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Cardiology > Heart Failure, Valve > Flashcards

Heart Failure, Valve Flashcards

1
Q

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

A

heart failure

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2
Q

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)

A

Forward or Low output heart failure

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3
Q

heart failure where elevated venous pressures lead to congestion of organs and fluid accumulations (edema, effusion)

A

Congestion heart failure

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4
Q

How do you determine CO

A

CO (ml/min) = HR (beat/min) x SV (ml/beat)

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5
Q

What 5 factors influence stroke volume

A

Preload (+)
Afterload (-)
Contractility (+)
Valve function
Ventricular Synchrony

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6
Q

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

A

Diuresis or Vasodilators

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7
Q

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

A

Give Inotropy or Vassopressors

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8
Q

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

A

Hard to treat
-Inotropy
-Vasopressors
-Diuresis (when the perfusion is restored)

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9
Q

What are causes of heart failure due to increased afterload (pressure overload)

A

1) Aortic or subaortic stenosis
2) Pulmonary valve stenosis
3) Tetralogy of Fallot
4) Pulmonary or systemic hypertension

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10
Q

What are causes of heart failure due to volume overload

A

1) valve insufficiencies (MR, TR, AI, PI)
2) Shunting lesions (VSD, ASD, PDA)

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11
Q

What can cause impaired contractility leading to heart failure

A

DCM phenotype

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12
Q

T/F: arrhythmias can lead to heart failure

A

true- loss of synergy
tachy or bradyarrhythmias

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13
Q

What can cause impaired diastolic filling leading to heart failure

A

1) HCM phenotype
2) Restrictive cardiomyopathy
3) Pericardial effusion
4) Constrictive pericarditis

*Heart cant relax

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14
Q

what are the causes of heart failure

A

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

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15
Q

What are compensatory mechanisms in patients with heart failure to buffer the fall in CO and help preserve perfusion

A

1) Frank-Starling Mechanism
2) Neurohormonal alterations (Sympathetic NS, RAAS, ADH, natiuretic peptides)
3) Development of ventricular hypertrophy and remodeling

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16
Q

Frank-Starling
As there is __________ stretch on myofibers it induces a ________ stroke volume on subsequent contraction

A

greater; greater

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17
Q

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

A

Frank-Starling Mechanism

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18
Q

Acute neurohormonal activation during decreases in cardiac output are ________________ while chronic effects are

A

acute: compensatory and beneficial

chronic: maladaptive and harmful

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19
Q

baroreceptor response

A

in response to heart failure signal in brain causes SNS activation to increase HR and contractility to increase cardiac output

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20
Q

RAAS activation in heart failure causes

A

decreased GFR to retain fluid thus increasing preload to increase cardiac output

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21
Q

Increased ventricular wall tension in heart failure causes

A

myocyte growth leading to hypertrophy and increases cardiac output (with limit)

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22
Q

Where are decreases in cardiac output detected

A

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

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23
Q

where are the baroreceptors

A

carotid sinus and aortic arch

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24
Q

What is the SNS response to decreases in cardiac output

A

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

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25
Q

What are the effects of long-term activation (maladaptive) of the sympathetic nervous system in response to decreased cardiac output

A

1) Increased myocardium oxygen demand (MVO2)

2) Chronic RAAS activation -> cardiac fibrosis ->arrhythmias

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26
Q

What occurs when Renin-Angiotensin Aldosterone System is activated

A

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

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27
Q

What are the 3 stimuli for renin secretion from the juxtaglomerular cells

A

1) Decreased renal artery perfusion pressure

2) Decreased sodium delivery to macula densa in kidney

3) Direct stimulation of juxtaglomerular B-receptors by SNS

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28
Q

where is renin secreted from

A

juxtaglomerular cells

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29
Q

short term RAAS activation leads to

A

-Na+ and H20 retention (increased SV)
-Vasoconstriction (increased SVR)

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30
Q

long term RAAS activation leads to

A

-myocardial O2 demand (MVO2)
leading to hypertrophy, fibrosis, and arrhythmias

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31
Q

A competitive aldosterone antagonist

A

spironolactone

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32
Q

Does RAAS blockade in heart failure, using ACE inhibitor or aldosterone blockers (spironolactone) improve survival in CHF?

