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NSU AA Denver: Summer 2025 (2nd Semester) > Applied Physiology: Lecture 10 - Valve Lesions > Flashcards

Applied Physiology: Lecture 10 - Valve Lesions Flashcards

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1
Q

Valvular Heart Disease: Left Sided Lesions

A

Aortic Stenosis
Aortic Regurgitation
Mitral Stenosis
Mitral Regurgitation

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2
Q

Valvular Heart Disease: Right Sided Lesions

A

Tricuspid Regurgitation

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3
Q

Preload

A

Defined as:
- End Diastolic fiber length or volume.
- Best defined as End Diastolic Volume (EDV).

According to the Frank-Stalling relationship, increases in LVEDV produces increases in CO until excessive filling leads to failure.

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4
Q

Which of the following factors do not affect preload?

Contractility
Venous Tone
Intravascular Volume
Total body Sodium

A

Contractility
Preload is affected by fluid load, which all three others effect

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5
Q

Afterload

A

It is the stress (force/unit area) encountered by the myocardial fibers throughout systole.

The external forces opposing ejection and often approximated by the SVR.

SVR=[(MAP-CVP)/CO] x 80
- Normal = 900-1500 Dynes –sec/cm5

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6
Q

Calculate the SVR given the following information.

BP 136/78, HR 78, SpO2 98%, LVESV 35, LVEDV 120, Right atrial Pressure of 9

A

1066

MAP = DBP+((SBP-DBP)/3)
CVP = Right Atrial Pressure
SV = LVEDV-LVESV
CO = SV x HR

SVR=[(MAP-CVP)/CO] x 80
Normal = 900-1500 Dynes –sec/cm5

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7
Q

Afterload – Right Ventricular (Dependent on what?)

A

Mainly dependent on Pulmonary Vascular Resistance (PVR).

PVR=[ (PAP- PCWP or LAP)/CO ]x 80
50-150 dynes-sec/cm5

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8
Q

Compliance

A

Compliant hearts are able to accommodate increases in volume without significant changes in pressure.
- Curves B and C

Noncompliant hearts undergo significant increases in pressure in response to volume
- Curve A

Decreases in compliance are seen with diastolic dysfunction and infiltrative diseases

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9
Q

What is BP?

A

BP = CO x SVR

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10
Q

What are CO and SVR dependent on?

A

CO depends on:
HR
SV

SV depends on:
Preload
Afterload
Contractility

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11
Q

Aortic Stenosis Etiology

A

Congenital
- Most common type
- In absence of rheumatic fever
- Most common congenital abnormality is a Bicuspid aortic valve > 50%

Acquired
- Calcific (degenerative) most common
- Seen with advanced age (senile)

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12
Q

Aortic Stenosis: Symptoms

A

Angina

Syncope

CHF (congestive heart failure)

Long asymptomatic period (up to 50 years)

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13
Q

Aortic Stenosis Pathophysiology: LVH

A

Concentric Left Ventricular Hypertrophy (wall thickness)
- Due to increased wall tension, which decreases diastolic compliance
- Hypertrophy enables Left Ventricle to maintain Stroke volume
- Stiffening of the ventricle can lead to a diastolic dysfunction due to a non compliant (elastic) ventricle.

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14
Q

Aortic Stenosis Pathophysiology: Diastolic Compliance (Diastolic HF)

A

Decreased compliance:
- Increased LVEDP required to provide adequate preload
Filling a smaller ventricle increases stretch (Increased LVEDP), passive filling is reduced due to the higher pressures at lower volumes which leads to the need for the atrial kick (forcing volume into the ventricle to preserve preload)
- Increased contribution of the atrial kick to CO
Up to 40% instead of usual 15-20%

Increases Pressures to keep volume
Increases Atrial kick to keep volume needed

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15
Q

Aortic Stenosis Pathophysiology Overview

A

Decreased compliance
- Hypertrophied myocardium
- Higher LVEDP

Ischemia
- Angina
- Arrhythmias
- Sudden Cardiac Death

Longer systolic ejection times (less diastolic time)
- Reduced time to perfuse coronary vessels

All of these sequelae lead to lower Coronary Perfusion Pressures and Cerebral Perfusion Pressures… due to decreased diastole time

Know coronary perfusion pressure formulas

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16
Q

Aortic Stenosis Pathophysiology: Contractility

A

May be preserved by increasing wall thickness
- Hyperdynamic LV

May also be depressed with chronic subendocardial ischemia.

