Heart Failure, Valve Flashcards
a pathological state/clinical syndrome where heart is impaired in ability to eject (systolic) or receive blood (diastolic)
cardiac output does not meet perfusion needs of metabolizing tissues and limited exercise capacity
and elevated venous pressures lead to congestion of organs
heart failure
heart failure where cardiac output does not meet perfusion needs of metabolizing tissues and exercise capacity is limited despire normal or higher than normal filling pressure (preload)
Forward or Low output heart failure
heart failure where elevated venous pressures lead to congestion of organs and fluid accumulations (edema, effusion)
Congestion heart failure
How do you determine CO
CO (ml/min) = HR (beat/min) x SV (ml/beat)
What 5 factors influence stroke volume
Preload (+)
Afterload (-)
Contractility (+)
Valve function
Ventricular Synchrony
How do you treat a warm/wet patient (CHF) indicated by jugular distension, dyspnea, cavity effusion, elevated filling pressure with normal cardiac ouput and normal SVR
Diuresis or Vasodilators
How do you treat a cold/dry patient (forward failure) indicated by weak pulse, Low CO, normal filling pressure, low temperature, pain at extremities, arrhythmias, and collapsed
Give Inotropy or Vassopressors
How do you treat a cold/wt patients indicating forward failure and CHF) indicated by cold extremities, collapsed, dyspnea, cavity effusion, Low CO, altered SVR
Hard to treat
-Inotropy
-Vasopressors
-Diuresis (when the perfusion is restored)
What are causes of heart failure due to increased afterload (pressure overload)
1) Aortic or subaortic stenosis
2) Pulmonary valve stenosis
3) Tetralogy of Fallot
4) Pulmonary or systemic hypertension
What are causes of heart failure due to volume overload
1) valve insufficiencies (MR, TR, AI, PI)
2) Shunting lesions (VSD, ASD, PDA)
What can cause impaired contractility leading to heart failure
DCM phenotype
T/F: arrhythmias can lead to heart failure
true- loss of synergy
tachy or bradyarrhythmias
What can cause impaired diastolic filling leading to heart failure
1) HCM phenotype
2) Restrictive cardiomyopathy
3) Pericardial effusion
4) Constrictive pericarditis
*Heart cant relax
what are the causes of heart failure
A) Increased Afterload 1) Aortic or subaortic stenosis
2) Pulmonary valve stenosis
3) Tetralogy of Fallot
4) Pulmonary or systemic hypertension
B) Volume overload
1) valve insufficiencies (MR, TR, AI, PI)
2) Shunting lesions (VSD, ASD, PDA)
C) Impaired contractility
1) DCM phenotype
D) Arrhythmias- loss of synergy; brady or tachyarrhythmias
E) Impaired diastolic filling (heart cant relax)
1) HCM phenotype
2) Restrictive cardiomyopathy
3) Pericardial effusion
4) Constrictive pericarditis
What are compensatory mechanisms in patients with heart failure to buffer the fall in CO and help preserve perfusion
1) Frank-Starling Mechanism
2) Neurohormonal alterations (Sympathetic NS, RAAS, ADH, natiuretic peptides)
3) Development of ventricular hypertrophy and remodeling
Frank-Starling
As there is __________ stretch on myofibers it induces a ________ stroke volume on subsequent contraction
greater; greater
States that with increased stretch on myofibers, it induces a greater stroke volume on subsequent contraction
helps empty enlarged ventricle and preserve forward CO
beneficial compensatory but has limited effect in severe HF cases
Frank-Starling Mechanism
Acute neurohormonal activation during decreases in cardiac output are ________________ while chronic effects are
acute: compensatory and beneficial
chronic: maladaptive and harmful
baroreceptor response
in response to heart failure signal in brain causes SNS activation to increase HR and contractility to increase cardiac output
RAAS activation in heart failure causes
decreased GFR to retain fluid thus increasing preload to increase cardiac output
Increased ventricular wall tension in heart failure causes
myocyte growth leading to hypertrophy and increases cardiac output (with limit)
Where are decreases in cardiac output detected
baroreceptors in the carotid sinus and aortic arch
signals transmitted to medulla
decreased inhibitory input from baroreceptors and mechanoreceptors leading to increase sympathetic tone and decreased parasympathetic activiation causing NE release and stimulation of a and beta receptors
where are the baroreceptors
carotid sinus and aortic arch
What is the SNS response to decreases in cardiac output
1) baroreceptors in the carotid sinus and aortic arch detect decreases in CO
2) signals transmitted to medulla
3) decreased inhibitory input from baroreceptors and mechanoreceptors leading to increase sympathetic tone and decreased parasympathetic activiation
4) NE release and stimulation of a and beta receptors
5) Increased HR, contractility, vasoconstriction (a receptor on systemic veins and arties), RAAS activation
What are the effects of long-term activation (maladaptive) of the sympathetic nervous system in response to decreased cardiac output
1) Increased myocardium oxygen demand (MVO2)
2) Chronic RAAS activation -> cardiac fibrosis ->arrhythmias
What occurs when Renin-Angiotensin Aldosterone System is activated
1) Renin converts angiotensinogen to angiotensin I
2) ACE converts it to angiotensin II
3) Angiotensin II causes
a) Aldosterone secretion in adrenal gland cortex
b) Sympathetic activity
c) Arteriolar vasoconstriction to increase in blood pressure
d) ADH secretion in pituitary gland posterior lobe
e) tubular Na Cl and H20 reabsoprtion and K excretion
What are the 3 stimuli for renin secretion from the juxtaglomerular cells
1) Decreased renal artery perfusion pressure
2) Decreased sodium delivery to macula densa in kidney
3) Direct stimulation of juxtaglomerular B-receptors by SNS
where is renin secreted from
juxtaglomerular cells
short term RAAS activation leads to
-Na+ and H20 retention (increased SV)
-Vasoconstriction (increased SVR)
long term RAAS activation leads to
-myocardial O2 demand (MVO2)
leading to hypertrophy, fibrosis, and arrhythmias
A competitive aldosterone antagonist
spironolactone
Does RAAS blockade in heart failure, using ACE inhibitor or aldosterone blockers (spironolactone) improve survival in CHF?
