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VTS(ECC) Study > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What does the T-wave indicate?

A

Ventricular repolarization

Ventricles relax

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2
Q

How many seconds is each small square on ECG paper @ 25mm/sec?

A

0.04 seconds

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3
Q

How many seconds is each large square on ECG paper @ 25mm/sec?

A

0.2 seconds

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4
Q

What conditions make up Tetralogy of Fallot

A

Pulmonic stenosis, ventricular septal defect, right ventricular hypertrophy, overriding aorta

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5
Q

What do Beta Blockers do?

A

Antagonize sympathetic nervous system

Slow HR, decrease cardiac oxygen demand, control of some arrhythmias

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6
Q

What are some adverse effects of beta blockers?

A

Excessive bradycardia, worsening heart failure, bronchospasm, hypotension, depression, mask hypoglycemia

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7
Q

What is the flow of blood through the cardiovascular system? Starting with deoxygenated blood returning from body.

A

Deoxygenated blood moves from vena cava to right atrium
Through the tricuspid valve into right ventricle
Out pulmonary semilunar valve to pulmonary artery
Blood oxygenated in pulmonary circulation
Return to left atrium via pulmonary veins
Through bicuspid valve to left ventricle
Through aortic semilunar valve to aorta
Deliver oxygen via systemic circulation

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8
Q

Preload

A

Volume of blood in left ventricle before contraction

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9
Q

Afterload

A

Resistance to left ventricle ejection

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10
Q

Normal CVP

A

0-5 cm H2O

0-3mmHg

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11
Q

Normal Systolic BP

A

100-160mmHg

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12
Q

Normal diastolic BP

A

60-110mmHg

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13
Q

Normal MAP

A

80-120mmHg

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14
Q

Pathway of cardiac conduction

A 
Sinoatrial Node (SA)
Atrioventricular Node (AV)
Bundle of His
Bundle Branches
Purkinjie Fibers
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15
Q

Clinical signs associated with right sided heart failure

A

Weakness, syncope, exercise intolerance, pallor, jugular distention, large liver/spleen, tachypnea, peritoneal and/or pleural effusion

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16
Q

Clinical signs associated with left sided heart failure

A

Weakness, collapse, coughing, orthopnea, pulmonary edema, hemoptysis
Pulmonary edema exclusively from left sided heart failure

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17
Q

Milrinone and amrinone

A

Phosphodiesterase-3 inhibitor
Inotrope and arteriolar dilator
For decompensated systolic failure
Increase contractility, decrease preload and afterload
May cause hypotension and tachyarrhythmia

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18
Q

Dobutamine

A

Sympathomimetic amine
Stimulates B-adrenergic receptors and increase calcium availability
Increase contractility and stroke volume
Increase cardiac output
Increase myocardial O2 demand and cardiac workload
Blood pressure and heart rate - normal to slightly increased
Injectable pimobendan

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19
Q

Dopamine

A

Sympathomimetic amine
Precursor of norepinephrine
Has dose dependent effects
Low - Arterial vasodilation
Mid - systemic arteriolar vasoconstriction
High - Significant vasoconstriction
Do not use with beta blockers
Causes tissue necrosis and sloughing if extravasated
Stimulates beta adrenergic receptors and calcium availability

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20
Q

Positive Inotropes

A

Sympatomimetic amines, phosphodiesterase inhibitors, Ca sensitizers, digitalis glycosides
Increase strength of contraction and cardiac output

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21
Q

Thiazide Diuretics

A

Hydrochlorothiazide
Act in proximal portion of distal convoluted tubule
Inhibits Na resorption and increase K excretion

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22
Q

Potassium Sparing Diuretics

A

Spirinolactone
May increase potassium concentration
Inhibits action of aldosterone on distal tubular cells