A

it may improve survival but newer data suggests conflicting results

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33
Q

is there evidence for use in beta-blockers in heart failure of dogs and cats

A

not really known. be cautionous with b blockers as they decrease ionotropy

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34
Q

Why might there be ventricular remodeling

A

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

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35
Q

Chronic neurohormonal activation of _____ , ______, and ________ promtes ventricular hypertrophy and fibrosis, which can lead to arrhythmias

A

NE
AT II
Aldosterone

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36
Q

What is the mechanism of eccentric hypertrophy

A

1) Increased volume overload
2) Increase diastolic wall
3) Series of sarcomere replication leading to chamber dilation
4) Eccentric hypertrophy

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37
Q

What is the mechanism of concentric hypertrophy

A

1) Increased pressure overload
2) Increased systolic wall
3) Parallel sarcomere replication (wall thickening)
4) Concentric Hypertrophy

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38
Q

What are the benefits of concentric or eccentric remodeling

A

-Enhance cardiac performance
-Decreased wall stress (decreased MVO2
-Maintain stroke volume

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39
Q

Does degenerate mitral valve disease lead to eccentric or concentric hypertrophy

A

eccentric hypertrophy

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40
Q

T/F: activation of renin-angiotensin-aldosterone system (RAAS) is stimulated by increased perfusion sensed in renal artery

A

False

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41
Q

T/F: with stimulation of the RAAS, systemic vasodilation will occur

A

false

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42
Q

What are the clinical signs of heart failure

A

-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)

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43
Q

Is cardiac cachexia more rapid in left or right sided congestive heart disease

A

right sided congestive heart disease

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44
Q

Causes of left sided CHF (pulmonary edema)

A

1) degenerative mitral valve disease
2) dilated cardiomyopathy
3) hypertrophic cardiomyopathy
4) subaortic stenosis

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45
Q

How do you get pulmonary edema with left sided congestive heart failure

A

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)

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46
Q

What is seen in left sided congestive heart failure

A

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

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47
Q

Why can you see pleural effusion in cats

A

difference in feline pulmonary venous anatomy (bronchial veins drain into pulmonary veins) and porosity of sub-pleural capillary beds

*can be chylous effuson

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48
Q

You have a patient that you suspect left sided CHF in. What is your diagnostic you should do to support this?

A

thoracic radiographs to confirm pulmonary edema

to support diagnosis (POCUS, Echo, NT-proBNP)

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49
Q

you suspect left sided heart failure with pulmonary edema. You do radiograph to confirm this. What findings will confirm this?

A

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

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50
Q

T/F: a dog with a murmur in respiratory distress is always in failure

A

False

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51
Q

What are the differentials for respiratory distress

A

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)

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52
Q

What is a normal VLAS score

A

less than 2.3

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53
Q

How can you use VLAS to diagnose right sided heart failure

A

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

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54
Q

What would you see on echo of the the left atrium when a patient is in left sided heart failure

A

the left atrium will be larger than the aorta
(2x larger)
can also tell if there is pericardial effusion or pleural effusion

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54
Q

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

A

NT-PROBNP

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55
Q

what would you use NT-ProBNP for

A

for differentiating cardiac and non-cardiac causes of dyspnea
screening for cardiomyopathy

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56
Q

What are the 2 different ways you can test NT-ProBNP for differentiating cardiac and non-cardiac causes of dyspnea

A

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

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57
Q

Tells you normal or abnormal result of NT-PRoBNP
-bedside test
-whole blood or pleural effusion
-cats only

A

ELISA SNAP NT-proBNP

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58
Q

What species can you use the ELISA SNAP NT-proBNP in

A

only the cat

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59
Q

T/F horses rarely get left sided heart failure

A

True

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60
Q

Horses rarely get left sided heart failure but when they do it is because

A

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

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61
Q

Mares in late stages of gestation may develop

A

CHF due to hemodynamic burden of pregnancy

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62
Q

Why do patients with right sided heart failure typically get ascites

A

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)

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63
Q

What are the clinical signs of right sided CHF

A

-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)

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64
Q

pericardial effusion secondary to heart failure is usually________ while pleural effusion is _______

A

a small volume

a large volume

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65
Q

What will you see in horses with right sided congestive heart failure

A

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

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66
Q

T/F: you see peripheral edema in BOTH left side and right sided congestive heart failure

