• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/114

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

114 Cards in this Set

  • Front
  • Back
What is the basis for Ischemic heart disease?
There is a misbalance in the supply and demand of O2 for the heart
The heart receives its O2 supply from which circulatory system?
Coronary circulation
Where do the coronary arteries branch from?
The aorta
What 2 main arteries branch from the aorta?
Right and left coronary arteries
What does the Left main coronary artery split into?
The Left circumflex artery and the left anterior descending artery
What does the LCA perfuse?
Different portions of the left atrium and left ventricle.

The inferior portion of the left ventricle as well as the posterior portion of the left atrium and ventricle
What is the LAD responsible for?
Perfusing the anterior wall of the left ventricle and the INTRAVENTRICULAR SEPTUM!
Why is the LAD so important?
Because it perfuses the intraventricular septum and thus allows for AP from the AV node to reach both ventricles.
What doe the right coronary artery perfuse?
Right atrium, right ventricle and a portion of the heart referred to as the inferior wall: bottom portion of the heart

Also perfuses the posterior portion of the right and much of the left vent.
What determines the workload on the heart (O2 demand)?
1. Heart rate
2. contractility
3. preload and afterload
4. wall tension
In reference to the wall tension equation, what could preload and afterload be in the equation?
Preload=radius (the more volume the wider the heart will have to stretch

Afterload= Systolic pressure
What is the myocardial O2 supply determined by?
1. Diastolic Perfusion Pressure
2. Coronary Vascular Resistance
3. O2 carrying capacity
4. O2 extraction by tissue
Why must the perfusion pressure that determines O2 supply for the heart be the diastolic value?
because the heart does not get blood during systole. Only at rest does it get blood flow.
What equation refers to the coronary vascular resistance?
The difference in pressure over the resistance
What does resistance refer to in coronary vascular resistance?
The diameter of the vessel. For resistance to go up, the vessel diameter must go down.

Inversely proportional
What issues can change the O2 carrying capacity?
Respiratory issue or potential anemic issue
What tissue extracts the most amount of O2 from hemoglobin?
Metabolically active tissue
What 2 aspects of the myocardial O2 supply are always at Max unless you have a ventilation or anemic problem?
O2 carrying capacity and O2 extraction
What happens to blood flow to the heart during systole?
It dramatically drops
What signals the beginning of diastole and the increase of blood flow to the heart?
The closing of the aortic valve
When does blood flow to the heart reach its peak?
At the beginning of diastole
What implications are there for blood flow to the heart occurring during diastole?
There is an increase in HR, contracility and workload on the heart which all require increase O2 demand. But diastole goes down!!
How does the heart compensate for O2 demands during times of increased CO?
It dilates its vessels!
What is the extrinsic mechanism for adjusting coronary vascular resistance?
Parasympathetic and sympathetic innervation
How does intrinsic mechanisms for coronary vascular resistance work?
It influences loca metabolites on endothelial releasing factors

Holds the greatest importance in matching O2 supply with demand
What metabolic factors are sensed by endothelial cells of the heart?
CO2, O2, acidity and adenosine
If the endothelial cells sense high O2, low CO2, low acidity and Low adenosine, what will they release? Why?
They will release endothelin: vasoconstrictor because they are sensing that that tissue is not metabolically active and does not need as much O2 supply
What levels of metabolites will be sense by an endothelial cell releasing nitric oxide?
Low O2, high CO2, high acidity, high adenosine!

This tissue is metabolically active
What happens to chronically injured endothelial tissue in terms of its ability to regulate vessel diameter?
The chronic injury decreases the tissue ability to vasoconstrict or dilate to meet the O2 demands for the heart
What often occurs to people with atherosclerosis of the coronary arteries during exercise? Why does this occur?
They cannot tolerate the exercise because the heart is becoming ischemic. This is due to a loss of function of the endothelial cells to regulate the diameter of the vessel to meet the O2 demands of the heart during increased CO.
What are the 2 types of ischemia that can occur in the heart?
1. Chronic ischemic heart disease
2. Acute coronary syndrom
What is chronic ischemic heart disease?
A manifestation of silent ischemia. You do not know that the heart is ischemic.

Can also have stable and variant angina
How does stable angina differ from variant?>
Stable angina is very predictable.

Variant angina is not predictable and may be caused by a vasospasm (cold)
Acute coronary syndrome is really about the change in a ____?
plaque
What can acute coronary syndrome, due to the rupture of a plaque, lead to?
1. Unstable angina
2. No ST-segment elevation MI
3. ST segment elevation MI
What is the difference between unstable angina and a MI?
a MI has loss of tissue, angina does not.
What does a the presence of an ST elevation on the EKG usually tell the HCP?
The severity of the MI

