ACUTE CANINE CHF TREATMENT: WHAT YOU NEED TO KNOW TO STABILIZE THE DYSPNEIC PATIENT

Transcription

1 1 ACUTE CANINE CHF TREATMENT: WHAT YOU NEED TO KNOW TO STABILIZE THE DYSPNEIC PATIENT JEREMY ORR DVM, DVSC, DACVIM (CARDIOLOGY) 2 CAUSES OF CHF IN CANINE PATIENTS Presentation will focus on left sided CHF today as cause for the dyspneic patient In general, older dogs who present with CHF have underlying degenerative mitral valve disease Small breed dogs most common, also diagnosed in Retrievers, Dobermans, Dalmatians and Poodles Dilated cardiomyopathy also noted in large & giant breed dogs Congenital cardiac disease: PDA, subaortic stenosis, mitral valve dysplasia 3 PRESENTING COMPLAINTS OF PATIENTS WITH CHF? Dyspnea/tachypnea/cough/orthopnea Not all dogs with CHF cough and not all coughing dogs have CHF Clinical signs may be worse at night with restless behavior noted Syncope/lethargy/exercise intolerance/weakness Abdominal distension Signs may be chronic & progressive but can be acute Acute chordal rupture in a dog with mitral valve disease Regardless, signs are often acute to the owner as other subtle signs may have been missed

2 4 COUGHING Cough is a normal protective reflex to expel material from the airways Also occurs in response to mechanical stimuli and inflammation Occurs in patients with tracheal, bronchial and pulmonary parenchymal disease Many clients have difficulty differentiating coughing from gagging, retching and even vomiting 5 COUGHING Nature of the cough Productive: moist sounding, patient swallows after coughing Usually associated with inflammatory/infectious disease or CHF Non-Productive: Dry or goose-honk, paroxysmal Often associated with tracheobronchial disease Hemoptysis Can be associated with severe CHF, coagulopathy, heartworm disease, neoplasia, fungal disease and airway foreign body 6 COUGHING History of the cough CHF cough tends to rapidly progressive, associated with tachypnea, orthopnea Airway disease cough has a long history (months) Timing of cough Many dogs with CHF have a nocturnal cough Cough intensity CHF cough may be softer

3 7 PHYSICAL EXAM FINDINGS Slow CRT, mucous membranes cyanosis Cool extremities, reduced rectal temperature Increased bronchovesicular sounds, crackles noted (often soft), +/- cough in exam room Thrill/cardiomegaly on precordial palpation Heart murmur (may be absent or quiet if DCM), gallop Abdominal effusion (generally occurs in DCM dogs, atrial fibrillation) Weak pulses, pulse deficits (due to arrhythmia) 8 WHAT IS CONGESTIVE HEART FAILURE? The heart is unable to meet body s metabolic demands at normal filling pressures Results from any condition that impairs the ventricles ability to fill with or eject blood Clinical signs are related to congestion/edema, decreased peripheral perfusion 9 JOB OF THE CARDIOVASCULAR SYSTEM In order of priority: Maintain normal systemic arterial pressure Maintain normal tissue blood flow Maintain normal systemic and pulmonary capillary pressures Why? Normal or adequate blood pressure to perfuse three critical vascular beds in the body: Brain, heart, kidneys - all have innate resistances to blood flow therefore require higher pressures to force blood through them

4 10 DETERMINANTS OF CARDIAC OUTPUT Preload Afterload Contractility Heart rate Our treatments of heart failure are targeted to these determinants of cardiac output 11 MITRAL REGURGITATION AS AN EXAMPLE Mitral Regurgitation (early) = less blood moving forward out the aorta A drop in blood pressure ensues Baroreceptors sense the fall in BP, as well as the kidneys Sympathetic nervous system activated Heart rate increased, contractility increased, systemic arterioles constrict Blood Pressure Increased, Improved renal perfusion However, beta receptor down-regulation occurs rapidly, therefore contractility decreases again and cardiac output falls 12 Volume overload hypertrophy ensues (eccentric hypertrophy), continued vasoconstriction via kidneys (angiotensin II, aldosterone, ADH) End result is a larger ventricle in diastole with an above normal stroke volume (to compensate for the regurgitation lost into the left atrium) With time as regurgitant fraction gets worse, forward stroke volume falls LV end diastolic pressure increases as body attempts to retain more fluid, but LV is approaching the end-stage of it s ability to increase in size Therefore, left atrial pressures increases as well Leads to increased pulmonary capillary wedge pressure and transduation of fluid into the lung tissue (edema)

