Lecture 2: Cardiac Pathology

Question 1

During exercise, a patient experiences angina that resolves after 10 minutes of rest. This symptoms is most consistent w/?

Answer 1

Stable angina

Question 2

Which cardiovascular risk factor is modifiable through patient education and lifestyle changes?

Answer 2

Dyslipidemia

Question 3

Which clinical manifestation may a patient with left ventricular failure present?

Answer 3

Pulmonary congestion

Question 4

Which coronary artery supplies the anterior portion of the heart

Answer 4

Left anterior descending artery
* NOTE: Its not the right coronary artery - this does more of the latearl portion while the circumflex does the back

Question 5

Which of the following structures forms the continuous lining of the mitral and tricuspid vales
1) Pericardium
2) myocardium
3) epicardium
4) endo cardium

Answer 5

Endocardium

Question 6

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

Answer 6

Pulmonary vein

Question 7

Cardio vascular disease and disorders

We have modifiable and non modifiable risk factors

Answer 7

Question 8

Which two groups is hypertension the most common in?

Answer 8

Highest in non-hispanic black and mexican americans
* NOTE: Hypertension is the most common cardiovascular disease in the world

Question 9

• What is primary hypertension?
• What causes it?
• What percent of hypertension does this make up

Answer 9

Primary hypertension = No known cause (idiopathic)
* seems to be connected to BMI/Diet

90-95% of cases

Question 10

What is essential hypertension?
* What causes it?
* What percent of hypertension does this make up

Answer 10

Same thing as primariy hypertension
* essential hyperteion = primary hypertension

essential hypertension = No known cause (idiopathic)

90-95% of cases

Question 11

What is seconday hypertension?
* Is it common?

Answer 11

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)

Question 12

What is Labile hypertension?

Answer 12

White coat syndrome
( Sporadic elevation

Question 13

What is mask hypertension?

Answer 13

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

Question 14

What is malignant hypertension?

Answer 14

Markedly elevated BP
* Think hyperetnsive crisis

Question 15

BP equation

Answer 15

CO * total peripheral resistance

Question 16

NOTE: Total peripheral resistance isnt just the stiffness of the arteries but anything that causes that stiffness in your vascular system

Question 17

What 3 things impact total peripheral resistance?
* Which one is the easist to modify
* When does hypertension develop?

Answer 17

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.

Question 18

Uncontrolled BP Does what to arteries? Why?

Answer 18

Arteriolar remodeling

Increased pressure on the arteries (think about a calus) we lead to those fibrotic changes

Question 19

uncontorlled BP does what to organs? Why?

Answer 19

Targeted organ damage

If you have pressure consistently hitting an organ you get this.

Question 20

With increased BP what part of heart suffers the damage?
* leads to what?
* A greater reliance on what contracting

Answer 20

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)

Question 21

How does hypertension present most of the time?

Answer 21

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)

Question 22

What is typically our first line of defense medication for hypertension?
* what are some others (6)

Answer 22

Diuretics
* Beta blockers
* Alpha blockers
* Calcium channel blockers
* ACE inhibitors
* Angiontensin 2 inhibitors
* Vasopeptidase inhibitors

Question 23

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)

Answer 23

age > 35

High BMI

Glucose intolerance (diabetes)

renal disease

Aortic anurysm

Question 24

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

Question 25

If wanting to do activity w/ a pt get medical clearance from a cardioologist of their systolic is _ **OR** their diastolic is _

Answer 25

Systolic > 200mmHg Diastolic > 110mmHg most of the time if they have a BP this high is already seeing a cardioologist

Question 26

Terminate exercise if systolic BP is _ **OR** Diastolic BP is _ **TEST**

Answer 26

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

Question 27

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

Answer 27

B A isnt out scope C/D = not interventions

Question 28

When does Coronary Artery Disease (CAD) begin? * explain how it develops? * What does it lead to?

Answer 28

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

Question 29

Single most significant cause of death?

Answer 29

CAD precedes MIs (so leads to heart attacks)

Question 30

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)

Question 31

Ischemia =

Answer 31

Decrease in BF to an area

Question 32

Infarction =

Answer 32

Cell death

Question 33

Imbalance between myocardial O2 supply and demand

Answer 33

Ischemia * its partially blocked so the tissue isnt getting the blood supply it needs

Question 34

How to we measure myocardial O2 supply (how much O2 the myocardium is using)

Answer 34

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

Question 35

The LV function is impaired. What happens the ejetion fraction? * What happens to CO over time?