it may improve survival but newer data suggests conflicting results
is there evidence for use in beta-blockers in heart failure of dogs and cats
not really known. be cautionous with b blockers as they decrease ionotropy
Why might there be ventricular remodeling
1) Increased wall tension is stimul for compensatory hypertrophy
a) Pressure or volume overload
b) genetics (sarcomere mutations)
c) Hyperthyroidism
2) Chronic HF- neurohormonal activation (NE, AT II, and aldosterone) promote hypertrophy and fibrosis
Chronic neurohormonal activation of _____ , ______, and ________ promtes ventricular hypertrophy and fibrosis, which can lead to arrhythmias
NE
AT II
Aldosterone
What is the mechanism of eccentric hypertrophy
1) Increased volume overload
2) Increase diastolic wall
3) Series of sarcomere replication leading to chamber dilation
4) Eccentric hypertrophy
What is the mechanism of concentric hypertrophy
1) Increased pressure overload
2) Increased systolic wall
3) Parallel sarcomere replication (wall thickening)
4) Concentric Hypertrophy
What are the benefits of concentric or eccentric remodeling
-Enhance cardiac performance
-Decreased wall stress (decreased MVO2
-Maintain stroke volume
Does degenerate mitral valve disease lead to eccentric or concentric hypertrophy
eccentric hypertrophy
T/F: activation of renin-angiotensin-aldosterone system (RAAS) is stimulated by increased perfusion sensed in renal artery
False
T/F: with stimulation of the RAAS, systemic vasodilation will occur
false
What are the clinical signs of heart failure
-exercise intolerance
-weakness
-syncope
-pale or grey mucous membrane, prolonged CRT
-Decreased arterial pulse quality
-Cool periphery
-Arrhythmias
-Cardiac cachexia (more commonly in R CHF)
Is cardiac cachexia more rapid in left or right sided congestive heart disease
right sided congestive heart disease
Causes of left sided CHF (pulmonary edema)
1) degenerative mitral valve disease
2) dilated cardiomyopathy
3) hypertrophic cardiomyopathy
4) subaortic stenosis
How do you get pulmonary edema with left sided congestive heart failure
left sided heart disease results in increased LA pressure and increased hydrostatic pressure in the pulmonary veins leading to post-capillary pulmonary hypertension
more plasma ultrafiltrate in lung interstitium
hydrostatic pressure >20mmHg and overwhelms lymphatics
fluid accumulates in itnerstitium (and alveoli when severe)
What is seen in left sided congestive heart failure
Pulmonary edema (dogs/cats): tachypnea, dyspnea, orthopnea with increased lung sounds, crackles and cough
Pleural effusion (cats). difference in feline pulmonary venous anatomy (bronchial veins drain into pulmonary veins) and porosity of sub-pleural capillary beds- can be chylous
subcutaneous edema (large animals)- brisket edema
Why can you see pleural effusion in cats
difference in feline pulmonary venous anatomy (bronchial veins drain into pulmonary veins) and porosity of sub-pleural capillary beds
*can be chylous effuson
You have a patient that you suspect left sided CHF in. What is your diagnostic you should do to support this?
thoracic radiographs to confirm pulmonary edema
to support diagnosis (POCUS, Echo, NT-proBNP)
you suspect left sided heart failure with pulmonary edema. You do radiograph to confirm this. What findings will confirm this?
1) Left atrial enlargement (splayed cowboy appearance on VD or backpack on lateral)
2) Left auricular enlargement
3) Pulmonary vein enlargement (ventral and central)
4) Left ventricular enlargement
5) Interstitial to alveolar infiltrate
T/F: a dog with a murmur in respiratory distress is always in failure
False
What are the differentials for respiratory distress
1) Primary respiratory disease (pulmonary fibrosis, bronchitis, pneumonia, upper airway disease, tracheal collapse
2) Pleural effusion (pyothorax, hemothorax, neoplastic, right sided congestive heart failure)
3) Pulmonary edema (cardiac or non-cardiogenic)
4) Pulmonary hypertension (secondary to PTE, respiratory disease, cardiac shunts, HW disease)
What is a normal VLAS score
less than 2.3
How can you use VLAS to diagnose right sided heart failure
comparing the Left Atrium to the vertebrae is important
Normal: VLAS <2.3
If VLAS <1.9- confidently rule out cardiogenic respiratory signs
If VLAS >3- can be confident of cardiogenic respiratory signs
What would you see on echo of the the left atrium when a patient is in left sided heart failure
the left atrium will be larger than the aorta
(2x larger)
can also tell if there is pericardial effusion or pleural effusion
a cardiac biomarker that is released at higher levels during ventricular wall stress
used for differentiating cardiac and non-cardiac causes of dyspnea. screening for cardiomyopathy
NT-PROBNP
what would you use NT-ProBNP for
for differentiating cardiac and non-cardiac causes of dyspnea
screening for cardiomyopathy
What are the 2 different ways you can test NT-ProBNP for differentiating cardiac and non-cardiac causes of dyspnea
1) Cardiopet NT-proBNP
-quantitative
-SEND OUT
-plasma
-dogs or cats
2) ELISA SNAP NT-proBNP
-normal (<100pmol/L) or abnormal (200pmol/L or >300pmol/L) result
-bedside test
-whole blood or pleural effusion
-cats only
Tells you normal or abnormal result of NT-PRoBNP
-bedside test
-whole blood or pleural effusion
-cats only
ELISA SNAP NT-proBNP
What species can you use the ELISA SNAP NT-proBNP in
only the cat
T/F horses rarely get left sided heart failure
True
Horses rarely get left sided heart failure but when they do it is because
1) Combo of structural heart disease (valvular or congenital) and atrial fibrillation
