Lecture 2: Cardiac Pathology Flashcards
During exercise, a patient experiences angina that resolves after 10 minutes of rest. This symptoms is most consistent w/?
Stable angina
Which cardiovascular risk factor is modifiable through patient education and lifestyle changes?
Dyslipidemia
Which clinical manifestation may a patient with left ventricular failure present?
Pulmonary congestion
Which coronary artery supplies the anterior portion of the heart
Left anterior descending artery
* NOTE: Its not the right coronary artery - this does more of the latearl portion while the circumflex does the back
Which of the following structures forms the continuous lining of the mitral and tricuspid vales
1) Pericardium
2) myocardium
3) epicardium
4) endo cardium
Endocardium
Which structures would be primarily affected due to increased pressure or load to the left atrium?
* Pulmonary artery
* pulmonary vein
* Aorta
* inferior and superior vena cava
Pulmonary vein
Cardio vascular disease and disorders
We have modifiable and non modifiable risk factors
Which two groups is hypertension the most common in?
Highest in non-hispanic black and mexican americans
* NOTE: Hypertension is the most common cardiovascular disease in the world
- What is primary hypertension?
- What causes it?
- What percent of hypertension does this make up
Primary hypertension = No known cause (idiopathic)
* seems to be connected to BMI/Diet
90-95% of cases
What is essential hypertension?
* What causes it?
* What percent of hypertension does this make up
Same thing as primariy hypertension
* essential hyperteion = primary hypertension
essential hypertension = No known cause (idiopathic)
90-95% of cases
What is seconday hypertension?
* Is it common?
Seconday to something else going wrong (think kidney being messed up)
* Renal endocrine, vascular, or neurological source - key is that it is caused by something else
* rare (makes sence, primary makes up most of the hypertension)
What is Labile hypertension?
White coat syndrome
( Sporadic elevation
What is mask hypertension?
Normal resting BP; however, it increases w/ ambulation / movement
* she said 200/100 but I don’t think these are the correct #’s - pull chart from old powerpoints
What is malignant hypertension?
Markedly elevated BP
* Think hyperetnsive crisis
BP equation
CO * total peripheral resistance
NOTE: Total peripheral resistance isnt just the stiffness of the arteries but anything that causes that stiffness in your vascular system
What 3 things impact total peripheral resistance?
* Which one is the easist to modify
* When does hypertension develop?
1) Blood viscosity - most easily modifiable
2) Elasticity of arterial walls - hard to modify short of surgery
3) Peripheral resistance
Hypertension develops when theres an imbalance of regulation. BP is supposed to icnrease / decrease, to keep CO/ keep homeostasis - however, when it gets out of balance is when we have problems.
Uncontrolled BP Does what to arteries? Why?
Arteriolar remodeling
Increased pressure on the arteries (think about a calus) we lead to those fibrotic changes
uncontorlled BP does what to organs? Why?
Targeted organ damage
If you have pressure consistently hitting an organ you get this.
With increased BP what part of heart suffers the damage?
* leads to what?
* A greater reliance on what contracting
LV suffers damage –> myocardial fibrosis (in that LV, the myocardium does that contraction. When you have fibrosis [scaring] keeps it from contracting as hard due to stiffness, and decreased distinsiability = decreased filling, due to that scaring) –> Greater reliance on atrial contraction (taking over for that LV because that fibrosis is keeping it from contracting/filling as much)
How does hypertension present most of the time?
Typically asymptomatic (they typically only find out through routine readings)
* however, they can present w/ s/s of HA, vertigo, and flushed face, spontaneous epitaxis (nost bleed), blurred vision
w/ progressive HTN
* cardiac: exertional dyspnea, fatigue, tachy, angina with exertion, exercise intolerance
* Neurological: N&V, drowsiness, confusion, and numbness or tingling in limbs - can easily confuse this w/ diabetes, stroke, vertigo, etc…
Lifestyle modifications: weight reduction, avoid tobacco, diet modification, PA, stress management, CAMs (alternative medication)
What is typically our first line of defense medication for hypertension?
