Ischemic Heart Disease Flashcards
Ischemic Heart Disease
Define Ischemic Heart Disease
imbalance between myocardial oxygen supply and demand
Ischemic Heart Disease
What does ischemic heart disease cause?
results in myocardial hypoxia and accumulation of metabolic waste products
Ischemic Heart Disease
What is the primary cause of ischemic heart disease?
narrowing of coronary artery as a result of athersclerotic plaque
Ischemic Heart Disease
What are “ischemic syndromes?”
manifestations of ischemic heart disease
Myocardial Oxygen Supply
What two things determine myocardial oxygen supply?
- O2 carrying capacity
- Coronary blood flow
Myocardial Oxygen Supply
What are the 2 factors effecting oxygen carrying capacity?
- blood oxygen saturation level (SaO2%)
- hemoglobin (Hg) content
Myocardial Oxygen Supply
What are considered normal levels of blood oxygen saturation level?
usually 97 - 100%
Myocardial Oxygen Supply
What are considered normal Hg content for men and women?
Men: 12 -15.5 mg/dl
Women: 13.5 -17.5 mg/dl
Myocardial Oxygen Supply
Key Point
oxygen carrying capacity is usuallt constant unless anemia or obstructive lung disease is present
Myocardial Oxygen Supply
What does coronary blood flow depend on?
- perfusion pressure
- vascular resistance
Myocardial Oxygen Supply
What is Darcy’s Law?
Q = (P1 - P2) / R
Myocardial Oxygen Supply
How is perfusion pressure (P) related flow?
P is directly related to flow (Q)
Myocardial Oxygen Supply
How is vascular resistance related to flow?
R is inversely proportional to flow (Q)
Myocardial Oxygen Supply
It is important to know that coronary blood flow occurs mainly during what portion of the heart cycle?
diastole (left coronary)
Myocardial Oxygen Supply
How can perfusion pressure (P) be estimated?
by diastolic pressure in aorta
Myocardial Oxygen Supply: Perfusion Pressure
The left main coronary blood flow is zero in early systole due to what?
extravascular myocardial compression of small coronary microvessels
Myocardial Oxygen Supply: Perfusion Pressure
Left coronary artery flow returns to diastolic level in systole but flow is maximum when?
during diastole
Myocardial Oxygen Supply: Perfusion Pressure
When does right coronary artery flow increases and why?
- during both systole and diastole
- this is due to less compression in right ventricle during systole
Myocardial Oxygen Supply: Perfusion Pressure
What is the typical aortic flow pressure? How is the accomplished?
- fairly constant flow between diastolic pressure of 60 - 150 mmHg
- this is done by autoregulation
Myocardial Oxygen Supply: Perfusion Pressure
Does P or R have greater contribution to flow alterations?
R is the major factoer that controls changes in coronary flow
Myocardial Oxygen Supply: Perfusion Pressure
Conditions that decrease aortic diastolic BP to less the 60 mmHg can cause what?
reduced coronary artery perfusion in left and right coronary artery; this increases risk of ischemia
- common issue in elderly
Myocardial Oxygen Supply
What is important to know about myocardial oxygen extraction?
it is almost maximal (75%) at rest
Myocardial Oxygen Supply
What is important to know about myocardium in regards to increased O2 requirement?
the demand must be met primarily by increased coronary blood flow (CBF)
Myocardial Oxygen Supply
What is the resting coronary blood flow and oxygen extraction?
- about 250 ml/min
- 70 - 80% in the heart
Myocardial Oxygen Supply
How does myocardial extraction differ from other parts of the body?
- it is much higher
- compared to about 25% in skeletal muscle
Myocardial Oxygen Supply
How is increased O2 consumption dealt with in the heart?
mainly be reducing vascular resistance
Myocardial Oxygen Supply: Vascular Resistance
Describe Poiseulle’s Law, Darcy’s Law, and the equation for resistance.
look them up
Myocardial Oxygen Supply: Vascular Resistance
What does it mean if:
1. flow (Q) through a tube is directly proportional to pressure gradient (delta P) and radius (r) of a vessel
2. Q is inversely proportional to resistance (R)
- R is indirectly proportional to r^4
- R is directly proportional to length (l) and viscosity of blood
Vascular Resistance and atherosclerotic
3 Key Points
- small resistance arterioles distal to plaque dilate (increase radius), which increases flow (Q) to tissue, in order to compensate for proximal stenosis and reduced flow
Maximal CBF is compromised when lesion damage is what?
greater than 60 - 70%
What effect does 60 - 70% lesion have on resting CBF?
no effect
When does resting CBF become compromised?
when the lesion is greater than 90%
Myocardial Oxygen Supply: Vascular Resistance
CBF is regulated by autoregulation of local vascular resistance via:
- Metabolic factors
- Endothelial factors
- Neural factors
Myocardial Oxygen Supply: Vascular Resistance
Examples of metabolic factors and what they do?
adenosine: dilation
hypoxia: dilation
Myocardial Oxygen Supply: Vascular Resistance
Examples of endothelial factors and what they do?