2) Mares in late stages of gestation -> CHF due to hemodynamic burden of pregnancy
Mares in late stages of gestation may develop
CHF due to hemodynamic burden of pregnancy
Why do patients with right sided heart failure typically get ascites
increased hydrostatic pressure in systemic venous causes hepatic capillaries to be leaky
increased formation of hepatic lymph (rate of formation exceeds ability of lymphatic system to drain cavity)
What are the clinical signs of right sided CHF
-Decreased CO and perfusion of tissues
-Increased systemic venous pressure leading to:
-Jugular vein distension or pulsation
-Hepatomegaly
-Ascites (palpable fluid wave)
-Pleural effusion (muffled lung sounds ventrally)- tachypnea, dyspnea, orthopnea
-Small volume pericardial effusion
-Subcutaneous edema (large animals)
pericardial effusion secondary to heart failure is usually________ while pleural effusion is _______
a small volume
a large volume
What will you see in horses with right sided congestive heart failure
1) peripheral edema
increased venous and capillary hydrostatic pressures overwhelm the lymphatic reserves and create a peripheral edematous state
(left sided, right sided, or biventricular failure)
2) jugular distension
T/F: you see peripheral edema in BOTH left side and right sided congestive heart failure
True
increased venous and capillary hydrostatic pressures overwhelm the lymphatic reserves and create a peripheral edematous state
(left sided, right sided, or biventricular failure)
What might you suspect if you see diagnostic findings associated with pulmonary edema and cavitary effusions
biventricular heart failure
-concurrent right and left sided heart disease present
can be seen in severe left sided heart disease such as DCM or MMVD complicated by atrial fibrillation
Biventricular heart failure
-concurrent right and left sided heart disease present
-pulmonary edema and cavitary effusions
can be seen in severe left sided heart disease such as DCM or MMVD complicated by atrial fibrillation
What is your go to diagnostic for congestive heart failure
thoracic radiographs
no audible heart murmur but an at risk breed (Cavalier King Charles Spaniels, Dachshunds, Miniature and Toy Poodles)
Class A MMVD
Audible heart murmur heard
Asymptomatic
Not severe enough to meet criteria for medical treatment
Class B1 MMVD
Audible heart murmur heard
Asymptomatic
Severe enough to result in cardiac remodeling sufficient to recommend treatment
Class B2 MMVD
audible heart murmur and severe neough to cause current or past clinical signs of heart failure (ex: pulmonary edema of CHF)
Class C MMVD
audible heart murmur and clinical signs of failure refractory to standard treatment for Stage c
Class D MMVD
At what ACVIM stage for MMVD/DMVD should Pimobendan be started
Stage B2
Audible heart murmur heard, Asymptomatic
Severe enough to result in cardiac remodeling sufficient to recommend treatment
can use +/- Ace-inhibitor (if cases of hypertension)
T/F: Starting dobermans on pimobendan for asymptomatic DCM is protective
Trie
At What ACIM stage for hypertrophic cardiomyopathy should Clopidogrel +/- atenolol be started
AVIM stage B2
Audible heart murmur heard, Asymptomatic
Severe enough to result in atrial enlargement sufficient to recommend treatment
What treatment should you do for asymptomatic heart disease (Stage B2)
MMVD/DMVD: Pimobendan +/- ACE Inhibitor (use in cases of hypertension)
DCM (Dobermans): Pimobendan
HCM: Clopidogrel +/- Atenolol
a prophylactic anti-thrombotic treatment for cats with left sided heart failure/ hypertrophic cardiomyopathy) to prevent thrombi formation
Clopidogrel
a calcium sensitizer (inodilator) that is used in contractility issues
functions to inrease contractility directly and increase calcium binding to troponin C
Pimobendan
What are the treatment strategies for congestive heart failure
1) remove congestion: diuretics to reduce preload
2) Supporting systolic (pump) function- positive inotropes
3) Blocking RAAS activation (chronically): ACE-I and aldosterone antagonism
4) Counteracting vasoconstriction: vasodilator- reduce preload (venodilator) and reduce afterload (arterial vasodilator)
What are the treatment strategies for forward heart failure
1) Supporting systolic (pump) function - positive inotropes
2) Removing congestion- if in concurrent CHF, diuretic to reduce preload (balance with perfusion)
what is the function of diuretics
promote increased production of urine
goal: to reduce preload
a) Loop diuretics- Furosemide and Torsemide
b) Potassium sparing diuretics- Spironolactone
c) Thiazide diuretics- Hydrochlorothiazide (HCTZ)
of goal of giving diuretics is to
reduce preload
what are your loop diuretics
Furosemide
Toremide
Bumetanide
Strongest class of diuretics
What is the mechanism of action of loop diuretics like furosemide, toremide, and bumetanide
inhibits Na+/K+/2Cl- co-transporter
thick ascending loop of henle
Na+, K+, Cl- and H20 excretion
rapid onset of action
affected by renal blood flow (decreased efficacy with renal failure and NSAIDS)
What decreases the efficacy of loop diuretics like Furosemide, Toremide, and bumetanide
affected by renal blood flow (decreased efficacy with renal failure and NSAIDS)
Where do loop diuretics like furosemid, toremide, bumetanide act
inhibits Na+/K+/2Cl- co-transporter
thick ascending loop of henle
Na+, K+, Cl- and H20 excretion
a more potent form of furosemide
most likely closer to 20 times in healthy dogs and requires 5-10% furosemide dose
given less frequently (12-24hours)
Torsemide
Is Furosemide of Torsemide more potent?