5 13 OUTCOMES OF COMPENSATORY MECHANISMS Elevated filling pressures = pulmonary edema Increased myocardial oxygen demand = myocardial necrosis Increased heart rate = promotion of arrhythmias and reduced time for diastolic filling & coronary perfusion ACUTE STABILIZATION DO NOT stress and handle these patients gently - sedation is much safer than struggling with them Oxygen - flow-by, oxygen kennel, nasal oxygen Attempt IV catheter if the patient is stable, avoiding stress Obtain renal values, electrolytes as baseline; PCV/TS, glucose Furosemide - dose dependent on presenting signs/radiographs Dog: 2-5 mg/kg IV (or IM) - not SQ!

6 16 ACUTE STABILIZATION Sedation if needed Butorphanol ( mg/kg), midazolam (0.25 mg/kg) AVOID acepromazine, dexmedetomidine, ketamine If catastrophic and gasping, INTUBATE If sedation required, can give hydromorphone ( mg/kg) with diazepam/midazolam ( mg/kg) Dump patient once tube in place and/or use suction to evacuate fluid from the airway Mechanical ventilation Thoracocentesis if indicated 17 ACUTE STABILIZATION Furosemide - continue therapy Generally dose 2 mg/kg every minutes until the respiratory rate has decreased by half of presenting rate - then reduce frequency Re-assess respiratory rate hourly Or, consider furosemide CRI in patients with fulminant pulmonary edema mg/kg/hr Furosemide should be diluted Furosemide is light sensitive Avoid giving too much fluid with a CRI 18 FUROSEMIDE MAINTENANCE DOSING Once respiratory rate has improved and patient is more stable, begin maintenance furosemide dosing 2-4 mg/kg q hrs (IV) Tailor the furosemide dose to the needs of the patient Titrated to renal values, respiratory signs Furosemide therapy reduces preload in an effort to resolve pulmonary edema by reducing pulmonary capillary pressures Also reduces afterload by reducing volume

7 19 WHAT ELSE? Any other drugs which can be used to further reduce preload and afterload? By decreasing afterload, we increase stroke volume and decrease myocardial oxygen consumption Increased stroke volume means more forward flow which therefore helps to alleviate congestion 20 PRELOAD REDUCERS Nitroglycerin 2% ointment Vasodilator via nitric oxide = venodilation Short half-life Transdermal Tolerance develops quickly (18-24 hours) Doses are anecdotal; 1 inch = 15 mg Small dog: 1/4-1/2 inch strip q. 8 hrs Large dog: 1/4-1 inch strip q. 8 hrs Remove after 6 hours for nitrate free period 21 SODIUM NITROPRUSSIDE Potent venodilator & arterial dilator Reduces both preload and afterload Rapidly metabolized with short half life No loading dose needed Cyanide toxicity possible (higher doses, prolonged treatment) Tolerance develops - generally by 48 hours Cost prohibitive at the present time Very useful in patients with severe MR, chordal rupture

8 22 SODIUM NITROPRUSSIDE Adverse effects: Hypotension, cyanide toxicity Monitor for metabolic acidosis Light sensitive and diluted in D5W Doses: Dogs: 1-5 ug/kg/min starting low and titrate up carefully while monitoring blood pressure Arterial BP preferred - maintain systolic > 90 mmhg, mean > 60 mmhg 23 SODIUM NITROPRUSSIDE ALTERNATIVE? Hydralazine Direct acting arterial vasodilator Has been shown in patients with MR to decrease mean blood pressure, systemic vascular resistance and PCWP May help to reduce volume of MR and improve forward flow Avoid in DCM Doses: 0.5 mg/kg PO q. 12 hrs Monitoring: Systemic blood pressure 24 DOBUTAMINE Beta agonist (β1 > β2 > α1) = inotropic, vasodilator Synthetic catecholamine with predominant β1 effects Ultra short half life At lower doses exhibits positive inotropy with minimal effects on HR and systemic vascular resistance; vasoconstrictor effects noted at higher dosages Useful in canine CHF for both MR and DCM patients Ideal to be given in patient with systolic dysfunction