50% of all AS patients have CAD

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17
Q

Aortic Stenosis Pathophysiology: PVR

A

Usually not a problem… due to left side of heart???

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18
Q

Progression of Aortic Stenosis

A
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19
Q

Normal Aortic Valve Size

A
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20
Q

Mild Aortic Valve Size

A
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21
Q

Moderate Aortic Valve Size

A
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22
Q

Severe Aortic Valvce Size

A
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23
Q

Aortic Stenosis Pressure Gradients

A

Transvalvular pressure gradients:
- Normal: <25mmHg
- Severe: 40-80mmHg
- Critical: >80mmHg

The transvalvular gradient represents the pressure drop that occurs as blood flows through a narrowed heart valve.

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24
Q

Critical Aortic Valve Area

A

0.5-0.7 cm2

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25
What does worsening Aortic Stenosis Yields?
Triad of: CHF Angina Syncope
26
Goals of Aortic Stenosis Anesthetic Management
Maintain preload, NSR, and afterload. Treat hypotension with vasoconstrictors
27
Anesthetic Management: Goals of AS LV Preload
Constant and/or Increased Keep intravascular volume normal to high Avoid venous dilation Keep the heart rate low to normal - CO is rate dependent 2/2 stiff LV Aggressive treatment of abnormal atrial rhythm (want to avoid A-Fib)
28
Anesthetic Management: Goals of AS HR
NSR Avoid Tachy Want to give more time during diastoles for cornoary perfusion
29
Anesthetic Management: Goals of AS Contractile State
Normal The heart must force the stroke volume through the constriction! Maintain inotropic state (contractility) Use beta blockers cautiously, may be dependent on HR to maintain CO
30
Anesthetic Management: Goals of AS SVR
Must Maintain!
31
Anesthetic Management: Goals of AS LV Afterload
Coronary perfusion to hypertrophied heart needs diastolic pressure. Aggressive treatment of hypotension with alpha agonist. Spinal/epidural with great caution. - Spinals likely contraindicated in severe/critical AS
32
You receive the following echo report: Aortic valve area 0.7cm2 EF 60% Mild Mitral regurgitation RVSP 30 mmHg What is your anesthetic plan and considerations for an emergent cystoscopy? A. Spinal with low dose bupivacaine B. General with Etomidate and pre-induction Arterial Line C. Cancel the Case D. General with Propofol and Central Line
B. General with Etomidate and pre-induction Arterial Line ## Footnote No Propofol as dont want to drop SVR
33
Aortic Insufficiency (AI) Etiology
Relatively uncommon unless accompanied by AS Congenital - Associated with other cardiac anomalies Acquired - Ankylosing spondylitis, Marfan’s syndrome - Endocarditis- acute AI - Aortic Dissection- acute AI - Rheumatic heart disease
34
Aortic Insufficiency Symptoms
CHF - Dyspnea - Fatigue - Palpations - Increased LVEDP and LVEDV Symptoms of LV failure with acute AI develop rapidly. - Acute: Endocarditis, Trauma, Dissection - Chronic: rheumatic, congenital
35
When might symptoms appear with AI
Can have an asymptomatic period for up to 20 years. Until regurgitant fraction exceeds 60% of SV (60% of blood falling back into left ventricle)
36
Can AI Symptoms progress rapidly?