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23
Q

Loop diuretics

A

Act on ascending Loop of Henle
Furosemide, torsemide
Decrease reabsorption of Na and Cl
Increase excretion of K, H2O, Cl, Ca, Mg, H
Possible decrease in kidney function, electrolyte disturbances, dehydration

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24
Q

Digitalis glycosides

A

Digoxin, digitoxin
Digitoxin only for dogs
Increase cardiac performance, decrease fluid retention, decrease heart rate, stop supraventricular tachyarrhymias
TOXIC - require serum monitoring, higher risk when combined with diazepam, anticholenergics, tetracycline, erythromycin

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25
Q

Pimobendan

A

Calcium sensitizer
Positive inotrope, Ca sensitization, vasodilaton
Platelet aggregation inhibitor
Monitor HR and rhythm

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26
Q

Sildenafil

A

Phosphodiesterase inhibitor
Inotrope and arteriolar dilator
5-Phosphodiesterase inhibition

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27
Q

What is special about the AV node?

A

Decremental conduction

More frequent stimulation leads to slower conduction

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28
Q

Depolarization

A

Systole, contraction, Na ions move into the cell

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29
Q

Repolarization

A

Diastole, relaxation, K ions move out of the cell

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30
Q

What does the P-wave indicate?

A

Atrial depolarization
Tricuspid & bicuspid valves open
Blood moving into ventricles

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31
Q

What does the QRS complex indicate?

A

Depolarization (Q- septal, R - ventricular, S - Purkinje)
Tricuspid and bicuspid valves close
Ventricular contraction

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32
Q

Pacemaker of the heart

A

SA node

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33
Q

Diltiazem

A

Ca Channel blocker
Non-Dihydropyridine
Negative inotrope
Vasodilator and negative chronotrope
Use for AFib, supraventricular tachycardia, HCM
Has GI side effects, cardiac blocking effects, CNS effects, peripheral and pulmonary edema, liver effects
DO NOT USE IN KIDNEY DYSFUNCTION

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34
Q

Amlodipine

A 
Calcium Channel Blocker
Blocks Ca channels from moving Ca across barrier
Used for systemic hypertension
Do not use in renal disease
Monitor blood pressure, vomiting
Arteriolar vasodilator
Dihydropyridine
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35
Q

ACE Inhibitors

A

Vasodilators
Decrease angiotensin II levels, allows for artery and venodilaton
Increase renal sodium and water excretion
Hypertension, valve disease, DCM, HCM
Enalapril, benazepril
Side effects - vomiting, diarrhea, hypotension, renal dysfucntion, hyperkalemia

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36
Q

Nitroglycerin

A

Vasodilators
Venodilator
Decrease preload
Monitor blood pressure, heart rate, sodium

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37
Q

Hydralazine

A

Vasodilator
Arteriolar vasodilator
Decreases afterload
Use in DCM, mitral valve regurgitation, intracardiac shunting

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38
Q

Nitroprusside

A 
Vasodilator
Arteriolar and venodilator (Combination vasodilator)
Decreases afterload
Decrease preload
May cause decreased BP and increased HR
Administration via CRI
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39
Q

Patent Ductus Arteriosus

A

Normally shuts 3-4 days after birth. If patent, flow of blood between aorta and pulmonary artery occurs. Blood moves from aorta to pulmonary artery (left to right shunt)
Congenital defect

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40
Q

Right side of heart carries _________ blood

A

Systemic

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41
Q

Left side of heart carries _________ blood

A

Pulmonary

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42
Q

Treatment for patent ductus arteriosus

A

Requires surgery - either coil or ligation

Stabilization with oxygen and diuretics and digoxin if needed

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43
Q

Which arrhythmia can be present in patent ductus arteriosis? Why?

A

AFib. Due to enlargement of left atrium from volume overload

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44
Q

Ventricular Septal Defect

A

Congenital defect
Hole in interventicular septum
Effect depends on size of defect and direction of flow
Small defect may have no effect
USUALLY - left to right shunting of blood (higher left sided pressure)

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45
Q

Treatment for ventricular septal defect

A

Palliative medical therapy - ACE inhibitors, symptomatic care
SURGERY REQURIED

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46
Q

What is the most common congenital cardiac defect in cats?