9 25 DOBUTAMINE Following administration there is down-regulation of beta receptors which blunts the response over time (48 hrs) In severe CHF cases beta receptors may be already down-regulated so may not be as effective as anticipated Doses: 2-10 ug/kg/min (start low, titrate up) - diluted with D5W Monitor: heart rate, potassium concentrations (potentially arrhythmogenic) May soon be unavailable Caution when combined with Vetmedin Caution in patients with atrial fibrillation - generally require concurrent diltiazem 26 VETMEDIN (PIMOBENDAN) If dobutamine is not available, then pimobendan is a consideration PDE inhibitor with calcium sensitization properties (inodilator) Leads to vasodilation and enhanced inotropy without significant increase in myocardial oxygen consumption Primarily afterload reducer with positive inotropy but does possess venodilator effects as well Doses: mg/kg PO q hrs If patient can take PO medications 27 BACK TO THE DETERMINANTS OF CARDIAC OUTPUT Preload Afterload Contractility Heart rate

10 28 29 ATRIAL FIBRILLATION Common in canine patients with CHF Rapid arrhythmia which contributes to increased left atrial pressures, reduced stroke volume (forward flow) and increased myocardial oxygen demand Will often decompensate a previously stable patient Rates generally exceed 200 bpm In patients being treated for fulminant CHF it also needs to be addressed 30 ATRIAL FIBRILLATION For the critical CHF patient, IV therapy is preferred for treatment Diltiazem Ca channel blocker Can have myocardial depressant effects Doses: Bolus mg/kg IV slowly (5 minutes) then start CRI at 1-5 mcg/kg/min while monitoring heart rate and blood pressure

11 31 ATRIAL FIBRILLATION If IV diltiazem is not available, then: Oral diltiazem dosed at 1-3 mg/kg PO q. 8 hrs in combination with digoxin dosed at mg/kg PO q. 12 hrs (round down to tablet size) CHF may be difficult to control until adequate heart rate control is achieved Ideal heart rate is bpm (patient dependent) 32 WHAT ABOUT OTHER ARRHYTHMIAS? Ventricular ectopy If single VPCs are present without complexity, specific anti-arrhythmic therapy is not warranted If frequent couplets, triplets and/or runs of ventricular tachycardia are noted (particularly in patient with DCM), then therapy with an antiarrhythmic is warranted Lidocaine CRI mcg/kg/min Procainamide CRI mcg/kg/min Oral sotalol (0.5-2 mg/kg PO q. 12 hrs) - caution in patient with fulminant CHF 33 ON-GOING MONITORING/CARE Hourly respiratory rate (normal SRR < 35 brpm) Body weight monitoring Ensure free access to water (DO NOT restrict!) ECG monitoring Particularly in patients with known arrhythmias and/or on dobutamine Blood pressure

12 34 BLOOD PRESSURE MONITORING Normal BP in hospital: mmhg systolic Goal in patient with CHF >90 mmhg systolic In patient with severe MR, want to avoid hypertension (BP > 150/160 mmhg systolic) I prefer Doppler BP in all patients in lateral recumbency, using the up limb and keeping it at the level of the heart during measurement 35 ON-GOING MONITORING Thoracic radiographs daily to assess response to therapy Renal values with electrolytes assessed every hours Particularly in patients receiving high doses of furosemide, those with historical azotemia, those receiving nitroprusside and those with arrhythmias Ensure potassium is normal Supplement if low Tumil-K PO : 2 meq / 4.5 kg body weight q. 12 hrs 36