Symptoms of LV failure with acute AI develop rapidly. - Acute: Endocarditis, Trauma, Dissection - Chronic: rheumatic, congenital
37
Stages of AI
Stage I = Mild AI: no symptoms - Normal LVEDP - Regurgitant fraction < 40% Stage II = Moderate AI: Symptoms - LVEDP rises - Regurgitant fraction 60% - Dyspnea and CHF Stage III = Severe AI: Terminal Failure EF is likely falsely elevated due to a percentage falling back into ventricle on relaxation.
38
Stage I of AI
Stage I = Mild AI: no symptoms - Normal LVEDP - Regurgitant fraction < 40%
39
Stage II of AI
Stage II = Moderate AI: Symptoms - LVEDP rises - Regurgitant fraction 60% - Dyspnea and CHF
40
Stage III of AI
Stage III = Severe AI: Terminal Failure
41
Aortic Insufficiency Pathophysiology
Eccentric Hypertrophy - Occurs due to the chronic volume overload from diastolic regurgitation. - Varies from Concentric Hypertrophy in AS Increased LV compliance - Initial Increase in LVEDV without increases in LVEDP. SV: effective SV may be reduced - Due to potentially large regurgitant fraction
42
Aortic Insufficiency: Acute vs Chronic
ACUTE disease causes: -Sudden rise in LVEDV->filling heart beyond Frank-Starling limits->increase LVEDP->acute pulmonary edema->effective SV rapidly declines CHRONIC disease causes - Slightly increased LVEDP but a large increase in LVEDV-> leading to eccentric hypertrophy and LV dilatation. The pulse pressure is wide, while stroke volume and EF are maintained. HR is normal and SVR is low. LVEDP increases in both acute and chronic AI CPP= DBP-LVEDP Decreased CPP and angina/ischemia ## Footnote Know the normal for LVEDP, etc.
43
Acute AI
ACUTE disease causes a sudden rise in LVEDV->filling heart beyond Frank-Starling limits->increase LVEDP->acute pulmonary edema->effective SV rapidly declines LVEDP increases in both acute and chronic AI CPP= DBP-LVEDP Decreased CPP and angina/ischemia
44
Chronic AI
CHRONIC disease causes a slightly increased LVEDP but a large increase in LVEDV-> leading to eccentric hypertrophy and LV dilatation. The pulse pressure is wide, while stroke volume and EF are maintained. HR is normal and SVR is low. LVEDP increases in both acute and chronic AI CPP= DBP-LVEDP Decreased CPP and angina/ischemia
45
Goals of Aortic Insufficiency Anesthetic Management
Management of regurgitant lesions require “Fast, Full, and Forward” HR faster to give less time to fall back into LV Lower SVR gives less pressure to push back against the Aorta
46
Goals of Aortic Insufficiency Anesthetic Management: Preload
Normal to elevated Keep intravascular volume high-maintain compensatory increase in preload Avoid significant venodilation Decreases preload High normal heart rate (90) is best Avoid bradycardia (more time in diastole = more time for regurgitation)
47
Goals of Aortic Insufficiency Anesthetic Management: Contractility
Elevated Maintain contractility as high cardiac output is compensation for regurgitation. Increase heart rate & contractility with beta-1 agonists. - Dobutamine - Dopamine - Ephedrine
48
Goals of Aortic Insufficiency Anesthetic Management: Afterload
Reduced afterload is essential Path of least resistance, if afterload is too high regurgitation volume will fall back into heart. Use arterial dilators (not venous): - SNP (nitroprusside) - Nicardipine
49
You receive the following echo: Severe Aortic Regurgitation EF 55% HR 65, BP 73/42, Spo2 93%, NSR Treatment? A. Nitroglycerin B. Phenylephrine C. Dobutamine D. Glycopyrrolate
C. Dobutamine (increase contractility) Glyco, would just increase HR, not terrible, but not best option
