Cardio disease PE findings
- tachypnea (c/d) and coughing (dogs esp)
- cachexia in chronic/severe
- long CRT = reduced CO, COULD be cardiac
- jugular pulses not distended unless R heart failure (elevated venous pressure)
- lung sounds crackling, wheezing, dull or absent
- ascites (R sided failure)
- possible weak or bounding femoral pulses
Systolic murmur ddx
- mitral regurg: PMI L 4-6, older, small-breed dogs
- tricuspid regurg: PMI R 3-5, labs
- subaortic stenosis: PMI L heart base or R cranial, maybe poor femoral pulses? boxers, labs, newfies
- pulmonic stenosis: PMI L heart base, normal femoral pulses, pitbulls and labs
- VSD: PMI R thorax
disastolic murmur ddx
- aortic insufficiency: bacterial endocarditis most common in dogs
- pulmonic insufficiency: rarely audible, may be ausculted secondary to pulmonic stenosis
continuous murmur ddx
PDA: machinery sounds loudest at cranial thorax, bounding femoral pulses
Cats with cardiac disease and coughing
cardiac disease weight changes
- cardiac cachexia: loss of lean muscle, most notable along topline and temporals
- ascites: accumulate of transudate in perionteal cavity, pot-belly. Could cause inappetance
clinical signs of degenerative mitral valve disease
- Sometimes none
- cough: soft or harsh. Airway compression from enlarged left atrium or pulmonary edema
- increased RR, resp distress: pulmonary edema
- syncope: reflex? Pulmonary hypertension, arrhythmia, left atrial tear
- weakness, exercise intolerance, weight loss: uncommon before end-stage
complications of degenerative mitral valve disease
- 1. left atrial volume and pressure increase = bronchus compression = COUGH, = syncope (unknown mech), = left atrial tear from jet lesions and can cause hemorrhagic pericardial effusion
- 2. increased pulmonary vein and capillary pressure (>20-25 mmHg)
- 3. increased systemic pressure in pulmonary arteries = pulmonary hypertension
- 4. pulmonary edema
cardiac auscultation findings typical of degenerative mitral valve disease
- systolic click: early stage due to mitral valve prolapse, lub-click-dub, gallop-like
- left apical systolic murmur: 5th space at level of apex beat, usually 2/6-4/6, NO CORRELATION between intensity and severity
ACVIM classification of degenerative mitral valve disease (cardiac size, clinical signs)
- A: at risk, all still normal
- B1: mild, mitral regurg but no other signs
- B2: moderate, mitral regurg and LA AND/OR LV ENLARGEMENT. Possible clinical signs in late B2
- C: severe, mitral regurg, LA and/or LV enlargement, PULMONARY EDEMA, possible clinical signs
- D: refractory, mitral regurg, enlargement of LA and/or LV, pulmonary edema, possible clinical signs
At what stage/ACVIM classification of degenerative mitral valve disease should medical treatment be initiated?
- B2 with clinical signs is controversial
- Yes for sure in C.
differences between degenerative mitral valve disease and endocarditis
- DMVD is endocardIOSIS.
- Endocarditis: RARE, appears in LARGE dogs, infection, NEW murmur, fever, lameness, lethargy, anorexia, CHF with pulmonary edema
- DMVD: COMMON, SMALL breed dogs, genetic or age-associated, murmur present for YEARS before clinical signs, CHF with pulmonary edema, cough, syncope
mitral valve insufficiency
- backflow from left ventricle (LV) to left atrium (LA)
- occurs during ventricular systole when mitral valve is closed
tricuspid valve insufficiency
backflow from right ventricle to right atrium, occurs during ventricular systole when AV valves are closed
aortic valve insufficiency
- backflow from aorta to left ventricle
- occurs in ventricular diastole when aortic valve is closed
pulmonic valve insufficiency
- backflow from pulmonary artery to right ventricle
- during ventricular diastole when pulmonic valve is closed
Pressures (diastolic, systolic) in chambers of the heart. LA, LV, Aorta, RA, RV, pulmonic
- LA: 5-7 mmHg on both
- LV: 0, 120
- Aorta: 80, 120
- RA: 3-5 mmHg on both
- RV: 0, 25
- Pulmonic: 15, 25
mechanisms for degenerative mitral valve disease
- leaflets: degenerative, infectious (endocarditis), congenital (dysplasia)
- valve annulus: enlargement with LV dilation
- chordae tendinae: rupture from dengeration, infection, trauma
- papillary muscles: displacement from LV dilation or thickening
- thickening of spongiosal layer (cartilage almost) of mitral valve, first degenerative changes. Accumulation of glycosaminoglycans, disruption of fibrosa.
