CLASS 21 - ISCHEMIC HEART DISEASE Flashcards
Which 2 coronary arteries does the myocardium recieve blood from?
L + R
Which 2 arteries does the Left Main Coronary Artery branch into?
Circumflex
Left Anterior Descending
What 2 areas of the heart does the LAD supply blood to?
Circumflex artery?
LAD: LV and septum
Circumflex: Lateral + posterior LV
What areas of the heart does the Right Main coronary artery and its branches supply blood to?
Anterior + posterior right vetricle
SA/AV nodes
What ares of the heart does the posterior descending artery supply blood to?
inf + apex of myocardium
When the heart rate or metabolic rate increases such as during exercise, smooth muscle in the arterioles supplying the heart muscle _______ causing _________ and increased blood flow.
relaxes
vasodilation
What are the 3 causes of local dilation in the smooth muscle of the arterioles supplying the heart?
1) metabolites
2) B-adrenergic stimulation (SNS reponse)
3) Release of NO from vascuar endothelium
Why does the heart muscle receive blood during diastole?
due to the high pressure during systole.
This is acheived by the aortic recoil which aids perfusion into the coronary arteries.
What is the effect of a high heart rate on diastolic time?
High HR decreases diastolic time.
Decreases the perfusion time of the coronary arteries which may contribure to ischemia in an individual w narrowed coronary arteries.
What is the most common form of heart disease?
CAD, also called IHD
What is the most common cause of CAD?
Atherosclerosis
What is an atheroma?
a fatty, fibrous mass, or a plaque
at what age does plaque formation usually begin in the body?
In your 20s.
the process of atheroslcerosis is usually asymptomatic until when? What symptoms show at this point?
asymptomatic until a vessel is 75% occluded.
at this time the heart shows signs of ischemia particularly during high times of physical exertion when the metabolic demand is higher.
What is collateral circulation?
additional arterial connections that can form around an area of increasing occlusion / blockage
What are the 9 clinical manifestations of CAD?
Chronic Stable Angina
Acute Coronary Syndrome
- Unstable Angina
- Acute MI
- Non-STEMI
- STEMI
Cardiac Arrhythmias
Heart Failure
Sudden Cardiac Death
when can ischemia occur at rest?
when lumen reduced by 90%
Describe the effects of a MI at a cellular level .
What happens if the blood flow returns in time?
myocardium hypoxic within first 10 seconds of blockage
total occlusion - contractility stops after several minutes
anaerobic metabolism begins
- lactic acid accumulates
- pain fibers stimulated
- crossover –> referred pain –> left shoulder and arm
cardiac cells begin dying ~ 20 mins
IF blood flow returns in time, process reverses, contractility restored and repair begins
Identify the 5 possible effects of Cardiac Ischemia
1) Diastolic Dysfunction
2) Systolic Dysfunction
3) Electric disturbance in heart rhythm
4) Angina pectoris (chest pain)
5) Cardiac muscle death (necrosis), MI
What is angina? Where is the pain typically located? What is the pain sensation often described as?
angina is chest pain resulting from reversible myocardial ischemia
pain typically located in substernal region and may radiate to the arm
visceral + referred pain
pressure, aching, heaviness, choking, suffocating, or squeezing
what are the 4 typical presentations of angina?
1) midsternal, neck, L shoulder and down both arms
2) substernal radiating to neck and jaw, radiating down left arm
3) epigastric, radiating to neck, jaw, and arms
4) intrascapular
describe stable angina in terms of how long it lasts, what causes it and induces it, and how we can control it.
- thought to be caused by an advanced plaque that is hightly fibrotic and contains little lipid (stable)
- usually brief (3-5 mins), relieved by rest and / or nitroglycerine (which causes vasodilation)
- may be induced by specific levels of activity
- can often be controlled with medications
what is the effect of Stable Angina on an ECG?
ST depression
What is prinzmetal’s angina (variant angina)?
what causes it? when does it occur?
occurs at rest due to coronary artery spasm
may occur w or w/o coronary artery disease (can occur if someone has a history of migraines or raynaud’s phenomenon)
may be in response to a stimulant
Describe Acute Coronary syndrome and its 3 components
when does it typically occur?
acute coronary syndrome develops when myocardial ischemia is prolonged and not immediately reversible.
- unstable angina
- non-STEMI (non ST-segment elevation myocardial infarction)
- STEMI (ST-segment elevation myocardial infarction)
Typically occurs when a coronary artery is greater than 90% occluded.
Describe Unstable Angina as an Acute Coronary Syndrome.
rupture of plaque with subsequent coronary vasoconstriction and occlusive thrombus formation.
