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141 Cards in this Set

  • Front
  • Back
The heart, like other organs, has it's own what? It requires lots of what?
Has it's own blood supply, requires lots of O2.
Up to 40% of a cardiac muscle cell's volume is what? What is this important for? What is required?
Mitochondria. Supplies the Energy needed for contraction.

Requires oxygen (aerobic metabolism).
Mitochondria are the "?" of cells.
Mitochondria only depend upon what kind of metabolism?
Only aerobic.
Cardiac muscle cells have lots of what? What do these store?
Have lots of myoglobin, storing limited amount of oxygen in the heart for immediate use.
Can blood passing through the heart muscle supply Oxygen or nutrients to the heart itself? So what does this imply?
NO...So the heart needs it's own blood supply.
List 2 reasons why blood passing through the heart muscle can't supply oxygen or nutrients to the heart?
1. Endocardium lining muscle prevents blood from passing into myocardium (the muscle itself)

2. Heart muscle walls too thick for diffusion of oxygen and nutrients
What is the heart's own blood supply known as?
Coronary Circulation
The left and right ? ? branch from the aorta just beyond the aortic valve.
The coronary arteries (for oxygen delivery)
The ? ? empty into the right atrium.
The coronary veins.
The heart gets most of its blood supply (O2) via what?
Gets most of its blood supply via coronary circulation during diastole.
Blood flow to the heart is reduced during what?
Reduced during systole.
Explain how the blood flow to the heart is reduced during systole.
1. Major branches of coronary arteries compressed by contracting myocardium (so decreased blood flow and decreased oxygen)

2. Entrance to coronary vessels are partially blocked by open aortic valve
Approximately what percentage of arterial flow occurs during diastole?
So coronary circulation occurs via what two arteries?
Right coronary artery and left coronary artery.
Coronary circulation is increased (blood flow is increased) when the heart is ?.
Relaxed (diastole)
Coronary blood flow matches the heart's ? demands.
List 2 ways in which blood delivery to cardiac cells is increased.
1. Via vasodilation of coronary vessels

2. Coordination of coronary flow with O2 needs is adenosine, formed from ATP during cardiac metabolism
The heart, unlike other tissues, is unable to remove what?
Unable to remove extra O2 from blood passing through vessels to meet increased metabolic needs.

(this is related to why the coronary vessels vasodilate to increase blood delivery to cardiac cells)
Under resting conditions, the heart removes ?% of available O2 from blood.

Other tissues use about ?%.
Heart = 65% (this meets metabolic needs...your heart can't extract anymore than this...even when working out)

Other tissues = 25%
What metabolite is key to keeping coronary vessels open? What is this known as?

Called metabolic auto-regulation.

Helps the heart extract oxygen.
What does increased adenosine formation and release do to coronary blood vessels?
Increased adenosine formation and release induces dilation of coronary blood vessels.
Epinephrine causes ?.

Norepinephrine causes ?.
Epi = dilation

NE = constriction
Increased metabolic activity of cardiac muscles leads to an increased need for what?
Increased met. activity of cardiac muscles (more oxygen needed) does what to adenosine?
Increases it.
Increased adenosine leads to ? of coronary vessels.
Vasodilation of coronary vessels does what to the blood flow to cardiac muscle cells?
Increases blood flow to cardiac muscle cells.
Increased blood flow to cardiac muscle cells does what to oxygen?
Increases oxygen available to meet the increased oxygen needs of cardiac muscle cells with increased metabolic activity.
What is CHD?
Disease of heart due to impaired coronary flow. What happens when heart doesn't get enough O2.
CHD can be ? or ?.
Chronic or Acute.
Diseases of the coronary arteries can cause what?
1. Angina

2. Myocardial infarction (MI)

3. Arrythmias

4. Congestive Heart Failure (CHF)

5. Sudden death
What is the most common cause of coronary heart disease (CHD)?
What are the two main classes of CHD?
1. Chronic Ischemic Heart Disease

2. Acute Coronary Syndrome
What is ischemia?
Restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue
What are 3 subclasses of CHD that fall under the category of 'Chronic Ischemic Heart Disease'?
1. Stable Angina

2. Variant Angina

3. Silent Myocardial Ischemia
Acute coronary syndromes are classified according to what?
EKG characteristics.
What are the two subclasses of CHD that fall under the category of 'Acute Coronary Syndrome'?
1. No ST-segment elevation

2. ST-segment elevation
'No ST-segment elevation' CHD can lead to what?
1. ST-segment elevation CHD

2. Non-ST-segment elevation AMI

3. Unstable Angina
What does AMI stand for?
Acure myocardial infarction...a heart attack
'ST-segment elevation' CHD can lead to what?
1. Non-ST-segment elevation AMI