A

Ventricular septal defect

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47
Q

What is the most common congenital cardiac defect in dogs?

A

Patent ductus arteriosus

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48
Q

Tricuspid valve dysplasia

A

Congenital malformation of tricuspid valve caused by pathologic lesion to the valve
Usually leads to tricuspid regurgitation and right sided heart failure

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49
Q

Treatment for tricuspid valve dysplasia

A

Reduce preload - diuretics and ACE inhibitors
May need antiarrhythmics long term (CCBs, digoxin)
If ascites present may require abdominocentesis
Surgery possible

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50
Q

Mitral valve dysplasia

A

Can be from various causes - leaflet deformity adhering to adjacent structures, cleft leaflet, inappropraite length of chordae tendonae, abnormal valve annuls, or fibrous ring/membrane above valve
Often causes volume overload, dilation, hypertrophy of left atrium and ventricle - left sided heart failure

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51
Q

Treatment for mitral valve dysplasia

A

ACE inhibitors (reduce preload), diuretics and/or digitalis if needed

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52
Q

Tetraology of Fallot

A

Pulmonic stenosis, VSD, secondary right ventricular hypertrophy, overriding aorta

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53
Q

Treatment for tetraology of Fallot

A

Palliative medical management, surgery required

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54
Q

Pulmonic stenosis

A

Right ventricular outflow obstruction, more common in small breeds
Clinical signs of right sided heart failure

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55
Q

Feline hypertrophic cardiomyopathy

A

Disorder of myocardium with left ventricular hypertrophy and impaired myocardial relaxation
Decreased diastolic function
Leads to left atrial enlargement

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56
Q

What are some consequences of feline hypertrophic cardiomyopathy

A

Circulatory stasis, thormboembolism, pulmonary congestion and edema, pleural effusion

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57
Q

What are treatment options for feline hypertrophic cardiomyopathy?

A 
Increase diastolic function, decrease myocardial ischemia, decrease circulatory congestion and hypoxemia
Calcium channel blockers - diltiazem
Furosemide for congestion
Vasodilators (nitroglycerin)
ACE inhibitor
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58
Q

Canine dilated cardiomyopathy

A

Decreased myocardial contractility leading to end systolic ventricular volume increasing, increased chamber volume

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59
Q

What are treatment goals for canine DCM?

A

Decrease preload, decrease afterload, improve contractility
Loop diuretics, vasodilator, dobutamine in emergency
Calcium channel blockers and beta blockers contraindicated

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60
Q

Which drug classes are contraindicated in DCM? Why?

A

Calcium channel blockers, beta blockers

Negative inotropes

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61
Q

Degenerative valvular disease

A

Most common cardiac disease in dogs

Mitral valve regurgitation or tricuspid valve regurgitation

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62
Q

What is the treatment for degenerative valvular disease

A

ACE inhibitors for vasodilation
Calcium channel blockers
Diuretics in case of edema

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63
Q

Infective endocarditis

A

Bacteria colonization of heart valves

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64
Q

Heartworm disease

A

Result of infection with Dirofilaria immitis

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65
Q

Potential complications of heartworm disease

A

Caval syndrome, obstruction of pulmonary circulation (leads to pulmonary hypertension), death, PTE

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66
Q

What is the treatment for heartworm disease

A

Doxycycline, immitacide, crate rest

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67
Q

Caval Syndrome

A

Large number of adult heartworms lodged in cranial and caudal vena cava and right atrium

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68
Q

ECG - undulating baseline with no normal p waves
Irregularly irregular R-R intervals
Normal - wide QRS complexes