* what are some others (6)
Diuretics
* Beta blockers
* Alpha blockers
* Calcium channel blockers
* ACE inhibitors
* Angiontensin 2 inhibitors
* Vasopeptidase inhibitors
Name 5 things that would make you think to check someones BP in the clinic (like 5 things about the person)
* age
* BMI
* sugar
* kidney
* vessel
NOTE: w/ these conditions you would want to take BP at rest and w/ activity (remember, we learned that when monitoring BP w/ activity you need to take it very fast (~15 seconds) following activity to get an acurate reading)
age > 35
High BMI
Glucose intolerance (diabetes)
renal disease
Aortic anurysm
Moderate hypertension –> blunted reduction to TPR –> isometric and dynamic exercise affected
* basically saying that BP will not increased and decrease w/ exercise the same way as a healthy person
* So when you’re in moderate hypertension, you’re not going to get the response in TPR as strongly. You’re going to get responses in CO (so changes in HR and SV) first before you see adjustments to TPR (because all 3 factors in TPR take longer / are harder to adjust) with exercise.
* She said to know that regardless of the class of hypertension its going to respond differently to differently to cardio/isometric/plyometric activity
* Just because you see a normal increase in BP w/ one of those exercises does not mean that the BP is not altered.
* So I think its saying that dependening on what kind of activity you’re doing you can see different kinds of jumps in BP
BP = CO * TPR
w/ moderate hypertension your CO wants to maintain homeostasis, so HR and SV are going to alter CO output first. TPR is not going to be whats changing first.
* Essentially saying that CO is going to be altering that BP not TPR. At least not first
TPR =
* Blood viscosity - this can altered fairly easy (think appropriate hydration). This is how sticky the blood is. If you are under hydrated the blood becomes more dense and sticky.
* Elasticity of arterial walls - not easily altered w/o surgery. Once this changes its not easily altered (only dietary changes can alter and that takes longer to do)
* Peripheral resistance - altered based on hormone levels (think parasympathetic / sympathetic NS) - this is most easily altered
If wanting to do activity w/ a pt get medical clearance from a cardioologist of their systolic is _ OR their diastolic is _
Systolic > 200mmHg
Diastolic > 110mmHg
most of the time if they have a BP this high is already seeing a cardioologist
Terminate exercise if systolic BP is _ OR Diastolic BP is _
TEST
Systolic = >250 mmHg
Diastolic = >115mmHg
question will look like this: “What would you do if the BP of a pt is the following…”
* diliniate between this crisis and just needing medical clearance.
If patient hasnt been diagnosed w/ hypertension don’t see pt back after terminating EX
* If they are you either need to send them to their cardiologist or look at your exercises and see if you were pushing the pt too hard.
* So if they have seen a cardiologist you would let that pt rest for a few minutes and if the BP drops back down then you can continue EX - so it doesnt have to be an absolute termination of EX
Which of the following interventions addressing cardiovascular risk factors is most appropriate for PT intervention?
A) Recommendations for hormone replacement therapy post menopause
B) Patient education on smoking cessation
C) Asking about familial cardiovascular medication hx
D) Taking pts BP
B
A isnt out scope
C/D = not interventions
When does Coronary Artery Disease (CAD) begin?
* explain how it develops?
* What does it lead to?
Childhood
Endothelial damage –> inflammation –> lesions/plaques
* whenever there is damage body responds w/ inflammation. The cycle that continues is abnormal, inflammation leads to plaque due to the constant remodeling.
CAD leads to CHF
Single most significant cause of death?
CAD
precedes MIs (so leads to heart attacks)
Coronary artery disease in women (striking gender disparities)
* Despite equal profiles, women are labled not at risk
* ECGs are limited in value for women (they look normal even though there are issues)
* Estradiol (form of estrogen) decreases after menopause and if women are not undergoing hormone replacement therapy they are not getting the affects from it (remember, its a natural vaso dilator similar to Ca2+ blockers)
Women have significantly greater adverse effects from CAD because it doesnt get treated as fast as it does in men
Psychosocial issues - women do care giving and don’t have time to go to Dr. (this may change as traditional roles are shifting)
Ischemia =
Decrease in BF to an area
Infarction =
Cell death
Imbalance between myocardial O2 supply and demand
Ischemia
* its partially blocked so the tissue isnt getting the blood supply it needs
How to we measure myocardial O2 supply (how much O2 the myocardium is using)
Rate Pressure Product
* measures the amount of O2 the myocardium in the heart utilizes (higher numbers are better, typically seen in younger people)
* HR * Systolic BP
The LV function is impaired. What happens the ejetion fraction?
* What happens to CO over time?
