Cardiology Objectives Flashcards

(35 cards)

1
Q

Lecture 8

Formulate a differential diagnosis for syncope in dogs.

what about left basilar systolic heart murmurs?

A

Cardiac
* Tachyarrhythmia
* Bradyarrhythmia
* Low CO
Neurogenic
* Reflex-mediated or situational
Exertional syncope
Cyanotic heart disease
Drug-related
Hyperviscosity

  • Aortic Stenosis
  • (Subvalvular
  • Valvular
  • Mass obstruction)
  • Functional
  • (Elevated outflow velocity
  • Anemia
  • Thyrotoxicosis
  • Pyrexia)
  • Pulmonary valve stenosis
  • (Congenital
  • Secondary to increased flow (ASD))
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2
Q

Lecture 8

Characterize the diagnostic work-up for a dog with syncope. How would you prioritze testing?

A
  • Blood Pressure
  • Electrocardiogram
  • Echocardiogram
  • Bloodwork - CBC & Chemistry (+/- cardiac troponin I)
  • Splenic ultrasound
  • +/- Holter or Event Monitor
  • +/- Thoracic radiographs
  • (FNA of dermal masses)
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3
Q

Lecture 8

Describe the electrocardiographic features of ventricular
tachycardia. How do you determine from which ventricle a PVC is likely originating?

A

PVCs have a QRS that is wider and much different in appearance than the sinus complex

Starts in RV: depolarization along lead II; positive R
Starts in LV: depolarization direction oppositie lead II; negative S.

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4
Q

Lecture 8

Know the first line therapy for acute in-hospital treatment of ventricular tachycardia. At-home therapy options include…?

A
  • Intravenous antiarrhythmics
    – Lidocaine (sodium channel blocker), procainamide, amiodarone
  • Oral antiarrhythmics
    – Sotalol
    – Amiodarone
    – Mexiletine
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5
Q

Lecture 8

List 5 categories/causes of ventricular arrhythmias in dogs.

A
  • Heart disease
    – Cardiomyopathy, myocarditis, etc.
  • Endocrine / Metabolic
    – Thyroid excess, hypokalemia, etc.
  • Autonomic imbalance
    – Elevated sympathetic tone
  • Drugs/Toxins
    – Digoxin, cocaine, etc.
  • Systemic Issues
    – Splenic disease, GDV, sepsis, DIC, etc.
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6
Q

Lecture 9

What is the most common form of congenital heart disease in the dog?
in the cat?

A

PDA
VSD

VSD was googled

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7
Q

lecture 9

List 5 differentials for a loud systolic heart murmur in a puppy. Where
would the heart murmur be loudest for each differential?

A
  • Subaortic stenosis
    – Left heart base, poor femoral pulse
  • Pulmonary valve stenosis
    – Left heart base, normal pulse
  • Ventricular septal defect
    – Right thorax
  • Tricuspid valve dysplasia – regurgitation
    – Right apex
  • Mitral valve dysplasia – regurgitation
    – Left apex
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8
Q

lecture 9

Characterize the auscultatory features of an innocent/functional heart murmur.

A

Decreased blood viscosity, increased velocity from stress or athleticism, or unknown causes can all
result in an innocent heart murmur. Innocent or physiologic heart murmur often have characteristics that differ
from pathologic murmurs – innocent murmurs may be sensitive (changes with position / respiration), of short
duration (early systolic), single (no associated clicks/gallops), small (limited to a small area, does not radiate), soft (low amplitude), and systolic in timing. These six ‘S’s can help to decide if a murmur is of pressing concern or can
be monitored less intensively.

from spring 24 cardio lectures

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9
Q

lecture 9

Discuss the diagnostic strategy for evaluating a young dog or cat with a
loud heart murmur

A
  • Thoracic radiographs
  • Echocardiogram
  • Blood pressure
  • +/- Bloodwork
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10
Q

lecture 10

List differential diagnoses for a dog that is coughing.

A

§ Laryngeal disease
§ Tracheal disease (tracheal or bronchial
collapse)
§ Hilar lymphadenopathy
§ Left atrial enlargement, bronchial compression
§ Heart base mass or parenchymal neoplasia
§ Airway disease/Chronic bronchitis
§ Pneumonia
§ Congestive heart failure
§ Heartworm disease

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11
Q

lecture 10

What diagnostics may be helpful to further investigate the
cause of the cough?

