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55 Cards in this Set
- Front
- Back
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Canine myxomatous valvular degeneration
-prevalence |
-older (ex. CKCS)
-small breed -more rapid onset of CHF, w/ worse prognosis |
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Canine myxomatous valvular degeneration
-Aetiology |
-hereditary, complex inheritance pattern
-may be an inflammatory process superimposed on genetic disposition |
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Canine myxomatous valvular degeneration
-Pathophysiology |
-proliferation of loose fibroblastic tissue in the spongiosa of mitral valve=severe distortion and prolapse
-mild: small discrete nodules on margins of valves -severe: gross distortion of valves by grey-white nodules and plaques -left ventricular dilation +/- eccentric ventricular hypertrophy -prolapse of mitral valve into the LA during systole |
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Canine myxomatous valvular degeneration
-CS |
-incidental heart murmur
+/- cough, tachypnoea, dyspnoea (pulmonary oedema) -CHF (w/ increased HR) -+/- atrial fibrillation -syncope (secondary to coughing) -sudden death (usu. due to left atrial tear and acute haemopericardium) |
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Canine myxomatous valvular degeneration
-Dx |
1. PE
-regurgitant murmur -S1 increased in intensity +/- crackles on thoracic auscultation (pulmonary oedema) -increased HR, arrhythmia 2. Rads -evaluate LA size -evaluate lungs for presence of pulmonary oedema 3. ECG -if arrhythmia 4. Echocardiogram -only for staging and monitoring |
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Canine myxomatous valvular degeneration
-Tx |
Treat CHF:
1. Loop diuretics (frusemide) 2. Vasodilators (Amlodipine if chronic outpatient, nitrates for short term in hospital; +/- ACE inhibitors; Pimobendan**) |
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DOGMA for treating endocariosis
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ACEi
frusemide pimobendan |
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Clinical approach to syncope
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1. Full PE and history (e.g. neurological vs. cardio)
2. full CBC, biochem, electrolyte and urinalysis 3. resting ECG 4. Thoracic rads 5. Echocardiogram 6. systolic BP |
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DCM
-CS |
-large or giant breed dogs (exc. CSp)
-middle anged to older +/- sudden death, syncopal episodes or signs of CHF -LSCHF signs predominate (tachypnoea at rest or exercise intolerance) -tachyarrhythmia (+/- atrial fibrillation due to enlarged L atrium) -mitral murmur (stretching of the annulus) +/- cardiac cachexia |
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DCM
-Dobermans |
-'occult DCM'
-no associated CS -poor functional shortening on echocardiogram -pimobendan improves survival |
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DCM
-American Cocker Spaniels |
-taurine deficiency (however not responsive to taurine alone)=transport across mitochondrial membrane decreased=reduced myocardial fxn.
-supplement w/ Taurine and L-carnitine |
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DCM
-Boxers |
-ventricular tachyarrhythmia (precedes development of systolic failure
-arrhytmogenic R ventricular cardiomyopathy -Category 1: mild ventricular arrhythmias (intermittent VPCs) -Category 2: severe ventricular arrhythmias (syncope, prone to sudden death) -Category 3: myocardial and heart failure (LSCHF AND RSCHF) |
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DCM
-Diagnosis |
2. Radiography
-assess whether pulmonary oedema present -generalised heart enlargement (except Dobermans-may only have increased LA) 2. Echocardiography -FS <15% of DCM 3. ECG -halter monitors -ALWAYS in Boxers and Dobermans |
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DCM
-Tx 1. Acute/fulminant CHF 2. Occult disease w. systolic dysfunction on echocardiography 3. Chronic CHF 4. CHF and atrial fibrillaiton 5. Ventricular arrhythmias |
1. sedation, O2 supp, IV frusemide, vasodilators (WITH CARE avoid hypotension as no compensatory mechanisms)