A

True

increased venous and capillary hydrostatic pressures overwhelm the lymphatic reserves and create a peripheral edematous state
(left sided, right sided, or biventricular failure)

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67
Q

What might you suspect if you see diagnostic findings associated with pulmonary edema and cavitary effusions

A

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

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68
Q

Biventricular heart failure

A

-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

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69
Q

What is your go to diagnostic for congestive heart failure

A

thoracic radiographs

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70
Q

no audible heart murmur but an at risk breed (Cavalier King Charles Spaniels, Dachshunds, Miniature and Toy Poodles)

A

Class A MMVD

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71
Q

Audible heart murmur heard
Asymptomatic
Not severe enough to meet criteria for medical treatment

A

Class B1 MMVD

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72
Q

Audible heart murmur heard
Asymptomatic
Severe enough to result in cardiac remodeling sufficient to recommend treatment

A

Class B2 MMVD

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73
Q

audible heart murmur and severe neough to cause current or past clinical signs of heart failure (ex: pulmonary edema of CHF)

A

Class C MMVD

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74
Q

audible heart murmur and clinical signs of failure refractory to standard treatment for Stage c

A

Class D MMVD

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75
Q

At what ACVIM stage for MMVD/DMVD should Pimobendan be started

A

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)

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76
Q

T/F: Starting dobermans on pimobendan for asymptomatic DCM is protective

A

Trie

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77
Q

At What ACIM stage for hypertrophic cardiomyopathy should Clopidogrel +/- atenolol be started

A

AVIM stage B2
Audible heart murmur heard, Asymptomatic
Severe enough to result in atrial enlargement sufficient to recommend treatment

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78
Q

What treatment should you do for asymptomatic heart disease (Stage B2)

A

MMVD/DMVD: Pimobendan +/- ACE Inhibitor (use in cases of hypertension)

DCM (Dobermans): Pimobendan

HCM: Clopidogrel +/- Atenolol

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79
Q

a prophylactic anti-thrombotic treatment for cats with left sided heart failure/ hypertrophic cardiomyopathy) to prevent thrombi formation

A

Clopidogrel

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80
Q

a calcium sensitizer (inodilator) that is used in contractility issues
functions to inrease contractility directly and increase calcium binding to troponin C

A

Pimobendan

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81
Q

What are the treatment strategies for congestive heart failure

A

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)

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82
Q

What are the treatment strategies for forward heart failure

A

1) Supporting systolic (pump) function - positive inotropes

2) Removing congestion- if in concurrent CHF, diuretic to reduce preload (balance with perfusion)

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83
Q

what is the function of diuretics

A

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)

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84
Q

of goal of giving diuretics is to

A

reduce preload

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85
Q

what are your loop diuretics

A

Furosemide
Toremide
Bumetanide
Strongest class of diuretics

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86
Q

What is the mechanism of action of loop diuretics like furosemide, toremide, and bumetanide

A

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)

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87
Q

What decreases the efficacy of loop diuretics like Furosemide, Toremide, and bumetanide

A

affected by renal blood flow (decreased efficacy with renal failure and NSAIDS)

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88
Q

Where do loop diuretics like furosemid, toremide, bumetanide act

A

inhibits Na+/K+/2Cl- co-transporter
thick ascending loop of henle
Na+, K+, Cl- and H20 excretion

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89
Q

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)

A

Torsemide

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90
Q

Is Furosemide of Torsemide more potent?

A

Torsemid
most likely closer to 20 times in healthy dogs and requires 5-10% furosemide dose

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91
Q

When should you consider switching a patient from furosemide to torsemide

A

if the patient is receiving >8mg/kg/d furosemide and having refractory symptoms you may need to move to the more potent torsemide

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92
Q

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

A

spironolactone

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93
Q

where does spironolactone act

A

Distal Tubule

it acts to be a mineralocorticoid receptor antagonist (MRA) that blocks action of aldosterone at distal tubule

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94
Q

T/F: Spironolactone is a strong diuretic

A

weak- it is potassium sparing but not that good at diuresis

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95
Q

What is a side effect of spironolactone (potassium sparing diuretic)

