L&J Chi 26 Pathophysiology, Ax Management of Patients with CV Disease Flashcards
What are conditions associated with pressure overload?
Subaortic Stenosis
Pulmonic stenosis
Consequences of SAS
- Chronic systolic pressure increase in left ventricle
- Results in increased wall tension, compensatory increase in ventricular wall thickness (concentric hypertrophy)
Consequences of PS
- Chronic systolic pressure increase in right ventricle
- Results in increased wall tension, compensatory increase in ventricular wall thickness (concentric hypertrophy)
Consequences of concentric hypertrophy of L/R ventricle associated with SAS and PS?
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
When is the resulting risk for ischemia the greatest?
-During periods of tachycardia –> myocardial necrosis, replacement fibrosis, development of ventricular arrhythmias
In young dogs with severe SAS
- Risk for syncope, sudden arrhythmogenic death is high
- Left-sided congestive failure only seen in much older dogs
Which is tolerated better?
Right concentric hypertrophy, even in cases of severe PS, appear to be better tolerated than cases of LV hypertrophy
In which condition (SAS or PS) is CHF more common?
PS
Chronic medical management of severe SAS, PS
Often involves beta blockers to reduce HR and myocardial oxygen demand
Echocardiography
-Useful to assess severity of SAS, PS lesion and extent of ventricular hypertrophy
Utility of Holter/24hr ECG in SAS, PS
- Evaluation of cardiac rhythm
- Detection of elevation/depression of ST segments which can be suggestive of myocardial ischemia
What drugs should be used with caution in SAS, PS patients?
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
How common is PS?
Third most common heart defect in dogs
Pathophysiology of PS
- 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
Consequences of RV Concentric Hypertrophy
- 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
What are clinical signs of R CHF?
Jugular distention
Ascites
Pleural effusion
Classifications of PS Severity
Mild
Moderate
Severe
What happens with dogs >125 mm Hg?
Frequently develop secondary tricuspid regurgitation, heart failure, exertion scope, serious cardiac arrhythmia
Mild
PG <50 mm Hg
Moderate
PG 50-80 mm Hg
Severe
PG >80 mm Hg
What are the types of PS?
Subvalvular, Valvular (A, B, Mixed), supravalvular
Valvular PS: Type A
- 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
Valvular PS: Type B
- 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