2. pimobendan, ACE inhibitors; -repeat chest rads and ECG q 3-4 mo -repeat echo q 6 mo 3. low salt, high energy diet, exercise restriction -frusemide (lowest dose once CS resolve; ACE inhibitor +/- pimobendan** 4. Treat CHF (frusemide, ACEi, pimobendan) -digoxin 5. treat CHF if present |
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HCM (cats)
-pathophysiology |
-hypertrophy of L ventricular free wall and the intraventricular septum
-LA enlarged -increased chamber stiffness -increased diastolic intraventricular pressures, LA enlargement and CHF |
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HCM (cats)
-Clinical features |
-CHF w/ pulmonary oedema or pleural effusion (NB Chylothorax can develop from CHF)
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HCM (cats)
-Dx |
1. ECG
-arrhythmias (supraventricilar +/- sinatrial blocks) 2. Radiography -valentine heart shape -large LA and left auricle causes bulge and apex shifts to the midline +/- pleural effusion and/or pulmonary oedema -lungs: increased interstitial pattern +/- air bronchograms 3. Echocardiography** -essential for Dx -increase in diagnostic wall thickness -M mode: thickened AV septum |
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HCM (cats)
-Tx 1. Severe, acute CHF 2. Chronic CHF 3. Asymptomatic animals 4. Prevention of ATE 5. Refractory CHF |
1. sedation, O2 supplementation
-thoracocentesis if pleural effusion -frusemide IV every 2-4 hours (swap to oral as son as possible and monitor e-lytes carefully-hypokalemia but don't put on fluids, need to get to start eating) 2. Frusemide at lowest possible dose -Beta-blockers or calcium channel blockers (atenolol b.i.d +/- ACEi 3. ACEi/ atenolol? 4. aspirin, clopidogrel, low molecular weight heparin 5. Increase dose of primary drug (CCB or Beta blocker) -change to diff. class of primary drug -add a second primary agent: ACEi, spirinolactone |
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HCM (cats)
-Follow-up |
-limit stress triggers
-rechecks (PE, ECG, echo, systolic BP) q 12 mo -symptomatic w/ pulmonary oedema: check bloods 2 weeks after discharge then systolic BP, bloods and physical exam every 3 months with ECG, Echo and rads every 6-12 mo -symptomatic w/ pleural effusion: checkups at least every 3 months |
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Restrictive cardiomyopathy (cats)
-definition |
-restrictive diastolic filling and reduced diastolic functino of one or both ventricles, w/ normal or near-normal systolic function and wall thickness
-significant diastolic dysfunction without concentric hypertrophy (w/o=unclassified cardiomyopathy) |
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Restrictive cardiomyopathy (cats)
-CS |
-gallop rhythm (ventricular diastolic dysfunction)
-systolic murmur -paresis (thromboembolism) -dyspnoea -hypothermia -muffled heart and lung sounds (if pleural effusion) -lung crackles -irregular heart rate/rhythm |
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Restrictive cardiomyopathy (cats)
-Dx |
1. ECG
-atrial ectopics of atrial fibrillation -interventricular conduction disturbances 2. Echo -MARKED LA or BILATERAL DILATION -hyperechoic wall segments may indicate fibrosis -absence of hypertrophy of myocardium (unlike HCM) 3. Rads -non specific and reflective of cardiomegaly and whether presence of pleural effusion or pulmonary oedema |
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Restrictive cardiomyopathy (cats)
-Tx |
1. Acute CHF
-as for HCM 2. Chronic management: -frusemide to lowest dose -ACE inhibitors -Aspirin and anti-platelet drugs (prevent thromboembolism) |
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Thyrotoxic heart disease (cats)
-Aetiology |
-direct and indirect effects of excessive thyroxine
-excess T4 may increase beta 1 receptors in LA and LV and increase basal metabolic rate -increased HR, contractility and metabolic rates -increased cardiac protein synthesis and myocardial hypertrophy |
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Thyrotoxic heart disease (cats)
-CS |
-systemic signs of hyperthyroidism (weight loss, poor hair coat, palpable goitre)
-tachycardia, systolic murmur, S4 gallop and bounding cardiac impulse may be present -CHF (rare) |
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Thyrotoxic heart disease (cats)
-Dx |
-demonstration of excess circulating T4
-T3 suppression test |
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Thyrotoxic heart disease (cats)
