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Unit 6: LGS > Week 2 > Flashcards

Week 2 Flashcards

1
Q

two components of the heart

A
  • Electrical is heart rate

- Mechanical is stroke volume

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2
Q

Calculating cardiac output

A
  • One way is to look at stroke volume and heart rate.

- increases in stroke volume or heart rate allows for an increase in cardiac output

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3
Q

What things can regulate stroke volume

A

Preload, afterload, and contractility

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4
Q

Preload

  • what does it deal with?
  • what dertermines it?
A
  • It has to deal with stretch and is your end diastolic volume (EDV)
  • Venous return
  • this is volume
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5
Q

Afterload

- what is it?

A
  • It’s the pressure that the heart/or chamber has to pump against in order to allow blood to move from one area to the next
  • Afterload is PRESSURE
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6
Q

Contractility

  • what is it
  • hat effects it?
A
  • How hard the heart pumps

- calcium cycling to allow for the force of contraction, independent of EDV

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7
Q

Cardiac cycle

  • what does blood enter?
  • what does blood come back through?
  • flow
A
  • arteries
  • veins
  • right atrium –> right ventricle –> pulmonary arteries –> pulmonary capillaries –> pulmonary veins –> left atria –> left ventricle –> aorta
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8
Q

how do we get blood to move from one area to the next?

A

High pressure to low pressure

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9
Q

Flow

A

change in pressure/resistance

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10
Q

Right side of heart CO

A

(mean pulmonary arterial pressure − left atrial pressure) / (pulmonary vascular resistance)

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11
Q

Left side of heart CO

A

(mean arterial pressure − right atrial pressure) / (systemic vascular resistance)

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12
Q

Wiggers diagram

A
  • left atrial pressure
  • left ventricle pressure
  • aortic pressure
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13
Q

isovolumic contraction

  • what is happening
  • why?
A
  • The valves are closed, the volume is constant but the pressure is increased
  • the pressure needs to exceed the pressure of where the blood needs to go– in left ventricle it needs to increase to greater than pressure in aorta
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14
Q

as the blood is flowing out of the ventricle, what’s going to happen to the pressure in the ventricle compared to that of the aorta

A
  • the pressure will decrease and then the aortic valve will close
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15
Q

isovolumic relaxation

  • what is happening
  • why?
A
  • reducing pressure in comparison to the atria, because the atria has lower pressure.
  • in order to have ventricular filling, the atria need to be a greater pressure than that of the ventricles.
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16
Q

Stroke volume

A
  • the amount of blood ejected in one pump

- SV = EDV - ESV

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17
Q

Ejection fraction

  • what is it?
  • formula
  • normal
  • EF for heart failure
A
  • tells you about the efficiency of the pump, the function of the ventricles
  • EF = SV/EDV
  • Normal ejection fraction is 50-60%
  • Ejection fraction of 20% indicates heart failure and that your ventricles aren’t pumping as efficiently as they should
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18
Q

ECG correlation; what does it correspond to with electrical and mechnical function of heart

  • P wave
  • QRS complex
  • T wave
A
  • P wave: correlates in response to atrial depolarization, which correlates in response to atrial contraction
  • QRS complex: ventricular depolarization; it’s seen right in front of ventricular contraction
  • T wave: Ventricular repolarization is right before ventricular relaxation
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19
Q

Heart Sounds

A
  • S1: Corresponds to mitral valve and tricuspid valve closing
  • S2: Corresponds to the aortic and pulmonic valve closing
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20
Q

Identify and explain the cause of the splitting of S2

A
  • During inspiration you have an increase in the intrathoracic pressure, and there’s more volume of blood in the pulmonary vessel, and so your diastolic pressure back to the right side of the heart is altered and your pulmonic valve shuts a little later than your aortic valve, and the reason your aortic valve shuts a little quicker is because there’s less filling and less venous return, so the cycle is a little quicker and so the valve will close a little quicker than the pulmonic valve
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21
Q

Varying widening of S2

  • cause? dx?
  • how?
A
  • Delayed closure of pulmonic valve
  • Pulmonic valve stenosis
  • RBBB: You have slow conduction on right side of heart, which delays that closure of pulmonic valve
  • Pulmonary hypertension: Right ventricle has to try and exceed pulmonic artery
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22
Q

Fixed splitting of S2

- causes, how?

