2. Outline
• Cardiac Auscultation and History
–Useful tools for distinguishing cardiac
and respiratory disease
• Radiographs
• Pathophysiology of Heart Failure
• Treatment of Heart Failure
3. Cardic Auscultation: Tips
• Take your time
• Adequately restrain
• Minimize panting, growling, purring
• Focus on heart sounds first, breath sounds second
• Develop a repeatable pattern
• Listen for 3rd heart sounds (clicks, gallops)
• Consider the signalment of the patient
– Common things happen commonly
– Congenital vs. Acquired
– Breed-specific defects
4. Cardiac Auscultation:
Quick Review
• Determine heart rate and rhythm
• Correlate with femoral pulses
• Auscult over all heart valves
– Cranially - PDAs in big dogs
• Normal Sounds
– S1 - closure of MV and TV
• Onset of systole
• High frequency, PMI left apex
• Pulse occurs just after S1
– S2 - closure of AoV and PV
• Onset of diastole
• High frequency, PMI left base
5. Cardiac Auscultation:
Quick Review
• Transient Heart Sounds
– Systolic Click
• Dogs - usually associated with DMVD (prolapse of AMVL)
• Cats - hyperdynamic function, systolic contact of LV walls
– S3 Gallop (ventricular gallop)
• Low frequency
• Represents ventricular stiffness
(diastolic dysfunction - reduced compliance while filling)
• Caused by sudden termination of expansion of LV walls during period of rapid
ventricular filling
• HCM, DCM, Severe DMVD
– S4 Gallop (atrial gallop)
• Low frequency
• Represents ventricular stiffness
• Caused by atria trying to force blood into an already over-distended ventricle; atria
forcing blood into stiff ventricle
(atrial contraction - late ventricular diastole)
• HCM
• Can also hear S4 with some 3rd degree AVB
7. Cardiology Auscultation:
Quick Review
• I - faint, requires
concentration/quiet room
• II - soft, consistently
ausculted over 1 valve area
• III - radiates on the same
side of the chest
• IV - radiates to both sides
of the chest
• V - loud with palpable
precordial thrill
• VI - audible with
stethoscope off chest wall
8. Cardiac Auscultation: Summary
• Slow down and take your time
• It matters - YOU are the gate keeper
• Making the correct diagnosis makes a difference
in outcome and survival
• 30% of Boxers, 1st sign to owner = SCD
• Does the presence of crackles = CHF?
• Document…Document…Document
– Vital signs and trends matter
– Can you explain changes?
• If present, when did arrhythmia start?
9. Dyspneic Patient:
Recognizing Breathing Patterns
• Upper Airway Disease
– Obstructive breathing pattern
• Long, slow inspiration
– Exception - intrathoracic obstruction can cause expiratory distress
– Narrowing of airway causes reduced and turbulent airflow
– Animal works harder to breathe against obstruction exacerbating edema and
inflammation - vicious cycle
• Stridor or Stertor
• Increased RE +/- abdominal component
• Orthopnea
– +/- Hyperthermia
– Auscultation
• Referred upper airway sounds, be sure to listen over trachea
• Obstructions can cause non-cardiogenic pulmonary edema (crackles)
10. Dyspneic Patient:
Recognizing Breathing Patterns
• Lower Airway Disease
– Expiratory distress
• Normal inspiration, exaggerated and prolonged expiration
• Edema and cellular infiltrates of bronchiole walls lead to thickening and
weakening of bronchial walls, excessive secretion, mucus plugs
• Narrowing causes acute bronchospasm
• As animal inhales, radial traction on the lungs pull the airways open and allows
air to enter alveolus
• As animal exhales, negative intrathoracic pressure causes airways to collapse,
trapping air in alveolus
– Alveolus full on next inspiration - reduced gas exchange
– Marked expiratory abdominal “push”
– Cats - cough (“coughing up hairballs”)
– Auscultation
• Expiratory wheezes
• Loud crackles
• No murmur
– Exception - presence of cor pulmonale or concurrent cardiac disease
11. Dyspneic Patient:
Recognizing Breathing Patterns
• Pulmonary Parenchymal Disease
– No specific respiratory pattern
– Respirations usually short, rapid, and deep
• Can mimic nearly any respiratory pattern
– +/- Abdominal component
– Dogs - cough
– Auscultation
• Soft crackles
– Sound of collapsed alveoli and lower airways “popping” open at end-
inspiration (indicate fluid-filled alveoli)
– Fluid - water, hemorrhage, pus
• +/- Murmur
12. Dyspneic Patient:
Recognizing Breathing Patterns
• Pleural Space Disease
– Restrictive breathing pattern
• Short, shallow, and rapid respirations
– Presence of air/fluid/organs/masses prevents expansion of
lungs
– Intrapleural pressure > Intrapulmonary pressure
» Causes increased tidal volume - animals must breathe
faster that normal to maintain minute volume
– Auscultation
• Dull lung +/- heart sounds
– Fluid - lungs loudest dorsal, dull ventral
– Air - lungs loudest ventral, dull dorsal
13. CARDIAC RESPIRATORY
Cough Soft +/- productive (mucus)
Occurs at rest
Harsh/honking
Occurs w/ activity/excitement
Activity +/- Exercise intolerance Normal
Weight/BCS +/- Weight loss +/- Obese
Lungs Sounds Normal to BV sounds
+/- Soft crackles (dyspneic)
BV sounds (pleural effusion)
Normal to BV sounds
+/- Loud crackles (eupneic)
+/- Wheezes
RR/RE/Pattern Usually short, rapid, deep +/-
abdominal effort
Exaggerated, prolonged expiration
+/- exp abd. push
HR/Rhythm Normal to Sinus Tachycardia
Possible arrhythmia
Normal to sinus bradycardia
+/- RSA
Murmur Often L apex in dogs +/- Cor pulmonale, Concurrent
cardiac disease (R vs L?)