Answer 35

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.

Question 36

What would someone w/ low CO present like?

Answer 36

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

Question 37

Clinical manifestations of myocardial ischemia (not enough O2 to heart muscle)

Answer 37

Angina lasting 3-15 min anginal equivalents arrythmias ECG changes hypotension (indiactes cardiac output issue) stable angina unstable angina Prinzmental (variant) angina

Question 38

Angina that occurs w/ rest or is unperdictable

Answer 38

unstable angina (doesnt resolve w/ rest and can occur at rest)

Question 39

What is Prinzmetal (variant) angina

Answer 39

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.

Question 40

What is acute coronary syndrome (2) * What is it caused by

Answer 40

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

Question 41

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

Answer 41

>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)

Question 42

Acute Coronary Syndrome typically procedes an MI in about _ % of cases?

Answer 42

In about 80% of cases you get acute coronary syndrome before MI

Question 43

What is the most leath occulsion of a cornary artery?

Answer 43

STEMI

Question 44

Is STEMI full thickness or partial thickness?

Answer 44

Full thickness (transmural MI)

Question 45

A STEMI is associated with a pathologic _ wave

Answer 45

Q wave

Question 46

NOTE: A full thickness necrosis affects all 3 layers of the heart including the valves

Question 47

How many layers of the heart does a NSTEMI impact.

Answer 47

Only affects 1 layers

Question 48

In a MI (Stemi or NSTEMI) you have 3 pathologic zones following the infarct. What are the 3

Answer 48

1) Zone of infarct 2) Zone of injury 3) Zone of ischemia

Question 49

Describe the zone of ischemia

Answer 49

Reduced BF, this is typically where the blood clot happens in the coronary artery

Question 50

Descirbe the zone of injury

Answer 50

Damaged but not yet dead tissue

Question 51

Describe the zone of necrosis?

Answer 51

Dead heart tissue

Question 52

where are coronary blood vessels housed?

Answer 52

Epicardium

Question 53

What does Transmural mean?

Answer 53

Full thickness MI (think STEMI)

Question 54

What does Nontransmural mean?

Answer 54

Typically spares the **endocardium** * Think NSTEMI

Question 55

Do you want to move soon after an MI

Answer 55

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

Question 56

NOTE: After you've had an MI another one is likely - they're at high risk

Question 57

EF < _ = increased chance of cardiac event?

Answer 57

40%

Question 58

If you notice a patient is taking nitro you're thinking they're at risk for MI * take vitals and be prepaird

Question 59

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

Question 60

Question 61

Which of the following is MOST likely classified as a STEMI? a) Transmural MI b) Non transmural MI c) Unstable Angina d) Myocardial injury

Answer 61

A

Question 62

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])

Question 63

What is venous return like in HF

Answer 63

Normal, the issue is that the pump doesnt work well

Question 64

If the LV doesnt work well what gets backed up * What happens to CO / EX tolerance?

Answer 64

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.

Question 65

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

Answer 65

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)

Question 66

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)?

Answer 66

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

Question 67

**TEST**: Class 1 stage of heart failure

Answer 67

No symptoms and no limitations in ordinary PA. * Would not have SOB while walking and climbing stairs

Question 68

**TEST**: Class 2 stage of heart failure

Answer 68

Milk symptoms (mild SOB and/or angina) and slight limitation during ordinary activity * Only you would notice

Question 69

**TEST**: Stage 3 stage of HF: * What are they like at rest?

Answer 69

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

Question 70

**TEST**: Stage 4 Heart failure

Answer 70

Severe limitations. Experiences symptoms even while at rest. These patients are mostly bedbound (due to those symptoms at rest).

Question 71

# 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?

Answer 71

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)

Question 72

Left ventricular failure Diastolic: * What happens to SV?

Answer 72

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

Question 73

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

Question 74

Didnt fully understand

Question 75

Compenstory methods for body to stablize BP

Question 76

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

Question 77

What causes R sided HF? * Leads to hypertension where * If this hypertension is chronic what happens to the RV?