This is followed by spontaneous thrombolysis (resolves it)
requires immediate hospitalization
identify the 3 clinical manifestations of unstable angina
1) chest pain - onset, duration, and intensity of symptoms lasting up to 20 minutes and is not relieved by rest or nitroglycerine
2) dyspnea - may occur due to myocardial cysfunction and pulm edema
3) reduced CO may occur bc of systolic dysfunction
what are the 5 typical progressions of angina?
1) angina that develops w less exertion
2) angina at rest or during sleep
3) angina pain that isn’t relieved properly w nitroglycerine but once was
4) angina that gradually worsens over a period of days
5) cardiac biomarkers remain normal or are only very minimally elevated.
how can a ventricle become “stunned”?
Ventricle can become stunned if ischemia is persistent but lasts less than 30 minutes
Results in mild decrease in ventricular function that can last for weeks.
if blood flow is not restored within ____ to ____ minutes, cardiac cells begin to die, resulting in permanent myocardial dysfunction.
40 - 60 minutes
What is the cause of myocardial infarction ?
Where does necrosis begin?
usually caused by plaque rupture and subsequent occlusive thrombus formation.
necrotic death of cardiac muscle results from prolonged ischemia (~ 20-60 minutes) and leads to irreversible dysfunction
necrosis begins on the endocardial (inside) surface of the heart and progresses to the pericardial (outside) surface.
What is it called when the infarction involves the entire thickness of the ventricle?
Transmural infarction
If the only inner portion of the ventricle has died, what is it called?
Subendocardial infarction
Why doesn’t a previous history of ischemic heart disease always precede myocardial infarctions?
rupture-prone plaques can be less than 50% occlusive.
what are the 7 clinical manifestations of a myocardial infarction?
1) Chest pain
2) Dyspnea, orthopnea, increased JVP, leg edema, and syncope
3) skin cold and clammy, reflex tachycardia, SNS stimulation
4) bradycardia
5) increased temp
6) ECG changes (such as STEMI)
7) elevated cardiac-specific biomarkers in the blood
how does the conc of troponin in the blood change in the hours after an MI to days after an MI?
Troponin can be 5x higher than normal level during an MI and reduces to 4x higher 6 hours later
returns to normal range around 2 days after a heart attack
how does the conc of myoglobin in the blood change in the hours after an MI to days after an MI?
myoglobin can be 4x higher 3 hrs after an MI
returns to normal about 4 days later
how does the conc of CK-MB in the blood change in the hours after an MI to days after an MI?
CK MB gradually rises
spikes 6 h after MI and reached 5x higher then steadily declines, reaches normal within 5 days after
______ of heart muscles results in an inflammatory response, infiltration of macrophages, small rise in temperature
necrosis
why does scar tissue form after a myocardial infarction? what damage occurs as a result of this?
cardiac cells cannot regenerate
leads to scar tissue formation
cannot contract and permanent ventricular dysfunction results
Why would a transmural MI result in a permanent change in the ECG?
Because scar tissue is not excitable.
Following an MI, ____________ reduces the risk of life threatening arrhythmias (increased circulating catecholamines), lower the myocardial oxygen demand, and reduce mortality.
Beta-blockade
what is an arrthythmia?
Arrhythmias are atrial and ventricular rhythms resulting in tachycardia, bradycardia, or AV conduction blockage.
True or false: cardiac arrest rhythms such as pulseless VT or VF require immediate hospitalization.
true
what is acute heart failure / cardiogenic shock?
failure to pump adequate blood results in hypotension and hypoperfusion of all organs, particularly the kidneys and brain.
Describe how tamponade occurs due to pericarditis, effusion, and myocardial rupture.
fluid around heart compresses the heart wall
the heart cannot expand to fill
backup into systemic circulation
decreased blood flow to lungs
reduces output to body (tamponade).
describe mural thrombosis and embolism as a complication of MI
stasis of blood in the ventricle can cause thrombus and embolism (ex - cerebral or pulmonary embolism)
describe valve disorders as a complication of MI
damage to papillary muscles can cause AV valve disorders such as mitral valve regurgitation
what is sudden cardiac death?
immediate loss of cardiac output, cerebral blood flow, or LOC
Death usually within 1 hour of symptom onset
what are the 2 highest predictors of sudden cardiac death?
ventricular EF < 30%
Ventricular arrhythmia post-MI
T or F: sudden cardiac death may be the first sign in 25% og people who die of heart disease
true
define angina
when the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle “aches”.
what increases myocardial oxygen demand?
increased physical activity stress SNS input tachycardia increased afterload volume overload cardiac hypertrophy
what decreased myocardial oxygen supply?