A

facial dermatitis in cats

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96
Q

spironolactone can be an adjunct treat for

A

heart failure or ascites

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97
Q

where do thiazide diuretics (hydrochlorothiazide) act

A

proximal distal convoluted tubule
inhibits Na+/Cl- co-transporter

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98
Q

What is the mechanism of hydrochlorothiazide

A

inhibits Na+/Cl- co-transporter in the
proximal distal convoluted tubule

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99
Q

inhibits Na+/Cl- co-transporter in the
proximal distal convoluted tubule
side effects:
hypokalemia
hypercalcemia
ventricular arrhythmia
nausea

A

hydrochlorothiazide (thiazide diuretics)

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100
Q

What are the side effects of hydrochlorothiazide (thiazide diretics)

A

hypokalemia
hypercalcemia
ventricular arrhythmia
nausea

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101
Q

What are different positive inotropes you can use to treat heart failure

A

1) Pimobendan (Ca2+ sensitizer)
2) Digitalis glycosides (Digoxin)
3) Catecholamines (Dobutamine, dopamine, epinephrine)

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102
Q

Pimobendan is an inodilator, what does that mean

A

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

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103
Q

What is the mechanism of action of Pimobendan

A

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

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104
Q

T/F: Pimobendan is a Phosphodiesterase-5 inhibitor

A

False

Phosphodiestrase-3 inhibitor
-Increased cAMP mediated peripheral vasodilation to decrease preload and afterload

105
Q

T/F: Pimobendan is not FDA approved in cats

A

true
used off label

106
Q

T/F: Pimobendan does not help in patients with asymptomatic MMVD and DCM

A

False

107
Q

Dobutamine is a potent

A

positive inotrope (B1>B2>a)

108
Q

What receptor does Dobutamine have the greatest effect at

A

(B1>B2>a)

109
Q

Why is Dobutamine used in heart failure

A

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)

110
Q

T/F: Dobutamine has less effect on heart rate and blood pressure than dopamine

A

True

-At higher doses see more alpha effects

111
Q

What should you do if you see a patient on dobutamine is developing tachycardia or ventricular ectopy

A

Decrease infusion rate (it is given as a CRI)

112
Q

what is the mechanism of action of digoxin

A

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

113
Q

What are the indications for using digoxin

A

rate control of atrial fibrillation

114
Q

When should you be careful giving digoxin

A

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

115
Q

What are the clinical signs of digoxin toxicity

A

arrhythmias: ventricular arrhythmias and bradycardia

anorexia, nausea, vomiting, diarrhea

116
Q

oral vasodilator
dihydropyridine calcium channel blocker
smooth muscle relaxation
long half life

A

Amlodipine

117
Q

What is Amlodipine’s mechanism of action

A

dihydropyridine calcium channel blocker
to cause vasodilation

118
Q

Venodilators (increase/decrease) preload

A

Decrease preload

119
Q

Arteriodilators (increase/decrease afterload)

A

decrease afterload

120
Q

a direct oral arteriodilator
acts on intracellular calcium hemostasis

A

Hydralazine

121
Q

What is Hydralazine’s mechanism of action

A

a direct oral arteriodilator
acts on intracellular calcium hemostasis

122
Q

How is Amlodipine administered

A

orally (vasodilator)

*dihydropyridine calcium channel blocker

123
Q

How is Hydralazine administered

A

orally (arteriodilator)

124
Q

How is sodium nitroprusside administered

A

IV (CRI)
-Vasodilator

125
Q

How is nitroglycerin administered

A

topical (ointment)
-vasodilator

126
Q

Sodium nitroprusside mechanism of action

A

Produces NO and results in vascular smooth muscle relaxation
given IV (CRI)

127
Q

Nitroglycerin prefers to act on (arteries/veins)

A

veins > arteries
vasodilator

128
Q

What are the most common ACE inhibitors used

A

Enalapril
Benazepril

129
Q

What is the mechanism of action of Enalapril and Benazepril

A

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

130
Q

Enalapril, Benazepril arent really used in patients with asymptomatic heart failure unless they are

A

hypertensive

ACE inhibitors decrease AT-II mediated vasoconstriction and volume retention

131
Q

How do you treat acute left sided congestive heart failure in dogs

A

SPOF
Sedation- Butorphanol (because in respiratory distress)
Pimobendan- inodilator
Oxygen Supplementation
Furosemide (Lasix)- diuretic
-can give CRI in life threatening case of pulmonary edema