Torsemid
most likely closer to 20 times in healthy dogs and requires 5-10% furosemide dose
When should you consider switching a patient from furosemide to torsemide
if the patient is receiving >8mg/kg/d furosemide and having refractory symptoms you may need to move to the more potent torsemide
a mineralocorticoid receptor antagonist (MRA) that blocks action of aldosterone at the distal tubule
antagonizes the cardiotoxic effects of aldosterone -cardioprotection
weak diuretic effect
can cause facial dermatitis in cats
adjunct treatment for heart failure or ascites
spironolactone
where does spironolactone act
Distal Tubule
it acts to be a mineralocorticoid receptor antagonist (MRA) that blocks action of aldosterone at distal tubule
T/F: Spironolactone is a strong diuretic
weak- it is potassium sparing but not that good at diuresis
What is a side effect of spironolactone (potassium sparing diuretic)
facial dermatitis in cats
spironolactone can be an adjunct treat for
heart failure or ascites
where do thiazide diuretics (hydrochlorothiazide) act
proximal distal convoluted tubule
inhibits Na+/Cl- co-transporter
What is the mechanism of hydrochlorothiazide
inhibits Na+/Cl- co-transporter in the
proximal distal convoluted tubule
inhibits Na+/Cl- co-transporter in the
proximal distal convoluted tubule
side effects:
hypokalemia
hypercalcemia
ventricular arrhythmia
nausea
hydrochlorothiazide (thiazide diuretics)
What are the side effects of hydrochlorothiazide (thiazide diretics)
hypokalemia
hypercalcemia
ventricular arrhythmia
nausea
What are different positive inotropes you can use to treat heart failure
1) Pimobendan (Ca2+ sensitizer)
2) Digitalis glycosides (Digoxin)
3) Catecholamines (Dobutamine, dopamine, epinephrine)
Pimobendan is an inodilator, what does that mean
it is a positive inotrope and vasodilator
increases the interaction between calcium and troponin C
-increased actin-myosin cross binding
-greater force of contraction (positive inotrope)
Phosphodiestrase-3 inhibitor
-Increased cAMP mediated peripheral vasodilation to decrease preload and afterload
What is the mechanism of action of Pimobendan
increases the interaction between calcium and troponin C
-increased actin-myosin cross binding
-greater force of contraction (positive inotrope)
Phosphodiestrase-3 inhibitor
-Increased cAMP mediated peripheral vasodilation to decrease preload and afterload
T/F: Pimobendan is a Phosphodiesterase-5 inhibitor
False
Phosphodiestrase-3 inhibitor
-Increased cAMP mediated peripheral vasodilation to decrease preload and afterload
T/F: Pimobendan is not FDA approved in cats
true
used off label
T/F: Pimobendan does not help in patients with asymptomatic MMVD and DCM
False
Dobutamine is a potent
positive inotrope (B1>B2>a)
What receptor does Dobutamine have the greatest effect at
(B1>B2>a)
Why is Dobutamine used in heart failure
positive inotrope (B1>B2>a)
Increases cardiac output and decreases edema formation
Improved arterial blood pressure
give as CRI
less effect on HR and BP than dopamine (at higher doses, see more alpha effects)
monitoring for tachycardia and ventricular ectopy (decrease infusion rate)
T/F: Dobutamine has less effect on heart rate and blood pressure than dopamine
True
-At higher doses see more alpha effects
What should you do if you see a patient on dobutamine is developing tachycardia or ventricular ectopy
Decrease infusion rate (it is given as a CRI)
what is the mechanism of action of digoxin
Inhibits Na+/K+ ATPAse to increase intracellular Na+
activation of Na+/Ca2+ exchanger and increased intracellular Ca2+ -> positive inotropy
sensitizes the barocreceptors leading to increased vagal tone
What are the indications for using digoxin
rate control of atrial fibrillation
When should you be careful giving digoxin
1) Kidney disease - it is excreted by kidneys and has long half life so you could cause toxicity
2) When the patient is hypokalemic (dont give with furosemide) it is exacerbated
Toxicity: anorexia, nausea, vomiting, diarrhea, and can cause arrhythmias: ventricular arrhythmias and bradycardia
What are the clinical signs of digoxin toxicity
arrhythmias: ventricular arrhythmias and bradycardia
anorexia, nausea, vomiting, diarrhea
oral vasodilator
dihydropyridine calcium channel blocker
smooth muscle relaxation
long half life
Amlodipine
What is Amlodipine’s mechanism of action
dihydropyridine calcium channel blocker
to cause vasodilation
Venodilators (increase/decrease) preload
Decrease preload
Arteriodilators (increase/decrease afterload)
decrease afterload
a direct oral arteriodilator
acts on intracellular calcium hemostasis
Hydralazine
What is Hydralazine’s mechanism of action
a direct oral arteriodilator
acts on intracellular calcium hemostasis
How is Amlodipine administered
orally (vasodilator)
*dihydropyridine calcium channel blocker
How is Hydralazine administered
orally (arteriodilator)
How is sodium nitroprusside administered
IV (CRI)
-Vasodilator
How is nitroglycerin administered
topical (ointment)
-vasodilator
Sodium nitroprusside mechanism of action
Produces NO and results in vascular smooth muscle relaxation
given IV (CRI)
Nitroglycerin prefers to act on (arteries/veins)
veins > arteries
vasodilator
What are the most common ACE inhibitors used
Enalapril
Benazepril
What is the mechanism of action of Enalapril and Benazepril
inhibits angiotensin converting enzyme (ACE) from converting angiotensin (AT) I to Angiotension II and decreases aldosterone production
this decreases AT-II mediated vasoconstriction and volume retention
used chronically in CHF in dogs but unclear benefit in asymptomatic dogs
Enalapril, Benazepril arent really used in patients with asymptomatic heart failure unless they are
hypertensive
ACE inhibitors decrease AT-II mediated vasoconstriction and volume retention
How do you treat acute left sided congestive heart failure in dogs
SPOF
Sedation- Butorphanol (because in respiratory distress)
Pimobendan- inodilator
Oxygen Supplementation
Furosemide (Lasix)- diuretic
-can give CRI in life threatening case of pulmonary edema
SPOF protocol is used to treat
acute left sided CHF
When should you continue dosing Furosemide in a patient with acute left sided CHF
continue hourly until RR is improved or total of 8mg/kg has been reached over 4 hours then decrease frequency
Why might there be inadequate response to initial therapy to acute left sided CHF (SPOF failed)
1) Is there arrhythmia present?
2) What is systolic BP?