-Tx |
-treat hyperthyroidism:
neomercazole, radioactive iodine, surgery (last two if concurrent renal insufficiency) -CHF w/ systolic dysfunction: frusemide, ACEi, digoxin -CHF w/ diastolic dysfunction: dilitiazem or atenolol |
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Aortic thromboembolism (cats)
-aetiology |
-cardiomyopathy: enlarged LA, sluggish blood flow in LA +/- increased platelet aggregability
-most common site is aortic trifurcation (causes release of vasoactive substances-serotonin and thromboxane-impairs collateral circulation) -ischaemic neuromyopathy developes (damage to nerve sheaths, Wallerian degeneration of peripheral nerves and ischaemic muscle damage) |
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List factors that predispose to thrombi formation (4):
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1. Venous stasis
2. turbulent blood flow 3. hypercoagulability 4. endothelial damage |
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Aortic thromboembolism (cats)
-CS |
SUDDEN ONSET OF PARESIS/PARALYSIS OF HINDLIMBS
(DDx: snake envenomation, trauma, IV disc disease, spinal lymphoma, FCE) -may see right forelimb lameness if right brachial artery involved +/- ischaemic necrosis of one footpad -distress/pain -tachypnoea and dyspnoea -heart murmurs/gallop rhythm -hypothermia -**femoral artery pulses absent or weak** -cold legs and feet -cyanotic footpads and nailbeds -no haemorrhage when toenail cut short -muscles painful, firm and swollen |
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Aortic thromboembolism (cats)
-Clin path |
-SK muscle damage and necrosis (Increased ALT/AST w/in 12 hours, peaking at 36 hours; increased CK)
-stress hyperglycaemia and azotemia -metabolic acidosis -hyperkalemia w/ reperfusion if rapid |
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Aortic thromboembolism (cats)
-Dx |
-PE
-Echo |
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Aortic thromboembolism (cats)
-Tx |
-ANALGESIA (buprenorphine+/- ACE as anxiolytic)
-treat underlying heart condition (avoid propranolol-may cause vasoconstriction) -Palliative (cage rest) -**Clopidegrel* or LMWH + Aspirin** -**DO NOT PERFORM SURGERY** |
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Congenital murmurs
-PDA -definition |
-diverts blood from the pulmonary artery into the aorta which closes functionally w/in hours of birth
-dogs, females -left to right shunt from the aorta to the pulmonary artery -continuous murmur |
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Congenital murmurs
-PDA -Pathophysiology |
-increased venous return from the pulmonary circulation causes VOLUME OVERLOAD on the LA and ventricle=compensatory dilation and hypertrophy
-increased AFTERLOAD on right ventricle |
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Congenital murmurs
-PDA -PE |
-continuous/'machinery' murmur
-widened pulse pressure and 'water hammer' pulses (lower aortic diastolic pressure) -PRE CORDIAL THRILL low on L heart base |
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Congenital murmurs
-PDA -Dx |
-PE
-Rads: Lateral: cardiac enlargement (LA and auricle), pulmonary over circulation, evidence of CHF in severe cases DV: triple bulges: 1 o clock pulmonary trunk, 2 o clock aorta, 3 o clock left auricle -ECHO: left heart enlargement and dilation of the pulmonary trunk; Doppler: turbulent blood flow in pulmonary artery |
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Congenital murmurs
-PDA -Tx |
-manipulate ductus closure after birth-surgical ligation**
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Pulmonic stenosis
-pathophysiology |
-English bulldogs, boxers, beagles; males
-increased afterload on the right ventricular wall and concentric hypertrophy -post-stenotic dilation of main pulmonary artery |
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Pulmonic stenosis
-CS |
-usually none, murmur incidental
-RSCHF (RARE) |
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Pulmonic stenosis
-Dx |
1. PE:
-ejection murmur at left heart base -normal femoral pulses 2. ECG -evidence of RV enlargement 3. Rads: -RV enlargement -lateral apex elongation 4. ECHO: -grading -RV hypertrophy/dilation -RA enlargement -deformity/narrowing of pulmonic valve -post-stenotic dilation -measure jet velocity |