2. Q-wave AMI
What does unstable angina make an individual prone to?
Makes you very prone to MI or thrombosis.
What does 'angina' mean?
a painful constriction or tightness
What does thrombosis refer to?
Formation of a clot or thrombus inside a blood vessel, obstructing the flow of blood through the circulatory system.
'Non-ST-segment elevation AMI' is indicative of ? definitely.
Q-wave AMI is indicative of what?
Atherosclerosis is the most common cause of what?
CHD...Plaque disruption is the most frequent cause of MI and sudden death.
Atherosclerosis is a ?, ? arterial disease. It leads to an ? of affected vessels.
A progressive, degenerative arterial disease, leading to an occlusion (closing) of affected vessels.
What happens to blood flow through occluded vessels?
Blood flow is reduced.
Atherosclerosis is characterized by the formation of what?
Plaques within arterial walls.
What do the plaques of arthersclerosis contain?
1. Lipid-rich core

2. Abnormal overgrowth of smooth muscle cells

3. Covered with collagen-rich connective tissue cap
A plaque bulges from where into where?
Bulges from vessel lining into lumen.
Plaques can occur where?
Anywhere...cause occlusion...disrupt blood flow...decrease oxygen delivery.
Atherosclerosis can affect which epicardial arteries? What does this include?
Can affect one or all three of the epicardial arteries and their branches.

1. Right coronary artery

2. Left main coronary artery

3. Circumflex artery

4. Left anterior descending artery
Coronary artery disease involves pathologic changes where? What is diminished?
Within the walls of coronary arteries that diminish blood flow.
Ordinarily blood flow through coronary vessels increases when?
Blood flow through these vessels increases as O2 demands increase.
Coronary artery disease may prevent blood flow from ? to meet increasing ? ?.
May prevent blood flow from increasing to meet increasing O2 demands.
How do Coronary artery disease complications rank among diseases in the US? What do these complications include?
Complications are the number one cause of death in the US.

Complications include:
Myocardial ischemia (possibly leading to acute MI)
Myocardial Ischemia may possible lead to acute MI via what? (3)
1. Vascular spasm of arteries

2. Formation of atherosclerotic plaques

3. Thromboembolism
List the two types of atherosclerotic plaques.
1. Unstable Plaque

2. Fixed/Stable Plaque
Unstable plaques have the ability to do what? What does this cause to happen?
Unstable plaques have the ability to rupture. This leads to platelet adhesion and thrombus formation. Eventually occludes the vessel and leads to a heart attack (MI).
Unstable plaques are implicated in what conditions?
Unstable angina, myocardial infarctions
Unstable plaques release what if ruptured?
Leads to secretion of platelet activating factors.
Fixed/Stable plaques cause what to occur?
Obstruction of blood flow.
Fixed/stable plaques are implicated in what conditions?
Chronic ischemic heart disease (stable, variant angina)
What does IHD stand for?
Ischemic heart disease
What kind of disorders are IHDs?
Disorders in coronary blood flow due to stable atherosclerotic plaques.
List the 3 ways in which Chronic Ischemic Heart Diseases are classified.
1. Stable (aka exertional or classic) angina

2. Variant (Prinzmetal's) angina

3. Silent myocardial ischemia
What is stable angina aka?
Exertional angina or Classic angina
What is variant angina aka?
Prinzmetal's angina
Describe stable angina?
Stable atherosclerotic plaques produce a fixed obstruction to blood flow with myocardial ischemia occurring during periods of increased metabolic needs.

(develop over a long period of time)
List 4 characteristics of stable angina?
1. Chest pain

2. Provoked by exertion of emotional stress

3. Reduced oxygen supply

4. Relieved within minutes of rest or nitroglycerin
What is a great drug to relieve the sx of angina?
What is angina?
A type of temporary chest pain, pressure, or discomfort.
A ? artery results in ischemia.
A narrowed artery results in ischemia. (the heart muscle is not receiving enough oxygen due to a narrowed coronary artery)
Describe Variant (Prinzmetal's) angina?
Abnormal spastic constriction, TRANSIENTLY narrowing coronary vessels.
Why might one describe Variant (Prinzmetal's) angina as 'peculiar'?
Because you don't see any overt plaques but the patient still has pain. (it is still an indicator associated with the early stages of coronary artery disease)
In Variant (Prinzmetal's) angina what causes angina?
INTENSE vasospasm reduces coronary oxygen supply.
What distinguishes Variant Angina from stable angina?
Occurs at rest, or with minimal exercise and frequently occurs at night.
What is a possible cause of Variant Angina?
Abnormal release of Platelet Activating Factor (PAF) from endothelium to smooth muscle causing a spastic contraction.
Describe Silent Myocardial Ischemia?
Ischemia occurs in absence of angina pain. (NO PAIN)
What three populations are affected by Silent Myocardial Ischemia?
1. Asymptomatic w/out evidence of coronary artery disease (CAD)

