Lect 5- Ischemic Heart Disease Flashcards
Ischemic heart disease definition
inadequate supply of blood and oxygen to a portion of the myocardium
occurs when there is an imbalance b/w oxygen supply and demand
what is the most common cause of myocardial ischemia?
atherosclerotic disease
atherosclerotic lesions reduce blood flow to the myocardium
what are powerful risk factors for IHD?
obesity, insulin resistance, and Type 2 DM
overlap b/w risk factors
major pathophysiological mechanism behind IHD
imbalance b/w myocardial oxygen demand (MVO2) and delivery
hypoxia vs ischemia
• 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)
the oxygen-carrying capacity of the blood is determined by:
the inspired level of O2, pulmonary function, Hb conc and function
coronary blood flow
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
Coronary blood flow is controlled by what?
Metabolic regulation= exercise, emotional stress, etc
Autoregulation= blood flow is kept at certain range independent to changes in BP (protective mechanism)
Rupture of a plaque
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
other causes of IHD
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
where is there coronary atherosclerosis?
sites of increased turbulence in coronary flow and branch points in the epicardial arteries
what are the risk factors for coronary atherosclerosis?
exactly the same as for atherosclerosis
high LDL, low HDL, smoking, HTN, DM
severity of symptoms in IHD
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)
50% stenosis in IHD
Usually pts do not have sx if they do regular activities but they might have sx if they do cardio/ exercise
80% stenosis in IHD
blood flow AT REST may be reduced
which arteries are particularly hazardous to develop stenosis?
left main coronary artery or the proximal left anterior descending
formation of collateral vessels
GOOD!
Collateral circulation affects the way the disease is produced
Formed when gradually developing stenosis
effects of ischemia
inadequate perfusion; decreased myocardial O2 tension; mechanical, biochemical and electrical disturbances
what are the mechanical effects of ischemia?
regional disturbances of ventricular contractility; segmental hypokinesia; segmental akinesia; segmental dyskinesia
all eventually lead to reduced myocardial pump function
effects of acute ischemia
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
what effect of transient ischemia would we see in clinic?
angina pectoris= chest pain
what effect of prolonged ischemia would we see in clinic?
acute MI
• Prolonged ischemia= severe narrowing/ blockage
• Myocardial infarction= tissue necrosis
○ Irreversible tissue damage/ cells are dying
ECG in IHD
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
what will you find on an ECG of a pt with IHD?
- Ischemia= problems with ventricular repolarization
- ST depression= indicates ischemia (partial thickness)
- Dramatic ST elevation= entire thickness
effects of ischemia
electrical instability, which may lead to ventricular arrhythmia’s or ventricular fibrillation
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
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
classification of IHD
- ) chronic coronary artery disease (CAD)= stable angina
- ) acute coronary syndromes (ACSs)= progressive; acute MI, unstable angina, NSTEMI, sudden cardiac death, Prinzmetal’s Variant Angina (special type)
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
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
STEMI
assoc w/ complete occlusion
NSTEMI
assoc w/ partial occlusion
stable angina pectoris age
male over 50 and women over 60 (since until 50 women are protected by estrogen)
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
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
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)
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)
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
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
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
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
coronary plaques prone to disruption
Thin fibrous cap
Thick fibrous cap and thin lipid core= safe; not likely to rupture
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
risk factors for STEMI
multiple: UA (can progress to clinically obvious MI), hypercoagulability, collagen vascular diseases, cocaine abuse, intracardiac thrombi, coronary emboli
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
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
diagnosis of STEMI
ECG, biomarkers, imaging, non-specific indicators of tissue necrosis and inflammation
biomarkers for STEMI
cardiac-specific troponin, cardiac-specific troponin-1, CK, CKMB (MB isoenzyme)
released when there is tissue damage
what chemical is used as a dye in autopsies to see a fresh MI better?
triphenyltetrazolium chloride
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
stages and histology of MI
LOOK AT SLIDE
reperfusion
RESCUE!=Critical to restore circulation!
however sometimes there are complications to reperfusion
preconditioning
situation in which repetitive ischemia is preparing myocardium to survive long periods of ischemia
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
complications of myocardial ischemia
acute left ventricular failure, pulmonary edema, shock, arrhythmias, myocardial rupture, hemopericardium (hemorrhage in myocardial cavity), pericarditis (Dressler Syndrome)
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
global cerebral ischemia
mild cases= transient post-ischemic confusional state
severe cases= persistent vegetative state; “Respirator brain”
focal cerebral ischemia
If sustained, leads to infarction
- Thrombotic occlusion due to atherosclerosis
- Embolism
- Vasculitis
2 types of brain infarction
- ) hemorrhagic= with blood
2. ) non-hemorrhagic (pale, anemic)= due to ischemia