Ejection fraction is decreased
* This is the amount of blood pumped out by the LV per beat
* If the LV isnt pumping well (isnt shooting as much out per beat) than note as big of a % of that blood comes out
Over time this hinder CO and decreases it. Meaning they would present w/ lots of fatigue w/ ex
* It decreases CO over time because the body tries really hard to stabilize CO (HR * SV) but over time it decreases.
What would someone w/ low CO present like?
Weak and fatigued, espically w/ EX.
* Very limited amount of time able to maintain EX.
* theres going to be changes in HR and SV before you see a change in CO
Clinical manifestations of myocardial ischemia (not enough O2 to heart muscle)
Angina lasting 3-15 min
anginal equivalents
arrythmias
ECG changes
hypotension (indiactes cardiac output issue)
stable angina
unstable angina
Prinzmental (variant) angina
Angina that occurs w/ rest or is unperdictable
unstable angina
(doesnt resolve w/ rest and can occur at rest)
What is Prinzmetal (variant) angina
Coronary vasospasm that causes angina
* they’re severe because we dont know when they happen. Keeps you from getting BF to your heart. Can happen w/ EX or at rest.
What is acute coronary syndrome (2)
* What is it caused by
Acute MI (that coronary pathology is causing a heart attack) - happens w/ a block in a cornary artery and a part of the heart does not get blood flow - similar to an ischemic stroke
Unstable angina
usually caused by ruptured plaque
When a patient has a myocardial infarction (interruption of BF to the heart) for how long till they typically call the hospital
* does this lead to tissue necrosis
> 20 minutes of interuption those symptoms typically becoming severe enough that they call 9-1-1
causes tissue necrosis
* depending on what coronary artery is involved, when you lack BF for an extended period of time you do have cell death (placement of that cell death depends on the artery involved)
Acute Coronary Syndrome typically procedes an MI in about _ % of cases?
In about 80% of cases you get acute coronary syndrome before MI
What is the most leath occulsion of a cornary artery?
STEMI
Is STEMI full thickness or partial thickness?
Full thickness (transmural MI)
A STEMI is associated with a pathologic _ wave
Q wave
NOTE: A full thickness necrosis affects all 3 layers of the heart including the valves
How many layers of the heart does a NSTEMI impact.
Only affects 1 layers
In a MI (Stemi or NSTEMI) you have 3 pathologic zones following the infarct. What are the 3
1) Zone of infarct
2) Zone of injury
3) Zone of ischemia
Describe the zone of ischemia
Reduced BF, this is typically where the blood clot happens in the coronary artery
Descirbe the zone of injury
Damaged but not yet dead tissue
Describe the zone of necrosis?
Dead heart tissue
where are coronary blood vessels housed?
Epicardium
What does Transmural mean?
Full thickness MI (think STEMI)
What does Nontransmural mean?
Typically spares the endocardium
* Think NSTEMI
Do you want to move soon after an MI
Yes! Early mobilization
* w/ the medication that reduces dilation we want to spread that blood around the heart to reduce the total amount of necrosis
NOTE: After you’ve had an MI another one is likely - they’re at high risk
EF < _ = increased chance of cardiac event?
40%
If you notice a patient is taking nitro you’re thinking they’re at risk for MI
* take vitals and be prepaird
NOTE: Arrhythmias may develop due to remodeling post MI
* depending on where the heart attack occured this can be more likely
* the ellectrical system in the heart is picky and small things can easily throw them into an MI
Which of the following is MOST likely classified as a STEMI?
a) Transmural MI
b) Non transmural MI
c) Unstable Angina
d) Myocardial injury
A
KNOW: Heart failure can be a result of papillary muscle dysfunction
KNOW: Heart failure can be due to transmural, anterior infarct (think full thickness necrosis in LV [which is anterior])
What is venous return like in HF
Normal, the issue is that the pump doesnt work well
If the LV doesnt work well what gets backed up
* What happens to CO / EX tolerance?
backs up to lungs
* we get pulmonary congestion (think that cough)
* Most common cause of hospitalized older adults - they’re used to not being able to do much but then breathing becomes an issue
Decreased CO because SV is lower which will lead to that decreased EX tolerance.
What causes a large dilated heart, systolic heart failure or diastolic heart failure?
* What is it caused by?
* What happens to ejection fraction? Why?