132
Q

SPOF protocol is used to treat

A

acute left sided CHF

133
Q

When should you continue dosing Furosemide in a patient with acute left sided CHF

A

continue hourly until RR is improved or total of 8mg/kg has been reached over 4 hours then decrease frequency

134
Q

Why might there be inadequate response to initial therapy to acute left sided CHF (SPOF failed)

A

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)

135
Q

How does a left atrial tear occur

A

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

136
Q

Systemic hypertension increases LV _______

A

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

137
Q

How do you treat acute forward heart failure in dogs

A

1) oxygen supplementation
2) Pimobendan- inodilator +/- dobutamine (CRI)
3) Furosemide- based on whether concurrent left sided CHF- balance while monitoring BP and perfusion

138
Q

How do you treat acute left sided CHF in cats

A

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

139
Q

How do you treat acute right side CHF in dogs

A

1) Sedation - Butorphanol
2) Thoracocentesis/ Abdominocentesis
3) Furosemide (Lasix) Continue q8-12hours

+/- Pimobendan- be cautious in cases of outflow obstruction

+/- oxygen supplementation

140
Q

How do you treat chronic CHF in dogs

A

1) Diet- low sodium
2) ACE Inhibitor (Enalapril or Benazepril)
3) Furosemide
4) Spironolactone
5) Pimobendan

+/ - Thoracocentesis/ Abdominocentesis
“Dogs are For Special People”

141
Q

What kind of diet is good for managing dogs in chronic CHF

A

low sodium

142
Q

How do you treat cats with chronic CHF

A

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

143
Q

Clopidogrel tastes bitter and cats dont like it. What should you do if you need to give it to them to manage chronic CHF

A

administer in empty gel capsule

144
Q

How do you manage heart failure in horses

A

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

145
Q

What is the prognosis with horses in heart failure

A

you can go therapy with Furosemide and Digoxin but it is poor and horses usually do not survive >6months after diagnosis

146
Q

How should you treat dogs with refractory CHF (Stage D)

A

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

147
Q

How should you treat cats with refractory CHF (Stage D)

A

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

148
Q

How might an animal develop diuretic tolerance

A

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

149
Q

How do you overcome diretic resistance

A

1) Add ACE inhibition (and/or spironolactone)
2) Sequential nephron blockage (add additional diuretics)
3) Torsemide

150
Q

What are dietary recommendations for dogs and cats with heart disease

A

-Adequate calorie intake
-High quality/adequate protein
-Moderate Na+ restriction
-K+ supplementation if hyperkalemic

151
Q

How can the owner monitor patients with congested left sided heart failure at home

A

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

152
Q

Is canine degenerative valve disease congenital or acquired

A

Chronic, acquired valvular disease that is progressive

153
Q

What are other names for canine degenerative valve disease

A

myxomatous mitral valve disease
endocardiosis

154
Q

What is the most common cause of cardiac morbidity and mortality in dogs?

A

canine degenerative valve disease

155
Q

What kind of dogs typically get degenerative valve disease

A

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

156
Q

90% of small breed dogs >8 years of age have

A

canine degenerative valve disease

157
Q

What valves are typically affected by canine degenerative valve disease

A

Mitral Valve (MV) is most affected
-60% MV alone
-30% MV and TV
occasionally affects TV alone (1%)
-rarely affects aortic valve

158
Q

What breed typically gets canine degenerative valve disease at younger age

A

Cavalier King Charles Spaniel

159
Q

How many leaflets does the mitral valve typically have

A

2 leaflets- anterior and posterior

160
Q

What are the components in the normal mitral valve apparatus

A

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

161
Q

What are the layers of mitral valve leaflets

A

1) Atrialis- mainly elastin
2) Spongiosa- GAGs+proteoglycans
3) Fibrosa- dense collagen for main load bearing layer
4) Ventricularis- mainly elastin

*ASFV

162
Q

What is the spectrum of disease of degenerative mitral valve disease

A

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

163
Q

What is the earliest gross finding of degenerative mitral valve disease

A

Edematous nodules of varying size and location
Plaque like elevations

then the chordae tendinae begin to become thickened

164
Q

what are the histopath findings of degenerative mitral valve disease

A

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

165
Q

What are the cardiac sequelae to degenerative mitral valve disease

A

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

166
Q

How might a small breed old dog with a history of heart murmur get pericardial effusion