A

THORACIC
RADIOGRAPHS
THORACIC
POCUS
+/- BLOOD
GAS
+/- ECHO

additional diagnostics for PH:
§ CBC, Chemistry panel, UA
§ Coagulation profile
§ Heartworm test
§ (Full assessment for possibility of hypercoagulable state)
§ Thoracic CT
§ Bronchoscopy

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12
Q

lecture 10

What are causes of pulmonary hypertension?

A

increased pulmonary blood flow
increased pulmonary vascular resistance
increased pulmonary venous pressure

  1. Pulmonary arterial hypertension
    a) Idiopathic, heritable, drugs/toxins
    b) Congenital cardiac shunts
  2. PH due to left heart disease
  3. PH due to respiratory disease, hypoxia, or both
  4. PH due to pulmonary thromboemboli (PTE)
  5. Parasitic disease (heartworm)
  6. Multifactorial causes or masses compressing PAs

More on PH due to respiratory disease
(Group 3)
§ Chronic obstructive airway disorders
§ Tracheal or mainstem bronchial collapse
§ Bronchomalacia
§ Primary pulmonary parenchymal disease
§ Interstitial lung disease
§ Infectious pneumonia
§ Diffuse pulmonary neoplasia
§ Obstructive sleep apnea
§ Chronic exposure to high altitude

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13
Q

lecture 10

Describe treatment strategies for a patient with pulmonary
hypertension.

A

§ Sildenafil or tadalafil
§ Phosphodiesterase 5 Inhibitor (PDE5 I)
§ Vasodilation of pulmonary arteries
§ 1-3 mg/kg PO q8hrs (sildenafil)
§ 1-2 mg/kg PO q24hrs (tadalafil)
§ Oxygen supplementation
§ Potent vasodilator
§ Sedation (butorphanol 0.2mg/kg IV or IM)
§ +/- Pimobendan (support right heart function)
§ Phosphodiesterase 3 Inhibitor (PDE3 I)
§ 0.25-0.3 mg/kg PO q12hrs

§ If group 2 – treat left heart disease
§ If group 3 - respiratory disease, hypoxia
§ Cough suppressants – hydrocodone
§ Treat secondary infection
§ Steroids
§ If group 4 – PTE
§ Tissue plasminogen activator (TPA)
§ Anticoagulants – heparin, apixaban,
rivaroxaban
§ Anti-platelet - clopidogrel

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14
Q

lecture 11

Describe abnormal physical exam findings that raise suspicion for
cardiomyopathy in the cat. What is a gallop sound and what is its
significance?

A

Pleural effusion
Gallop sound
Tachypnea
Weight loss

Gallop sound
◦ S3 or S4 heart sound audible
◦ S3 – vibration of ventricular walls during active
ventricular filling
◦ S4 – final ventricular filling by atrial contraction
in a poorly compliant ventricle
◦ Differentiate from systolic clicks and
split heart sounds

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15
Q

lecture 11

What diagnostics may you consider in a cat in respiratory distress in
which cardiac disease is suspected?

A

◦ Initial:
◦ Thoracic POCUS
◦ Consider point-of-care NTproBNP

◦ When stable:
◦ Thoracic radiographs
◦ Echocardiogram
◦ Bloodwork
◦ Blood pressure

consider a thoracocentesis if cat is in crisis

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16
Q

lecture 11

List three common causes of left ventricular concentric hypertrophy
in the cat.

A

HYPERTHYROIDISM
SYSTEMIC HYPERTENSION
PRIMARY HYPERTROPHIC
CARDIOMYOPATHY

17
Q

lecture 11

What is NT-proBNP and how do you interpret an elevated value?

A

◦ N-terminal pro B-type natriuretic peptide
◦ BNP is a hormone secreted by cardiomyocytes
that causes renal and sodium loss, as well as
vasodilation
◦ Production and excretion is increased in response
to stretch of the heart

18
Q

lecture 11

Be familiar with the staging of feline cardiomyopathy and treatment
for asymptomatic cats and cats in congestive heart failure (acute
and chronic therapy).

