Emergency Management of Congestive Heart Failure in Small

Emergency Management of Congestive Heart Failure in Small Animal Practice **Name**, DVM, DACVIM-Cardiology **Date**

Outline • Cardiac Auscultation and History – Useful tools for distinguishing cardiac and respiratory disease • Radiographs • Pathophysiology of Heart Failure • Treatment of Heart Failure

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 3 rd heart sounds (clicks, gallops) Consider the signalment of the patient – Common things happen commonly – Congenital vs. Acquired – Breed-specific defects

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 – S 1 - closure of MV and TV • Onset of systole • High frequency, PMI left apex • Pulse occurs just after S 1 – S 2 - closure of Ao. V and PV • Onset of diastole • High frequency, PMI left base

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 – S 3 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 – S 4 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 S 4 with some 3 rd degree AVB

Cardiac Auscultation: Quick Review • Heart Murmurs – Timing • Systolic - b/w S 1 and S 2 (“lub-shh-dub”) • Diastolic - after S 2 (“lub-dub-shh”) • Continuous – PMI (base vs. apex, L vs R) – Intensity (I-VI) – Quality • Regurgitant = plateau shape – MR, TR • Ejection = crescendo-decrescendo – SAS, PS • Machinery (PDA) • Decrescendo (VSD, MR, TR)

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

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, 1 st sign to owner = SCD • Does the presence of crackles = CHF? • Document…Document – Vital signs and trends matter – Can you explain changes? • If present, when did arrhythmia start?

Dyspneic Patient: Recognizing Breathing Patterns • Upper Airway Disease – Obstructive breathing pattern • Long, slow inspiration – Exception - intrathoracic obstruction 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)

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

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 endinspiration (indicate fluid-filled alveoli) – Fluid - water, hemorrhage, pus • +/- Murmur

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

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

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

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/d. L – 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

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)

Chest Radiographs: Quick Review

Chest Radiographs: Quick Review • <3 ICS - Avg Dog – <3. 5 - Small Breeds – < 2. 5 - Deep-Chested • A = 1/3 -1/4 (A+B) • B = 2/3 -3/4 (A+B) • Cats - <70% height of chest; < 2 -3 ICS • Greatest horizontal dimension should be <2/3 chest dimension at that location • Cats - <50% width of chest

Chest Radiographs: Quick Review • Normal dogs: 8. 5 -10. 7 (9. 7 +/- 0. 5) • Boxers: 10. 3 -12. 6 • Labrador Retrievers: 9. 7 -11. 7 • CKCS: 9. 9 -11. 7 • Cats: 6. 7 -8. 1 (mean 7. 5)

Cat in a Box Radiograph Trick

Ok…. so it’s CHF… Now what? ? ?

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

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

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

CHF - Mechanisms • 5 Mechanisms of CHF – Volume overload • MR, PDA – Pressure overload • SAH, SAS, PS – Myocardial failure • DCM – Diastolic dysfunction • HCM – Arrhythmias • AFib, SVT, VT

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

CHF - Consequences • CHF results in reduction of cardiac output - triggers cascades of physiologic events to restore BP (CV System 1 st priority) – Sympathetic stimulation of the heart – Vasoconstriction – Redistribution of blood flow • • SNS RAAS Vasopressin Vascular endothelial systems – Na/H 2 O Retention • • Changes in RBF Aldosterone Vasopressin Inhibition of natriuretic hormones

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

CHF - ER Management • Goals – Reduce venous congestion, edema, and effusion formation – Increase CO – Normalize HR and rhythm – Address forward failure signs (hypotension, hypothermia) • O 2 – Pulmonary edema can case life-threatening hypoxemia d/t decreased ability of O 2 to diffuse from alveoli into pulmonary capillaries – Increased inspired O 2 concentration increases pressure gradient of O 2 from alveoli to capillaries – Emergency - 60 -100% Fi. O 2 – Chronic O 2 therapy - 35 -40% Fi. O 2

Methods for Supplemental O 2 Delivery • Blow-by O 2 • O 2 Hood (temporary treatment) – Place head inside plastic bag; O 2 tubing through small hole in front of bag; Back of bag left open for gas to escape; Monitor temp. – Provides 85 -95% O 2 • O 2 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; O 2 tubing placed along inside of collar and taped ventrally – O 2 concentration up to 80% can be achieved – Flow rate of 1 L / 10 kg of BW usually provides adequate Fi. O 2 • 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 m. L/kg, up to 5 -6 L/min Provides at least 40% O 2

Methods for Supplemental O 2 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 O 2 • O 2 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

Methods for Supplemental O 2 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 m. L/kg/min • 5 -8 Fr - medium dogs • 8 Fr - large dogs – 100 m. L/kg/min – Provides 40 -50% O 2 • If higher flow rates needed, – Place 2 nd nasal catheter – Nasopharyngeal O 2 catheter » Tip ends in proximal pharynx, ie. angle of mandible » Provides 60 -70% O 2 at same flow rates as nasal catheter – Nasotracheal O 2 catheter » Tip ends in proximal tracheal lumen, ie. level of thoracic inlet (elevated head to help facilitate blind passage) » Provides 80 -90% O 2 at 50% of nasal catheter flow rates » Remember to humidify O 2 – *Avoid in dogs w/ severe nasal/pharyngeal disease, thrombocytopenia, bleeding disorders, head trauma (sneezing increases ICP)

REMEMBER…it’s simple physiology…

Goal #1: Reduce Congestion, Edema, Effusions • Reduce vascular volume (preload) – Diuretics - Lasix • • Cats - 1 -3 mg/kg IM/IV q 1 -2 hr initially Dogs - 2 -4 mg/kg IM/IV q 1 -2 hr 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 q 1 -4 hr; 0. 2 -0. 5 mg/kg IM or SC q 3 -4 hr – Dogs - 0. 1 -1 mg/kg IV q 1 -4 hr; 0. 2 -2 mg/kg IM or SC q 2 -4 hr • 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

Goal #1: Reduce Congestion, Edema, Effusions • Effusions – If clinically significant, remove – Pericardial effusion • Caution in cats and small dogs…Why?

Goal #2: Improve CO • Decrease Afterload – Arterial vasodilators • Hydralazine – If BP >120 mm. Hg, ok to give PO meds – Monitor BP closely - want to decrease ~15 -20 mm. Hg – 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 q 5 -15 min – Goal - maintain BP ~100 mm. Hg 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 72 hr, then wean off over 8 -12 hours

Pimobendan vs. Dobutamine or Dopamine • Do. Butamine – B 1 > B 2 > A 1 – Synthetic direct beta-1 agonist – Mild beta-2 and alpha-1 • Balance effect on vasculature – Strongest + inotrope available – Less arrhythmogenic and effect on HR • Dop. Amine – Beta; High dose alpha – Precursor to Nor. Ep – 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

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 2 x dose for 2 doses (ie. 24 hr) – – 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

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. 1 mg/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

Goal #3: Continued • Frequent VPCs or Vtach – Reasons to Treat • Sustained VTach = >160 bpm for 30 seconds • R-on-T phenon (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 1 st dose of Mexitil, wait 4 -6 hours, then wean off Lidocaine over 4 -6 hours

Goal #4: Forward Failure, Cardiogenic Shock • Hypotension – Systolic BP < 90 mm. Hg – Consider dobutamine CRI • CRI total volume should be <25% maintenance fluid rates (ie. <15 m. L/kg/d) • What about hypotensive, dehydrated cats in active CHF? – IVF contraindicated – NE tube fluids better tolerated

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

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