A
  • Atrial septal defects can cause this: There is shunting of blood from the left to the right side of the heart, and you’re changing those volumes
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23
Q

Paradoxical splitting

  • what happens
  • causes
A
  • There’s delayed closure of aortic valve

- LBBB and Aortic stenosis

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24
Q

S4

  • cause
  • why?
A
  • Left ventricle stiffening

- When the atria is pumping into a stiff LV, the contraction of the atria actually causes an S4 sound

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25
Q

S3

- cause

A
  • Tells us that there’s a dilated LV
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26
Q

What causes the ejection click and OS (opening snap)

A
  • They’re occurring when the valves open

- Stenosis can cause a snap or click

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27
Q

How would you categorize, the different causes (etiologies) of mitral valve regurgitation

A
  • Primary vs Secondary

- Acute vs. Chronic

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28
Q

Primary vs secondary

A
  • primary: direct valvular issue being the root cause– structural problem
  • secondary: kind of disease that then causes valvular disease– functional problem
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29
Q

mitral valve prolapse

  • frequency
  • causes
  • what is happening?
  • abnormality of the valve
  • what happens to endothelial cells of the valve?
  • what you expect to find histologically
  • staining
  • what happens to valve chronically
  • murmur?
A
  • most common
  • Infectious Endocarditis, Rheumatic Fever
  • with every systolic contraction, you get a regurgitant volume going back into atria, so with every contraction some of that volume is going back into the atrium.
  • when the left ventricle contracts because of the pressure gradient that mitral valve closes, but the mitral valve is too lax, it balloons back and it actually snaps & hits the wall or the endocardium of the left atrium, when it does that it causes damage
  • first the endothelial cells are denuded and then all of these cytokines & all of these chemicals that are released causing inflammatory cells to come and there is going to be reparative process.
  • Myxoid Degeneration; Increased deposition of proteoglycans replacing collagen in the fibrous layer
  • Tri-chrome Stain, with proteoglycan being either blue or green
  • annulus of valves will be calcified
  • yes, holosystolic murmur between s1 and s2
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30
Q

Is connective tissue disorder primary or secondary, specifically marfans?

A
  • In marfans the Chordae Tendinea are STRUCTURAL abnormal so it would be primary.
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31
Q

If the patient has mitral valve regurgitation, how would this alter the Wiggers Diagram?

A
  • Increase in atrial pressure during systole
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32
Q

Effects of acute episode of mitral valve prolapse

- why?

A
  • The left atrium will have blood pushed back into it which will increase the volume and the pressure and since it is not yet compliant the extra volume will start to back into the lungs and cause pulmonary edema
  • pulmonary edema is caused by increased hydrostatic pressure on the venous side which prevents more fluid from being able to be absorbed on the venous end of the pulmonary circuit.
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33
Q

Effect of chronic mitral valve prolapse

- what happens when left untreated?

A

The atria start to become compliant to the extra volume causing an increase in the size of the atria. Since the artia can hold more they now push more fluid into the ventricle and the ventricle has to become compliant to hold that fluid so the ventricle enlarges but cannot pump as well because the muscle is hypertrophic
- chronic heart failure

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34
Q

Murmur for mitral valve prolapse

  • kind
  • when
A
  • holosystolic

- any time the ventricular pressure is higher than the atrial, so usually between s1 and s2

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35
Q

Aortic Stenosis

  • what is it?
  • causes?
  • most common? where?
  • effects?
  • etiologies/risk factors?
  • congenital risks
  • what happens to the wiggers diagram?
  • chronically?
  • murmur?
A
  • narrowing of aortic valve
  • calcification, congenital bicuspid disease, or rheumatic fever
  • calcification; interior surface of the valve leaflets
  • decrease in flexibility of the valve and so it does not open or close well
  • age, and hyperlipidemia
  • develop aortic stenosis at an earlier age because of the increase in sheer forces
  • increase pressure, in the left ventricle cause the blood cannot get into the aorta because of that stiff valve so you are increasing pressure which then forces
  • concentric hypertrophy which will cause thick wall with smaller chamber–> not as much filling
  • Systolic Murmur = Cresendo - Decresendo; a little after S1
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36
Q