- Thickened leaflets with ballooning and nodules at edges, thickened and elongated chordae tendinae
most common populations with degenerative mitral valve disease
- MOST COMMON cardiac disease in dogs, almost 100% prevalence in small breed old dogs
- middle age to old small breed most likely, more in CKCS (after 4 years old)
- more males than females (always in cardiac)
progression of degenerative mitral valve disease
- normal, starts prolapse or ballooning, no insufficiency/leakage yet. Then valve insufficiency, can be mild to severe in volume
- takes YEARS
rads (views) for cardio (DMVD)
B-type natriuretic peptide (BNP)
- secreted by ventricles in response to wall stress
- promotes natriuresis (losing Na, H2O).
- Prediction risk for CHF/cardiac death, helps differentiate cardio vs non-cardio death
wide P wave =
left atrium enlargement
tall R wave =
left ventricle enlargement
medications for mitral valve degeneration
- ACE-inhibitor (enalapril, benazepril): mild, increase natiuresis and vasodilation, decrease angiotensin II and aldosterone
- Pimobendan: inodilator, + inotrope, vasodilator
- furosemide: diuretic (most important, pulmonary edema)
- could add spironolactone, thiazide, torsemide (diuretics at different places)
Best indicator of pulmonary edema in DMVD
respiratory rate, have O monitor. >40 is a strong indicator
sound waves, shows cross-sectional slices of heart structures
ejection fraction (EF)
amount or percentage of blood that is pumped or ejected from ventricles at each contraction
- one-dimensional display. Cursor is one beam of sound, only that area seen. Scroll across the monitor and change thickness or position as heart fills or contracts.
- Used for assessment of size and function.
Fractional shortening (FS)
- fraction of any diastolic dimension that is lost in systole - looks at degree of shortening of left ventricular diameter between end-diastole and end-systole
- = percentage change in left ventricular size between filling and emptying.
- Measure of FUNCTION, not contractility. Can be affected by contractility, afterload, preload
E-point to septal separation (EPSS)
- measured from M-mode at mitral valve level -- distance between septum and peak opening of anterior mitral leaflet.
- Increased by left ventricular dilation, aortic insufficiency, and mitral valve dysplasia
uses doppler principle to calculate velocity of RBC - allows analysis of moving cells or myocardium to give direction, velocity, character, timing of blood flow, muscle motions
velocity of blood flow is calculated by moving a cursor
ultrasound pulses to examine flow at specific sites
continuous wave doppler
no limit to max velocity and not site-specific like pulsed-wave
- blood flow is coded in red (towards transducer) or blue (away from transducer), and superimposed on black 2-D image.
- High velocities are a mosaic of color
velocity of myocardial motion. Assesses systolic and diastolic function and synchronicity
- measures summed surface potential changes as a result of cardiac electrical activity to make a graph (ECG) of this activity.
- Takes longer = wide
- more cells depolarized = higher
vectors, leads and corresponding waves on ECG
- sum of vectors causes wave. Parallel or towards pole is highest, perpendicular is lowest.
- Lowest amplitude lead is isoelectric.
- Towards positive pole make an upward deflection.
results from depolarization of the ventricles
depolarization of the atria
represents time elapsed during AV node conduction
Mean electrical axis
axis along which summed vector of ventricular depolarization travels. Will be perpendicular to isoelectric (1, 2, 3, RLF)
- ventricular depolarization stimulation originated in the ventricles, not the His-Purkinje (slower).
- Can be VPC/VT. Could also be abnormal due to abnormal conduction pathway
- COuld be structural or physiologic block of His-Purkinje system (any part), causes wide and bizarre
- could be aberrancy
three or more consecutive VPCs. Can be non-sustained/paroxysmal (<30s) or sustained/non-paroxysmal (>30s)
- excitable tissue stimulated during relative refractory period = decreased conduction velocity.