CAD hypovolemia weakened heart muscle arrhythmias cardiac injury / remodelling valve disease anemia respiratory disease
What Class of Angina is this:
ordinary physical activity does not cause angina, such as walking or climbing stairs. angina occurs w strenuous, rapid, or prolonged exertion at work or recreation.
Class I
What Class of Angina is this:
slight limitation of ordinary activity. angina occurs on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or other emotional stress, or only during the few hours after awakening. angina occurs on walking more than 2 blocks on the level and climbing more than 1 flight of ordinary stairs at a normal pace and under normal coditions.
Class II
What Class of Angina is this:
marked limitations of ordinary physical activity. angina occurs on walking one to two blocks on the level and lcimbing one flight of stairs under normal conditions and at normal pace
Clas III
What Class of Angina is this:
inability to carry on any physical activity without discomfort; anginal symptoms may be present at rest.
Class IV
What are the 4 main goals of angina management?
minimize the frequency, duration, and intensity of anginal pain
improve or maintain functional capacity
prevent or delay MI, cardiac remodelling, arrhythmia
minimize adverse effects from medications
Identify 5 non pharmacological mgmt interventions for angina
diet
lifestyle modifications
treat underlying disorder (diabetes, htn, hyperlipidemia)
angioplasty
surgery
What is the MOA of antianginal medications?
Increase supply to ischemic heart muscle by dilating coronary arteries
Decrease myocardial workload by either:
- slowing HR
- Dilating veins in the body so the heart receives less blood (reduce preload)
- causing the heart to contract with less force
- dilating arterioles in the body to lower blood pressure (reduce afterload)
identify the 7 classes of antianginal medications
Beta blockers
Calcium channel blockers
Nitrates
Anticoagulants
Antiplatelets
Antilipemics
Thrombolytics
Provide 2 examples of nitrates and their ROA.
Nitroglycerine (SL tablet or spray, transdermal, IV)
Isosorbide dinitrate (Isordil) (PO)
What is the MOA of nitrates?
- dilate veins in body, decrease venous return which therefore decreases preload and workload
- dilate coronary arteries to increase blood supply to the heart
- used for prevention and treatment of angina
- artificial Nitric Ocide Donor
what needs to be assessed in a pt after administering nitro SL tabs or sprays? How should the doses be administered?
assess angina, BP, and HR after each dose
administering:
- first dose: wait 5 mins
- second dose: wait 5 mins
- third dose: not to exceed 3 doses in 15 mins
What are the adverse effects associated with nitrates?
headaches - usually diminish w continued use
orthostatic hypotension, reflex tachycardia
potential development of tolerance if taking 24/7
what steps need to be taken with transdermal forms of nitrates to prevent tolerance?
remove patch at bedtime for 8 hrs + apply a new patch in the morning
what is the purpose of nitroglycerine IV?
bp control in perioperative HTN
treatment of HF
ischemic pain
pulmonary edema associated w acute MI
hypertensive emergencies
provide 2 examples of beta blockers (the LOLs) and their ROA.
metoprolol (po, IV)
atenolol (po)
What is the MOA of beta blockers?
Selectively block beta-adrenergic stimulation of the heart
cardioprotective
slow heart rate and decrease workload
decrease contractility and decrease workload
decrease frequency of anginal attacks
first-line for chronic angina
anti-arrhythmic
what is the function of cardiac CCBs (non-dihydropyridines)?
dilate coronary arteries and slow condiction velocity to the heart to decrease HR (decrease workload)
provide 2 examples of cardiac CCBs
verapamil
diltiazem (Cardiazem)
what is the MOA of diltiazem (Cardiazem)?
what are some adverse effects? how can we treat it?
inhibits transport of calcium into myocardial cells
reduce vasospasm which is useful w variant angina
used to treat arrythmias
- very acceptable safety profile
- may increase digoxin levels
- caution with other blockers, can cause bradycardia or complete heart block (calcium chloride IV antidote)
what is the function of vascular CCBs (dihydropyridine)?
cause peripheral arterial vasodilation (decrease afterload to therefore decrease workload)
provide 2 examples of vascular CCBs (dihydropyridines)
the “dipine”s
amlodipine (norvasc)
nifedipine (adalat)
what is the MOA of nifedipine (adalat).
inhibits transport of calcium in smooth muscle cells
what are some adverse effects associated with vascular CCBs?
v acceptable adverse effect and safety profile
hypotension, headache, dizziness, edema of ankles and feet related to vasodilation
