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ACVIM: SAIM Specialty boards study 2023 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What disease accounts for 75% of cardiac cases in North America?

A

MMVD

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2
Q

What signalment of dog is more commonly affected with MMVD?

A

Males (1.5x), less than 20kg (85% show valve lesions by age 13)

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3
Q

What changes lead to progressive deformation of the valve structure in MMVD?

A

Dysregulation of the extracellular matrix
- Changes in collagen content and alignment of collagen fibrils
- Expansion of the spongiosa layer with changes in proteoglycans
Valvular interstitial cells aquire properties of activated myofibroblasts => increase in proteolytic enzymes (MMPs), which degrade collagen and elastin

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4
Q

What factors are moderately predictive of MMVD progression and can help identify dogs at risk for heart failure?

A
  • Progressive enlargement of the LA and LV
  • Increased transmitral E wave blood flow velocity
  • Increased NT-proBNP
  • Increased resting heart rate
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5
Q

What does the term heart failure refer to?

A

Clinical signs caused by heart dysfunction

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6
Q

What is “backward” heart failure?

A
  • AKA congestive heart failure
  • The heart fails to drain the veins adequately => increase in venous pressures => accumulation of fluid in the lungs or body cavities
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7
Q

What is “forward” heart failure?

A
  • The heart’s pumping ability is compromised such that it cannot meet the body’s demands during exercise or at rest
  • May or may not occur with backward heart failure
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8
Q

What is stage A MMVD?

A

Dogs at high risk for developing heart disease, but have no identifiable structural abnormalities (i.e. all Cavies without heart murmurs)

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9
Q

What is stage B MMVD?

A

Dogs with structural heart disease (murmur, etc) that have never developed clinical signs of heart failure

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10
Q

What is stage B1 MMVD?

A

Asymptomatic dogs with no radiographic or echocardiographic evidence of cardiac remodeling OR remodeling is present but mild (does not need criteria for treatment)

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11
Q

What is stage B2 MMVD?

A
  • Asymptomatic dogs that have more advanced mitral regurgitation (hemodynamically severe) => radiographic and echocardiographic left atrial and ventricular enlargement
  • Meet the criteria for treatment to delay the onset of CHF
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12
Q

What is stage C MMVD?

A

Dogs with current or past clinical signs of heart failure

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13
Q

What is stage D MMVD?

A

Dogs with end-stage MMVD - clinical signs of CHF are refractory to standard treatment and required advanced or specialized treatment strategies

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14
Q

How should patients with stage A MMVD be monitored?

A

Yearly physical examination with cardiac auscultation

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15
Q

If a murmur is identified during a routine examination, what diagnostics are always recommended?

A
  • Thoracic radiographs - look for evidence of cardiac enlargement (use vertebral left atrial size) and establish a baseline for the patient’s appearance before CHF develops
  • Blood pressure
  • Echocardiogram, if possible
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16
Q

When should an echocardiogram be repeated in dogs with MMVD stage B1?

A

6-12 months (potentially more frequent in large breed dogs, as the disease progresses faster)

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17
Q

What are the criteria for meeting MMVD stage B2?

A
  1. Murmur greater than or equal to 3/6
  2. LA:Ao ratio in the right sided short axis view in early diastole >1.6
  3. Left ventricular internal diameter in diastole >1.7
  4. Breed adjusted VHS >10.5 (or greater than 11.5 if echo cannot be performed)
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18
Q

How is the vertebral left atrial score measured?

A
  • Draw a line from the most ventral aspect of the carina to the the dorsal border of the caudal vena cava (the most caudal aspect of the LA)
  • Transpose that line to the cranial edge of the 4th thoracic vertebral body
  • > 3 likely = stage B2 MMVD
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19
Q

What are the treatment recommendations for MMVD stage B2?

A
  • Pimobendan (0.25-0.3mg/kg PO q12)
  • Mild dietary sodium restriction, highly palatable diet with adequate protein
  • ACEi is recommended by 5/10 panelists
  • Surgical valve repair can be considered
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20
Q

What two medications are currently not recommended for MMVD B2 patients?

A

Beta blockers, spironolactone - evidence is lacking

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21
Q

Name 3 potential complications of chronic mitral regurgitation

A
  • Pulmonary hypertension
  • Acquired atrial septal defect
  • Pericardial effusion from an atrial tear
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22
Q

What dose of furosemide should be given to a hospitalized patient with CHF? When should it be repeated?