- can cause wide QRS without leaving normal conductance pathway
Hyperpolarization/cyclic nucleotide gated channels (HCN)
voltage-gated channels in the SA node that are the ONLY ONES that open at relatively depolarized resting membrane potential of the heart.
- resting membrane potential
- absolute refractory period
- relative refractory period
- resting membrane potential
voltage-gated channels that stimulate heart tissue (atrial myocardium, ventricular myocardium, His-Purkinje, SA, AV nodes)
- Na+ channels in atrial and ventricular myocardium and his-purkinje tissue
- Ca2+ channels in SA node and AV node
- responsible for most clinically significant tachycardias (a-fib, v-tach, v-fib)
- requires: region of unidirectional block, region of non-conduction and region of slowed conduction. Could be refractory or permanent (infarct)
- critical number of reentry circuits required to cause/maintain fibrillation. More dilated chambers make more spiral waves
- causes tachycardia
- previous action potentials cause depolarizing afterdepolarizations, can self-perpetuate
- could be early afterdepolarization (before cell depolarizes back to resting membrane potential EAD) or delayed afterdepolarization after cell returns to restingMP, DAD)
non SA-node tissue that becomes automatic (happens in ischemia).
- for antiarrhythmic drugs
- Group 1A, 1B: sodium channel blockers
- Group 2: ligand-gated receptor blockers, beta-adrenergic blockers
- groups 3: prolong action potentials
- group 4: voltage-gated ion channel blockers
class I on vaughn-williams classification
- sodium channel blockers
- decrease phase 0 depolarization rate, decrease conduction
- variable effects on APD
- use, reverse use dependence
- Uses: atrial/ventricular myocardial and His-Purkinje tissue (bypass tracts)
class 1A drug examples and uses
- Procainamide: SVT/VT, minimal effect at APD. Reverse use dependence (increased affinity for Na+ channel rest state)
- Quinidine: SVT (especially a-fib), VT. Increases APD, peripheral alpha blockade.
class 1B drugs
- FIRST CHOICE for VPC, VT.
- SVT (esp opioid-induced atrial fib).
- Use dependence (increase affinity for Na channel active state)
- shortens APD
Class II drugs
- variable effect on APD
- subtype selectivity
- negative inotropes
- variable half-lives (esmolol: ultra-short)
- Atenolol, metoprolol = selective beta 1 blockers. NO REASON to use non-selective.
Class III drugs
- Prolong APD
- Prolong refractoriness
- potassium channel blockade (cause delayed repolarization, make ARP longer)
- minimal effects on inotropic function
Class IV drugs
- calcium channel blockers
- nodal tissue
- minimal effect on APD
- negative inotropes
- diltiazem, verapamil
- wide complex: originate outside His-Purkinje system in ventricle (VPC/VT) or depolarize ventricles outside normal His-Purkinje tract in normal sequence. Could also be caused by bypass tract (from atria by not through AV node)
- narrow complex: supraventricular reentry arrhythmias like a-fib or abnormal atrial automaticity like a-tach. Normal His-Purkinje causes narrow QRS
Wolf Parkinson White Syndrome
a bypass tract from atria bypasses AV node then travels retrograde up the AV node, causing a potential reentry circuit (atria, bypass tract, ventricle, AV node)
- most common supraventricular arrhythmia
- rapid chaotic electrical activity in atria (500bpm in dog! 400bpm in horse!)
- tachycardia, normal QRS and irregularly irregular R-R intervals (hits AV node at different times in cycle)
- quinidine or electrical cardioversion, but often Ca channel blockers to decrease AV node conduction and manage tachycardia, since normal may not be reachable. Digoxin (PNS) and or beta blockers too. Shoot for 90-100bpm in dog.
oxygen in cardio
antiarrhythmic! Normalizing O2 by giving more, fixing failure or tachyarrhythmias helps a lot!
Electrolytes in cardio
serum electrolyte abnormalities change membrane potential and ion channel function. This alters substrate and predisposes to arrhythmias.
causes of pericardial effusion in dogs (2-3 + examples)
- neoplasia: most common. hemangiosarc (lg breed middle age), chemodectoma (brachycephalic, mesothelioma, lymphoma, ectopic thyroid carcinoma
- non-neoplastic: idiopathic (very common), toxin (rodenticide), LA rupture (severe mitral regurg)
- other: pericardioperitoneal diaphragmatic hernia, hypoalbuminemia, congenital pericardial cyst, immune mediated vasculitis, bacterial/fungal pericarditis (penetrating wound)
causes of pericardial effusion in cats
- heart failure # 1!