3) recheck radiographs- has there been response to furosemide. Is there concurrent pulmonary disease and check VLAS
4) Check for pericardial or pleural effusion- MMVD patients can develop left atrial tear
5) Left atrial size on POCUS- is this a different disease process (pulmonary hypertension, pneumonia)
How does a left atrial tear occur
1) high velocity jet of mitral regurgitation (MMVD)
2) Injury to Left Atrium endocardium creating jet lesion
3) Atrial tear ranges from partial thickness atrial splitting (acute or subacute)
4) Creates pericardial effusion -> cardiac tamponade -> forward failure
Systemic hypertension increases LV _______
afterload
-failing LV (DCM patient) or patient with imcompetent mitral valve (MMVD patient) is sensitive to increases in afterload
-increased systemic BP worsens mitral regurgitation
How do you treat acute forward heart failure in dogs
1) oxygen supplementation
2) Pimobendan- inodilator +/- dobutamine (CRI)
3) Furosemide- based on whether concurrent left sided CHF- balance while monitoring BP and perfusion
How do you treat acute left sided CHF in cats
1) Furosemide
2) Oxygen Supplementation
3) Sedation- if needed Butorphanol IV,IM
4) Clopidogrel
+/- thoracocentesis (if pleural effusion is present)
+/- Pimobendan with signs of low cardiac output (if dynamic LV outflow tract obstruction is absent
How do you treat acute right side CHF in dogs
1) Sedation - Butorphanol
2) Thoracocentesis/ Abdominocentesis
3) Furosemide (Lasix) Continue q8-12hours
+/- Pimobendan- be cautious in cases of outflow obstruction
+/- oxygen supplementation
How do you treat chronic CHF in dogs
1) Diet- low sodium
2) ACE Inhibitor (Enalapril or Benazepril)
3) Furosemide
4) Spironolactone
5) Pimobendan
+/ - Thoracocentesis/ Abdominocentesis
“Dogs are For Special People”
What kind of diet is good for managing dogs in chronic CHF
low sodium
How do you treat cats with chronic CHF
1) Furosemide
2) Clopidogrel
3) +/- Pimobendan- consider patients without LV outflow obstructon
some do ACE-I but no evidence to show that it delayed onset of treatment failure
Clopidogrel tastes bitter and cats dont like it. What should you do if you need to give it to them to manage chronic CHF
administer in empty gel capsule
How do you manage heart failure in horses
usually secondary to valvular or myocardial diseases
1) Furosemide
2) Digoxin- especially when accompanied by atrial fibrillation
contraindicated in cases with ventricular ectopy
-monitor blood levels with chronic use
*Pimobendan and ACE-I have been used but very costly
Monitor: Resting HR and RR, body condition, jugualr venous pulsation and distension
What is the prognosis with horses in heart failure
you can go therapy with Furosemide and Digoxin but it is poor and horses usually do not survive >6months after diagnosis
How should you treat dogs with refractory CHF (Stage D)
1) Increased pimobendan frequency to 0.3mg/kg PO TID (off-label use)
2) Switch from Furosemide to Torsemide (a more potent loop diuretic)
3) Vigorous afterload reduction (Amlodipine- PO, Nitroprusside-IV or Hydralazine- PO)
+/- sildenafil for patients clinical for concurrent pulmonary hypertension
How should you treat cats with refractory CHF (Stage D)
1) Switch from Furosemide to Torsemide (a more potent loop diuretic)
2) Spironolactone- PO but monitor for side effect of ulcerative dermatitis
3) +/- taurine if systolic dysfunction
*as number of medications in cats increases, owner compliance will likely decrease
How might an animal develop diuretic tolerance
1) increased solute delivery to distal nephron segments- hypertrophy and up-regulation of ion channels, leads to increased Na+ retention
2) Chronic RAAS and SNS activation leads to decrease renal responsiveness to natriuretic peptides
How do you overcome diretic resistance
1) Add ACE inhibition (and/or spironolactone)
2) Sequential nephron blockage (add additional diuretics)
3) Torsemide
What are dietary recommendations for dogs and cats with heart disease
-Adequate calorie intake
-High quality/adequate protein
-Moderate Na+ restriction
-K+ supplementation if hyperkalemic
How can the owner monitor patients with congested left sided heart failure at home
look at sleeping respiratory rate
<30 breaths per minute
detect pulmonary edema early and prevent severe episode of CHF
-if elevated sleeping RR, owner can give extra dose of furosemide at home
Is canine degenerative valve disease congenital or acquired
Chronic, acquired valvular disease that is progressive
What are other names for canine degenerative valve disease
myxomatous mitral valve disease
endocardiosis
What is the most common cause of cardiac morbidity and mortality in dogs?
canine degenerative valve disease
What kind of dogs typically get degenerative valve disease
small to medium breed dogs (but can occur in larger breed dogs)
usually older patients
90% of small breed dogs >8 years of age
can affect younger dogs -ex: CKCS and Dachshund
90% of small breed dogs >8 years of age have
canine degenerative valve disease
What valves are typically affected by canine degenerative valve disease
Mitral Valve (MV) is most affected
-60% MV alone
-30% MV and TV
occasionally affects TV alone (1%)
-rarely affects aortic valve
What breed typically gets canine degenerative valve disease at younger age
Cavalier King Charles Spaniel
How many leaflets does the mitral valve typically have
2 leaflets- anterior and posterior
What are the components in the normal mitral valve apparatus
1) 2 leaflets- anterior and posterior
2) Valve annulus
3) Chordae tendineae
4) Papillary muscles
5) Posterior left atrial wall
6) Left ventricular free wall
Normal structure and function of al lcomponents required for valve competence
What are the layers of mitral valve leaflets
1) Atrialis- mainly elastin
2) Spongiosa- GAGs+proteoglycans
3) Fibrosa- dense collagen for main load bearing layer
4) Ventricularis- mainly elastin
*ASFV
What is the spectrum of disease of degenerative mitral valve disease
1) Edematous nodules of varying size and location
2) Plaque like elevations
3) Thickened chordae tendinae (proximal and then more generalized)
4) Distortion and contraction of valve leaflets
What is the earliest gross finding of degenerative mitral valve disease
Edematous nodules of varying size and location
Plaque like elevations
then the chordae tendinae begin to become thickened
what are the histopath findings of degenerative mitral valve disease