* What valves are impacted and how
Systolic heart failure
Caused by impaired myocardial contractility
Decreased ejection fraction because not as much blood is pumped out per beat (because of the reduced contractility)
* This not being able to pump all the blood out causes that backflow which leads to that large dilated heart (because it backs up and stretches)
* When you have a stretched out dilated muscle its not going to be able to create as much power which will further reduce contractility (positive feedback loop)
Causes functional mitral regurgitation, tricusipid regurgiation from ventricular dilation (so talking about the R/L ventricle)
* valves are not closing appropraitely because LV is so stretched out that those leaflets don’t close all the way (too much volume)
Patient has heart failure but has a normal ejection fraction. Is this systolic or diastolic heart failure?
* Whats going on in this pathology?
* Who is this primarily seen in (3)?
Diastolic (heart has problems at rest)
Impaired ventricular relaxation and increased passive stiffness (decreased compliance)
* So the ventricule can’t relax apparopraitely, so it cant fill appropriately because its not releaxed
* Ejection fraction is fine because if it doesnt have as much blood in it its easier to pump out a higher % of that ejection fraction
Primarily seen in:
* Women
* Hypertensives
* Older individuals
TEST: Class 1 stage of heart failure
No symptoms and no limitations in ordinary PA.
* Would not have SOB while walking and climbing stairs
TEST: Class 2 stage of heart failure
Milk symptoms (mild SOB and/or angina) and slight limitation during ordinary activity
* Only you would notice
TEST: Stage 3 stage of HF:
* What are they like at rest?
Marked limitation in activity due to symptoms, even during less-than ordinary activity, e.g. walking short distances (20-100m) comfortable at rest
* Others start to notice here
TEST: Stage 4 Heart failure
Severe limitations. Experiences symptoms even while at rest. These patients are mostly bedbound (due to those symptoms at rest).
1.
Left ventricular failure. During systole:
* What happens to EDV?
* What happens to SV?
* What happens to ejection fraction?
* is there backflow, if so what does it lead to?
* Because of the point prior, what floods?
* Which valve is pathologic?
Increased EDV (because of that decreased ability to pump all that blood out you keep more of it in)
Decreased SV (decreased contractility leads to that decreased SV –> leaving more of the blood in the heart)
Because our SV is low and our EDV is high that ejection fraction is low (out of all the volume of blood we have in the heart were not pushing out a very high % of it).
Backflow from the LV –> LA dilation and backflow –> pulmonary congestion
That pulmonary congestion leads to alveolar flooding
* meaning theres too much blood around the alveoli and proper gas exchange cannot take place.
Mitral regurgitation (essentially LV is so full that blood flows backwards)
Left ventricular failure Diastolic:
* What happens to SV?
Decreased SV, but higher HR reduces the filling time
* think tachy giving less time to fill
Gas exchanged is impaired due to the high pulmonar ypressure that leads to dyspnea
CO needs to be maintained, so there are compensatory mechanisms
KNOW: w/ left ventricular failure you’re at a risk of subendocardial ischemia (more in the endometrium of the lung) due to the higher pressure in the LV END
Didnt fully understand
Compenstory methods for body to stablize BP
What happens in left sided HF due to the backup of blood into the lungs
Confusion/REstlessness = due to not appropraitely being able to utilize O2
Dry cough at rest
What causes R sided HF?
* Leads to hypertension where
* If this hypertension is chronic what happens to the RV?
Increased pressure or volume laod on the LEFT atrium –> increased pressure on RV (has to pump harder to get it across the lungs into the LA)
Leads to pulmonary hypertension (trying to push blood through that pulmonary artery into the heart is harder = increased resistance = hypertension)
If this pulmonary pressure is chronic it results in RV dilation and hypertrophy (blood backing up = dilation, pushing harder = hypertorphy)
W/ R sided HF what happens to RV end diastolic pressure? Why?
Its increased because its having to push harder to get blood intot he pulmonary artery
What kind of HF leads to jugular venous distension, liver engorgement, ascites, and peripheral edema
This is more systemic so its the R side of the heart backing up
* R sided HF
What is Cor Pulmonale?
R sided HF
Notice the blood has backed up systemically in this R sided HF
This is common for pulmonary pts. remember while this backflows in the body the lungs are also impacted because the LA is backed up leading some blood back into the lungs
NOTE: If HF is unstable = rest (don’t try to EX0
Pleurocentesis = taking fluid out of thoracic cavity
What is decompensation?
* What are some signs of this?
