial ischemia
acute left ventricular failure, pulmonary edema, shock, arrhythmias, myocardial rupture, hemopericardium (hemorrhage in myocardial cavity), pericarditis (Dressler Syndrome)
56
acute ischemic injury
* Global cerebral ischemia= Usually assoc w/ systemic reasons (cardiac arrest, shock, severe hypotension) * Focal cerebral ischemia= Only the portion of brain is affect
57
global cerebral ischemia
mild cases= transient post-ischemic confusional state | severe cases= persistent vegetative state; "Respirator brain"
58
focal cerebral ischemia
If sustained, leads to infarction * Thrombotic occlusion due to atherosclerosis * Embolism * Vasculitis
59
2 types of brain infarction
1. ) hemorrhagic= with blood | 2. ) non-hemorrhagic (pale, anemic)= due to ischemia