A

Stage A: no treatment, +/- monitor
Stage B1: no treatment, +/- atenolol
therapy if documented dynamic left ventricular outflow tract obstruction (DLVOTO)
Stage B2: * Consider clopidogrel
* +/- antiarrhythmics (atenolol or
sotalol) if concurrent ventricular arrhythmias
Stage C (CURRENT/PREVIOUS CHF OR ATE):
◦ Acute decompensated HF
◦ Furosemide
◦ 1-2mg/kg boluses IM or IV or
CRI
◦ Supplementary oxygen
◦ Sedation (butorphanol)
◦ +/- thoracocentesis

◦ Chronic heart failure
Furosemide (1-2mg/kg PO
q12hrs)
◦ Titrated to maintain resting RR
<30 breaths per minute
Clopidogrel (18.75mg/cat
PO q24hrs)
◦ Can be given in empty gelatin
capsule due to bitter taste
◦ +/- ACE inhibitor
◦ Diet low in sodium

Stage D: * If furosemide dose
> 6mg/kg/day PO, consider torsemide
(0.1-0.2 mg/kg PO
q24hrs)
* +/- spironolactone (1-2mg/kg PO q12-24hrs)
* Monitor for facial dermatitis
* +/- pimobendan if systolic dysfunction present

19
Q

lecture 11

Discuss owner education and monitoring of cats with CHF.

A

Monitoring at home: Most important for owners to monitor RESTING or SLEEPING respiratory rate at
home (Ideally <30 breaths per min)

Also monitor for increased respiratory effort, syncope, inappetence, hiding, paresis or paralysis

Rechecks:
Stage B1
Monitored annually

Stage B2
* q6-12 months
*Consider effect of stress on patient

Stage C
CHF**
* 3-10 days after discharge from hospital
* q2-4 months, but consider effect of stress on
patient
**
ATE

* 3-10 days after discharge from hospital
* 2 weeks after discharge to recheck for distal
limb necrosis
* q1-3 months but consider effect of stress on
patient

20
Q

lecture 12

Describe the pathophysiology of feline aortic thromboembolism.

A

Thrombus originates in left heart and
dislodges to systemic arterial system

¬ Thromboembolism to ≥ 1 limb
¬ Most commonly associated with
cardiomyopathy, although cardiac disease
not present in all cats
¬ rarely associated with pulmonary
neoplasia

Poor prognostic indicators:
¬ Hypothermia
¬ ≥2 limbs affected
¬ Absence of motor function
¬ Bradycardia
¬ CHF

21
Q

lecture 12

What are 5 physical examination findings for a patient with FATE?

A

5 P’s!!
¬Pulselessness
¬ Pallor
¬ Pain
¬Paresis
¬Polar or poikilothermia
(cold)

Other tools to diagnose?
¬ Lactate and glucose on affected limb
¬ Lack of Doppler BP
¬ Increased creatinine kinase (CK) (and AST/ALT)

¬ With ATE:
¬ Glucose decreases
¬ Lactate increases

22
Q

lecture 12

What diagnostics may be helpful in diagnosing FATE?

A

¬ Lactate and glucose on affected limb
¬ Lack of Doppler BP
¬ Increased creatinine kinase (CK) (and AST/ALT)

¬ With ATE:
¬ Glucose decreases
¬ Lactate increases

23
Q

lecture 12

What treatment strategies are used in the setting of FATE?

A

STAGE C (ATE)
¬ Analgesia is PRIORITY
¬ Fentanyl, hydromorphone, or methadone

Anti-thrombotic therapy
¬ Low-molecular weight heparin (enoxaparin SQ)
¬ Unfractionated heparin
¬ Oral factor Xa inhibitor (PO) – apixaban or rivaroxaban $$

Anti-platelet therapy
¬ Clopidogrel as soon as cat can tolerate oral meds

Other therapies
¬ Sedation or anxiolytics
¬ Rule out CHF
¬ Treat if in CHF
¬ Caution to mistake tachypnea due to pain for CHF
¬ Careful to not make azotemic
Thrombolytic drug therapy is controversial (TPA tissue plasminogen
activator)
¬ Not recommended by ACVIM consensus statement
¬ Some may advocate in acute setting (<6 hours since event)
Confirm ATE
¬ Diagnostics such as cardiac POCUS or echocardiogram

24
Q

lecture 12

What is the prognosis for patients with FATE?

A

Poor
¬ Studies suggest ~1/3 of cats presenting to a University
hospital will be euthanized, 1/3 of cats will succumb to
disease, and 1/3 will live through event

If severe cardiac disease, overall prognosis post-ATE is
poor
Can consider 24-72 hours of hospitalization if owners are aware of risks
Patient will be at risk for future ATE