A
  • 2mg/kg IV or IM
  • Repeated doses of 2mg/kg hourly until the respiratory signs improve OR a total dose of 8mg/kg over 4 hours is reached
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23
Q

When should a furosemide CRI (1mg/kg/hr) be considered after the initial 2mg/kg bolus?

A

Life threatening pulmonary edema
- Expectoration of froth with severe dyspnea
- Radiographic “white out”
- Poor response to the initial furosemide bolus

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24
Q

Apart from furosemide, what other treatments are recommended for hospitalized patients with CHF?

A
  • Pimobendan 0.25-0.3mg/kg q12
  • Oxygen supplementation if needed
  • Abdominocentesis or thoracocentesis, if needed
  • Sedation to help with anxiety associated dyspnea (narcotics, anxiolytic agents)
  • ACEi
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25
Q

In hospitalized CHF patients that are failing to respond to normal treatments, what drug may be considered? Why? What should be monitored during administration?

A
  • Dobutamine - increased LV function
  • Monitor ECG, decrease dose if tachycardia or ectopic beats occur
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26
Q

In hospitalized CHF patients with life threatening pulmonary edema that is not responding to standard treatments, what drug may be considered?

A

Sodium nitroprusside CRI for up to 48 hours

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27
Q

What is the dose of torsemide compared to furosemide?

A

5% to 10%
- For example, if at home furosemide is 2mg/kg q12, may give 0.1-0.3mg/kg torsemide q24

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28
Q

A patient is considered stage D if what dose of furosemide is needed to control clinical signs?

A

> 8mg/kg q24 (or torsemide equivalent) with appropriate doses of pimobendan, ACEi, and spironolactone

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29
Q

When should a chemistry panel be performed after starting furosemide or ACEi therapy?

A

3-14 days

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30
Q

What clinical sign has the best predictive value for impending clinical decompensation in a controlled CHF patient?

A

Increased resting respiratory rate above normal baseline

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31
Q

In patients with atrial fibrillation, what drugs are used to control ventricular rate? What is the goal heart rate?

A
  • Diltiazem +/- digoxin
  • <125 BPM
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32
Q

What should the maintenance calorie intake be in patients with stage C MMVD?

A

60kcal/kg (~RER x2)

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33
Q

What drugs may be used to reduce afterload in patients with stage D MMVD?

A

Hydralazine or amlodipine

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34
Q

What clinical signs should raise concern for pulmonary hypertension in dogs with primary left sided heart disease?

A

Ascites, jugular distension

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35
Q

In the EPIC trial, dogs treated with pimobendan developed CHF in how many days compared to placebo?

A

Pimo 1228 days, Placebo 766 days
So essentially prolonged the preclinical period by 15 months
Hazard ratio 0.64

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36
Q

What is the definition of a cardiomyopathy?

A

A myocardial disorder in which the heart muscle is structurally and functionally abnormal WITHOUT other cardiovascular disease capable of causing these changes (MMVD, etc)

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37
Q

What is hypertrophic cardiomyopathy?

A

Diffuse or regional increased LV wall thickness without LV chamber dilation

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38
Q

What characterizes the endomyocardial form of restrictive cardiomyopathy?

A
  • Prominent endocardial scar that bridges the interventricular septum and LV free wall
  • May cause fixed, mid-LV obstruction, LV apical thinning or aneurysm
  • LA or biatrial enlargement common
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39
Q

What characterizes the myocardial form of restrictive cardiomyopathy?

A
  • Normal LV dimensions (including wall thickness) with LA or biatrial enlargement
  • Increased wall rigidity leads to diastolic dysfunction
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40
Q

What characterizes arrhythmogenic cardiomyopathy?

A
  • Severe RA and RV dilatation, RV systolic dysfunction, RV wall thinning
  • Left heart can be affected
  • Arrhythmias and right sided CHF common
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41
Q

What mutation causes HCM in Maine Coons?

A

A31P mutation in the myosin binding protein C (MyBPC3 gene)

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42
Q

What mutation causes HCM in Ragdoll cats?

A

R820W mutation in the myosin binding protein C (MyBPC3 gene)

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43
Q

What is the 5 year cumulative incidence of cardiac mortality in cats with HCM?

A

23% - so most cats are subclinical

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44
Q

What factors are associated with longer survival times in HCM cats with CHF?