When HF is not stable
Sudden weight gain (due to that fluid accumulation), increased SOB (lungs imapcted), increased LE edema, abdominal swelling/pain, cough, increased fatigue, lightheadnedness, dizziness
Weight gain of _ pounds or more is a sign of decompensation (When HF is unstable)
3 pounds or more
If HR is _ at rest and BP is _ at rest this is a sign of decompensation (unstable HF)
At rest: increased HR and low BP
NOTE: can’t use HR / BP to quantify activity in HF pts because they’re likely on beta blockers which blunt the responses. Use RPE
Which of the following medications are MOST commonly prescribed for heart failure management?
a) Thrombolytics
b) Antiarrhythmics
c) Angiotensin II Receptor Blockers
d) Heparin
C (ARB)
What kind of forces cause aneurysm?
* destruction of what layer of the artery are aneurysms?
*
Increased hearing foces
Destruction of the media and elastic tissue, arterial wall weakening
Can also result from trauma, infectoin, inflammation, cystic medial necrosis, congential vascular disease
W/ a dissecting abominal aneurysm is a tear in what layer of the artery?
* what does it feel like?
Tear in arterial intima
* Sudden pain/discomfort? / palpable mass
* in the abdomen
Arrhythmias are classified according to site of origin, type of cardiac activity, and presence of conduction block
What do tachy arrhythmias do to myocardial O2 demand
Increased HR increased O2 demand
* reduces filling time
* its also going to increase the demand of O2 because the heart is using more O2 (because its beating more)
* So you’re not getting as much and you need more
Brady arrhythmias lead to what in CHF pts
Pulmonary congestion
Atrial arrhythmias do what to EDV?
Reduce it by 20-30%
* this is because the atrium might be beating too quickly and not letting the ventricle fill all the way
Ventricular fibrilatoion –> not getting enough blood supply, are not contracting –> deadly
Treatment for arrythmias>
* antiarrhythmics
* Cardioversion
* DEfibrillation
* Surgical options
atrial Fibrillation does what to ventricular filling time
Leads to decreased ventricular filling time –> inadequate CO / reduced coronary BF
NOTE: Thrombus formation in the atria happens primarily due to atrial fibrillation which leads to a stroke
AFib leads to interference w/ organ perfusion - not all do
Clinical manifestations: palpitations, dizziness, syncope, fatigue, chest discomfort
PT: HR, BP, Graded EX testing, ECGs when available
Know the signs of inadequate CO
* this is exercise intolerance
Restricted valvular opening
Stenosis
* narrowing, obstruction of valve
* Concentric hypertrophy to normalize SV
Incomplete valve closure (comes w/ regurgitation)
Insufficiency
* backward BF
* Leads to dilation and hypertrophy
What 3 things cause mitral regurgitation?
LV dilation
Papillary m dysfunction
Calcification
NOTE: this is regurgitation in LV to LA
Acutely what happens w/ mitral regugitation to LA? What does that lead to? (2)
* what does it look like chronically?
* What are S/S consistent w/?
* What heart sounds are common w/ mitral regurgitation?
Acutely LA pressure increases (because blood is backing up from the LV into the LA because the valve isnt closing all the way)
That increased LA pressure causes pulmonary hypertension (blood has backed up into the lungs) and pulmonary edema (that increased fluid in the lungs)
KNOW: Chronically LA compensates at rest
* body can still keep going w/ mitral reguitation
* However, you’re going to see problems w/ EX.
S/S consistent w/ low CO s/s
S3 heart sounds common
Aortic Stenosis
* 2 causes?
* What happens to CO?
* What happens to the LV and why
* Prognosis
* Should we EX w/ this?
Congential or severe atherosclerosis
Failure to increase CO on exertion, often asymptomatic
* so arent going to meet bodies demands for EX
Aortic Valve is restricted = increased perssure in LV
* Stenosis = problems opening
NOTE: Prognosis is poor - symptom can be sudden death
EX is contraindicated in severe aortic stenosis
No valsalva maneuver (increases LV pressure)
Which of the following arrhythmias MOST LIKELY leads to myocardial ischemia?
a) Supraventricular tachycardia
b) Sinus bradycardia
c) Sinus arrest
d) Atrial fibrillation
D
What layer of heart muscle do cardiomyopathies originate in?
* what are the 3 kinds
* Which one is most common
* Which one leads to sudden cardiac death
Originate in the myocardium (contraction issue)
Classified according to structure and function
* Dilated - most common
* Hypertrophic - leads to sudden cardiac death (mostly atheltes)
* Restrictire
NOTE: you can have multiples of these going on at the same time
Explain what happens in dilated cardiomyopathies (to the ventricles)
* Does impact during systole or diastole?