25
# lecture 12 What are some possible complications of treating FATE?
Hyperkalemia ¬ Reperfusion injury ¬ Important to monitor electrolytes and rhythm throughout hospitalization Limb necrosis ¬ Requires careful monitoring If severe cardiac disease, overall prognosis post-ATE is poor Can consider 24-72 hours of hospitalization if owners are aware of risks Patient will be at risk for future ATE
26
# lecture 13 Appreciate the electrocardiographic features of atrial fibrillation | what does it look like?
ECG hallmarks of atrial fibrillation (Afib): * No discernable p waves * Chaotic (”irregularly irregular”) rhythm * Narrow complex/supraventricular tachycardia ## Footnote Differentiate from Vtach (usually regular rhythm, wide complex QRS) -> might sound similar on auscultation – VT requires urgent therapy -> life-threatening Afib: Urgent therapy rarely required à but need to figure out cause of Afib Afib+tachycardia usually associated with severe cardiac disease (severe atrial enlargement) & heart failure (in dogs & cats) Treatment goal: slow/delay AV node conduction
27
# lecture 13 Understand the physical exam findings that increase suspicion of DCM (preclinical vs clinical)
low left apical (systolic) heart murmur ## Footnote Radiographic hallmarks of congestive heart failure (CHF): * Severe left atrial and left ventricular enlargement * Pulmonary edema -> perihilar & caudodorsal interstial (+/- alveolar) pattern; diffuse distribution when severe * Pulmonary venous distension * When paired with clinical signs -> clinical diagnosis of CHF
28
# lecture 13 Understand the cause and cardiac auscultation characteristics of mitral regurgitation in dogs with DCM
* Dilated cardiomyopathy (DCM) “phenotype” – Caused by? (more work to do…) * Atrial fibrillation with tachycardia (“rapid ventricular response rate”) – Caused by DCM * Left-sided congestive heart failure (cardiogenic pulmonary edema + clinical signs) – Caused by DCM (+ Afib)
29
# lecture 13 Describe the 3 radiographic hallmarks of cardiogenic pulmonary edema (ie., left-sided congestive heart failure)
Radiographic hallmarks of congestive heart failure (CHF): * Severe left atrial and left ventricular enlargement * Pulmonary edema -> perihilar & caudodorsal interstial (+/- alveolar) pattern; diffuse distribution when severe * Pulmonary venous distension * When paired with clinical signs -> clinical diagnosis of CHF
30
# lecture 13 Appreciate the acute (in hospital) management of CHF in dogs with DCM
* Initiate acute (in-hospital) congestive heart failure therapy ASAP (Goal: alleviate suffering à ↓preload & ↑O2 delivery) * ”SPOF” Someone Please Obtain Furosemide * S = sedation (butorphanol) * P = pimobendan (↑contractility & vasodilator) * O = oxygen * F = furosemide (diuretic to ↓preload/venous pressure ## Footnote Management of preclinical DCM * Pimobendan +/- ACEi, spironolactone, beta-blockers? * Antiarrhythmics as needed (e.g., lidocaine, sotalol) * Treating underlying cause, if possible * Change the diet if “high-pulse”/nontraditional & supplement taurine if low Management of clinical DCM * If congestive heart failure -> treat accordingly, acute vs chronic * Antiarrhythmics as needed (e.g., lidocaine, sotalol) * Treating underlying cause, if possible * Change the diet if “high-pulse”/nontraditional & supplement taurine if low * Long-term prognosis of primary/idiopathic DCM is poor (~6-12 months), worse if atrial fibrillation L
31
# lecture 14 Appreciate the ACVIM stages of MMVD and their recommended treatment
Subclinical * At risk breeds with no current disease (Stage A) – No treatment, breed screenings * MMVD but without cardiac remodeling (Stage B1) – No treatment; watchful waiting * MMVD with significant cardiac remodeling (specific criteria defined) without CHF (Stage B2) – Pimobendan 0.3 mg/kg PO q12h (life-long) to delay onset of CHF and prolong survival Clinical * MMVD + HF (Stage C) àend-stage/refractory (Stage D) – Treatment for CHF (“Dogs are for special people“) and up-titrate drugs (furosemide) as needed
32
# lecture 14 Recognize the physical exam findings of preclinical and clinical MMVD
dyspnea., tachypnea, increased lung sounds/crackles and Grade V/VI left apical systolic murmur
33
# lecture 14 Understand how to quantitate VHS & VLAS
count with vertebral bodies 8.5-10.7 in dogs 6.8-8.1 in cats VLAS in dogs: 1.4-2.3
34
# lecture 14 Explain why checking blood pressure in dogs with MMVD is important
can also develop pulmonary hypertension
35
# lecture 14 Appreciate the chronic (at home) management of CHF in dogs with MMVD | it's lifelong
* Goal: prolong survival * ”Dogs Are For Special People” * D = Diet (↓sodium) * A = Angiotensin converting enzyme (ACE) inhibitors * F = Furosemide * S = Spironolactone * P = Pimobendan