CXR Interstitial to alveolar pattern
LAE
Bronchial and nodular patterns -
unlikely CHF
Bronchial, Broncho-interstitial
pattern
Peri-bronchial enhancement
14. Cardiac vs. Respiratory -
Dogs
• Causes of dyspnea
– Bronchitis
– Collapsing airway disorders
– Pulmonary interstitial disease (IPF)
– Pulmonary hypertension
– Pneumonia
• Cardiac cough = “hack/gag”
– Cardiomegaly and bronchial compression
– RR should be normal
• Sequence of pulmonary edema:
– Perihilar Cd-D (R then L) Cr-V
– Resolves in reverse order w/ Tx
15. Cardiac vs. Respiratory - Cats
• Causes of Dyspnea
– CHF
– Asthma / Inflammatory
bronchial disease
– Mycoplasma
– Pneumonia
• CHF Origin Pulmonary
Infiltrates (usually)
– Cardiomegaly
– No bronchial pattern
– Can put edema anywhere
• Cardiac Origin Pleural Effusion
– TP < 4.5 g/dL
– Mixed cell population with low
TCC
– No bacteria
• Arrhythmias
– CV disease
– Hypoxia (global or local)
– Metabolic disease
– Drugs / Toxins
– Infection (sepsis)
– Autonomic disease (usuall
diagnosis of exclusion
16. History and Presenting Complaint
• Early Signs of CHF
– Dogs
• Exercise intolerance
• +/-Coughing
– Cats
• Hiding, decreased
appetite, behavioral
change
– Both
• Increase
sleeping/resting RR
• Late Signs of CHF
– Rapid breathing
– Exaggerated chest
and abdominal motion
to respiration
– Extended head/neck
– Coughing up pink
foam (pulmonary
edema)
22. Congestive Heart Failure
• Syndrome, not a
disease
– Abnormality of
cardiac function that
results in the failure
of the heart to pump
blood at a rate
commensurate with
requirements of
metabolizing tissues
23. CHF - Classification
• Forward Failure
– Signs result from low CO and inadequate tissue perfusion
– Weakness, lethargy, pre-renal azotemia
• Backward Failure
– Failure of heart to empty blood from the veins - leading to
elevated venous and capillary pressures
– Pulmonary edema, ascites, pleural effusion
• Cardiogenic Shock
– Signs of forward and backward failure + systemic
hypotension
24. CHF: Classification
NYHA
Class I
(Mild)
Asymptomatic; Heart disease present but no CS
Class II
(Mild)
CS present with strenuous activity; Comfortable at rest
Class III
(Moderate)
CS with routine daily activities and mild exercise; Comfortable at rest
Class IV
(Severe)
CS severe, even at rest; Requires hospitalization
ACVIM 2009 Consensus Statement
A Dogs are risk for CHF; No apparent structural abnormality; No murmur
B-1 Structural heart disease present; Never had signs of CHF; Asymptomatic
B-2 Asymptomatic; Hemodynamically significant, remodeling noted on echo
C Past or current signs of CHF assoc w/ structural heart disease
D End stage heart disease; CHF refractory to standard therapy
26. CHF - CV System Priorities
• Priorities of the CV System
– Maintain normal systemic BP
– Maintain normal tissue blood flow
– Maintain normal systemic and pulmonary capillary
pressures
• Why does the CV system have priorities?