Elevated are usually more severe that non-elevated
What has been found to be the norm in terms of the prevelance of occult coronary artery disease?
It is so prevalent among industrialized countries that is it now the norm rather than the exception.
If ischemia is symptomatic, how does it manifest?
Cardiac ischemic PAIN: angina
What are the 3 categories of cardiac ischemic pain?
1. Diffuse visceral pain
2. a better defined somatic component conforming to a distribution by dermatones
3. An interpretive component modulated by psychological factors
What is the referred pain of ischemic heart disease?
Anginal pain
Describe the mechanism of "referred" anginal pain.
Referred pain is thought to come in when you have a strong signal and is picked up by the somatic sensory nerves in the spine. So if the sensation is sent to the spine at a location responsible for another part of the body, you will have CROSS WIRING of the sensory and get pain in that section of the body.
How is stable angina describe in terms of pain?
retro-sternal chest discomfort or distress rather than pain
What are the characteristic of anginal pain?
-heaviness, burning, tightness, choking
-discomfort in arms, shoulder, back, jaw or epigastrum
-dyspnea, profound fatigue, weakness, syncope
How long does stable angina usually last?
3-5 mins, usually no more than 10
What is stable angina brought on by?
Very predictable threshold

physical activity or emotional distress
What is warm up angina? how many people with angina have this?
Chest pain prior to "warming-up" for physical activity. Goes away after a period of time.

20%
What is the most common cause of angina chest pain?
CAD: with fixed obstructive coronary disease

-coronary disease with dynamic flow limitations
What are the causes of anginal chest pain other than CAD? What do they all have in common?
-aortic stenosis
-hypertrophic cardiomyopathy
-hypertensive Heart disease LVH
-Mitral valve prolapse

They will limit blood flow, but not form a plaque
How is anginal pain classified?
In terms of the degrees of activity that provoke its onset and how the pain affects the ADL.

There are a total of 4 classes, 4 being the worst
ST segment depression is most often associated with a _____ ischemia?
DEMAND

happens upon exertion because the heart needs more O2
A supply ischemia is often characterized by what EKG change?
ST segment elevation

usually an occlusion of the vessels
Why does ischemia effect the EKG?
Lack of O2 to the tissue causes a decrease in ATP production and thus an accumulation of Na inside the cell. The myocardium becomes slightly depolarized causing the EKG changes
What is the Dx for a person showing a ST segment depression on the EKG, but is asymptomatic?
Silent ischemia
What is the main pathological mechanism of acute coronary syndrome?
Rupture or fissure of a plaque with a superimposed thrombus
How do you clinically Dx unstable angina?
1. Hx of chest pain and have excluded the Dx of MI by EKG or biomarker
2. The chest pain will be prolonged at rest or of new onset
3. May also represent accelerating symptoms of previously stable angina
What are the 3 classes of unstable angina? List the other ways to group unstable angina patients.
I: new onset of severe pain, no pain at rest
II: Angina at rest within the past mont, but not within preceding 48 hours
III: Angina at rest within 48 hours

-Presence of extra-cardiac condition, previous MI, treatment for stable angina, transient ST changes during chest pain
When there is evidence of myocardial necrosis consistent with ischemia, what has occurred?
MI
What are the classical symptoms of MI?
1. Intense, oppressive, durable, excruciating chest pressure
2. impending sense of doom
3. radiation to left arm
4. chest heaviness or burning, radiation to jaw, neck, shoulder, back or both arms
What are the symptoms associated with MI, other than the classical?
Pale skin, significant Tachy, elevated BP, NV dyspnea
What are the SIGNS of a MI?
-Detection of Biomarkers
-EKG changes (ST elevation, Q wave, T wave inversion)
How can a MI be classified?
-Size: microscopic, moderate, large
-% of damage: 10%, 10-30% etc
-EKG changes: NSTEMI or STEMI
-Location: anterior/posterior etc
What are the 3 intracellular components that release when myocardial tissue dies?
1. Troponin
2. Lactate dehydrogenase
3. CK-MB
WHat is the most indicative biomarker used to Dx a MI?
Troponin
Why are CK-MB and LD not as reliable as troponin?
They can spike dues to death of any other tissue in the body
Would a STEMI/Q wave MI be considered severe or less severe?
SEVERE
What is a transmural MI?
the entire wall is infarcted in a particular portion of the heart
What is non-transmural MI?
less than 100% of the wall is infarcted
What portion of the wall of the heart infarcts first?
The inner portion
List everything you DON"T want to see on an EKG?
ST elevation
T wave inversion
Q wave
What occurs in an obstruction of the right coronary artery?
1. If proximal is occluded: moderate to large inferior wall MIs
2. Distal occlusion: small inferior wall MI
An obstruction in what artery is deemed the Widow maker? Why?
the PROXIMAL LAD

-it perfuses the intraventricular septum and thus loss of O2 will stop electrical conduction of APs to the ventricles
An occlusion in which portion of the LAD is least common?
The distal LAD
What occurs when an obstruction occurs in the LCA?
Can have a moderate to large infarction in inferior portion of the heart and the left lateral and middle of the left
What is the process of cardiac remodeling?
When infarcted tissue is replaced by fibrotic tissue
Once scar tissue has formed in the myocardium, what happens to the contractility of the heart?
It goes down.