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Pulmonic stenosis
-Tx |
closed patch graft
closed valvulotomy balloon dilation (valvuloplasty)*** |
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Aortic stenosis or subaortic stenosis
-Pathophysiology |
-resistance to left ventricular outflow=increased afterload on the left ventricle and concentric let ventricular hypertrophy
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Aortic stenosis or subaortic stenosis
-CS |
-exertional syncope and sudden death (acute peripheral arterial and venous dilation and BRADYCARDIA; +/- arrhythmias)
-large breed dogs |
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Aortic stenosis or subaortic stenosis
-Dx |
1. PE
-harsh systolic ejection murmur left heart base -precordial thrill low on LH base -Pulses weak ** (low systolic presure) and late rising 2. Rads: -LV enlargement -cranial mediastinal widening (post stenotic dilation) 3. Echo: -LA enlargement and dilation of ascending aorta -LV hypertrophy -systolic turbulence -**measure velocity across aortic valve** |
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Aortic stenosis or subaortic stenosis
-Tx |
-not indicated for mild SAS
+/- prophylactic a/b for potential bacteraemia episodes due to risk of endocarditis -exercise restriction -Beta blockers may decrease myocardial oxygen demand -surgery (balloon dilation) |
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Ventricular Septal Defects
-Aetiology/Pathophysiology |
-failure of closure of the interventricular foramen (high in the membranous portion of interventricular septum)
-part of Tetralogy of Fallot -English Springer Spaniels -pressure and volume overloads on the right ventricle -increased preload may result in LEFT VENTRICULAR FAILURE |
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Ventricular Septal Defects
-CS |
-murmur on Right parasternal edge
+/- heart failure (LS) |
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Ventricular Septal Defects
-Dx |
1. Small defects:
-loud murmur -may resolve spontaneously 2. Moderate defects: -loud heart murmur -rads: cardiomegaly and pulmonary over-circulation 3. Large Defects: -rare (most animals die w/in first few weeks of age from CHF) -heart murmur often softer than w/ smaller defects -easily visible on 2D echo |
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Ventricular Septal Defects
-Tx |
-treat large defects
-treat CHF as standard -reduce shunt flow: medically w/ vasodilator; surgically by creating a pulmonic stenosis, ideally close defects |
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Pericardial effusion
-DDx (causes) |
Dog:
-NEOPLASIA AND IDIOPATHIC (haemangiosarcoma of RA, aortic body tumour [chemodectoma], ectopic thyroid carcinoma, metastatic) -other: coagulopathies, infection, CHF, hypoalbuminaemia, ureamia, preicardial cysts, left atrial tear, pericardial FB Cat (less common): -FIP -CHF (esp. if pleural effusion) -Bacterial pericarditis -uraemia -coagulopathies -lymphoma -metastatic neoplasia -left atrial tear -idiopathic pericarditis |
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Pericardial effusion
-signalment |
-large breed dogs >5y
-Haemangiosarc: GSD, GR, male Chemodectoma: Boxers, E. Bulldogs, BT |
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Pericardial effusion
-CS |
1. Chronic: RSCHF (end-point)
-lethargy, anorexia, weakness, collapse, abdominal distension, tachypnoea, -ascites, muffled heart sounds, audible fluid on thoracic auscultation (modified transudate: increased hydrostatic pressure), jugular venous distension tachycardia -pulsus paradoxus: exaggerated fall in blood pressure during inspiration 2. Acute: -sudden collapse -weak pulses +/- pulsus paradoxus -sudden death |
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Pericardial effusion
-Dx |
-lab tests if suspect systemic disease
-Rads: mild to severe enlargement of cardiac shadow; heart may be obscured (pleural effusion) -ECG: sinus tachycardia, low voltage QRS complexes, variations in QRS amplitudes -ECHO: definitive; diastolic collapse of RA and or RV look for heart base masses |
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Pericardial effusion
-Tx |
DO NOT USE DIURETICS (will further decrease preload and CO)
**Pericardiocentesis** -ultrasound guided |