Side effects of chronic aortic stenosis

  • exertional syncope
  • angina
A
  • exertional syncope because during exercise your body needs more blood and the heart cannot keep up, adding to that there is vasodilation in skeletal muscle which deacreased venous return and so pre-load decreases so there is even less blood in the left ventricle being pushed out when there is high demand for oxygen
  • angina: coronary arteries have less blood flow so you have an imbalance in myocardial supply & demand
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37
Q

chronotropy

A
  • heart rate
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38
Q

inotropy

A
  • contractility
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39
Q

MOA of drugs that increase inotropy

  • Target L-type Ca2+ channels
  • ryanodine receptors (RyR2)
  • phospholamban
  • troponin
A
  • L-type Ca2+ channels: activating them to allow more Ca2+ influx into the cell which will help facilitates contraction
  • ryanodine receptors (RyR2) on the sarcoplasmic reticulum (SR): allow for release of SR Ca2+ stores through the calcium-induced calcium release mechanism –> Calcium release into the cytosol facilitates muscle contraction because Ca2+ is now available to bind troponin to allow for cross-bridge formation between actin and myosin.
  • inhibit phospholamban a SERCA inhibitorso that
    SERCA ican increase Ca2+ reuptake into the SR –> important so Ca2+ can cycle adequately to allow for muscle relaxation (Ca2+ reload into SR) and subsequent contractions (Ca2+ release from SR) of the beating heart
  • troponin directly by phosphorylating it to facilitate quick bind (better contraction) and release (better relaxation) of Ca2+
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40
Q

how we can affect cardiac output physiologically?

A
  • increase heart rate

- increase stroke volume

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41
Q

How can we increase HR?

A

With sympathetics (increase HR) and parasympathetics (decrease HR

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42
Q

How can we increase SV?

A
  • By changing preload, contractility, and/or afterload
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43
Q

Cardiac Output

- what is on the graph?

A
  • y= muscle tension and x= muscle length
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44
Q

stroke volume

  • intrinsic
  • extrinsic
A
  • preload

- contractility

45
Q

Preload

  • what is it?
  • how to change it?
A
  • The volume of blood in the ventricle preceding contraction. Also known as end diastolic volume
  • Increase in venous return–> increase in EDV–> increases stretch (in a healthy heart)–> sarcomeres stretch apart–> less overlap of thick and thin filaments—> more available binding sites for actin and myosin–> more cross-bridge formation (known as cross-bridge optimization)–> increased force of contraction
46
Q

Contractility

  • what is it?
  • how to change it??
A
  • strength/force of contraction determined by tension and velocity of shortening at the level of the sarcomeres
  • Changes in sympathetic tone through beta adrenergic stimulation–> will increase Ca2+ cycling—> will increase both cardiac contraction and relaxation
47
Q

Afterload

  • what is it??
  • condition with increase afterload
  • what happens when afterload is increased? why?
A
  • is the pressure required to overcome the pressure in the next chamber in order to move blood from one chamber to the next or from the ventricles into the vessels
  • Atrial valve stenosis
  • SV goes down because the heart uses a lot of its energy to just build up the pressure to open the valve that it doesnt have a lot left to actually push the blood through
48
Q

EF

- equation

A
  • (SV / EDV)
49
Q

SXS of right sided heart failure

A
  • JVD

- lower extremity edema

50
Q

How can prior MI cause CHF?

A
  • ## Prior MI caused damage to inferior wall–>damage to myocytes–>decreased contractility–>decreased EF.
51
Q

How can you tell if the patient has compensated or decompensated CHF?

A
  • compensation: vitals fairly normal

- decompensated will show high HR, increased RR, low SPO2

52
Q

How does a body compensate for heart failure?

A
  • increase sympathetic tone -> increase in venous return
53
Q

How does sympathetic tone increase venous return?