A

1) Degenerative mitral valve disease leading to left atrial tear

2) Neoplasia

167
Q

Describe the pathophysiology of degenerative mitral valve disease leading to mitral regurgitation

A

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)

168
Q

degenerative mitral valve disease causes (concentric/eccentric) left ventricular hypertrophy

A

eccentric from a volume overload

169
Q

What diagnostics are helpful for degenerative mitral valve disease

A

-Physical exam
-Echo (definitive diagnosis)
-Thoracic radiograph
-Electrocardiogram
-Systemic blood pressure

170
Q

What is the definitive diagnosis for degenerative mitral valve disease

A

echo

171
Q

why do you hear a systolic murmur with degenerative mitral valve disease

A

during systole you want the AV valves to be closed but if there is disease, there will be regurgitation and cause systolic murmur

172
Q

What kind of murmur is heard with degenerative mitral valve disease

A

apical systolic heart murmur
-initially focal and low intensity
-progressively louder with disease progression, becoming holosystolic
-point of maximum intensity (left mitral; right tricuspid)

173
Q

If you hear a left apical systolic heart murmur, you should be suspicious of

A

degenerative mitral valve disease

174
Q

What are the physical exam findings of a patient with degenerative mitral valve disease

A

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)

175
Q

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

A

True

176
Q

What will you see on echo in a dog with degenerative mitral valve disease

A

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)

177
Q

Echo is the definitive diagnosis to degenerative mitral valve disease but what should you do if you dont have access to echocardiography

A

Thoracic radiographs
-LA and LV enlargement
-Mainstem bronchus compression
-Congestive heart failure (pulmonary edema and pulmonary venous congestion)

178
Q

What will you see on thoracic radiography of a dog with degenerative mitral valve disease

A

-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)

179
Q

What is a normal vertebral heart score

A

8.5-10.7 but range with breeds

around 10.5 is normal

180
Q

pulmonary edema that is cardiogenic is usually _______ on radiography

A

perihilar or caudodorsally distributed

181
Q

What will you see on electrocardiogram in a dog with degenerative mitral valve disease

A

*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

182
Q

Patients with degenerative mitral valve disease have LA enlargement. How is this reflected on ECG

A

wide p wave (>40mseconds)

183
Q

Patients with degenerative mitral valve disease have LV enlargement. How is this reflected on ECG

A

tall QRS complex (QRS amplitude >2.5mV)

184
Q

What can worsen mitral insufficency

A

systemic hypertension can increase LV afterload and worsen mitral insufficiency

*Important to monitor blood pressure

185
Q

Why is it important to monitor blood pressure in patients with mitral insufficency

A

systemic hypertension can increase LV afterload and worsen mitral insufficency

186
Q

How does systemic hypertension worsen mitral insufficiency

A

systemic hypertension can increase LV afterload and worsen mitral insufficiency

*Important to monitor blood pressure

187
Q

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)

A

Stage A

188
Q

T/F: potential breeding animals should not be bred if murmur is identified during nx breeding range (<6-8 years)

A

True

189
Q

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

A

Stage B1

190
Q

How should you re-evaluate a patient that is Stage A

A

small breed dogs including breeds with known predispositions should be evaluated yearly (auscultation by vet)

191
Q

How should you re-evaluate a patient that is Stage B1

A

Re-evaluate by echocardiography (or radio if unavailable) in 6-12 months

192
Q

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

A

Stage B2

193
Q

At what stage of DMVD is treatment of dogs recommended

A

B2- start pimobendan

194
Q

How do you distinguish between B1 and B2

A

Echo

if you do not have access to echo then radiographs are best

195
Q

al arge randomized multinational, multicenter study designed to investigate the effect of pimobendan of DMVD

A

EPIC trial (Evaluation of Pimobendan in Dogs with Cardiomegaly)

196
Q

What stage of DMVD is a dog with a vertebral heart score of less than <10.5 on radiography and is asymptomatic

A

B1- recheck in 12 months

197
Q

What stage of DMVD is a dog with a vertebral heart score of >11.5 and is asymptomatic