The scar tissue is only there for structural value of the heart
What are the 3 categories of Acute Heart Failure
1. Fatal MI
2. Sudden cardiac death
3. Acute decompensation of chronic heart failure
Describe sudden cardiac death?
Failure of the conduction system.
Fatal arrhythmias that can lead to cardiac death.

Can occur due to an inherited mutation in the ion channel of cardiac cells.
What are channelopathies?
Abnormalities in the ion channel of the heart
who is at risk for sudden cardiac death?
Anyone that has any structural remodeling: remodeling post MI
Why does a person die from acute decompensation of Chronic heart Failure?
Generally either from severe acute pulmonary edema or from cardiorenal syndrome (poor response to diuretics)
Other than acute pulmonary edema, what other occurrence can lead to acute decompensation?
A huge dinner!!
What are the 4 causes of Chronic heart Failure?
1. Abnormal cardiac muscle function
2. Abnormal left ventricular volume
3. Abnormal left ventricular pressure
4. Abnormal left ventricular filling
What are the examples of abnormal caridac muscle function?
-Myocardial Infarction
-Cardiomyopathies
What can lead to abnormal left ventricular volume?
1. Valve insufficiency
2. Blood volume expansion associated with high out-put states
a. Chronic anemia
b. infusion of a large volume of IV fluid in a short period of time
c. Pregnancy
Why is chronic anemia cause chronic ventricular volume?
An adaptation of chronic anmeia is plasma volume expansion
What is characteristic of abnormal ventricular pressure?
Increase afterload

-HTN
-COPD
-Aortic/pulmonic valve stenosis
Why does pts with COPD have abnormal ventricular pressure?
Pulmonary arteries constrict when low O2. When they constrict the RV is pumping against pressure. Never designed to pump against pressure. High risk for right sided HTN and can lead to pulmonary HTN
What disorders lead to abnormal ventricular filling?
1. Mitral valve stenosis
2. Tricuspid valve stenosis
3. Atrial fibrillation
What sided heart failure can lead to GI distress?
Right
Dependent edema and ascites is characteristic of heart failure on which side?
Right
A cough with frothy sputum is a sign what what disorder and results from which sided heart failure?
Pulmonary edema; left sided heart failure
What are the 2 components of CHF that represent the 2 phases?
1. Structural remodeling of cardiac tissue as a result of tissue death= reduction in cardiac function
2. Multiple compensatory events in response to decreased function makes up the majority of the pathological issues. (viscous cycle of cardiac failure)
the pathophysiology of heart failure involves changes in ____ and _____?
Cardiac function; Neurohumoral responses
What can cause changes in cardiac function that can lead to heart failure?
1. cardiac remodeling
2. decreased cardiac output
What are some examples of neurohumoral responses leading to heart failure?
-activation of SNS
-activation of renin-angiotensin system
-increase release of ADH and ANP
what is the net effect of neurohumoral responses leading to heart failure?
-produce arterial vasoconstriction
-produce venous constriction
-increased blood volume
When the body experiences a drop in CO, what does it assume is the problem? Why is this bad?
Blood volume

The body will try to fix it by activating the SNS and retaining fluid which in turn increases the workload of the heart. Vicious cycle
In heart failure, why is Frank Starling law maladaptive?
The heart knows that by increasing its volume it should be able to increase its volume output, but with Heart failure, the increase in preload actually injures the heart further and drops the output
By what stage is a person considered to be in heart failure?
Stage C
How many stages are there for heart failure?
4
Stages A, B, C, D
What is Stage A of heart failure?
Just at high risk for developing HR.

ie. HTN, DM, hyperlipidemia etc
What is end-stage HF?
Stage D
What are the functions of ACE inhibitors for Heart failure?
Prils

-block angiotensin II which will block volume expansion and vasoconstriction.

-Some evidence that they enhance contractility of the heart
What do Beta Blockers do to help treat Heart failure?
Reduce O2 demands of the heart. Block acceleration of HR and contractility that is part of the SNS.
Describe digoxin?
+ inotropic drug. Increases the contractility of the heart. Tries to enhance CO
What are the most powerful diuretics used to Tx HF?
Loop diuretics
What must be monitored with loop diuretics?
Loss of too much K
What is the classic drug combination for HF?
Dig and Lasix
Why are diuretics used to Tx HF?
They reduce volume and control its expansion. Thus they reduce preload and workload on the heart
What are the types of diuretics used for HF?
1. Loop diuretics
2. Thiazide diuretics
3. K sparing diuretic
4. Sequential nephron blockade
List all the classes of drugs used to treat the various stages of heart failure.
1. ACE inhibitors
2. Angiotensin Receptor Blockers
3. Aldosterone Antagonists
4. Beta Blockers
5. Dig
6. Diuretics
How do ARBs help treat Heart failure?
They block angiotensin from attaching to its receptor and thus prevent vasoconstriction, which will decrease the workload of the heart.
Aldosterone antagonist act in which way to treat HF?
They prevent fluid volume excess by blocking aldosterone's reabsorption on Na and Water and thus they reduce the preload on the heart.