- NO, prostacyclin, EDHF: dilation
- Endothelin-1: constriction
- Angiotensin II: constriction
Myocardial Oxygen Supply: Vascular Resistance
Examples of neural factors and what they do?
sympathetic nerve and circulation NE/Epi:
- alpha-1 adrenergic activation: constriction from sympathetics
- beta-2 adrenergic activation: dilation from Epi
Myocardial Oxygen Demand
What 3 physiological factors create myocardial oxygen demand?
- wall stress
- heart rate
- contractility
Myocardial Oxygen Demand
Define Myocardial Oxygen Demand.
indicates metabolic rate or oxygen consumptoin of myocardium (MVO2)
Myocardial Oxygen Demand: Wall Stress
Define wall stress
tangential force activation on the LV myocardial fibers tending to pull them apart
wall stress = (P * r) / h
Myocardial Oxygen Demand: Wall Stress
What happens to wall stress, if P or r increases?
it increases; examples:
- hyoertension or aortic stenosis increase LV P and increases wall stress
- conditions (aortic regurg; heart failure) that augment LV chamber size via excess LV filling will increase wall stress
Myocardial Oxygen Demand: Wall Stress
What may happen to h when P increases to maintain wall stress?
it increases, example:
- LV hypertrophies in response to chronic high BP to decrease wall stress
Myocardial Oxygen Demand: Heart Rate
When does the number of contraction increase?
during exertion
Myocardial Oxygen Demand: Heart Rate
What two things does increased contraction of the heart lead to?
- increase in ATP per minute consumed
- increased MVO2
Myocardial Oxygen Demand: Heart Rate
Conversely, a decrease in HR can be caused by what? What will become reduced?
- beta-blocker medication
- MVO2
Myocardial Oxygen Demand: LV myocardial contractility
What are three ways an increase in MVO2 can be caused?
- increase in circulating norepinephrine
- direct sympathetic nerve stimulation on LV myocardium
- positive iontropic drugs will increase MVO2
Myocardial Oxygen Demand: LV myocardial contractility
What can cause a decrease in MVO2?
beta-blockers or Ca+2 channel blockers
Ischemic ‘Syndromes’
What are 5 types of ischemic syndromes?
- angina pectoris
- stable vs. unstable angina
- variant angina
- silent ischemia
- myocardial infarction
Ischemic ‘Syndromes’: Angina Pectoris
What can the pain of angina pectoris be described as?
strangling in the chest
Ischemic ‘Syndromes’: Angina Pectoris
Where do people typically feel discomfort?
substernal chest area from ischemia
Ischemic ‘Syndromes’: Angina Pectoris
What are nociceptors in myocardial tissue stimulated by?
ischemic metabolites send afferent signals to brain
Ischemic ‘Syndromes’: Angina Pectoris
Where else can someone feel pain radiate in their body?
- left shoulder/arm
- epigastric
- neck/jaw
- upper back
(known as referred pain)
Ischemic ‘Syndromes’: Angina Pectoris
What are precipitating causes?
physical exertion, emotional stress; relieved by rest
Ischemic ‘Syndromes’: Angina Pectoris
Key Point
Angina results from imbalance between myocardial oxygen suppply and demand (MVO2)
Ischemic ‘Syndromes’: Angina Pectoris
Quality of symptoms?
usually described as pressure, tightness, burning, squeezing
- last 5-10 minutes
Ischemic ‘Syndromes’: Angina Pectoris
What could a time frame of longer than 10 minutes signify?
may be the start of myocardial infarction
Ischemic ‘Syndromes’: Angina Pectoris
What are NOT symptom qualities?
sharp and stabbing pain
- change of pain with inspiration/expiration
- change of pain with palpating chest wall
Ischemic ‘Syndromes’: Angina Pectoris
What are common associated symptoms?