2. Previous myocardial infarct with continued episodes of silent ischemia

3. Angina with episodes of silent ischemia
Describe the mxm responsible for the painless episodes of Silent Myocardial Ischemia?
Defects in pain threshold/transmission. Perhaps due to genetic reasons you may have a high threshold for pain.
Silent Myocardial Ischemia has an increased incidence in people with what disease state?
Diabetes mellitus.
Why do people with diabetes mellitus have an increased incidence of silent myocardial ischemia?
Because of autonomic neuropathy (degeneration of nerves)
In a normal heart oxygen supply = ?.
Oxygen supply = oxygen demand
Angina occurs when ? ? does not equal ? ?.
Oxygen supply does not = oxygen demand
Angina is caused by a reduction in what? This reduction is caused by what?
A reduction in blood flow.

Reduction caused by:

1. Vessel narrowing (stable angina)

2. Abnormal vascular tone (Prinzmetal's)
A plaque in what artery could cause the most extensive damage?
Left main coronary artery
Abnormal vascular tone is caused by the release of what?
Endothelial cells of heart and coronary vessels may release vasoactive substances that alter contractile and relaxation state of blood vessels.
What are the vasoactive substances released by the endothelial cells of the heart and coronary vessels that may result in abnormal vascular tone?
1. NO (nitric oxide)

2. Endothelins (eg. ET-1)
What does NO cause?
Dilates vessels by relaxing smooth muscle.

Also prevents coagulation.
What do endothelins cause?
Endothelins (eg. ET-1) cause vasoconstriction. So they restrict blood flow.

Also promotes coagulation.
When is ET-1 elevation observed?
In atherosclerosis, acute MI, CHF, HTN.
The oxygen carrying capacity of the blood doesn't typically change. What are some exceptions? What is subject to change instead?
Anemia or increases in altitude.

Coronary blood flow is subject to change.
What are the key determinants of Myocardial oxygen SUPPLY?
1. O2 carrying capacity of blood (not subj. to change usually)

2. Coronary blood flow (subject to change)...

A. Coronary perfusion pressure

B. Coronary vascular resistance
a. external compression
b. intrinsic regulation
i. local metabolites
ii. endothelial factors
iii. neural innervation
What are the key determinants of myocardial oxygen DEMAND?
1. Preload / Afterload

2. Heart rate (faster = more Oxygen)

3. Contractility
Venous tone is aka?
What diastolic factors increase the heart's oxygen reqts?
1. Increased blood volume

2. Increased Venous tone

(1 & 2 = preload)

Increase intramyocardial fiber tension thus increasing the myocardial oxygen reqt (demand).
What does peripheral resistance do to the heart's oxygen reqts?
Peripheral resistance (AFTERLOAD) increases intramycardial tension thus increasing the myocardial oxygen reqt (demand).
What systolic factors increase the heart's oxygen reqts?
1. Increased heart rate

2. Increased heart force

3. Increased ejection time

All increase intramyocardial fiber tension thus increasing myocardial oxygen reqts (demand)
What happens to the heart during angina?
1. Oxygen supply is decreased.
(coronary arteries cannot supply sufficient oxygen to myocardium)

2. Oxygen demand is increased.
(Afterload, Preload, Heart Rate, and Contractility all cause work for the heart)
What is the goal of angina therapy?
To restore balance between oxygen supply and demand by either :

1. Increasing oxygen supply by increasing blood flow to the ischemic myocardium


2. Decrease myocardial oxygen demand


3. Both (1 and 2)
AMI is aka what?
Acute myocardial infarction = heart attack
What does ACS stand for?
Acute coronary syndromes (related to acute ischemic heart diseases)
What are ACSs?
Spectrum of acute ischemic heart diseases.