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14 40 SPECIFIC DISEASE CONSIDERATIONS Mitral Regurgitation If acute (due to suspected chordae tendinae rupture), these patients may not be necessarily volume overloaded (preload) Focus on afterload reduction When chronic with volume overload, focus on preload AND afterload reduction while addressing any tachyarrhythmias 41 SPECIFIC DISEASE CONSIDERATIONS Dilated Cardiomyopathy Focus on preload reduction and enhanced inotropy Heart rate monitoring is critical in these patients (especially when receiving dobutamine) and continuous ECG monitoring (telemetry) is preferred Treat any tachyarrhythmias 42 KEY POINTS Be aware of how much IV fluids patient is receiving when on CRIs If using bolus furosemide therapy, flush with the smallest volume, particularly in small animals Free access to water at all times Oxygen, sedate if necessary Other supportive care: anti-nausea therapy, famotidine There is no cookbook treatment regimen - modify to your patient!

15 43 KEY POINTS CONTINUED When in doubt - furosemide! Don t wait - Lifesaving preload reduction! One dose in a patient without CHF is not deleterious Sometimes the most difficult step is determining if heart failure is present or not History, physical examination and diagnostics (thoracic radiographs) to help reach diagnosis If patient is not responding to CHF therapy: prior to being more aggressive with therapy ensure proper diagnosis 44 PULMONARY HYPERTENSION THE GREAT PRETENDER 45 PULMONARY HYPERTENSION Challenging as clinical signs overlap with mitral valve disease/chf Similar patient population at risk Clinical signs: Cough, dyspnea, exertional syncope, lethargy, exercise intolerance, ascites

16 46 PULMONARY HYPERTENSION DIAGNOSIS Physical exam findings +/- murmur Typically right apical PMI Split heart sound Significant crackles, dyspnea Ascites if CHF present, hepatomegaly Jugular venous distension, positive hepatojugular reflux test 47 DIFFERENTIATING MR/CHF FROM PH Pulmonary Hypertension Murmur may not be audible; right apex Murmur more recent Split S2 Ascites Coarse, loud and diffuse crackles Historical chronic cough (months-years) Mitral Valve Disease with CHF Historic chronic heart murmur (years) Murmur best head over the left apex Systolic click may be present in early stages Ascites uncommon unless atrial fibrillation or develop concurrent PH secondary to MR Crackles may be heard, but generally quiet, end-inspiration (unless fulminant alveolar CHF) Cough is more recent Jugular venous distension, positive hepatojugular reflux test 48 PULMONARY HYPERTENSION DIAGNOSIS Thoracic radiographs Pulmonary arterial vasodilation, tortuosity, abruptly tapered Pulmonary infiltrate not typical of CHF Concurrent bronchial pattern which can be significant Right heart enlargement Sternal contact, loss of cranial waist, reverse D Lack of left atrial enlargement

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19 55 PULMONARY HYPERTENSION DIAGNOSIS Echocardiography Gold standard in veterinary medicine Use tricuspid/pulmonic insufficiency jets to estimate pulmonary artery pressure RA/RV dilation, RV concentric hypertrophy, septal flattening, underperfused left heart 56 ECHOCARDIOGRAPHY 57 PULMONARY HYPERTENSION TREATMENT Address any underlying cause HWD, airway disease, Cushings, PLE/PLN Sildenafil for PA vasodilation mg/kg PO q. 8 hrs Oxygen (including at home oxygen if needed) Vetmedin (efficacy not well documented) Theophylline Clopidogrel, heparins = particularly if increased suspicion of PTE

20 58 PULMONARY HYPERTENSION TREATMENT CONTINUED Treat right sided CHF if present Diuretics ACE inhibitors Abdominocentesis as needed 59 PULMONARY HYPERTENSION PROGNOSIS Variable Patients require multi-modal, life-long therapy to manage Median survival in one study was 175 days (range days) In dogs with primary mitral valve disease, secondary pulmonary hypertension (>55 mmhg) predicted a worse outcome 60 WHEN TO REFER Acutely dyspneic/tachypneic patient with no previous history of a heart murmur Thoracic radiographs not suggestive of left sided heart disease/chf Failure of response to therapy for presumed left sided heart disease Clinical signs supportive of PH - exercise intolerance, syncope, cough, tachypnea

21 QUESTIONS? 61