* What happens to EF
* Where does the LV go/
* S/S?
* How do you treat this pt?
* Do they have trouble filling?
The ventricles are dilated. This is impaired systolic function of 1 or both ventricles
* So essentially the heart muscle is so stretched out and dilated that it cannot contract properly because the muscle is over stretched, leading to decreased blood being pumped out per beat.
* This leads to decreased ejection fraction (because less of that blood in the LV is pumped per beat and that EDV is higher because that LV has more volume because its dilated)
LV is often displaced when trying to hear it from the outside
* this being displaced tells us the size of the heart has increased (point of max impulse)
Typically idiopathic
Treat as a CHF patient
* the ventricles are also dilated w/ CHF so this makes sense
Do not have trouble filling, they have trouble contracting and shooting the blood out
Explain what happens in hypertrophic cardiomyopathies?
* what happens to ejection fraction?
* During diastole waht happens to ventricular complance and filling pressure?
* S/s?
* Heart sound?
* Should they do strenuous EX?
Symmetric/asymmetrical, normal or hyperdynamic systolic function
* essentially the ventricles have hypertrophy (1 or both)
Increased ejection fraction
* this is because it can’t fill as much and it can push super hard
LV affected - diastolic dysfunction
* Decreased compliance (increased stiffness) - do to the excess muscle mass
* Increased filling pressure - due to that increased stiffness
Clinical manifestations vary greatly in intensity
* Dyspnea, angina, fatigue, palpitations, S4 heart sounds, SVTs
Drug therapy or surgical; avoid strenous EX
Which cardiomyopathy leads to sudden cardiac death the most?
* This priamrily happens in what kind of people?
* Contraindication? (1)
Hypertrophic
Happens primarily to young atheletes.
* Black atheletes disproportionally affected
Contraindication = competitive sports w/ medium to high dynamic / static components
* things like bowling and golf are okay
After diagnosis - mitigate risk of complications and sudden cardiac death
With the cardiomyopathies what happens to diastolic function in resistrictive?
* What happens to ventricular filling?
* What happens to the atrium and why?
* What happens to CO?
* How to treat this pt?
Restrictive cardiomyopathies have dysfunction at rest
* because its a disastolic dysfunction
So the ventricule has issues fulling filling during diastole because its non compliant (can’t distend)
Typically theres atrial enlargement because that non compliant blood from the ventricle backs up into the atrium
Reduced CO, impaired ex tolerance (due to that reduced CO), jugular venous distention (the atrial enlargement backsflows through lungs and systemically), abnormal heart sounds
Treat the same as HF
Take pulse
Be aware of arrhythmias post EX
Exercise intolerance common
Valsalva maneuver reduces CO –> so they’ll need to coordinate breathing to cope w/ this
Rest between activities
* this is much easier for older adults to udnerstand than younger
What causes pericarditis?
* what is it?
* Why have there been more reciently?
* tx?
* The reoccurance causes what, leading to what?
Idiopathic and/or viral
These have increased since covid
Inflammatory reponse around the heart
Leads to chest pain, dyspnea, ECG abnormalitites, pericardial friction rub will be heard when listening w/ stethascope. Sounds like a rub - sacs rubbing against eachother since they’re enlarged
Cardoac tamponade
Tx = NSAIDS
can reoccur and cause fibrosis leading to s/s of HF
Cardiac tamponade
Low CO, fluid filling in pericardial sac, cardiac compression adn eventual decreased diastolic ventricular filling
* prevents adequate contraction because the heart is now being compressed
* Heart is compressed = no room to expand and fill
Common w/ pericarditis
medical emergency
This is showing what happens w/ pericarditis / pericardial effusion (just that extra fluid around the heart)
What causes endocarditits?
* what is it?
* What anatomical structure in the heart does it directly impact.
Endocarditis = inflammation of the endocardium
Its caused by a bacterial (often dentral) issue
Affects the valves because the endocardium is impacted
* it can impact them where they can’t open and close properly
Notice how inflammed the heart valves are
Which of the following pathologies is exercise contraindicated when pathology is severe?
a) atrial fibrillation
b) aortic stenosis
c) Dilated cardiomyopathy
d) HF
b
in aortic stenosis the aortic valve doesnt open causing increased pressure in the LV which could cause it to explode. w/ increased EX you’re putting even more pressure on it, which is bad.