A

Stage B2- start pimobendan

198
Q

How do you treat patients with Stage B2 DMVD

A

-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

199
Q

when DMVD is severe enough to cause current or past clinical signs of heart failure (not refractory to standard treatment)

A

Stage C

200
Q

How do you treat Stage C DMVD - Acute congestive heart failure

A

SPOF
Sedation-butorphanol
Pimobendan
Oxygen
Furosemide (access to water once diuresis has begun)

Make diagnosis with radiographs (definitive), echocardiogram, renal panel or blood pressure

201
Q

How do you treat Stage C DMVD- chronic congestive heart failure

A

Diet
Ace inhibitor
Furosemide
Spironolactone
Pimobendan
(dogs are for special people)

Re-evaluate in 5-10 days
Recheck: BP, Renal panel +/- chest radiographs

202
Q

How do you treat a patient with Stage D DMVD

A

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

203
Q

What are alternative options for DMVD, other than medical therapy

A

1) Do surgical mitral valve repair
2) V-Clamp (Mitral transcatheter edge to edge repair- TEER)

*expensive

204
Q

What is the prognosis for DMVD

A

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

205
Q

What factors impact vascular resistance

A

1) blood viscosity (increases cause increased resistance)

2) vessel length (longer vessels have more resistance)

3) Vessel radius (smaller vessels have more resistance)

206
Q

What determines blood pressure

A

Cardiac Output (HR x stroke volume) x Systemic Vascular Resistance

207
Q

What is the predominant factor for controlling systemic vascular resistance

A

arteriolar size- effected by many systemically circulating, local tissue, and endothelial-derived factors

208
Q

Blood volume is regulated by

A

kidneys- through pressure natruresos and RAAS

209
Q

How do we measure blood pressure

A

1) Invasive arterial measurement
2) Non-invasive measurement (Doppler and Oscillometric)

210
Q

what is gold standard for assessing blood pressure

A

direct-invasive
catherization of suitable artery and assessing arterial pressure using an electric transducer
not practical for routine screening

211
Q

occludes the artery with cuff and can hear pulse at systolic BP while deflating cuff

A

Doppler ultrasound

212
Q

measures oscillations of artery and provides systolic, diastolic, mean
can obtain inaccurate results with limb motion

A

oscillometric

213
Q

why might oscillometric blood pressure be inaccurate

A

limb motion

214
Q

Protocol for non-invasive blood pressure measurement

A

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

215
Q

What should the cuff width be?

A

Cuff width 30-40% circumference of cuff site

216
Q

What is a normal systolic BP for a dog

A

<140mmHg

217
Q

What is a normal systolic BP for cat

A

around 130-140mmHg

218
Q

What are the degrees of hypertension in a dog

A

Normotensive SBP<140mmHg

Prehypertensive SBP 140-159mmHg

Hypertensive SBP 160-179mmHg

Severely Hypertensive SBP>180 mmHg

219
Q

What are the causes of hypertension

A

-Situational (white Coat hypertension -sympathetic

-Secondary >80% (kidney, etc.)

-Idiopathic or primary

220
Q

situational hypertension

A

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

221
Q

What are secondary causes of hypertension

A

cats: chronic kidney disease and hyperthyroidism

dogs: chronic kidney disease/acute kidney injury, hyperadrenocorticism. diabetes, pheochromocytoma

222
Q

secondary causes of systemic hypertension in dog

A

-chronic kidney disease/acute kidney injury
-hyperadrenocorticism.
-diabetes
-pheochromocytoma

223
Q

secondary causes of systemic hypertension in cat

A

chronic kidney disease and hyperthyroidism

224
Q

T/F: heart disease does not result in hypertension

A

true- hypertension hurts the heart but it is not the cause

225
Q

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

A

idiopathic hypertension

226
Q

target organ damage

A

injury to tissues secondary chronic systemic hypertension
referred to as end organ
*Strong indication for anti-hypertensive therapy

227
Q

What is a strong indication for anti-hypertensive therapy

A

target organ damage: injury to tissues secondary chronic systemic hypertension
referred to as end organ
*Strong indication for anti-hypertensive therapy

228
Q

What organs are affected by chronic systemic hypertension

A

1) Eyes
2) Heart
3) Brain
4) Kidneys

229
Q

How do you screen for target organ damage

A

1) Diagnostic profile and renal ultrasound
2) Echocardiogram
3) Fundic exam
4) Neurologic examination