1) there begins to be a proliferation of glycoaminoglycan (GAG) and proteoglycan (PG) within the spongiosa
2) Alterations in valvular interstitial cells (VIC)
3) Loss of collagen-laden fibrosa layer
all causes mitral valve malformation and biomechanical dysfunction
What are the cardiac sequelae to degenerative mitral valve disease
1) Insufficiency of valve (leak) - regurgitation**
2) Chordae tendineae rupture- hyalinization and disintegration of collagen bundles leading to MV prolapse and flail
3) Left atrial tear - high velocity jet of mitral regurgitation (MR) leading to injury in left atrium endocardium causing a jet lesion
atrial tear ranges from partial thickness to full thickness atrial splitting (acute) and causes acute pericardial effusion
How might a small breed old dog with a history of heart murmur get pericardial effusion
1) Degenerative mitral valve disease leading to left atrial tear
2) Neoplasia
Describe the pathophysiology of degenerative mitral valve disease leading to mitral regurgitation
1) Mitral regurgitation: progressive over years as leaflet changes progress
2) Left-sided volume overload: LV eccentric hypertrophy, LA enlargement
annular stretch leads to progressive MR (functional), increased LA pressure
3) Left sided congestive heart failure: tachypnea, cough, syncope, develop pulmonary hypertension (post-capillary cause)
degenerative mitral valve disease causes (concentric/eccentric) left ventricular hypertrophy
eccentric from a volume overload
What diagnostics are helpful for degenerative mitral valve disease
-Physical exam
-Echo (definitive diagnosis)
-Thoracic radiograph
-Electrocardiogram
-Systemic blood pressure
What is the definitive diagnosis for degenerative mitral valve disease
echo
why do you hear a systolic murmur with degenerative mitral valve disease
during systole you want the AV valves to be closed but if there is disease, there will be regurgitation and cause systolic murmur
What kind of murmur is heard with degenerative mitral valve disease
apical systolic heart murmur
-initially focal and low intensity
-progressively louder with disease progression, becoming holosystolic
-point of maximum intensity (left mitral; right tricuspid)
If you hear a left apical systolic heart murmur, you should be suspicious of
degenerative mitral valve disease
What are the physical exam findings of a patient with degenerative mitral valve disease
1) Signs of cardiogenic pulmonary edema (cough, tachypnea, dyspnea, orthopnea, pulmonary crackles, grey mucous membranes and prolonged CRT)
2) Signs of decreased cardiac output and perfusion of tissues (exercise intolerance, weakness, syncope, arrhythmias)
3) Sinus tachycardia (Increased sympathetic)
T/F: the grade of the heart murmur in a dog with degenerative mitral valve disease cannot give you information on the severity of regurgitation
True
What will you see on echo in a dog with degenerative mitral valve disease
1) thickening of mitral valve leaflets
2) prolapse or flail of mitral valve leaflets
3) systolic jet of mitral insufficiency
4) Left ventricular dilation and eccentric hypertrophy
5) Left atrial enlargement
6) LA mixing of colors (turbulent flow backwards into the left atrium)
Echo is the definitive diagnosis to degenerative mitral valve disease but what should you do if you dont have access to echocardiography
Thoracic radiographs
-LA and LV enlargement
-Mainstem bronchus compression
-Congestive heart failure (pulmonary edema and pulmonary venous congestion)
What will you see on thoracic radiography of a dog with degenerative mitral valve disease
-LA and LV enlargement (vertebral heart score and left atrial score)
-Mainstem bronchus compression (can cause cough)
-Congestive heart failure (pulmonary edema and pulmonary venous congestion)
What is a normal vertebral heart score
8.5-10.7 but range with breeds
around 10.5 is normal
pulmonary edema that is cardiogenic is usually _______ on radiography
perihilar or caudodorsally distributed
What will you see on electrocardiogram in a dog with degenerative mitral valve disease
*Left atrial and ventricular enlargement pattern
1) LA: wide p wave (>40mseconds)
2) LV: tall QRS complex (QRS amplitude >2.5mV)
Also atrial premature contractions: comes a little early, foci fire prematurely
Patients with degenerative mitral valve disease have LA enlargement. How is this reflected on ECG
wide p wave (>40mseconds)
Patients with degenerative mitral valve disease have LV enlargement. How is this reflected on ECG
tall QRS complex (QRS amplitude >2.5mV)
What can worsen mitral insufficency
systemic hypertension can increase LV afterload and worsen mitral insufficiency
*Important to monitor blood pressure
Why is it important to monitor blood pressure in patients with mitral insufficency
systemic hypertension can increase LV afterload and worsen mitral insufficency
How does systemic hypertension worsen mitral insufficiency
systemic hypertension can increase LV afterload and worsen mitral insufficiency
*Important to monitor blood pressure
dogs at high risk for developing heart disease (every CKCS without murmur)
no treatment is recommended
no dietary treatment
small breed dogs including breeds with known predispositions should be evaluated yearly (auscultation by vet)
potential breeding animals should not be bred if murmur is identified during nx breeding range (<6-8 years)
Stage A
T/F: potential breeding animals should not be bred if murmur is identified during nx breeding range (<6-8 years)
True
spectrum of imaging findings ranging from normal left sided dimensions to evidence of LA and LV enlargement that does not meet specific criteria for next stage
-Treatment is not recommended
-No dietary treatment
-Re-evaluate by echocardiography (or radio if unavailable) in 6-12 months
Stage B1
How should you re-evaluate a patient that is Stage A
small breed dogs including breeds with known predispositions should be evaluated yearly (auscultation by vet)
How should you re-evaluate a patient that is Stage B1
Re-evaluate by echocardiography (or radio if unavailable) in 6-12 months
Asymptomatic DMVD causing MR severe enough to result in left-sided cardiac remodeling sufficient to recommend treatment before onset of clinical signs of heart failure
-Treatment recommended
Stage B2
At what stage of DMVD is treatment of dogs recommended
B2- start pimobendan
How do you distinguish between B1 and B2
Echo
if you do not have access to echo then radiographs are best
al arge randomized multinational, multicenter study designed to investigate the effect of pimobendan of DMVD