A
  • prompts kidneys to increase water reabsorption which leads to total body volume increase which allows for an increase in venous return which increases EDV
54
Q

What is isovolumic contraction

A

when the mitral valve has closed and pressure begins to increase in the ventricle but the aortic valve hasnt opened because the pressure in the ventricle isnt higher than the pressure in the aorta.

55
Q

What does increased pre-load look like on a pressure volume loop?

  • why?
  • what does it result in? why?
A
  • larger, same height but the end diastolic volume is greater so the loop is larger to the left.
  • Increased venous return–> Increase EDV–> increases stretch–> better cross-bridge optimization–> stronger contraction–> increased SV
  • increased stroke volume (SV), because there is more blood in the ventricle to push out so more is being pushed out
56
Q

What does increased contractility look like on a pressure volume loop?
- how?

A
  • the loop is taller and longer to right because the fore of the contraction leaves less of a end systolic volume
  • ncreased sympathetic tone–> increased Ca2+ cycling–> increased stroke volume
57
Q

What does increased after load look like on a pressure volume loop?
- what does it result in?

A
  • taller and skinnier because the end systolic volume is increased
  • decreased SV
58
Q

what happens in a healthy heart during exercise.

- how does healthy heart compensate?

A
  • Exercise–> increases metabolic demand–> need cardiac output (CO) to increase in order to reach homeostasis
  • increase heart rate or stroke volume
59
Q

How to increase SV?

A
  • intrinsically with increased venous return (increased preload)—> increases end diastolic volume (EDV)–> increases stroke volume (SV)
  • Extrinsically with sympathetics–> increases contractility
60
Q

What happens in heart with mitral regurg?

  • how does it compensate?
  • what happens after decompensation?
A
  • During every contraction, some of the blood is going back into the left atrium and some is going out into the aorta.
  • left atrium dilates out in order to increase volume and decrease stress on the pulmonary circulation.
  • Regurgitant volume will increase more and more as the atrium dilate over time–> some of this volume will start going into the left ventricle–> the left ventricle will similarly dilate out–> will have a greater end diastolic volume (EDV) –> the heart will try to increase contractility to compensate but may reach a point where it can’t keep up anymore–> can’t contract as well anymore–> contractility will decrease–> End systolic volume pressure relationship (ESPVR) will decrease–> will decrease cardiac output.
  • heart may try to compensate again and offset the loss in stroke by increasing EDV more–> increases stretch on muscle wall–> increases force of contraction through the Frank-Starling Mechanism.
61
Q

What happens to heart after MI?

A
  • Prior MI caused damage to inferior wall–>damage to myocytes–>decreased contractility–>decreased EF.
62
Q

compensation for heart failure/reduced EF/reduced systolic function

  • what is underlying mechanism?
  • what other parts of body are adding to this?
A
  • increase sympathetic tone to increase venous return
  • Increased tone and volume. There’s an increase in total body volume which is occurring in the kidneys leading to a compensatory state (this has happened over time). The increase in volume occurs in response to ischemic cardiomyopathy.
63
Q

What changes if the patient has contractile dysfunction?

  • compensation?
  • what happens to EF?
A
  • End-systolic pressure-volume relationship
  • To keep SV as close to normal as possible, you increase EDV (preload) by increasing sympathetic tone which increases venous return to heart–>healthy tissue stretches greater leading to greater force of contraction to try and maintain SV
  • decreased
64
Q

What is S3?

A
  • hearing blood flow into dilated ventricle
65
Q

What happens when a patient in compensated CHF has too much salt?

A
  • bunch of salt over the weekend–>fluid overload–>increases volume–>Circulating volume increases–>increases venous return–>increases EDV
66
Q

Why would patient having STEMI have low BP?

A
  • heart cannot contract during MI
67
Q

Side effect of MI to anterolateral portion of heart?

A

mitral valve regurgitation because anterolateral MI affects the myocardium that normally stabilizes those valvular structures.

68
Q

What happens to pessure volume loop in patient with STEMI?

- why is EDV that way?

A
  • EDV basically remains the same, then you have a really reduced stroke volume and ESV is significantly elevated which leads to symptomatic manifestations.
  • because it is an acute event and has not had time to compensate yet
69
Q

What do large QRS complexes mean?