A

Atrial fibrillation

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69
Q

Treatment for atrial fibrillation

A

Cardioversion, digoxin, calcium channel blockers

70
Q

ECG - Tachycardia, rhythm is regular and extremely fast, p waves may be regular or irregular but often hard to locate, can be continuous or paroxysmal

A

Supraventricular tachycardia

71
Q

Treatment for supraventricular tachycardia

A

Vagal maneuver, or calcium channel blocker, beta blocker, digoxin, diltiazem

72
Q

ECG - Pause between two normal complexes >2x normal R-R interval

A

Sinus arrest

May be normal in brachycephalic dogs

73
Q

ECG - Absence of P waves, wide bizarre QRS complexes, and bradycardia

A

Atrial standstill

74
Q

What causes atrial standstill?

A

Hyperkalemia >7.5mEq/L

Addison’s disease, anuric/oliguric renal failure, DKA, metabolic acidosis, UO, ruptured bladder

75
Q

Treatment of atrial standstill

A

IV dextrose, +/- insulin, IV bicabonate, calcium gluconate

76
Q

ECG - Prolonged P-R interval, normal rate and rhythm

A

First degree AV block

77
Q

What are some causes for first degree AV block?

A

Digitalis - most common

Any drug that delays AV conduction, hyperkalemia, increased vagal tone, myocarditis, doxorubicin, cardiomyopathies

78
Q

ECG - Progressively prolonging P-R interval until dropped beat occurs, after several prolonged beats P wave with no QRS

A

Second Degree AV block - Mobitz type 1 (Wenckebach)

79
Q

ECG - Consistent PR intervals, intermittent p wave with no QRS

A

Second degree AV block - Mobitz type 2

80
Q

Which type of second degree AV block is more serious?

A

Type 2

More likely to progress to third degree, more likely to cause reduced cardiac output

81
Q

What causes second degree AV block type 1?

A

Increased vagal tone, fibrosis, some drug/electrolyte imbalances

82
Q

ECG - Consistent P-P interval, consistent R-R interval, irregular P-R interval

A

Third degree AV block

Atria and ventricles acting independently of one antoher

83
Q

ECG - Bidirectional saw toothed atrial complexes, tachycardia

A

Atrial fluttter

84
Q

ECG - Premature P waves, QRS normal or abnormal

A

Atrial premature complexes

85
Q

Sick sinus syndrome

A

Any combination of sinus bradycardia, sinus arrest, SA block, vary/alternating brady/tachycardia, SA/AV conduction issues

86
Q

What breeds are predisposed to sick sinus syndrome?

A

Mini schnauzer, cocker spaniel, dachshunds, pugs, west highland terriers
Usually older females

87
Q

What is the treatment for sick sinus syndrome

A

Check atropine response -
If atropine responsive isoproteronol
If not atropine responsive, pacemaker required

88
Q

Heart rate is controlled by?

A

Sympathetic nervous system

89
Q

Heart failure

A

Inability to meet metabolic needs of peripheral tissues or instances when heart can only do so in presence of increased venous filling pressures

90
Q

Describe renin-angiotensin-aldosterone system

A

Inability of the heart to provide normal renal perfusion leads to decreased renal blood flow and Na delivery to distal portion of nephron which induces renin release
Renin converts angiotensinogen into angiotensin I
Angiotensin I is converted to angiotensin II by ACE in pulmonary vasculature
Angiotensin II used in responses that promote cardiac injury and heart failure (renal sodium and water retention, production of aldosterone, thirst, vasoconstriction)
RAAS activation causes retention of fluid and myocardial and vascular remodeling

91
Q

What causes renin release?

A

Decreased renal blood flow and Na delivery to distal portion of nephron

92
Q

What does renin do in the body?

A

Converts angiotensinogen to angiotensin I

93
Q

What is the significance of angiotensin I?

A

Converted into angiotensin II by angiotensin converting enzyme (ACE) in pulmonary vasculature

94
Q

What is the role of angiotensin II in the body?