EPIC trial (Evaluation of Pimobendan in Dogs with Cardiomegaly)
What stage of DMVD is a dog with a vertebral heart score of less than <10.5 on radiography and is asymptomatic
B1- recheck in 12 months
What stage of DMVD is a dog with a vertebral heart score of >11.5 and is asymptomatic
Stage B2- start pimobendan
How do you treat patients with Stage B2 DMVD
-Pimobendan
-Dietary treatment (mild dietary sodium restriction and highly palatable diet with adequate protein and calories for maintaining optimal body condition)
+/- ACE inhibitor (benazepril or enalapril) if the patient is systemically hypertensive or borderline
+/- cough suppressants- when cough is suspected from cardiac enlargement
when DMVD is severe enough to cause current or past clinical signs of heart failure (not refractory to standard treatment)
Stage C
How do you treat Stage C DMVD - Acute congestive heart failure
SPOF
Sedation-butorphanol
Pimobendan
Oxygen
Furosemide (access to water once diuresis has begun)
Make diagnosis with radiographs (definitive), echocardiogram, renal panel or blood pressure
How do you treat Stage C DMVD- chronic congestive heart failure
Diet
Ace inhibitor
Furosemide
Spironolactone
Pimobendan
(dogs are for special people)
Re-evaluate in 5-10 days
Recheck: BP, Renal panel +/- chest radiographs
How do you treat a patient with Stage D DMVD
They are patients with clinical signs of failure refractory to standard treatment for stage C
require more than a total daily dosage (8mg/kg furosemide or equivalent doage or torsemide)
consider anti-arrhythmic therapy to regulate ventricular response to atrial fibrillation
consider switching diuretic from furosemid to torsemide
What are alternative options for DMVD, other than medical therapy
1) Do surgical mitral valve repair
2) V-Clamp (Mitral transcatheter edge to edge repair- TEER)
*expensive
What is the prognosis for DMVD
usually a slowly progressive disease
it may take years for some dogs to develop CHF and some dogs may never develop CHF
prognosis factors:
-cardiac size
-severity of MR
-Maintenance dose of furosemide
-Severity of exercise intolerance
-severity of cardiac cachexia
What factors impact vascular resistance
1) blood viscosity (increases cause increased resistance)
2) vessel length (longer vessels have more resistance)
3) Vessel radius (smaller vessels have more resistance)
What determines blood pressure
Cardiac Output (HR x stroke volume) x Systemic Vascular Resistance
What is the predominant factor for controlling systemic vascular resistance
arteriolar size- effected by many systemically circulating, local tissue, and endothelial-derived factors
Blood volume is regulated by
kidneys- through pressure natruresos and RAAS
How do we measure blood pressure
1) Invasive arterial measurement
2) Non-invasive measurement (Doppler and Oscillometric)
what is gold standard for assessing blood pressure
direct-invasive
catherization of suitable artery and assessing arterial pressure using an electric transducer
not practical for routine screening
occludes the artery with cuff and can hear pulse at systolic BP while deflating cuff
Doppler ultrasound
measures oscillations of artery and provides systolic, diastolic, mean
can obtain inaccurate results with limb motion
oscillometric
why might oscillometric blood pressure be inaccurate
limb motion
Protocol for non-invasive blood pressure measurement
1) Quiet, isolated environment with owner present if possible
2) Acclimate patient in room for 5-10min
3) Gently restrain in comfortable position (ideally ventral or lateral recumbency)
4) Cuff width 30-40% circumference of cuff site
5) trained individual perform 5-7 measurements (discard first measurement)
6)Average measurements
7) Limb should be at same height of heart
What should the cuff width be?
Cuff width 30-40% circumference of cuff site
What is a normal systolic BP for a dog
<140mmHg
What is a normal systolic BP for cat
around 130-140mmHg
What are the degrees of hypertension in a dog
Normotensive SBP<140mmHg
Prehypertensive SBP 140-159mmHg
Hypertensive SBP 160-179mmHg
Severely Hypertensive SBP>180 mmHg
What are the causes of hypertension
-Situational (white Coat hypertension -sympathetic
-Secondary >80% (kidney, etc.)
-Idiopathic or primary
situational hypertension
increases in BP as consequence of in-clinic measurement process in an otherwise normotensive animal
-influenced by autonomic nervous system caused by effects of excitement of anxiety
-resolves under conditions that decrease stress stimulus
-no treatment is necessary
What are secondary causes of hypertension
cats: chronic kidney disease and hyperthyroidism
dogs: chronic kidney disease/acute kidney injury, hyperadrenocorticism. diabetes, pheochromocytoma
secondary causes of systemic hypertension in dog
-chronic kidney disease/acute kidney injury
-hyperadrenocorticism.
-diabetes
-pheochromocytoma
secondary causes of systemic hypertension in cat
chronic kidney disease and hyperthyroidism
T/F: heart disease does not result in hypertension
true- hypertension hurts the heart but it is not the cause
increased BP in absence of an overt clinically apparent disease that is known to cause secondary hypertension
due to prevalence of subclinical kidney disease and other comorbidies can be challenging to diagnose
accounts for 13-20% of cases of hypertension in cats
idiopathic hypertension
target organ damage
injury to tissues secondary chronic systemic hypertension
referred to as end organ
*Strong indication for anti-hypertensive therapy
What is a strong indication for anti-hypertensive therapy
target organ damage: injury to tissues secondary chronic systemic hypertension
referred to as end organ
*Strong indication for anti-hypertensive therapy
What organs are affected by chronic systemic hypertension
1) Eyes
2) Heart
3) Brain
4) Kidneys
How do you screen for target organ damage
1) Diagnostic profile and renal ultrasound
2) Echocardiogram
3) Fundic exam
4) Neurologic examination
How does chronic systemic hypertension impact the kidneys
Enhanced rate of decline of renal function (increased glomerulosclerosis and arteriosclerosis
-Increased magnitide of proteinuria
-Azotemia
Up to 65% of cats with CKD are
hypertensive
and azotemia is seen in 70% of hypertensive cats
How does systemic hypertension impact the kidneys
RAAS activation leads to efferent arteriole constriction leading to elevated intraglomerular pressure and progressive glomerular and tubulointerstitial damage.
