Treatment of heart failure Flashcards
What is pathophysiology of CV disease?
heart failure or cardiac insufficiency prsent when heart cannot meet demands of the body at normal or elevated filling pressures
many heart diseases can remain compensated for some time
awareness of compensatory mechanisms vital to avoid iatrogenic problems with therapy
What are factors that influence cardiac output?
- preload–increased preload improve stroke volume up to a pount then get congestion
- afterload–reduce, improve CO
- contractility–increase, improve CO
- heart rate: incrased HR improves CO up to a point
What is an issue with ramapril?
drops blood pressure a lot and makes dog feel weak
What might be an issue with increasing cardiac contractility?
can increased work of heart (increased oxygen consumption) with possibly impaired perfusion
Why do we reduce preload?
to decrease congestion
What is the benefit of reducing afterload?
reduces stretch, work of the heart–reduction of heart remodelling, arrythmias
What is the RAAS system
renin-angiotensin-aldosterone system. renin released by kidney in response to hypoperfusion, decreased slat delivery and adrenergic stimulaition. Renin converts angiotensinogen to angiotensin I which is converted to AT II by angiotensin converting enzyme
What do ace inhibitors do?
they inhibit angiotensin converting enzyme. in people they cause pril cough in animals don’w
What are two drugs that interrupt RAAS?
ace inhibitor
angiotensin II receptor blocker
What are the effects of angiotensin II?
- vasoconstrictor–increased afterload
- increased aldosterone–increased salt and water retension
- increased thirst
- increased GFR
- myocardial hypertrophy
deleterious in long term
What is the classification scheme of heart disease?
Stage A-risk for HR dz stage B-structural HR dz no signs (B1 normal imaging, B2 abnormal) Stage C: past or current HR failure Stage D current failure refractory to standard therapy
Dobermans and cavalier king charles spaniels are considered in what stage when born?
stage A
What is an example of stage B1
heart murmur, no heart enlargement
What is an example of stage B2
enlarged heart but no cough etc
What are the general recommendations for stage A
- routine monitoring–holter monitor every 6mo, echo
2. no treatment recommended
What are the general recommendations for stage B
- imaging–differentiate B1 or B2
- BP measurement recommended
- echo when rads and physical not adequate to assess patient
- basic lab work
- large breed dogs–echo + radiograph
- treatment? no consensus–differnet for endocardiosis vs DCM
- consider ACE inhibitors–reduce preload, afterload, intefere with production of hormones–scar tissue formation in heart
What are the benefits of ACE inhibitors?
- mild preload reduction
- afterlaod reduction
- interfere with RAAS activation
If you give an ACE inhibitor to stage B DCM animals (asymptomatic) before heart failure, what happens?
improves quality of life and prolonges life span?
If you give an ACE inhibitor to an animal in heart failure what happens?
improves quality of life and lifespan
If you give an ACE inhibitor to an animal that is asymptomatic that has endocardiosis (heart murmur) some B1, some B2 is there a benefit?
no–not to onset of failure or lifespan
What can cockers get?
DCM or endocardiosis. if give DCM thiamine they survive much longer
What are the recommendations for stage C?
- reduce preload to reduce congestion
What animals benefit from pimobenan in stage B?
e.g. dobermans with DCM
no data on endocardiosis
What should you do with dogsin stage B?
if DCM dog, give ACE inhibitor, pimobendan. if endocardiosis don’t do anything
What is furosemide/features
REDUCES PRELOAD powerful loop diuretic: potassium wasting--predisposition to arrhythmia, digoxin toxicity--rarely issue in dog, may be in cat activates RAAS!!! (low volume) can cause low output failure (powerful) only indicated for pulmonary edema
If you have an animal with evidence of forward failure, what should you be cautious using?
drugs like furosemide that can cause low output failure