A
  • Cause of CHF: iatrogenic (IV fluids, general anesthesia, corticosteroids) do better than cats that develop CHF naturally
  • Greater decrease in NT-proBNP concentrations during hospitalization
  • Resolution of CHF at reexamination
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45
Q

How should the results of genetic testing influence breeding in Maine Coon or Ragdoll cats?

A
  • Cats homozygous for mutations should not be bred
  • Cats that are heterozygous but have other outstanding characteristics may be bred to genotype negative cats
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46
Q

A palpable thrill (grade 5-6/6 murmur) in cats is most likely to be associated with what?

A

Congenial malformations - rarely appreciated in HCM

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47
Q

What point of care test has reasonable diagnostic accuracy for differentiating between cardiac and non cardiac causes of respiratory distress in cats?

A

NT-proBNP

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48
Q

What cardiac biomarker is prognostic in cats with HCM, independent of left atrial size?

A

Cardiac troponin I - increases are associated with increased risk of cardiovascular death

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49
Q

For most normal sized cats, what is a normal end diastolic LV wall thickness?

A

<5mm
>6 mm = hypertrophy

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50
Q

When echocardiography is not available, what test can be used to screen cats for HCM? How do you interpret the results?

A
  • NT-proBNP: increased = clinically significant heart disease is likely and an echocardiogram is recommended
  • May be normal in early HCM (without LA enlargement), so it does not tell you that a cat is free of the disease
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51
Q

In older cats with heart murmurs, gallop sounds or arrhythmias, what tests should be performed?

A
  • Serum T4
  • Blood pressure
  • Echo
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52
Q

What are the radiographic findings of CHF in cats?

A
  • Pulmonary infiltrates
  • Cardiomegaly
  • LA enlargement and distended pulmonary vessels are inconsistently identified in cats!
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53
Q

For cats with stage B1 cardiomyopathy, how frequently is monitoring recommended?

A

Annual echocardiogram

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54
Q

What is the clinical significance of dynamic left ventricular outflow tract obstruction in HCM cats?

A
  • No evidence for increased morbidity/mortality
  • Atenolol does not increase the 5 year survival rate in cats with subclinical HCM
55
Q

What drug was more effective in preventing ATE in cats that had survived a previous ATE episode?

A

Clopidogrel&raquo_space;» aspirin

56
Q

In two randomized, placebo controlled clinical trials, what drugs had no effect on LV mass or diastolic function in cats with subclinical HCM?

A

ACEi or spironolactone

  • Note: No studies on pimobendan in subclinical cats
57
Q

Ventricular ectopy is common in cats with HCM. What drug can be used for treatment?

A

Atenolol or sotalol

58
Q

When should pimobendan be considered in cats with CHF?

A

In cats with signs of low cardiac output (hypotension, hypothermia, bradycardia) without DLVOTO

59
Q

When should cats with CHF be re-evaluated after discharge from hospital?

A

3-7 days - evaluate for resolution of CHF, renal function, electrolytes

60
Q

In cats, did benazepril delay the onset of treatment failure in cats with CHF?

A

Not in the randomized, placebo controlled study

61
Q

What nutrient deficiency results in DCM in cats?

A

Taurine

62
Q

What treatment is recommended for cats with ATE?

A
  • Clopidogrel + heparin or an oral anti-Xa inhibitor
  • Thrombolytic treatment NOT recommended
63
Q

What are the most common congenital heart defects in dogs? Cats?

A

Dogs - PDA, PS > SAS
Cats - VSD others depend on the survey

64
Q

What heart murmur is appreciated with a reverse PDA?

A
  • Often none due to severe pulmonary hypertension
  • Can often hear a tympanic or split second heart sound
65
Q

Hyperkinetic pulses are felt with what type of disorders?

A

Abnormal diastolic run off and low arterial diastolic pressure - PDA, severe aortic regurgitation

66
Q

What is Eisenmenger’s syndrome?

A

Circumstances where increased pulmonary vascular resistance causes reversal of left to right shunt development => cyanotic heart disease

67
Q

What factors may lead to the development of Eisenmenger’s syndrome?

A

Physiology not completely known, but likely shear stress caused by high flow rates in the pulmonary vasculature leads to proliferative changes in the vessel walls => increased resistance

68
Q

In dogs, Eisenmenger’s syndrome usually develops before what age?

A

6 months
Cats can be older

69
Q

How is Eisenmenger’s syndrome treated?