A
  • L ventricular hypertrophy
70
Q

L ventricular hypertrophy

  • causes
  • what happens?
  • ef?
  • kind of dysfunction? why?
A
  • High BP
  • eccentric hypertrophy, thicken the wall muscle which makes L ventricle stiffer
  • preserved
  • diastolic, because the patients cavities have gotten smaller and cannot fill as much
71
Q
  • point of the cardiovascular system
A

meet the metabolic demand of the body.

72
Q

What happens if you increase metabolic demand?

A

increase your CO to compensate for it bc you wanna allow for more circulation of your blood so you’re getting more oxygen there.

73
Q

tissue oxygen level

A
  • oxygen supply is gonna allow for more oxygen to be there where the oxygen demand is going to utilize it more
74
Q

What do you think happens to the myocardial supply and demand during exercise?

  • depends on?
  • where does it come from?
A
  • Demand increases so supply should increase to offset the demand.
  • amount of coronary blood flow and the arterial oxygen content
  • Blood
75
Q

concentric hypertrophy of the ventricle

  • what is it?
  • What happens to O2 demand?
  • If that person was exercising, what happens to oxygen supply?
  • What do you happens to the pressure gradient on those coronary arteries?
  • What happens to the supply in that type of individual?
  • sxs during running?
  • what part of the myocardial tissue is not getting as much of the supply?
A
  • Thick, mass of ventricle is increased
  • Increases
  • It would not match it, filling is decreased but you also have thickened wall.
  • increases
  • Decreases bc of the thickness of the mass of the heart itself.
  • Angina
  • subendocardial layer is getting less oxygen. Bc the coronary arteries are outside
76
Q

What is angina?

- why does it occur?

A
  • chest pain

- sx of imbalance of supply and demand, usually is youre having more demand than you are supply

77
Q

what happens to the coronary blood flow during normally during …..?

  • systole
  • diastole
A
  • During systole youre contracting so pressure is increasing, blood flow decreases
  • During the diastole, your pressure gradient is less so those vessels open back up
78
Q

Changes seen on EKG when oxygen supply to heart does not meet the demand?

A
  • ST depressions or T wave inversions
79
Q

Cardiac remodeling

  • what is it?
  • kinds?
A
  • something your heart will undergo to offset stress. Could be
  • concentric or eccentric
80
Q

Concentric remodeling

  • myocyte formation?
  • sarcomeres functioning?
  • induced by? example.
  • chamber?
  • causes what type of dysfunction?
A
  • stack in parallel and they become shorter and get thicker
  • yes, even though there are more sarcoemres they all function correctly
  • Pressure overload; aortic stenosis
  • decreases in diameter
  • diastolic, smaller chamber means you cannot fill
81
Q

Cardiac remodeling in athlete?

  • what is it?
  • why?
  • fibrosis?
  • term
A
  • thickening of the wall to overcome the new CO that your body is undergoing
  • body undergoes constant exercise induced stress -> heart needs to meet metabolic demand -> heart remodels in physiological way to match that new CO demand that the body now needs
  • no
  • physiological remodeling
82
Q

Pathological remodeling

  • what is it? example.
  • types
  • fibrosis?
  • effects?
A
  • remodeling of heart due to pathological problem (HTN)
  • concentric and eccentric
  • yes
  • systolic and diastolic functions are not gonna be as effective
83
Q

Eccentric hypertrophy

  • myocyte formation
  • functioning sarcomeres?
  • cause?
  • chamber?
  • causes what type of dysfunction?
A
  • elongating the myocytes
  • thick and thin filaments start to elongate out as well and so your ability to form cross bridges are not as efficient
  • can be physiologic change due to increase in venous return from exercising
  • increases in diameter
  • systolic, chamber filling with lots of blood but area is so much bigger than the walls that they cannot effectively push out as much blood
84
Q

Timeline of cardiac remodeling in patient with chronic, uncontrolled HTN

  • type at beginning
  • type at end?
A
  • diastolic dysfunction, the patients heart has to work harder to overcome the increased afterload and so it has concentric hypertrophy but chronically the heart cannot handle this for too many years.
  • start to dilate out and you will start to get an eccentric hypertrophy which is a systolic dysfunction because the heart walls are too thin in comparison the the cavity and they cannot pump the blood out effectively
85
Q

what happens to oxygen demand in the setting of hypertrophy

- what happens if demand outweighs supply for long period of time? effect?