This leads to loss of nephrons with further activates RAAS and causes afferent arteriole dilation also leading to elevated intraglomerular pressure and proteinuria. Only perpetuating systemic hypertension
How does systemic hypertension impact the heart
Echo: Left ventricular concentric hypertrophy (indistinguishable from primary HCM in cat)
Physical exam: systolic murmurs and/or gallop sounds
Sequelae: CHF after fluid therapy, less likely aortic aneurysm or aortic dissection
What would you see on echo of an animal with chronic systemic hypertension
Left ventricular concentric hypertrophy (indistinguishable from primary HCM in cat)
-Wall thickening
-Smaller LV lumen
On echo you see left ventricular concentric hypertrophy in a cat. What are the three possible causes
1) Chronic systemic hypertensiokn
2) Hyperthyroidism
3) Primary Hypertrophic Cardiomyopathy (sarcomere mutation seen in Maine-Coon)
What changes to the eyes will you see in cats with chronic hypertension
Hypertensive retinopathy, choroidopathy, optic neuropathy
-Retinal detachment is the most common finding
Retinal changes can occur when
the systemic blood pressure reaches 160 or above
hemorrhages of varying size and numbers in the retina due to hypertension
hypertensive retinopathy
appear more commonly with chronic hypertension
changes to appearance of retinal vessels; retinal detachement
hypertensive choroidopathy
appear more commonly with acute elevations in BP
does retinal detachment happen with more acute or chronic elevations in blood pressure
acute elevation in blood pressure
if you see hemorrhages of varying size and numbers upon a fundic exam, is this more due to acute or chronic elevation in BP
hypertensive retinopathy seen in chronic hypertension
What is the prognosis for retinal detachment (hypertensive choroidopathy)
effective antihypertensive treatment an lead to retinal reattachment but restoration of vision only occurs in a minority
What does retinal detachment (hypertensive choroidopathy) look like on fundic exam
large bullous retinal detachement with smaller foci of detachement
What effects to the brain do you see with systemic hypertension
1) Hypertensive encephopathy (dogs and cats)- occurs when BP is high enough and sustained long enough to overcome the autoregulatory ability of the cerebral vasculature leading to cerebral edema and arteriosclerosis
signs: disorientation, seizures, ataxia, depression, vestibular signs
occurs when BP is high enough and sustained long enough to overcome the autoregulatory ability of the cerebral vasculature leading to cerebral edema and arteriosclerosis
signs: disorientation, seizures, ataxia, depression, vestibular signs
improves when normalization of BP
hypertensive encephalopathy
What is the definitive diagnosis for hypertensive encephalopathy
Imaging
Vasogenic edema in occipital and parietal lobes of the brain in affected cats and dogs
-Risk for ischemic myelopathy of cervical spinal cord (tetraparesis or paralysis)
typically just treat hypertension and see if it resolves
a 10yo domestic shorthair cat presents for increased hiding and episodes of disorientation. Systolic blood pressure measures 225mmHg today. A fundic examination is performed which finds evidence of retinal hemorrhage and focal retinal detachment. What are the next MOST appropriate diagnostic test to pursue for this cat.
A) CBC, blood culture, and echo
B) Serum biochem profile, total T4
C) Thoracic and abdominal radiographs
D) 24h ambulatory ECG and NT-proBNP
E) No further test
B) Serum biochem profile, total T4
need to rule out causes of systemic hypertension
CKD and hyperthyroidism
When do you treat systemic hypertension
1) signs of target organ damage
2) >180mg: repeat BP twice within 14 days and recheck for target organ damage with recheck if >160 then start antihypertensive therapy
3) If 160-179mmHg then repeat BP twice within 8 week and recheck for TOD and >160 then start antihypertensive therapy
How do you treat hypertension in dogs
1) RAAS inhibition using ACE-1, angiotensin receptor blockers (ARBs), or aldosterone antagonists
IF severely hypertensive SBP>200mmHg then use RAAS inhibition +Calcium channel blocker (Amlodipine)
How do you treat severe hypertension (>200mmHg) in a dog
IF severely hypertensive SBP>200mmHg then use RAAS inhibition +Calcium channel blocker (Amlodipine)
but never use Amlodipine as a sole therapy (dilates renal afferent arteriole and can expose glomerulus to increased glomerular capillary hydrostatic pressure)
How do you treat hypertension in a dog that is <200mmHg
RAAS inhibition using ACE-1 (Benazepril, enalapril), angiotensin receptor blockers (ARBs) like Telmisartan, or aldosterone antagonists
Why should you never use Amlodipine (Ca2+ channel blocker) as a monotherapy for severe hypertension >200mmHg in a dog
never use Amlodipine as a sole therapy (dilates renal afferent arteriole and can expose glomerulus to increased glomerular capillary hydrostatic pressure)
RAAS inhibitors (ACE-1 and ARBs dilate the renal efferent arteriole so together the CCB has little effect on hydrostatic pressures)
*This is not the case in cats (Amlodipine can be used solely)
Calcium-channel blockers, like Amlodipine dilate the renal afferent arteriole and expose the glomerulus to increased glomerular capillary hydrostatic pressure. What can you give with this to counteract this in a dog
RAAS inhibitors (ACE-1 and ARBs dilate the renal efferent arteriole so together the CCB has little effect on hydrostatic pressures)
What RAAS inhibitors should you use to treat hypertension that is less than 200mmHg in a dog
ACE Inhibitors (benazepril and enalapril)
Angiotensin II Receptor Blockers (Telmisartan)
How do you treat systemic hypertension in a cat
First Line: Amlodipine (Calcium Channel Blocker)
*titrate doses
or Telmisartan
2) Double dose of amlodipine. (cant do this with telmisartan)
3) Combine amlodipine and telmisartan if either drug alone doesn’t result in adequate control of BP
How does systemic hypertension treatment differ in dogs vs cats
Cats: First line is Amlodipine (or Telmisartan)
Dogs: First line is a RAAS inhibitor but in severe cases (>200mmHg) you should also add Amlodipine
What is not recommended as first line in the treatment of systemic hypertension in cat
ACE-Inhibitors like Benazepril and Enalapril (this is not the case in dogs)
You are treating a cat with Amlodipine for systemic hypertension. It still isnt working as much as you’d like (>160mmHg). What should you do
2) Double dose of amlodipine. (cant do this with telmisartan)
if nothing
3) Combine amlodipine and telmisartan if either drug alone doesn’t result in adequate control of BP
What is the goal of systemic hypertension treatment
1)Institute first line therapy
2) Check in 7-10 days or 1-3 if TOD to measure blood pressure
3) <160mmHg is the minimal goal but <140 is optimal goal. recheck in 4-6 months
How often should you be monitoring blood pressure in catts
Healthy adult (3-6yo): Consider every12 months
Healthy senior cats (7-10): At least every 12months
Healthy geriatric (>11 years): At least every 6-12 months
Cats with recognized risk factors: CKD, hyperthyroidism, PHA, HAC, pheochromocytoma, drug therapy (erythropoeitin), of TOD evidence: Measure immediately and reassess at least every 3-6 months
