L&J Chi 26 Pathophysiology, Ax Management of Patients with CV Disease

Question 1

What are conditions associated with pressure overload?

Answer 1

Subaortic Stenosis

Pulmonic stenosis

Question 2

Consequences of SAS

Answer 2

• Chronic systolic pressure increase in left ventricle

- Results in increased wall tension, compensatory increase in ventricular wall thickness (concentric hypertrophy)

Question 3

Consequences of PS

Answer 3

• Chronic systolic pressure increase in right ventricle

- Results in increased wall tension, compensatory increase in ventricular wall thickness (concentric hypertrophy)

Question 4

Consequences of concentric hypertrophy of L/R ventricle associated with SAS and PS?

Answer 4

Increase in ventricular muscle mass and increase in myocardial work required to generate increased systolic pressures –> increased demand for coronary blood flow and myocardial oxygen delivery

Question 5

When is the resulting risk for ischemia the greatest?

Answer 5

-During periods of tachycardia –> myocardial necrosis, replacement fibrosis, development of ventricular arrhythmias

Question 6

In young dogs with severe SAS

Answer 6

• Risk for syncope, sudden arrhythmogenic death is high

- Left-sided congestive failure only seen in much older dogs

Question 7

Which is tolerated better?

Answer 7

Right concentric hypertrophy, even in cases of severe PS, appear to be better tolerated than cases of LV hypertrophy

Question 8

In which condition (SAS or PS) is CHF more common?

Answer 8

PS

Question 9

Chronic medical management of severe SAS, PS

Answer 9

Often involves beta blockers to reduce HR and myocardial oxygen demand

Question 10

Echocardiography

Answer 10

-Useful to assess severity of SAS, PS lesion and extent of ventricular hypertrophy

Question 11

Utility of Holter/24hr ECG in SAS, PS

Answer 11

• Evaluation of cardiac rhythm

- Detection of elevation/depression of ST segments which can be suggestive of myocardial ischemia

Question 12

What drugs should be used with caution in SAS, PS patients?

Answer 12

Arterial vasodilators
-Decrease in arterial blood pressure increases the pressure gradient across stenotic valve –> can increase myocardial work, severe hypotension, and decreased coronary perfusion pressure

Question 13

How common is PS?

Answer 13

Third most common heart defect in dogs

Question 14

Pathophysiology of PS

Answer 14

• Obstruction to RV outflow tract increases resistance to injection so have a proportional increase in ventricular systolic pressure
• Concentric hypertrophy of RV occurs in an attempt to normalize wall stress (LaPlace’s Law)
• During systole, blood ejected from the RV accelerates as it travels the obstructive orifice –> blood velocity increases –> becomes turbulent as it travels through the obstructive orifice
• Poststenotic dilation develops in the main PA as turbulent jet flow decelerates and expends some of the kinetic energy against the wall

Question 15

Consequences of RV Concentric Hypertrophy

Answer 15

• Reduces right ventricular diastolic compliance, which impairs ventricle’s ability to fill –> can result in increased RA pressure
• Tricuspid regurgitation from progressive ventricular dilation +/- valvular dysplasia can contribute to further increases in atrial pressure
• As RA pressure approaches 15 mm Hg, see signs of R CHF

Question 16

What are clinical signs of R CHF?

Answer 16

Jugular distention
Ascites
Pleural effusion

Question 17

Classifications of PS Severity

Answer 17

Mild
Moderate
Severe

Question 18

What happens with dogs >125 mm Hg?

Answer 18

Frequently develop secondary tricuspid regurgitation, heart failure, exertion scope, serious cardiac arrhythmia

Question 19

Mild

Answer 19

PG <50 mm Hg

Question 20

Moderate

Answer 20

PG 50-80 mm Hg

Question 21

Severe

Answer 21

PG >80 mm Hg

Question 22

What are the types of PS?