A

causes renal sodium and water retention, production of aldosterone, myocardial apoptosis, cardiac and vascular remodeling/fibrosis, thirst, vasoconstriction

95
Q

How is angiotensin II produced?

A

Both by being converted from angiotensin I into angiotensin II by ACE
AND by independent generation - can be elevated despite ACE inhibitor therapy

96
Q

What is the role of aldosterone in the RAAS system

A

Contributes to further retention of water and sodium in the body

97
Q

What are the main effector molecules of the sympathetic nervous system?

A

Epinephrine and norepinephrine

98
Q

What is the purpose of the sympathetic nervous system?

A

Evolutionary response to stress

Increase HR, CO, blood flow increase to stress-response organs (skeletal muscle)

99
Q

What is the natriuretic peptide system?

A

Two hormones produced by myocardial tissue - induce natriuresis, diuresis, and vasodilation
Atrial natriuretic peptide and b-type natriuretic peptide (ANP & BNP)
Produced in response to stretch or stress of myocardial tissue
Counter regulatory system to RAAS and SNS

100
Q

What is endothelin 1?

A

Vasoconstrictor produced by vascular endothelial cells in response to stress, angiotensin II, and other cytokines
Alters Ca cycling in muscles

101
Q

What is arginine vasopressin?

A

Antiduretic hormone

Increases reabsorption of free water in renal collecting duct

102
Q

What happens in a normal heart if preload increases?

A

Cardiac contraction increases

103
Q

What can happen in a diseased heart if preload increases too much?

A

Cardiac contraction does not improve - excess preload leads to CHF
Poor contractility leads to low output heart failure

104
Q

Generally, what are causes of diastolic heart dysfunction?

A

Primary impairments of ventricular filling, relaxation, compliance, or secondary to pericardial disease

105
Q

What are the four clinical stages for grading heart failure?

A

Class A - overtly healthy animals at risk for developing heart disease (Dobermans >4 yrs, adult Maine Coons)
Class B - Diagnostic evidence of heart disease without clinical signs
- Asymptomatic
-Class B1 - No radiographic or echocardiographic changes
-Class B2 - Radiographic or echocardiographic changes
Class C - Cardiac remodeling and current or historical signs of heart failure
Class D - Severe and debilitating signs of heart failure -even at rest

106
Q

Most dogs and cats develop (low output or congestive failure)?

A

Congestive failure

107
Q

Congestive heart failure clinical signs

A

Pulmonary edema, effusion, ascities, increased RR/RE, coughing, activity intolerance, abdominal distention

108
Q

Low output heart failure clinical signs

A

Weakness, depression, cardiogenic shock, syncope, hypotension, hypothermia, oliguria/anuria, lactic acidosis

109
Q

How is low output heart failure treated

A

Positive inotropes

110
Q

Causes of left sided heart failure in dogs

A

Degenerative mitral valve disease, DCM, patent ductus arteriosus

111
Q

Causes of left sided heart failure in cats

A

Hypertrophic and restrictive cardiomyopathy

Pleural effusion

112
Q

Causes of right sided heart failure in dogs

A

DCM, degenerative or congenital tricuspid valve disease, pulmonary hypertension

113
Q

Causes of right sided heart failure in cats

A

Rare. Even if ascites, usually non-cardiac in origin

114
Q

Forward flow failure with hypoperfusion

A

Cardiogenic shock

115
Q

Cardiac output

A

Stroke volume x heart rate = cardiac output

116
Q

Stroke volume

A

Preload x afterload x contractility

117
Q

Clinical signs of cardiogenic shock

A

Altered mentation, pale MM, prolonged CRT, cool extremities, tachycardia

118
Q

Which metabolic abnormality is often seen on blood gas results of a patient in cardiogenic shock?