- neoplasia common (lymphoma, carcinoma)
presenting complaint in pericardial effusion
- increased RR
- abdominal distension
physical exam findings in pericardial effusion
- muffled heart sounds
- weak +/- variable pulses (pulses paradoxus = decreased systemic BP with inspiration (tampanade)
- decreased CRT, pale mm
- +/- jugular pulses
- +/- ascites or hepatosplenomegaly
Diagnostics for pericardial effusion
- ECG: sinus tachycardia, low amplitude on QRS, VE or SVE, electrical alternans
- Minimum BW: QATs may be normal, Coags - rule out. Troponin in older dogs indicates neoplasia.
- T FAST: confirm pericardial fluids, tamponade
- Thoracic rads: globoid heart, distended cd VC, pleural effusion, mass lesion at heart base, cranial thorax or mets.
- Echo: amt and echogenicity of fluid, thickness of peircardium and presence of a mass. Free fluid gives great contrast but tap if hypotensive, tachycardic or shocky
When to tap in pericardial effusion
- R atrial or ventricular tampanade
- Clinical signs
when not to tap in pericardial effusion
- no tampanade or clinical signs, not much fluid
- abnormal coag
- suspected LA rupture (small breed dog with history of murmur, CKCs, maltese, poodle, etc)
Pericardiocentesis: DO _________ and _______! Check for _________
DO NOT _______
- DO: IV catheter and give fluids! Need to improve CO and treat hypovolemic shock.
- Check for: Rule out CHF first, esp in cats and small breed dogs
- DO NOT: give lasix or vasodilators (reduce ventricular filling and worsen hypotension
How to pericardiocentesis!
- sedate if anxious, torb is better because methadone causes panting
- sternal or lat recumbancy
- Right side of thorax ALWAYS (may hit coronary groove otherwise, which is arrhythmogenic)
- fluid in red and purple top. LOOK FOR clotting in red, this tells you you're in the heart. Submit both.
- Monitor overnight
- IV fluids, continuous ECG, check for more fluid before discharge.
- Pericardectomy may be necessary if needs second tap
Risks of pericardiocentesis
- laceration of coronary or atria
- intra-cardiac puncture
- death VERY rare.
- Prognosis good for idiopathic pericardial effusion, though often need pericardectomy
- prognosis fair for chemodectoma (may live over a year with pericardectomy)
- poor for hemangiosarc (days to weeks)
define occult cardiomyopathy
- disease of the cardiac muscle (myocardium) with NO CLINICAL SIGNS but WITH cardiac dysfunction
- can be dilated, restrictive or hypertrophic
Echo and ECG characteristics of doberman cardiomyopathy
- genotypic (carrying mutation), occult (arrhythmias and dysfunction but no clinical signs) or overt (signs).
- premature beats, tachycardia, gallop rhythm, murmur due to mitral regurg because of annulus dilation
- present with syncope, weakness, dyspnea/cough.
- ECG/Holter: ventricular premature beats (>100/24h or coupling) and/or ventricular tachycardia
- echo: left ventricular dilation (eccentric hypertrophy and decreased systolic function)
Echo and ECG characteristics of Boxer ARVC
- arrhythmogenic right ventricular cardiomyopathy (ARVC)
- desmosomal abnormalities, fatty infiltrates in RV.
- ECG: VPCs, couplets, V-tach.