A
  • Some response can occur with sildenafil (pulmonary vasodilation).
  • However, if plexiform lesions are present, they are not reversible. Closure of the shunt may force the RV to work against high pulmonary resistance => RV failure, circulatory collapse and death
70
Q

What is the primary cause of morbidity and mortality in patients with right to left shunting? When does it occur?

A
  • Hyperviscosity syndrome => thrombosis, microvascular complications
  • Occurs when the PCV > 68%
71
Q

How does exercise worsening right to left shunting?

A

Exercise promotes systemic arteriolar vasodilation => decreased systemic vascular resistance => worse right to left shunting

72
Q

In cases of RV hypertrophy and VSD, why does tachycardia/sympathetic tone increase the magnitude of R to L shunting? What treatment may help?

A
  • Worsens dynamic obstruction of the right outflow tract from hypertrophy, increasing resistance to RV ejection
  • Beta-adrenergic blocking drugs can help (especially in Tetralogy of Fallot patients)
73
Q

Name 5 congenital differentials for right to left shunting

A
  1. Tetralogy of Fallot
  2. Transposition of the great vessels
    With elevated right sided pressures:
  3. PDA
  4. VSD or ASD
  5. PS or TVD with a patent foramen ovale
74
Q

Visible cyanosis occurs when the partial pressure of arterial oxygen drops below what?

A

45 mmHg

75
Q

A splintered QRS complex is indicative of what congenital heart disease?

A

TVD

76
Q

What other cardiac arrhythmia has been noted in Labs with TVD?

A

Ventricular pre-excitation and re-entrant supraventricular tachycardia

77
Q

What embryonic structure does the ductus arteriosus develop from? What is its function?

A
  • Left sixth aortic arch
  • Shunts unoxygenated blood from the pulmonary artery through the descending aorta to the placenta, where the blood is oxygenated
  • So the majority of the RV output is diverted away from the nonfunctional fetal lungs
78
Q

Why does the ductus arteriosus close at birth?

A
  • Breathing => decrease in pulmonary vascular resistance => reversal in the flow through the ductus
  • Rising arterial oxygen tension inhibits local prostaglandin release => constriction of the vascular smooth muscle and closure
79
Q

How long does the ductus arteriosus take to close?

A

Fully closed by 7-10 days old

80
Q

What is a ductus diverticulum?

A
  • A mild form of PDA, where the vessel completely closes at the pulmonary arterial end, resulting in a blind pocket in the ventral aspect of the aorta
  • Not clinically significant, but the dog likely carries the genes for PDA
81
Q

In the most common form of PDA, which direction does the blood flow? What does this lead to?

A
  • From the aorta to the pulmonary artery (high to low pressure)
  • In these cases, the PDA is funnel shaped, with the smaller end at the pulmonary artery
  • Causes pulmonary overcirculation => higher LV stroke volume => eccentric hypertrophy of the LV
  • RA and RV will be normal in size
82
Q

In a reverse PDA, what direction is the blood flowing? What does this lead to?

A
  • From the pulmonary artery to the aorta
  • In this case, the PDA is cylindrical, not funnel shaped, so there is no resistance to flow and the aortic and pulmonary pressures equilibrate
  • RV hypertrophy occurs, but do to diminished pulmonary flow, the LA and LV are normal in size
83
Q

What is the only congenital heart defect where there is a published sex predisposition for females?

A

PDA

84
Q

Describe the murmur with a PDA

A

Continuous murmur, loudest over the pulmonary artery in the left axially region. May palpate a thrill here as well

85
Q

What is a “ductus bump” on thoracic radiographs?

A

Aortic bulge followed by abrupt narrowing of the descending aorta

86
Q

What form of cyanosis is commonly with a reverse PDA? Why?

A
  • Differential cyanosis
  • The PDA shunts deoxygenated blood from the pulmonary artery to the descending aorta, sparing the proximal branches of the aorta, which provide normal oxygen to the cranial portion of the body
87
Q

Flow across an ASD occurs primarily during what phase of the cardiac cycle?

A

Ventricular diastole

88
Q

Flow across a VSD occurs primarily during what phase of the cardiac cycle?

A

Ventricular systole

89
Q

What cardiac structural changes occur with a left-to-right ASD?

A
  • Dilation of the RA, eccentric hypertrophy of the RV
  • No or only mild change to the LA as most of the blood shunts to the right side again
90
Q

Subvalvular PS has been associated with abnormal development of what arteries, especially in Bulldogs and Boxers?