A
  • increases
  • we can get ischemia which can progress to infarction
  • infarcting pieces of the heart dont work correctly and can contribute to dilating the heart out.
86
Q

what does it mean when HF is in compensated state

A
  • trying to compensate for the changes in the structure of the heart and keep stroke volume normal
87
Q

Laplace’s law

A

alter the wall thickness to reduce the tension on the wall of the heart

88
Q

Overt heart failure

  • what is it?
  • effects
A

stretch out walls of heart too much, they begin to thin out and heart is unable to function
- can lead to death

89
Q

What are the steps of compensation?

A
  • pressure has been increase -> autonomic addaptation -> increase in contractility -> cant go for long -> increase in volume -> become volume overloaded ->
90
Q

Autonomic adaptation

  • what is it?
  • mediators? how?
A
  • increased SNS activation and RAAS activation

- catecholamines; ind to beta receptors and increase Ca2+ in myocytes and increase heart rate in nodal cells

91
Q

What happens with increased contractility in the pressure volume loop?

A

heart is trying to compensate and it is doing so for a while, but over time those compensatory mechanisms can only keep up for so much before they fail so the we start to get volume overload

92
Q

Impedance changes

  • what is it looking for?
  • how can it be measured?
  • chamber specifically being looked at? organ?
A
  • alteration in the amounts of fluid in the chest
  • place external leads on the skin or we can also place impendence leads inside the heart
  • LV
  • lungs -> see if there is any fluid backing up into the lungs
93
Q

How can fluid back into the lungs?

A

LA pressure increases –> Pulmonary venous pressure increases –> pressure in capillaries increases -> increased hydrostatic pressure in pulmonary vessels –> pushed into the lungs

94
Q

Heart failure sxs

  • normal
  • chronic
  • kussmaul sign
A
  • Dyspnea on exertion, edema (lungs & LE), fatigue, JVD, weight gain, Orthopnea, PND, angina
  • hepatomegaly with RUQ pain due to stretching of the capsule; syncope/ light headedness or altered mental status
  • paradoxical rise in jugular venous pressure (JVP) on inspiration
95
Q

hepatojugular reflex

A
  • so volume overloaded that when you press on the RUQ over the liver it pushes fluid back up toward where you can see distention in the jugular veins
96
Q

Hypertrophic cardiomyopathy

  • presentation
  • structural changes
  • Etiology
  • Functional changes
  • what happens with asymmetric HCM
  • treatment
  • abnormality with EF?
A
  • Cardiac arrest after exercising OR SOB when exercising
  • myofiber/sarcomere disarray, Increase in size of myocyte and disconnect with mitochondria and sarcomeres
  • genetic with incomplete variance or idiopathic
  • Heart failure with preserved EF, Decreased EDV, No change in end systolic volume or contractility, obstruction depending on whether or not it is symmetrical or asymmetrical
  • puts pressure on the mitral valve and there can be mitral valve regurg
  • beta blocker and stop exercising
  • can be increased early on in disease because since there is an increase in sarcoemeres there is harder contraction so ESV would be decreased along for EF to be above average
97
Q

Explain HCM to patients mother

A

Your son has a genetic abnormality that causes the wall between his two ventricles to become thickened (enlarged). When his heart tries to contract the wall becomes even thicker and can block the space where the blood usually exits the heart in order to travel to the body which makes it harder to pump blood to the rest of the body. When you exercise your body needs more energy and blood carries a lot of things to help with energy (such as oxygen and nutrients). So, because of the abnormality and the blockage making it harder to send blood to the rest of the body, your son is unable to meet his body’s needs for the extra oxygen and nutrients. The fact that your son has SOB and syncope when exercising is his bodys way of showing that they aren’t getting the nutrients they need fast enough to be able to perform as fast as they need to as so they begin to almost start shutting down. For instance, the reason your son faints is because the brain isn’t getting the oxygen it needs. The reason your son has this condition and you don’t could be for multiple reasons. Since it is genetic it could mean that you do have a similar problem but not to the severity he does or you may not have the problem at all and he inherited from his dad.