Answer 22

Subvalvular, Valvular (A, B, Mixed), supravalvular

Question 23

Valvular PS: Type A

Answer 23

• Most frequent
• Normal annular size with various degrees of valve leaflet thickening, incomplete separation of valve commissures to almost complete fusion
• Causes systolic doming of the valve
• Post-stenotic dilation of pulmonary trunk present with various degrees of severity

Question 24

Valvular PS: Type B

Answer 24

• Hypoplastic osmium with various degrees of valvular leaflet thickening and immobility but little commissural fusion
• Main pulmonary trunk often hypo plastic –> rarely presents post-stenotic dilation

Question 25

Valvular PS: Mixed type

Answer 25

A + B

Question 26

Anesthetic Considerations for PS

Answer 26

• Poor ventricular compliance
• Avoid tachycardia to limit myocardial oxygen deficit
• Afterload is elevated but remains fixed due to stenosis at level of the valve so VD/reductions in vascular tone do very little to address after load so end up reducing preload, reduce coronary perfusion pressure
• Critically important to maintain adequate preload

Question 27

Why is it important to maintain adequate preload in PS patients?

Answer 27

Maintaining adequate venous return by insuring a full intravascular volume to fill the non-compliant ventricle chamber will help optimize diastolic filling and CO

Question 28

How is the severity of the obstruction accurately quantified?

Answer 28

• Peak velocity of blood flow jet recorded on spectral Doppler tracing acquired with continuous wave Doppler beam in parallel alignment with direction of flow
• Modified Bernoulli equation: P=4V^2
• Relates instantaneous pressure gradient across an obstruction to the peak velocity of the jet distal to the obstruction

Question 29

What is important to remember about Doppler-derived gradients?

Answer 29

• 40-50% higher than the gradient measured during cardiac catheterization
• Doppler studies performed in awake dogs –> transvalvular flow considerably higher in these circumstances

Question 30

Dilated Cardiomyopathy

Answer 30

• Idiopathic systolic dysfunction –> accompanied by eccentric dilation, volume overload
• Decrease in heart’s generation of normal forward stroke volume
• Resulting LV dilation –> dilation of MV annulus –> secondary MR that contributes to volume overload

Question 31

DCM Breeds

Answer 31

-Large breed dogs –> Irish Wolfhound, Doberman Pinscher, Great Dane

Question 32

Is DCM common in cats?

Answer 32

No, relatively uncommon since recognized taurine deficiency

–can see taurine deficiency in dogs fed grain-free diet

Question 33

What see with DCM

Answer 33

• Mostly L CHF (pulmonary edema), sometimes R CHF (pleural effusion, ascites)
• Ventricular arrhythmias that can cause activity tolerance, syncope, sudden death

Question 34

How diagnose, stage severity

Answer 34

ECG, echo, TXR

Also perform Holter monitoring to screen at-risk dogs for ventricular premature beats, which is an early sign of disease

Question 35

Chronic DCM Therapy

Answer 35

1. Reduction of preload - diuretics (furosemide, spironolactone)
2. Reduction of afterload - ACEIs, pimobendan
3. Increased contractility - positive inotropes (pimo, digoxin)

Question 36

Acute DCM Anti-Arrhythmic Therapy

Answer 36

Lidocaine

Procainamide CRI

Question 37

Chronic DCM Anti-Arrhythmic Therapy

Answer 37

Sotalol, amiodarone

Question 38

Why use caution with beta blockers as anti-arrhythmic therapy with DCM?

Answer 38

Negative inotropic effects but use with caution in animals with severe systolic dysfunction or active CHF

Question 39

AF and DCM

Answer 39

Common in Great Danes, Irish Wolfhounds, Mastiffs, other giant breeds

Question 40

Consequences of AF

Answer 40

• Rapid ventricular rate associated with AF increases myocardial oxygen demand
• Reduces CO as diastolic filling time decreases

Question 41

Treatment for AF

Answer 41

• Reduction of AV nodal conduction
• Slowing ventricular HR
• Drugs: Ca channel blockers (diltiazem), beta blocks, digoxin

Question 42

Occult DCM

Answer 42

Asymptomatic

See unexplained VPCs before/during anesthesia that do not resolve