sympathetic response
- tachycardia, diaphoresis, dyspnea, fatigue, nausea
Ischemic ‘Syndromes’: Stable vs Unstable Angina
Define stable angina.
chronic pattern of angina has 3 features:
- exacerbated during physical exertion or emotion
- relieved with rest within 3-5 minutes or with sublingual nitroglycerin
- ST segment depression or T wave inversion on ECG
Ischemic ‘Syndromes’: Stable vs Unstable Angina
Define unstable angina
- pattern of increased “frequency or duration of anginal episodes” or “anginal symptoms at rest
- indicates progression of disease and likely from partial thrombosis
- high risk for progressing to myocardial infarction
Ischemic ‘Syndromes’: Variant angina
What other name is this known as?
prinzmetal’s angina
Ischemic ‘Syndromes’: Variant angina
How is the pain caused?
anginal discomfort comes from coronary vasospasm
Ischemic ‘Syndromes’: Variant angina
What is the result of a coronary vasospasm?
decreased myocardial oxygens supply because of constriction (rather than increased MVO2)
Ischemic ‘Syndromes’: Variant angina
When can this occur?
at rest or due to physical exertion
Ischemic ‘Syndromes’: Variant angina
What groups of people experience this more commonly?
females and smokers
Ischemic ‘Syndromes’: Variant angina
What is the estimated mechanism?
a result in part from impaired nitric oxide release or other dilators from endothelium, but cause is unknown
Myocardial Ischemia on ECG
Subendocardial ischemias can be determined by what two things on an ECG?
- T wave inversion
- ST segment depression
Myocardial Ischemia on ECG
Describe a subendocardial ischemia T wave inversion.
- usually appears within seconds of onset of ischemia
- due to delat in repolarization
Myocardial Ischemia on ECG
Describe a subendocardial ischemia ST segment depression.
- usually from severe subendocardial ischemia
- leads to delayed repolarization in subendocardium
- sometimes associated with inverted T wavs (but not always)
Myocardial Ischemia on ECG
Define an ST segment depression.
depression of ST segment in mm below PQ segment (baseline)
- 0.08 msec (two small boxes) after the J point
Myocardial Ischemia on ECG
3 Key ST segment characteristics used for determination.
- magnitude: in mm (severity of ischemia)
- distribution: # of leads
- slope of ST depression is significant
Myocardial Ischemia on ECG
Describe what differing ST segment slopes mean.
- downsloping = severe ischemia
- horizontal = moderate ischemia
- upsloping = non-diagnostic of ischemia
Ischemic ‘Syndromes’: Silent Ischemia
Define Silent ischemia.
myocardial ischemia without symptoms of angina
Ischemic ‘Syndromes’: Silent Ischemia
How does it present on an ECG?
- may show up as ST segment depression or T wave inversion on ECG
- difficult to diagnose without ECG
Ischemic ‘Syndromes’: Silent Ischemia
What is the cause?
unknown
Ischemic ‘Syndromes’: Silent Ischemia
Who experiences this more commonly?
- patients with diabetes because of impaired pain sensation from peripheral neuropathy
- women or has an unusual presentation then typical chest discomfort
Pharmacological Treatment of Angina
What is the goal?
to prevent symptoms
Ischemic ‘Syndromes’: Myocardial Infarctions
MI
discussed in next leture
Pharmacological Treatment of Angina
What do nitrates do?
vaso and venodilator
- decrease MVO2 demand
- increase MVO2 supply
Pharmacological Treatment of Angina
How do nitrates decrease MVO2 demand?
reduce preload via venodilation:
- decrease venous return back to heart
- decrease LV flling (decrease wall stress)
Pharmacological Treatment of Angina
How do nitrates increase MVO2 supply?
- increase coronary blood flow via vasodilation
- decrease coronary vasospasm
Pharmacological Treatment of Angina
What do beta-blockers do?
block cardiac beta-1 adrenergic receptors
- decrease MVO2 demand
Pharmacological Treatment of Angina
How do beta-blockers decrease MVO2 demand?
decrease HR and contractility (decrease wall stress)
Pharmacological Treatment of Angina
What do calcium channel blockers do?
blocks cardiac and VSMC L-type Ca2+ channels
- decrease MVO2 demand
- increase MVO2 supply
Pharmacological Treatment of Angina
How do calcium channels blockers decrease MVO2 demand?
- decrease preload, contractility, HR
Pharmacological Treatment of Angina
How do calcium channel blockers increase MVO2 supply?
- increase coronary blood flow via vasodilation
- decrease coronary vasospasm