A

Metabolic acidosis, often compensated with respiratory alkalosis
Due to poor cellular oxygenation leading to anaerobic metabolism

119
Q

One possible cause of increased A-a gradient in cardiogenic shock?

A

Pulmonary edema

120
Q

Radiographic signs of CHF

A

Enlarged pulmonary veins, alveolar or interstitial pattern in perihilar region of dogs
Cats patchy lung pattern and pleural effusion

121
Q

What is the most common cause of cardiogenic shock from systolic dysfunction?

A

Dilated cardiomyopathy

122
Q

What dog breeds are predisposed to DCM?

A

Boxer, Great Dane, Labrador, Cocker Spaniel, Doberman

123
Q

Is DCM a failure of flow or contractility?

A

Flow. Forward failure. Decreased myocardial contractility leads to decreased stroke volume

124
Q

What is the treatment for cardiogenic shock when caused by DCM?

A

Maximize CO by increasing SV
Monitor preload closely, diuretics for left sided failure, positive inotropes (dobutamine), Phosphodiesterase inhibitors (amrinone, pimobendan), cardiac glycossides

125
Q

What can happen with the heart in sepsis to cause cardiogenic shock

A

Decreased ejection fraction caused by decreased contractility, biventricular dilation, and reduced ventricular compliance

126
Q

When does myocardial dysfunction peak in sepsis?

A

Within days of onset

127
Q

When does myocardial dysfunction resolve in sepsis?

A

Within 7-10 days of resolution

128
Q

Endomyocarditis

A

Rare condition in cats - occurs within several days of routine anesthetic procedure
Cardiac dysfunction, hypotension, pulmonary edema, and interstitial pneumonia

129
Q

Mechanical failure of the heart in dogs and cats

A

Rare. Possible chordae tendonae rupture. May have reduction of forward flow from left ventricular outflow obstruction (aortic stenosis or HCM)

130
Q

Diastolic failure occurs due to?

A

Inadequate ventricular filling (decreased preload)

131
Q

When is a fluid bolus warranted in a patient with cardiogenic shock?

A

If cardiogenic shock due to cardiac tamponade

132
Q

What causes cardiogenic shock in cardiac tamponade?

A

Decreased diastolic filling leading to decreased SV and CO

Inability to continue to compensate with tachycardia leads to severe hypotension and cardiovascular collapse

133
Q

What is the most commonly diagnosed feline cardiac disease?

A

Hypertrophic cardiomyopathy

134
Q

What type of flow failure happens in HCM?

A

Backward flow failure

135
Q

How does HCM cause cardiogenic shock

A

Decreased end-diastolic ventricular volume - leads to decreased SV and CO

136
Q

What is the most common tachyarrhythmia to cause cardiogenic shock?

A

Supraventricular tachycardia

137
Q

Which are the most common bradyarrhythmias to cause cardiogenic shock?

A

Second or third-degree AV block and severe sick sinus syndrome

138
Q

Systolic heart failure

A

Defect in pumping or contractile function of heart

139
Q

Diastolic heart failure

A

Defect in filling or relaxation function of heart

140
Q

Forward heart failure

A

Decreased CO results in inadequate delivery of blood to arterial system. Leads to reduced organ perfusion, accumulation of plasma volume, and ECF.

141
Q

Backward heart failure

A

Elevated filling pressures - causes increased pressure in left atrium and pulmonary vasculature. Elevated capillary hydrostatic pressure, pulmonary edema, if right sided heart disease may lead to ascites

142
Q

Primary causes of ventricular (systolic) failure

A

DCM, arrhythmogenic right ventricular cardiomyopathy

143
Q

What other cardiac diseases may cause ventricular failure?

A

Chronic volume or pressure overload, congenital disease like PDA or VSD, or chronic valve disease

144
Q

What are possible extracardiac causes of ventricular failure?

A

Sepsis, cardiotoxic drugs, nutritional deficiency, myocarditits

145
Q

Which disease processes may cause true myocardial infarction in animals?