A

Coronary arteries - both left and right coronary arteries branch from a single large coronary artery arising from the right aortic sinus of Valsalva

91
Q

Why is it important to rule out coronary abnormalities before balloon valvuloplasty in dogs with subvalvular PS?

A

Balloon dilation can lead to rupture of the left coronary artery and sudden death

92
Q

What structural cardiac abnormalities develop due to PS?

A
  • RV concentric hypertrophy due to increased resistance to ejection and increase in ventricular systolic pressure
  • Post-stenotic dilation of the main pulmonary artery as the turbulent jet of blood decelerates and expends energy against the vessel wall
93
Q

What structural cardiac abnormalities develop due to SAS?

A
  • LV concentric hypertrophy
  • Abnormal coronary blood flow in severe cases => focal areas of myocardial infarction and fibrosis in the papillary muscles and subendocardium - may lead to malignant arrhythmias and sudden death
94
Q

Dogs with mild SAS (pressure gradient <50 mmHg) may lead normal lives. What treatment is recommended?

A
  • Prophylactic antibiotics during anticipated periods of bacteremia - dentals, surgery, infectious disease
95
Q

Does balloon dilation of SAS improve the severity of obstruction or MST?

A

Severity improves by up to 50% but no improvement in survival vs medical treatment with atenolol

96
Q

What are the defining anatomic features of Tetralogy of Fallot?

A
  • RV outflow obstruction due to infundibular obstruction
  • Secondary RV hypertrophy
  • Large perimembranous VSD
  • Rightward positioned aorta (dextroaorta)
97
Q

What direction does blood shunt in Tetralogy of Fallot?

A

Right to left through the VSD

98
Q

What are the common causes of pericardial effusion in cats?

A
  • Most common: CHF secondary to HCM
  • Neoplasia (lymphoma, thymoma, etc)
  • FIP
99
Q

In dogs >15kg with MMVD, how did the development of atrial fibrillation affect outcomes?

A
  • AF increased risk of cardiac death (HR = 2.5)
  • MST was longer for dogs who achieved rate control (<160 bpm, 171 days vs 61 days)
  • However, MST for any dog with AF was lower than for dogs without (142 vs 234 days)
100
Q

In dogs >15kg with MMVD, what drugs were most effective in controlling atrial fibrillation?

A
  • Combination diltiazem and digoxin significantly improved MST over diltiazem alone
101
Q

Measurement of POC NT-proBNP in what sample can help distinguish cardiac from non-cardiac causes of pleural effusion in cats?

A

Plasma
NOT pleural effusion - specificity sucks on the POC test

102
Q

Which adipokine is higher in dogs with MMVD? Which is lower?

A

Leptin = higher
Adiponectin = lower

103
Q

A significant, direct correlation exists between MMVD stage and what other chronic disease condition?

A

CKD - MMVD stage correlates with IRIS staging

104
Q

The prevalence of CKD was how much higher in dogs with MMVD than in the normal population?

A

25% vs 5-15%, depending on the study

105
Q

What effect did treatment with pimobendan have on heart size in dogs with MMVD?

A
  • At day 35, heart size was reduced (both LVIDDN and La:Ao)
  • Associated with an increased time to CHF
  • When the dogs receiving pimobendan did go into CHF, their hearts had become larger again (no change from placebo)
106
Q

In dogs with atrial fibrillation, every 10 bpm increase in HR incensed the risk of all cause mortality by what percent?

A
  • 35%
  • Dogs with HR <125 lived significantly longer
107
Q

What was the MST of dogs after the diagnosis of advanced (stage D) heart failure? What was associated with longer survival?

A
  • 281 days
  • Dogs receiving higher doses (>6.7 mg/kg/day) of furosemide lived longer
108
Q

In cats with preclinical HCM, what percent will eventually develop CHF or ATE?

A

30%

109
Q

Are cats with HOCM at higher risk for cardiovascular morbility/mortality than cats with HCM?

A

No

110
Q

Dogs with cardiac cachexia were more likely to have what PE findings and clinicopathologic abnormalities?

A
  • Cardiac arrhythmias
  • Higher chloride
  • Lower hematocrit
  • Lower albumin
111
Q

In dogs with CHF, what factors are associated with shorter survival time?

A
  • Cardiac cachexia, low BCS or high BCS
  • Clinically important tachyarrhythmias
  • Azotemia
112
Q

What percent of dogs and cats with CHF display evidence of cardiac cachexia?