- Echo: normal or LV dilation, reduction in systolic function
Common causes of myocarditis
- cardiotropic viruses: parvo, adenovirus, herpesvirus
- Bacterial agents: borrelia
- protozoal agents: trypanosoma cruzi
- toxins: anthracyclines
- hypersensitivity: cephalosporins, digoxin, diuretics
- immunological syndromes: post-infectious, inflammatory bowel disease, lupus
Common causes for cardiomyopathies
- inherited/genetic (primary), juvenile vs breed
- drug toxicity/toxins, hypersensitivity
- infectious/inflammatory, virus, bacteria, protozoa, parasite, fungal
- arrhythmias (tachycardia-induced)
- immune mediated
clinical signs of left heart failure and right heart failure
- left: pulmonary edema (d/c), pleural effusion (cats)
- right: pleural effusion (cats), ascites (dogs), SQ edema (horses and cattle)
list 4 diuretics and main characteristics, potency
- torsemide: ascending loop of henle, most potent/strongest
- Furosemide: ascending loop of henle, 2nd most potent
- hydrochlorothiazide: distal tubule, third most potent
- spironolactone: collecting duct, so weak/not potent that may not even be a diuretic (in healthy animals) - never use alone!
Furosemide: mode of administration in acute tx of stage C heart failure
- IV! Diuresis within 30 minutes (PO takes 2-3 hours). Bolus then CRI
- High ceiling, so dose gets VERY high before it stops increasing diuresis
how to monitor response to diuretics in stage C heart failure
- increase in BUN and reduction in electrolytes means it's working.
- monitor RR hourly (<40 at rest)
drugs recommended for chronic treatment of stage C heart failure
- furosemide/diuretics (can increase/combine): decrease backlog and PE, pressure
- pimobendan: +inotrope, vasodilator
- ACE Inhibitors/Enalapril: block RAAS, allow diuretics to work (USE WITH DIURETICS)
- +/- O2 supplementation, sedation, K+
- inability of the heart to provide optical O2 and nutrient supply to body, maintain CO without COMPENSATORY MECHANISMS
- compensated (B1, B2) or decompensated (C, D) stages
stages of heart failure
- A: at risk
- B1: heart disease, no cardiomegaly, NO SIGNS
- B2: heart disease, cardiomegaly, NO SIGNS
- C: clinical signs
- D: clinical signs, refractory to tx
problems with large volume ascites
- renal congestion
- intestinal edema (decrease absorption, bacterial translocation)
- hepatic congestion
- impairs diaphragmatic function
- cachexia (increase protein! Boiled egg)
tx of pulmonary edema vs ascites
- PE: diuretics
- ascites: abdominocentesis. Can use diuretics to prevent/limit ascites from returns AFTER tap
what is a cardiac emergency?
anything that diminishes the heart's ability to pump so that organ perfusion is vitally decreased (or has potential to do so)
pericardial effusion and PE
- fluid accumulation in pericardial space
- causes tampanade when exceeds right atrial pressure, decreases venous return and preload = decreased SV
- muffled heart sounds, tachycardia, jugular pulses, poor femoral pulses, ascites
factors that progress pericardial effusion to tampanade (3)
- fluid accumulation
- fluid characteristics
- pericardial compliance
pericardial effusion and imaging
- Electrocardiogram: decreased R wave amplitude, tachycardia, electrical alternans
- Thoracic rads: globoid silhouette, pericardiomegaly, +/- dilated caudal VC
- echo: pericardial fluid +/- tampanade, +/- space occupying lesion (neoplasia, fibrin, thrombus), +/- pleural fluid
pericardial effusion therapy
- pericardiocentesis: sterile, lido block, ECG monitor, IV catheter and fluids, over-needle catheter, stopcock with extension set, bowl, syringe, Right Hemithorax, penetrate at cardiac impulse cranial to rib. May scratch epicardium. COllect samples for cytology and culture, should not clot (clotting factors used up)
- NO LASIX
More than ____________ pericardiocentesises requires ____________
- more than three consecutive ventricular Premature Complexes (VPC). Paroxysmal or non-sustained VT = <30s, non-paroxysmal or sustained = >30s
- increases myocardial O2 = hypoxia/ischemia, decrease systolic function and more arrhythmias. Tachycardia decreases diastolic filling time = decreased preload, SV, CO
- wide bizarre QRS not preceeded by P wave. Uniform or multiform, rate varies.
- R on T is more malignant
Ventricular tachycardia therapy
- NOT ALWAYS AN EMERGENCY (but monitor)
- post-trauma is slow, benign, transient. So perfusion compromise or progression? then OK.
- Therapy: poor perfusion (low BP etc), multimorphic VPC, R on T, rapid rate, syncope.