230
Q

How does chronic systemic hypertension impact the kidneys

A

Enhanced rate of decline of renal function (increased glomerulosclerosis and arteriosclerosis
-Increased magnitide of proteinuria
-Azotemia

231
Q

Up to 65% of cats with CKD are

A

hypertensive

and azotemia is seen in 70% of hypertensive cats

232
Q

How does systemic hypertension impact the kidneys

A

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

233
Q

How does systemic hypertension impact the heart

A

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

234
Q

What would you see on echo of an animal with chronic systemic hypertension

A

Left ventricular concentric hypertrophy (indistinguishable from primary HCM in cat)
-Wall thickening
-Smaller LV lumen

235
Q

On echo you see left ventricular concentric hypertrophy in a cat. What are the three possible causes

A

1) Chronic systemic hypertensiokn
2) Hyperthyroidism
3) Primary Hypertrophic Cardiomyopathy (sarcomere mutation seen in Maine-Coon)

236
Q

What changes to the eyes will you see in cats with chronic hypertension

A

Hypertensive retinopathy, choroidopathy, optic neuropathy

-Retinal detachment is the most common finding

237
Q

Retinal changes can occur when

A

the systemic blood pressure reaches 160 or above

238
Q

hemorrhages of varying size and numbers in the retina due to hypertension

A

hypertensive retinopathy

appear more commonly with chronic hypertension

239
Q

changes to appearance of retinal vessels; retinal detachement

A

hypertensive choroidopathy

appear more commonly with acute elevations in BP

240
Q

does retinal detachment happen with more acute or chronic elevations in blood pressure

A

acute elevation in blood pressure

241
Q

if you see hemorrhages of varying size and numbers upon a fundic exam, is this more due to acute or chronic elevation in BP

A

hypertensive retinopathy seen in chronic hypertension

242
Q

What is the prognosis for retinal detachment (hypertensive choroidopathy)

A

effective antihypertensive treatment an lead to retinal reattachment but restoration of vision only occurs in a minority

243
Q

What does retinal detachment (hypertensive choroidopathy) look like on fundic exam

A

large bullous retinal detachement with smaller foci of detachement

244
Q

What effects to the brain do you see with systemic hypertension

A

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

245
Q

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

A

hypertensive encephalopathy

246
Q

What is the definitive diagnosis for hypertensive encephalopathy

A

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

247
Q

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

A

B) Serum biochem profile, total T4

need to rule out causes of systemic hypertension
CKD and hyperthyroidism

248
Q

When do you treat systemic hypertension

A

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

249
Q

How do you treat hypertension in dogs

A

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)

250
Q

How do you treat severe hypertension (>200mmHg) in a dog

A

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)

251
Q

How do you treat hypertension in a dog that is <200mmHg

A

RAAS inhibition using ACE-1 (Benazepril, enalapril), angiotensin receptor blockers (ARBs) like Telmisartan, or aldosterone antagonists

252
Q

Why should you never use Amlodipine (Ca2+ channel blocker) as a monotherapy for severe hypertension >200mmHg in a dog

A

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)

253
Q

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

A

RAAS inhibitors (ACE-1 and ARBs dilate the renal efferent arteriole so together the CCB has little effect on hydrostatic pressures)

254
Q

What RAAS inhibitors should you use to treat hypertension that is less than 200mmHg in a dog

A

ACE Inhibitors (benazepril and enalapril)

Angiotensin II Receptor Blockers (Telmisartan)

255
Q

How do you treat systemic hypertension in a cat

A

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

256
Q

How does systemic hypertension treatment differ in dogs vs cats

A

Cats: First line is Amlodipine (or Telmisartan)

Dogs: First line is a RAAS inhibitor but in severe cases (>200mmHg) you should also add Amlodipine

257
Q

What is not recommended as first line in the treatment of systemic hypertension in cat

A

ACE-Inhibitors like Benazepril and Enalapril (this is not the case in dogs)

258
Q

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

A

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

259
Q

What is the goal of systemic hypertension treatment

A

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

260
Q

How often should you be monitoring blood pressure in catts

A

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

Cardiology (8 decks)

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