A

~40% for both

113
Q

Compared to furosemide, how did torsemide treatment affect outcomes in dogs newly diagnosed with CHF secondary to MMVD?

A
  • Torasemide was non inferior to furosemide for controlling new onset CHF
  • Torasemide significantly decreased risk of cardiac related death
114
Q

In dogs with DCM eating nontraditional diets, what effect did changing to a more traditional diet have?

A
  • Diet change lead to a larger percentage decrease in systolic LV internal dimension and La:Ao compared to dogs that did not change their diet
  • Diet change also lead to longe surgival (337 days vs 215)
115
Q

What percent of dogs with hyperadrenocorticism are hypertensive?

A

82% (severe in 46%)

116
Q

In dogs with hyperadrenocorticism, what clinicopathologic changes correlated with hypertension?

A
  • All dogs with thrombocytosis were hypertensive: platelet count >438K was 100% specific and 61% sensitive for hypertension
  • Dogs with UPC >0.5 had higher median SBP
117
Q

In dogs with pulmonary hypertension, what echocardiographic findings were associated with shorter survival?

A

Right atrial enlargement
Right sided CHF

118
Q

What is the mechanism of action of class I anti-arrhythmics? What are the subclasses?

A

Na channel blockers: block fast sodium channels, slowing conduction in fast-channel tissues (atrial and ventricular myocytes, Purkinje system)
- Class Ia: intermediate kinetics, also block repolarizing K channels and prolong the refractory period
- Class Ib: fast kinetics, not very potent
- Class Ic: slow kinetics

119
Q

When are class I anti-arrhythmic drugs indicated?

A
  • All: Ventricular tachyarrhythmias (V tach, V fib)
  • Class Ia and Ic: supra ventricular tachyarrythmias (A fib, A flutter, etc)
120
Q

Give 3 examples of class I anti-arrhythmic drugs

A

Class Ia: Procainamide
Class Ib: Lidocaine, mexiletine
Class Ic: Propafenone

121
Q

What is the mechanism of action of class II anti-arrhythmic drugs?

A

Beta blockers
- Primarily affect slow-channel tissues (SA and AV nodes)
- Decrease the rate of automaticity, slow condition velocity, and prolong refractoriness
- Slow HR, lengthen PR interval

122
Q

When are class II anti-arrhythmic drugs indicated?

A
  • Supraventricular tachycardia (A fib, A flutter, sinus tachycardia)
  • HOCM
123
Q

Name 2 class II anti-arrhythmics

A

Atenolol: beta1 specific
Propanolol: non-specific, poor bioavailability

124
Q

What is a potential side effect of class II anti-arrhythmias?

A

Bronchoconstriction if beta 2 activity is blocked

125
Q

What is the mechanism of action of class III anti-arrhythmics?

A
  • Potassium channel blockers
  • Prolong action potential duration and refractoriness in slow and fast channel tissues
126
Q

When are class III anti-arrhythmic drugs indicated?

A
  • Supraventricular tachycardias (A fib, A flutter)
127
Q

Name 2 class III anti-arrhythmics

A
  • Amiodarone
  • Sotalol (also beta blocker)
128
Q

What is the mechanism of action of class IV anti-arrhythmics?

A

Calcium channel blockers (non-dihydropyridine)
- Act on slow channel tissues to decrease conduction velocity, rate of automaticity, prolong refractoriness

129
Q

When are class IV anti-arrhythmic drugs indicated?

A
  • Supraventricular tachycardia (A fib, A flutter)
130
Q

Name a class IV anti-arrhythmics

A
  • Diltiazem
131
Q

What is the mechanism of action of digoxin?

A
  • Inhibits Na/K ATPase in the myocardium => increase in intracellular Na => decrease in the activity of the Na/Ca exchanger => increase intracellular Ca => increased contractility
  • Stimulates the parasympathetic nervous system to slow AV nodal conduction
  • Overall slows HR while increasing stroke volume
132
Q

What are two scenarios when digoxin may be used?

A
  • A fib
  • CHF
133
Q

Overall, what classes of anti-arrhythmics can be used to treat supraventricular tachycardias?

A

Class Ia, II, III (amiodarone), IV

134
Q

Overall, what classes of anti-arrhythmics can be used to treat ventricular tachycardias?

A

Class Ia, Ib, II, III (sotalol)

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