– 3 critical vascular beds in the body (brain, heart, kidneys)
have high innate resistance to blood flow
• Ie. They need high pressures to force blood through them
27. CHF - Consequences
• CHF results in reduction of cardiac output - triggers
cascades of physiologic events to restore BP
(CV System 1st priority)
– Sympathetic stimulation of the heart
– Vasoconstriction
– Redistribution of blood flow
• SNS
• RAAS
• Vasopressin
• Vascular endothelial systems
– Na/H2O Retention
• Changes in RBF
• Aldosterone
• Vasopressin
• Inhibition of natriuretic hormones
28. CHF - Systems altered…
What’s the harm?
• So, if these events are beneficial, why do we try to
block them with medications?
– No permanent harm if systems return to normal
– Chronic activation - physiologic balance shifts toward
• Vasoconstriction
• Na retention
• Mediators of inflammation
• Mediators of tissue growth
• Remodeling/fibrosis
– Structural and functional damage to heart muscle
29. CHF - ER Management
• Goals
– Reduce venous congestion, edema,
and effusion formation
– Increase CO
– Normalize HR and rhythm
– Address forward failure signs
(hypotension, hypothermia)
• O2
– Pulmonary edema can case life-threatening hypoxemia d/t decreased ability
of O2 to diffuse from alveoli into pulmonary capillaries
– Increased inspired O2 concentration increases pressure gradient of O2 from
alveoli to capillaries
– Emergency - 60-100% FiO2
– Chronic O2 therapy - 35-40% FiO2
30. Methods for Supplemental
O2 Delivery
• Blow-by O2
• O2 Hood (temporary treatment)
– Place head inside plastic bag; O2 tubing through small hole in front of bag;
Back of bag left open for gas to escape; Monitor temp.
– Provides 85-95% O2
• O2 Collar (short or long-term treatment)
– Cover ventral 50-75% E-collar with plastic wrap; E-collar should be 1 size
larger than normally used; O2 tubing placed along inside of collar and taped
ventrally
– O2 concentration up to 80% can be achieved
– Flow rate of 1L / 10kg of BW usually provides adequate FiO2
• Nasal Cannula (long-term)
– Infant - cat and small dogs (2-5 kg)
– Pediatric - medium dogs (11-24 kg)
– Adult - large dogs (>25 kg)
– Flow rate 50-100 mL/kg, up to 5-6L/min
– Provides at least 40% O2
31. Methods for Supplemental
O2 Delivery
• Transtracheal Catheter
– Patient with upper airway obstruction
– Large-bore over-the-needle catheter or commercial
tracheal catheter placed between tracheal rings in
midcervical region
– Humidify O2
• O2 Cage
– Easy
– Disadvantage - time it takes to oxygenate cage (up to
30 min to reach 45% at 15 L/min), inability to
evaluate/treat patient, opening doors for
evaluation/treatment
32. Methods for Supplemental
O2 Delivery
• Nasal Catheter (long-term)
– One of the most effective methods
– Red rubber tube placed in ventral nasal meatus and sutured to face
• Measure from tip of nose to lateral canthus
• 3.5-5 Fr - small dogs and cats
– 50 mL/kg/min
• 5-8 Fr - medium dogs
• 8 Fr - large dogs
– 100 mL/kg/min
– Provides 40-50% O2
• If higher flow rates needed,
– Place 2nd nasal catheter
– Nasopharyngeal O2 catheter
» Tip ends in proximal pharynx, ie. angle of mandible
» Provides 60-70% O2 at same flow rates as nasal catheter
– Nasotracheal O2 catheter
» Tip ends in proximal tracheal lumen, ie. level of thoracic inlet (elevated head to help facilitate
blind passage)
» Provides 80-90% O2 at 50% of nasal catheter flow rates
» Remember to humidify O2
– *Avoid in dogs w/ severe nasal/pharyngeal disease, thrombocytopenia, bleeding
disorders, head trauma (sneezing increases ICP)
34. Goal #1: Reduce Congestion,
Edema, Effusions
• Reduce vascular volume (preload)
– Diuretics - Lasix
• Cats - 1-3 mg/kg IM/IV q1-2hr initially
• Dogs - 2-4mg/kg IM/IV q1-2hr initially
• Then reduce to 2 mg/kg TID-QID
• If RR/RE not improving to <40-50/min within 2-3 hours (ie. 2-3 doses), consider
additional therapies or incorrect Dx
– Nitroprusside +/- Dobutamine
• Morphine
– Anxiolytic and may increased pulmonary venous compliance
– Cats - 0.02-0.1 mg/kg IV q1-4hr; 0.2-0.5 mg/kg IM or SC q3-4hr
– Dogs - 0.1-1 mg/kg IV q1-4hr; 0.2-2 mg/kg IM or SC q2-4hr
• Reduce venous tone (vasodilators - increase venous capacitance)
– Pimobendan - 0.2-0.3 mg/kg PO BID
– Dobutamine - 1-10 mcg/kg/min (max. 5-8 in cats)
– Nitroglycerine - 1/4” small dog, 1/2’ large dog
35. Goal #1: Reduce Congestion,
Edema, Effusions
• Effusions
– If clinically significant, remove
– Pericardial effusion
• Caution in cats and small dogs…Why?