50
Mitral Valve
Very Rare
51
Mitral Stenosis Etiology
Delayed complication of Rheumatic Fever - Rare in most developed countries Can occur in Hemodialysis dependent patients - Calcific in nature 2/3 are female
52
Mitral Stenosis Symptoms
Congestive Heart Failure Pulmonary Edema Pulmonary HTN – and Right Heart Failure. - Avoid hypoxia, hypercarbia, and acidosis Atrial Fibrillation (a result of stretching the Atria) Develop after asymptomatic period of 20-30 years
53
Mitral Stenosis Pathophysiology: LA "Size"
Left Atrium: - Hypertrophy (Increased pressure needed for atrial kick) - Markedly dilated - Chronic volume and pressure overload. - LV filling is impeded. - LV filling is achieved by increases in LAP - LA:LV pressure gradient increased because of the stenotic valve.
54
Mitral Stenosis Pathophysiology: LA Rhythm
Chronic distention of the LA eventually leads to atrial fibrillation - Distension/Stretching of electrical system Blood flow stasis promotes thrombi formation, usually in LAA (Left atrial appendage) No atrial systole, necessitates higher diastolic flow to maintain CO
55
Mitral Stenosis Pathophysiology: Pulmonary Effects
Pulmonary edema Pulmonary HTN, marked dilation of RV RV failure – cor pulmonale Pulmonary and tricuspid insufficiency All due to back up of blood flow
56
Mitral Stenosis Pathophysiology: Left Atrial Function
LA chronically overloaded, HOWEVER... ... Contractility is usually preserved - Unless in atrial fibrillation
57
Mitral Stenosis Pathophysiology: Emboli
Embolic events common with MS/Afib Increased incidence of: - Systemic and pulmonary emboli - Pulmonary infarction - Hemoptysis (coughing up blood) LEADS TO LV chronically underloaded, SV reduced ## Footnote Crisis Management Book in Library to look at PE treatment!!!
58
Mitral stenosis: Quantification (Valve Area)
Normal opening: - 4 - 6 cm2 Mild stenosis: - 1.5 -2.5 cm2 (symptom free) Moderate stenosis: - 1 – 1.5 cm2 (CHF easily induced) Critical Stenosis: - 0.6-1.0 cm2 (Symptoms at rest)
59
What is Normal Mitral Valve Area?
Normal opening: - 4 - 6 cm2
60
What is Mild Mitral Stenosis?
Mild stenosis: - 1.5 -2.5 cm2 (symptom free)
61
What is Moderate Mitral Stenosis?
Moderate stenosis: - 1 – 1.5 cm2 (CHF easily induced)
62
What is Critical Mitral Stenosis?
Critical Stenosis: - 0.6-1.0 cm2 (Symptoms at rest)
63
Goals of Mitral Stenosis Anesthetic Management
May be susceptible to worsening Pulmonary HTN (Avoid Hypercarbia)
64
Goals of Mitral Stenosis Anesthetic Management: Preload
Maintain but Avoid Volume Overload (Fragile pts) Keep intravascular volume high (not too high!) Avoid vasodilation Low normal heart rate is best - Ventricle needs time to fill Aggressive treatment of tachycardia Cardioversion for atrial fibrillation (Look more about A-Fib and this!!!)
65
Goals of Mitral Stenosis Anesthetic Management: Contractility
Maintain Constant Contractility is only an issue for end-stage disease
66
Goals of Mitral Stenosis Anesthetic Management: Afterload
Maintain in normal range Large increases/decreases should be avoided because of possible LV dysfunction. - Again, careful with neuraxial anesthesia - Potentially avoid spinal anesthesia
67
Mitral Regurgitation: Acute vs Chronic
68
Acute Mitral Regurgitation
Usually due to ischemia/infarction of chordae or papillary m. rupture Prosthetic valve dysfunction Endocarditis
69
Chronic Mitral Regurgitation
Most due to rheumatic fever/coexists with mitral stenosis Congenital Annular dilation - Secondary to cardiomyopathy