98
Q

Why is there preserved EF in HCM?

A

It is percentage of the blood that is returning to the ventricle so it is preserved because the percentage of blood that is returning to the heart is the same but stroke volume is significantly diminished because he is not getting enough blood into the chamber

99
Q

What is the difference between aortic stenosis and hypertrophic murmur is depending upon different movements?
- valsava and standing

A
  • decrease in ventricular cavity
  • Hypertrophic murmur: murmur intensifies
  • Aortic stenosis murmur: murmur reduces
100
Q

Left sided hypertensive heart disease

  • structural changes, type of compensation?
  • diff between a hypertensive induced hypertrophy and a hypertrophic cardiomyopathy
  • dysfunction acutely
  • dysfunction chronically? Why?
A
  • Myocardium are slightly thicker, concentric; myocardial disarray, dilated left atrium
  • Even though there is hypertrophy it is organized remodeling with interstital and perivascular collagen deposition
  • diastolic
  • Systolic dysfunction–cannot pump; The patient transitioned from concentric hypertrophy to eccentric hypertrophy which decreases systolic function so forward cardiac output decreases
101
Q

Why does left sided hypertensive heart disease cause dilated atrium? What can this lead to?

A
  • increased pressure in the left ventricle cause increased pressure in the right atrium which increase pressure all the way to the lungs -> to prevent pulmonary edema the atrium will dilate out over time
  • A fib- increased pressure in the left ventricle -> left atria enlarges -> enlargement is stretching the myocytes causing them to be irritated so you start having ectopic foci and breaking away gap junctions so the conduction does not travel as well.
102
Q

What is Myocardial disarray

  • why is it seen in hypertensive left sided heart disease?
  • effect
A
  • cells being stretched and fibrosis filling up area
  • Fibrosis around the myofibers will then cause a decrease in the diameter of the myofiber and there is problem with conduction
103
Q

What kind of dysfunction does patient with left sided hypertensive heart disease….

  • start out with?
  • progress to
A
  • diastolic dysfunction
  • the muscle hypertrophy and causes the cavity to become smaller so the heart does not fill as well during diastole
  • Systolic dysfunction
104
Q

Presentation of left sided hypertensive cardiac disease

  • early in disease
  • middle of disease
  • late disease
A
  • Earlier in disease: Asymptomatic, but w/ HTN.
  • Pulm HTN–rales
  • JVD and pitting edema
105
Q

Why do patients with left sided hypertensive cardiac disease progress to having pulmonary HTN?

  • what does this do to CO?
  • compensation?
A
  • Increase in left ventricular pressure -> increase in left atrial pressure -> increase in pressure in pulmonary veins -> increase in hydrostatic pressure in pulmonic capillaries -> fluid pooling in the lung tissue because the hydrostatic forces are messed up and fluid is not being pulled into the venule side of the capillary
  • It decreases because you have less volume coming back
  • Atrium dilates
106
Q

How and why do patients with left sided hypertensive cardiac disease progress to having JVD and edema?

A
  • back up into Left atrium and pulmonic system cause back up into right ventricle then right atria and then into the veins draining into the right atrium.
  • increased pressure in right atria is same amount of pressure in the venous circulation and since there is no valves that lead towards the atrium there becomes a back up of pressure. Since the largest vein going to the atria that we can see is the jugular we see can see distention (pooling of blood) in that vein.
107
Q

Sxs when patient with left sided HTN induced hypertrophy transitions from concentric to eccentric hypertrophy

A
  • Fatigue/syncope
108
Q

Can late stage left sided hypertensive heart disease have a murmur?

  • why?
  • what would it sound like?
A
  • yes

- Pansystloic/Holosystolic murmur between S1 and S2

109
Q

Treatment for concentric vs eccentric in left sided hypertensive heart dx?

A
  • Treatment plan for concentric would be to reduce BP since the afterload is what induces the hypertrophy
  • when it swithced to eccentric hypertrophy then we start adding meds to control the sxs for heart failure

Unit 6: LGS (10 decks)

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