Answer 77

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)

Question 78

W/ R sided HF what happens to RV end diastolic pressure? Why?

Answer 78

Its increased because its having to push harder to get blood intot he pulmonary artery

Question 79

What kind of HF leads to jugular venous distension, liver engorgement, ascites, and peripheral edema

Answer 79

This is more systemic so its the R side of the heart backing up * R sided HF

Question 80

What is Cor Pulmonale?

Answer 80

R sided HF

Question 81

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

Question 82

NOTE: If HF is unstable = rest (don't try to EX0 Pleurocentesis = taking fluid out of thoracic cavity

Question 83

What is decompensation? * What are some signs of this?

Answer 83

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

Question 84

**Weight gain of _ pounds or more is a sign of decompensation (When HF is unstable)**

Answer 84

3 pounds or more

Question 85

If HR is _ at rest and BP is _ at rest this is a sign of decompensation (unstable HF)

Answer 85

At rest: increased HR and low BP

Question 86

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

Question 87

Which of the following medications are MOST commonly prescribed for heart failure management? a) Thrombolytics b) Antiarrhythmics c) Angiotensin II Receptor Blockers d) Heparin

Answer 87

C (ARB)

Question 88

What kind of forces cause aneurysm? * destruction of what layer of the artery are aneurysms? *

Answer 88

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

Question 89

W/ a dissecting abominal aneurysm is a tear in what layer of the artery? * what does it feel like?

Answer 89

Tear in arterial intima * Sudden pain/discomfort? / palpable mass * in the abdomen

Question 90

Arrhythmias are classified according to site of origin, type of cardiac activity, and presence of conduction block

Question 91

What do tachy arrhythmias do to myocardial O2 **demand**

Answer 91

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

Question 92

Brady arrhythmias lead to what in CHF pts

Answer 92

Pulmonary congestion

Question 93

Atrial arrhythmias do what to EDV?

Answer 93

Reduce it by 20-30% * this is because the atrium might be beating too quickly and not letting the ventricle fill all the way

Question 94

Ventricular fibrilatoion --> not getting enough blood supply, are not contracting --> deadly

Question 95

Treatment for arrythmias> * antiarrhythmics * Cardioversion * DEfibrillation * Surgical options

Question 96

atrial Fibrillation does what to ventricular filling time

Answer 96

Leads to decreased ventricular filling time --> inadequate CO / reduced coronary BF

Question 97

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

Question 98

Restricted valvular opening

Answer 98

Stenosis * narrowing, obstruction of valve * Concentric hypertrophy to normalize SV

Question 99

Incomplete valve closure (comes w/ regurgitation)

Answer 99

Insufficiency * backward BF * Leads to dilation and hypertrophy

Question 100

What 3 things cause mitral regurgitation?

Answer 100

LV dilation Papillary m dysfunction Calcification NOTE: this is regurgitation in LV to LA

Question 101

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?

Answer 101

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

Question 102

Aortic Stenosis * 2 causes? * What happens to CO? * What happens to the LV and why * Prognosis * Should we EX w/ this?

Answer 102

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)

Question 103

Which of the following arrhythmias MOST LIKELY leads to myocardial ischemia? a) Supraventricular tachycardia b) Sinus bradycardia c) Sinus arrest d) Atrial fibrillation

Answer 103

D

Question 104

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

Answer 104

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

Question 105

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?

Answer 105

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

Question 106

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?

Answer 106

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

Question 107

Which cardiomyopathy leads to sudden cardiac death the most? * This priamrily happens in what kind of people? * Contraindication? (1)

Answer 107

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

Question 108

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?

Answer 108

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

Question 109

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

Question 110

What causes pericarditis? * what is it? * Why have there been more reciently? * tx? * The reoccurance causes what, leading to what?

Answer 110

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

Question 111

Cardiac tamponade

Answer 111

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

Question 112

This is showing what happens w/ pericarditis / pericardial effusion (just that extra fluid around the heart)

Question 113

What causes endocarditits? * what is it? * What anatomical structure in the heart does it directly impact.

Answer 113

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

Question 114

Which of the following pathologies is exercise contraindicated when pathology is severe? a) atrial fibrillation b) aortic stenosis c) Dilated cardiomyopathy d) HF

Answer 114

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.