36. Goal #2: Improve CO
• Decrease Afterload
– Arterial vasodilators
• Hydralazine
– If BP >120 mmHg, ok to
give PO meds
– Monitor BP closely - want to
decrease ~15-20 mmHg
– Hydralazine - 0.5-1 mg/kg
PO QD-BID (cats -2.5 mg
PO BID)
– Balanced vasodilators
• Nitroprusside - 1-10
mcg/kg/min
– Light sensitive
– Monitor BP closely - titrate
q5-15 min
– Goal - maintain BP ~100
mmHg systolic
– Do NOT use >48 hours
• Increase Contractility
– Pimobendan
– Dobutamine
• Consider early in Tx plan if
DCM suspected
• Greatest clinical benefit
when left on CRI for 72hr,
then wean off over 8-12
hours
37. Pimobendan vs.
Dobutamine or Dopamine
• DoButamine
– B1 > B2 > A1
– Synthetic direct beta-1 agonist
– Mild beta-2 and alpha-1
• Balance effect on vasculature
– Strongest + inotrope available
– Less arrhythmogenic and
effect on HR
• DopAmine
– Beta; High dose alpha
– Precursor to NorEp
– Direct and indirect (via NE)
effects on alpha and beta-1
rec.
– More arrhythmogenic and
tachycardia-inducing
• Pimobendan
– Inodilator
• PDEIII inhibtor
• Ca sensitizer
– Contractility
– Vasodilator
• Balanced systemic
• Pulmonary
– Myocardial blood flow
– LV filling pressures
– *Requires oral dosing and
absorption to be effective
38. Goal #3: Normalize HR
and Rhythm
• Arrhythmias further compromise cardiac function
– Atrial fibrillation
– VPCs / Vtach
• Stick to medications that do NOT significantly worsen
cardiac function
– Digoxin - 0.003-0.005 mg/kg of LBW PO BID
• Can “load” by giving 2x dose for 2 doses (ie. 24hr)
– Diltiazem - 0.5-2 mg/kg PO TID
– Mexilitine - 5-8 mg/kg PO TID
– Lidocaine - 40-80 mcg/kg/min
– (Sotalol) - 1-3 mg/kg PO BID
• Ideally know systolic function
• Beta-blockers are contraindicated in active CHF
39. Goal #3: Continued
• Atrial Fibrillation
– Digoxin in acute setting
• Primary SE = inappetance
– May present inappetant, but you can’t eat if you can’t breathe
– +/- Diltiazem
• Delay combination if inappetant
• If Pt laterally recumbent due to arrhythmia and unable to take oral
medications, can give diltiazem IV as CRI
– Bolus 0.1mg/kg SLOW (over 3 minutes)
– CRI 1-5 mcg/kg/min
– Do NOT expect conversion to NSR
– Goal is rate control
• < 160 bpm in stressful setting ultimately
• Start drugs low, then increase based on rate response every 24
hours
40. Goal #3: Continued
• Frequent VPCs or Vtach
– Reasons to Treat
• Sustained VTach = >160 bpm for 30 seconds
• R-on-T phenonenon (risk factor for VFib)
• Mutlifocal VPCs, Couplets, Triplets
– Lidocaine
• Bolus - 2 mg/kg IV slow (1-2 min)
– Repeat up to 4 times
• CRI - 40-80 mcg/kg/min
– Mexilitine
• 5-8 mg/kg PO TID
• Primary SE - GI - Recommend giving w/ food
• Start Mexitil prior to discontinuing Lidocaine
– Give 1st dose of Mexitil, wait 4-6 hours, then wean off Lidocaine
over 4-6 hours
41. Goal #4: Forward Failure,
Cardiogenic Shock
• Hypotension
– Systolic BP < 90 mmHg
– Consider dobutamine CRI
• CRI total volume should be <25% maintenance
fluid rates (ie. <15 mL/kg/d)
• What about hypotensive, dehydrated cats
in active CHF?
– IVF contraindicated
– NE tube fluids better tolerated
42. CHF and Cats
• Hypotensive + Hypothermic + Dehydrated
= Poor prognosis for short term survival
– Need NE tube for caloric and rehydration
needs
• Cats that do not respond to standard
therapy have a poor prognosis
• Cats are more sensitive to CRIs in general
– Nitroprusside can be useful