A

In hypercoagulable or hyperfibrinolytic states. End-stage feline or canine cardiomyopathy

146
Q

What are clinical signs consistent with ventricular failure?

A

May be consistent with right, left, or both side heart failure

147
Q

Dobutamine has what effect?

A

Positive inotrope with peripheral vasodilation

148
Q

Dopamine has what effect?

A

Low dose - positive inotrope with peripheral vasodilation, higher doses peripheral vasoconstriction

149
Q

Treatment goals for ventricular failure

A

Support contractility, relieve congestion, suppressing arrhythmia, maximize cardiac output

150
Q

What type of heart diseases do cats usually get?

A

Myocardial diseases. Rare for valve, pericardial, or conduction disease

151
Q

Hypertrophic cardiomyopathy

A

Primary heart muscle disease in which ventricular hypertrophy develops without cause

152
Q

Restrictive cardiomyopathy

A

Ventricular filing impaired in absence of myocardial hypertrophy or pericardial disease
Atrial enlargement associated with ventricle that has normal or near normal appearance

153
Q

Diastolic dysfunction

A

Happens when there is impaired myocardial relaxation and poor chamber compliance
Alters pressure volume relationship leading to high diastolic pressure with normal to low ventricular volume

154
Q

What is the predominant pathophysiologic mechanism responsible for signs in HCM and RCM?

A

diastolic dysfunction

155
Q

What is systolic anterior motion of mitral valve? Why is it significant?

A

Systolic anterior motion (SAM)
Occurs in 65% of cats with HCM
Movement of mitral leaflets leading to dynamic left ventricular outflow tract obstruction and concurrent mitral valve regurgitation
Associated with asymptomatic status in cats, most important cause of heart murmur in cats with HCM

156
Q

What is important about gallop rhythms in cats?

A

It is a more specific than a murmur for diagnosing cardiac disease

157
Q

Feline hypertrophic cardiomyopathy usually results in dilation of which chamber?

A

Left atrium - due to diastolic dysfunction and mitral valve regurgitation

158
Q

If a feline patient has respiratory signs and a normal left atrial size, what is the cause of the respiratory signs?

A

Difficult to say without more information but NOT due to cardiomyopathy

159
Q

What causes pseudohypertrophy?

A

Dehydration - causes temporary thickening of cardiac wall due to low volume within chambers

160
Q

Feline aortic thromboembolism often lodges where?

A

Usually lodges at aortic trifurcation

161
Q

Is FATE caused solely from arterial occlusion?

A

No, likely other vasoactive mediators released from thrombus decrease blood flow through collateral circulation and contribute to development of ischemia

162
Q

What is the role of furosemide or nitroglycerin in treatment of congestive heart failure?

A

Reduces preload but does not improve cardiac performance

163
Q

What are treatment goals for long-term management of feline chronic heart failure?

A

Slow heat rate, speed myocardial relaxation

164
Q

What types of cardiomyopathies are most common in dogs?

A

Dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy
Hypertrophy cardiomyopathy has been reported

165
Q

What type of dog is arrhythmogenic cardiomyopathy reported in?

A

Boxers

166
Q

What dog breeds most commonly get dilated cardiomyopathy

A

Dobermans, dalmatians, Portuguese water dog, cocker spaniel, giant breeds

167
Q

What breed of dog gets pediatric onset dilated cardiomyopathy?

A

Portuguese water dogs

168
Q

Do dogs with DCM have a significant heart murmur?

A

Often no, usually low grade (I-III/VI)

169
Q

What might be auscultated on a dog with DCM?

A

Low grade murmur along with A-Fib or APCs or VPCs, tachycardia

170
Q

What medications are used for long-term treatment of DCM?

A

Diuretics PRN, ACE inhibitors, Digoxin, Pimobendan, pimobendan

171
Q

How many VPCs daily warrants treatment of ARVC?

A

> 500-1000

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