- Lidocaine, procainamide, Mg Sulfate, amiodarone, esmolol
all _____________ can cause arrhythmias
- sodium channel blocker
- use-dependent, good for RAPID VT
- failure due to inadequate dose or hypokalemia
- sodium channel blocker
- prolongs action potential duration
- reverse use dependence
- watch for QT prologation
- Na/K pump cofactor
- calcium channel antagonist
- non-long QT ventricular arrhythmias controversial
- prolongs action potential duration (potassium channel blocker). Can also block some Na, Ca, beta blocker. MIXED ANTIARRHYTHMIC DRUG
- may cause hypotension, anaphylaxis
- ULTRA-short-acting beta blocker
- may cause hypotension secondary to negative inotropic effects
- rapid cardiac rhythm originating or sustained in SA node, atria and/or AV node, decreases ventricular filling, preload, SV, CO, myocardial O2.
- Tachycardia with NARROW QRS, may have altered P wave axis (junctional tachycardia) vs absent P waves with fibrillation (a-fib). P could be buried in previous T. R-R regular (a-tach) or irregularly irregular (A-fib)
supraventricular tachycardia therapy
- convert to normal sinus, but may not be possible so control rate and BP.
- vagal manuvers: ocular pressure (retropulse), carotid sinus massage, cold water immersion
- Quinidine, amiodarone?, diltiazem, esmolol
- Na channel blocker
- watch for QT prolongation
- Requires patient stabilization (not possible in sx)
- Ca channel blocker
- negative inotrope
- combined with digoxin +/- beta blocker for rate control in a-fib.
- oral for a-fib rate in non-ER situation
- disordered asynchronous electrical depolarization of the ventricles
- usually reentry-mediated. Severe, life-threatening emergency
- rapid, irregular undulations without QRS
Equine heart has very high ____________, which causes their __________ and _________, ___________, ___________
- vagal tone
- low heart rate
- tendency toward atrial fibrillation (shortens action potential duration, predisposes to reentry). Also respiratory sinus arrhythmia and bradyarrhythmias (sinus bradycardia and second degree AV block)
Horses extra cardiac sound
Split S2 sound - aortic and pulmonic at different times.
common murmurs in horses
- tricuspid regurg most common
- mitral regurg common
- aortic insufficiency, musical diastolic murmur in left hemithorax (older horses, seem normal)
what do we look for on equine ECG
intervals only, don't worry about mean electrical axis in a horse
most common arrhythmia in a horse and tx
- atrial fibrillation
- predisposed due to large atrial mass and high vagal tone (shortens action potential). Usually have normal cardiac structure and function ("lone" AF) but poor performance due to no diastolic filling.
- try chemical cardioversion with quinidine THEN electrical cardioversion (anesthesia risk).
- Could cause increase in ventricular rate, give digoxin (decrease AV conduction, but could make a-fib more likely)
- no antiarrhythmic has been shown to reduce fibrillatory threshold in ventricles of horses.
given to decrease AV nodal conduction (parasymp) and slow ventricular tachycardias, but can increase action potential duration in atria so could make more prone to a-fib. Also, hypotension (alpha1 block) and colic
bioavailability of heart failure meds in horses
poor due to hind gut fermentation. Esp ACE inhibitors
bacterial endocarditis in horses
- pasteurella and streptococcus
- usu mitral valve, followed by aortic valve
most common congenital cardiac defects in horse (3)
- ventricular septal defect
- tetraology of Fallot
- tricuspid valve atresia
- chronic severe heart failure
- loss of lean muscle mass, esp along topline and temporal region
jugular pulse distension
- indicative of elevated venous pressure due to R heart failure
- pericardial effusion with cardiac tamponade, heartworm disease, severe tricuspid valve insufficiency, congenital defects leading to right heart failure
systolic murmurs (5)
- mitral: L 4-6, older small-breed dogs
- tricuspid: R 3-5, labs
- subaortic stenosis: L heart base or R cranial, may have poor femoral pulses, Boxers, labs, Newfies.
- pulmonic stenosis: L heart base, normal femoral pulses, Pit Bulls, labs
- VSD: R thorax
diastolic murmurs (2)
- aortic insufficiency: bacterial endocarditis most frequent cause in dogs
- pulmonic insufficiency: rarely audible, maybe secondary to pulmonic stenosis
PDA: machinery sound loudest at cranial thorax, bounding femoral pulses