Norton - IHD Flashcards
IHD - general
imbalance - supply and demand for oxygenated blood for the heart
reduced nutrients, waste removal
IHD is also called
CAD, coronary heart disease
> 90% of IHD is caused by
reduced coronary blood flow due to atherosclerotic coronary arterial obstruction
Clinical manifestation - IHD
angina pectoris
MI
Chronic IHD w/ HF
Sudden cardiac death
1 cause of death of both men and women in US
IHD
Pathogenesis IHD
demand > coronary perfusion
What can increase the demand while perfusion is low
Fixed obstruction
acute plaque change
coronary thrombus
vasospasm
obstruction needed to cause symptomatic ischemia with:
exercise
at rest
> 70% w/ exercise
> 90% at rest
what can protect distal myocardium from ischemia
collateral
triggering factors for acute plaque change
- adrenergic stimulation
- dynamic changes of the structure and composition of plaque
- moderately stenotic are most dangerous
most dangerous trigger factor for acute plaque change
moderately stenotic
Coronary thrombus can
- partial occlusion – eventually lead to total occlusion
- emolize
- activate SM growth-related signals
Vasoconstriction is stimulated by
adrenergic agonist
platelet contents
How does angina pectoris present?
Paroxysmal
Recurrent
Substernal/precordial chest discomfort - constricting, squeezing, choking, knifelike
lasts at most 15 min - no infarction
what is angina pectoris due to
myocardial ischemia
Stable angina - decreased coronary perfusion due to
fixed obstruction
Unstable angina is due to
disruption of atherosclerotic plaque with superimposed partially occluding thrombus
1 of the acute coronary syndromes
unstable angina
Prinzmetal angina is not related to
physical activity
HR
BP
2 of the acute coronary syndromes
MI
Acute plaque disruption
- hemorrhage
- erosion/ulceration
- rupture or fissuring
90% of transmural infarcts
acute plaque disruption – platelets adhere to exposed subendothelial collagen/necrotic plaque contents, release aggregators – vasospasms – other extrinsic coag pathway also gets activated – Thrombus quickly occludes lumen
myocardial response to ischemia at ~ 1 sec
cessation of aerobic glycolysis
decreased creatine phosphate, ATP
Accumulate lactic acid
when does loss of contractility occur
after 2 min
when does injury to myocyte become irreversible?
20-40min
microvascular injury occurs
after 1 hr
_____ may occur even due to ischemia
arrhythmias
Subendocardial infarct is NOT due to
plaque disruption
superimposed thrombus
Subendocardial infarct is majorly due to
diffuse stenosing coronary atherosclerosis with reduction of blood flow
Morphology of MI depends on
- Location, severity and rate of dev of coronary obstruction
- size of area perfused by obstructed vessel
- duration of occlusion
- metabolic/oxygen demand
- extent of collateral
- coronary vasospasm
- BP, HR, rhythm
- Necrosis (complete in 6 hrs)
Infarct modification by reperfusion
Thrombolysis
Angioplasty w/ stent placement
CABG
Grafting of
RCA
LAD
RCA - saphenous vein
LAD - internal mammary artery
Factors associated with poor prognosis (MI)
Advanced age
female gender
DM
previous MI
Consequence and complications of MI
Contractile dysfunction (htn, pulmonary vascular congestion, cardiogenic shock if severe)
Arrhythmias
Myocardial rupture
Pericarditis
right ventricular infarct
Mural thrombus
Ventricular aneurysm
Papillary m. dysfunction
Progressive late heart failure
Most common to least common myocardial rupture
Ventricular free wall – cardiac tamponade
Intraventrucular septum – L-R shunting
Papillary m. – severe mitral regurgitation
What is a later complication of MI
ventricular aneurysm
is rupture common with ventricular aneurysm?
no - scar tissue is strong
Complications of MI depend on
infarct size, site, transmural extent
Large transmural infarct
Cardiogenic shock
Arrhythmias
late CHF
Anterior transmural infarct
Free-wall rupture expansion Mural thrombi aneurysm worse clinical course
Inferior transmural infarct
conduction blocks
RV involvement
Most important factors affecting prognosis after an MI
- quality of LV function
- extent of vascular obstruction perfusing viable myocardium
Often elderly, ptns develop ________ due to ischemic myocardial damage
progressive HF
Chronic ischemic heart dz
hypertrophy, dilation, stenosis of coronary, healed previous infarcts
is prior sx or history necessary to present with CHF?
no
Sudden Cardiac death
Unexpected death from cardiac causes - no symptomatic heart dz or early after the onset of sx (less than 1 hr)
Sudden cardiac death is usually due to
IHD
Other causes of Sudden cardiac death
- congenital
- valvular issues (aortic)
- myocarditis
- cardiomyopathy
Ultimate mechanism of Sudden cardiac death
lethal ARRHYTHMIA
3 of the acute coronary syndromes
Sudden cardiac death
Morphology of sudden cardiac death
- coronary artery occlusion 75% in one or more of the three major vessels
High grade stenosis
Prognosis in survivors of sudden cardiac death is improved by
implanting automatic cardioverter-defibrillator
The acute coronary syndromes:
unstable angina
acute MI
sudden cardiac death
What do acute coronary syndromes share?
- common pathophys -
coronary atherosclerotic plaque disruption and assoc. intraluminal platelet-fibrin thrombus formation