70
Mitral Regurgitation Symptoms Progression
20-40 year asymptomatic period Gradual onset of: - Fatigue - Dyspnea Rapid downhill course (5 years)
71
Mitral Regurgitation Pathophysiology: Chronic
LA and LV dilation and hypertrophy - Annular dilation, prevents coaptation of valve leaflets Pulmonary Congestion/edema - More typical with severe LV dysfunction LV failure - Regurgitant factor > 60% - EF < 50%
72
Mitral Regurgitation Pathophysiology: Acute
LA and LV volume overload Low CO Hypotension Pulmonary edema Increase HR and contractility may increase the risk of MI (Careful!)
73
Stages of Chronic MR
Stage I: Mild MR with compensation - LV dilatation, increase LVEDV with normal LVEDP - CO maintained Stage II: Moderate MR with symptoms - Low cardiac output - Patients become symptomatic Stage III: Severe MR; terminal failure - Increased pulmonary artery pressure - RV failure
74
Stage I of Chronic MR
Stage I: Mild MR with compensation - LV dilatation, increase LVEDV with normal LVEDP - CO maintained
75
Stage II of Chronic MR
Stage II: Moderate MR with symptoms - Low cardiac output - Patients become symptomatic
76
Stage III of Chronic MR
Stage III: Severe MR; terminal failure - Increased pulmonary artery pressure - RV failure
77
Severity of MR
Mild MR - Less than 30% of total LV stroke volume Moderate MR - 30-60% of stroke volume Severe MR - >60% of stroke volume ## Footnote Looks similar to Aortic Insufficiency
78
Mitral Regurgitation Anesthetic Management
Again: Fast, Full, and forward!!! (Like Aortic Insufficiancy)
79
Goals of Mitral Stenosis Anesthetic Management: Preload
Increased Individualize - Preload augmentation may dilate LV and MV annulus High normal heart rate is best - Bradycardia increases LVEDV, further dilates MV annulus - Maintains heart size - Treat bradycardia aggressively ## Footnote Brady one of the worst things for a Regurg lesion (Aortic and Mitral)
80
Goals of Mitral Stenosis Anesthetic Management: Contractility
Normal to Increased Contractility is important Keeps ventricular size down Maintains forward cardiac output
81
Goals of Mitral Stenosis Anesthetic Management: Afterload
Afterload reduction is essential - Increases forward SV - Reduces regurgitant fraction
82
Big Takeaway from Mitral Regurgitation Anesthetic Plan (Aortic as well???)
Remember: faster, fuller, and vasodilator (forward)
83
Full Valve Lesions Comparison (AR vs MR vs AS vs MS)
84
Tricuspid Regurgitation Etiology
Chronic LV Failure to Pulmonary HTN to RV Dilation to TV Annulus Dilation to TR - Most typical etiology - Due to LV dysfunction Can also follow: - Endocarditis - Rheumatic fever
85
Goals of TR Anesthesia Management
TTE = TR will increase with RVSP > 40 mmHg and/or Pulm HTN - Conversely, pulmonary hypertension is often determined by amount of TR on echo Maintain RV and LV preload - Avoid hypovolemia, hypoxia, hypercarbia, acidosis - PEEP and increased PIP increase RV afterload
86
Which would you avoid in Aortic Stenosis?
Milrinone (decrease afterload?) Inodilator
87
When referrring to Severe Chronic Aortic Insufficincy which is true?
Stroke volume is increased
88
Which can lead to eccentric heart failure?
Chronic Arotic Regurgitation
89
Patient RVSP 60 pH 7.12, PaCO2 76, SpO2 83%, Base Excess +7 Vitals HR 120 BP 64/40 Which is best option for Treatment?
Dobutamine

NSU AA Denver: Summer 2025 (2nd Semester) (62 decks)

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