1. Unstable angina

2. Non-ST-segment elevation (non-Q-wave) MI

3. ST-segment elevation (Q-wave) MI
What are the determinants of ACS status (low or high risk)?
1. Presenting characteristics and timing

2. ECG variables (ST or Non-ST)

3. Serum Cardiac Markers
What are the serum cardiac markers that are indicative of myocardial injury?
1. myoglobin

2. creatine kinase (CK)(3 isoforms)

3. Troponin
What are the two basic subgroups of acute ischemic HD classified by EKG variables?
1. Non-ST-segment elevation (associated with unstable angina and non-st-seg AMI)(may or may not have heart attack)

2. ST-Segment elevation (assoc. with non-st-segment AMI and Q-wave AMI)(more associated with heart attacks than non-ST-segment)
Is ST-segment or Non-ST-segment elevation more associated with heart attacks?
ST-segment elevation is more associated. (however they can still occur with non-ST elevation)
Unstable angina is aka what?
Non-ST-segment elevation MI
Unstable angina/Non-ST-segment elevation MI is a clinical syndrome that ranges between what?
Clinical syndrome ischemia ranging between stable angina and MI.
What is the cause of Unstable angina/Non-ST-segment elevation MI?
Atherosclerotic plaque disruption, platelet aggregation with secondary hemostasis; coronary vasoconstriction.
How is unstable angina/non-ST-segment elevation MI diagnosed?
1. Pain severity and presenting sx

2. Hemodynamic stability

3. ECG and serum cardiac markers
How does the pain of unstable angina compare to stable?
Unstable has much greater pain
When diagnosing by observing hemodynamic stability what are you looking for?
Coagulation factors
What is the difference between the serum cardia markers of unstable angina verses non-st-segment elevation MI?
These are not elevated in unstable angina. These ARE elevated in Non-ST-segment (myoglobin, CK, troponin)
What does ST-segment elevation MI indicate?
Major myocardial injury...massive ischemia
What do you see when you observe a coronary artery in someone with ST-segment elevation MI?
Complete occlusion of coronary artery.
ST-segment elevation MI = what?
Heart Attack : Ischemic death of myocardial tissue associated with atherosclerotic disease of coronary arteries.

(associated with classic sx of heart attacks...pain in jaw, etc)
The area of infarct in ST-segment elevation MI is determined by what?
The artery affected.
ST-segment has an abrupt onset of progression from what?
Abrupt onset or progression from unstable angina/non ST-segment elevation MI.
What are the manifestations of ST-segment elevation MI?
Abrupt onset of severe, crushing pain.

30-50% die of ventricular fibrillation w/n hours of sx.

Females may present differently = more GI sx and back pain.
The majority of occlusions seen in fatal arrythmias occurs where?
In left main coronary artery. (higher up = more damage)
In an EKG what does the P wave represent?
Atrial depolarization (contraction)
In an EKG what does the QRS wave represent?
Ventricle depolarization (contraction)
In an EKG what does the T wave represent?
Ventricle repolarization
In an EKG what can appear abnormal during a myocardial infarction?
1. ST-segment elevated (hyperacute)

2. Q wave may be absent
ST-segment elevation indicates issues with ?.
Q-wave absence indicates issues with ?.
Myocardial infarction causes some tissue to do what?
To die (become necrotic) depolarizes...abnormal Q wave on EKG.
The extent of damage during ACS pathology depends upon what 6 things?
1. Location and Extent of occlusion

2. Amount of heart tissue supplied by vessels

3. Duration of occlusion

4. Metabolic needs of affected tissue

5. Extent of collateral circulation

6. Other factors (like pre-existing conditions)
How is the duration of an occlusion related to the extent of damage it might cause?
Increased time = increased ischemia = increased necrotic tissue...if you survive this may be replaced with fibrous tissue (less able to contract)
The rupture of an atherosclerotic plaque (that causes ischemia to develop and an ST-seg elevation to be observed) can develop in what two areas/degrees?
1. Transmural (100%, thru total thickness of heart muscle wall, whole ventricle wall)

2. Subendocardial (~50% of heart wall will become ischemic)
Ischemia leads to ? metabolism.
Anaerobic metabolism because of loss of myocardial function (diminished contractile function).
Early changes of ischemia to myocardial function are what?
There is a striking loss of contractile function of myocardia due to ischemia within what time frame?
By 60 seconds
Ischemia causes irreversible cells death w/n what time frame?
20-40 minutes
Early ? after onset of ischemia can prevent necrosis.
Early reperfusion (w/n 15-20 min) after onset.
Necrosis starts in ? tissue and moves how?
Starts in subendocardial tissue and moves out.

The necrotic areas are replaced with nonfunctional scar.
List 6 pharmacologic tx for ACS?
1. Oxygen

2. Nitroglycerin

3. ASA

4. Morphine

5. Beta-blocker

6. Thrombolytic (to avoid plaque rupture)
List 2 medical tx for ACS?
1. PTCA (angioplasty)(Percutaneous Transluminal Coronary Angioplasty )

2. CABG (coronary artery bypass graft)