Cardiology: Diagnostic Tools

Diagnostic Tools for Cardiology

• A physical exam includes using eyes, fingers and a stethoscope
• An ECG can evaluate changes in heart rhythm
• Use a modified lead, the base apex
• Place the LA over the left apex
• Place RA on top of the jugular furrow
• Then select lead 1 on the electrocardiograph
• ECG is not useful for cardiomegaly in equine medicine
• ECG can be used for continuous and exercise evaluation of the heart
• A normal P wave is typically notched, but can vary
• P waves can be single-peaked, diphasic, or polyphasic
• QRS and T wave morphology can vary and the T wave can be negative, positive, or biphasic
• Thoracic radiographs are limited in evaluating the heart
• Use radiographs to identify pulmonary diseases related to cardiac diseases
• Echocardiography includes 2-D, M-mode, and Doppler
• M-mode displays movement of cardiac structures over time
• Doppler includes pulsed wave, continuous wave, and color-flow Doppler
• Echocardiography technology and costs are decreasing
• Use a 2-3.5 mHz probe and understand anatomy to use echocardiography
• Measure Cardiac troponin I (CnI) concentrations as a biomarker of myocardial injury

Equine Heart Exam - History

• Exercise intolerance is the most important factor, but varies with severity
• Weakness, ataxia, fainting, collapse, ADR, and colic
• Coughing, nasal discharge, and exercise-induced pulmonary hemorrhage may be present
• Sudden death
• An incidental finding means there is no history

Equine Heart Exam - General Examination/Palpation

• Check the facial or another artery for pulse strength and rhythm
• Venous distention and a jugular pulse when the head is up are abnormal
• It is normal to see a jugular pulse in the distal 1/3 of the vein
• Palpate the left thorax for the left apical beat, to assess rhythm and rate
• Observe mucous membrane color, looking for pink or cyanotic
• Check capillary refill time as an indication of peripheral perfusion

Equine Heart Exam - Auscultation

• Normal heart rate is 28-44 bpm
• The Heart rate will be slower in athletic horses
• Foals, yearlings, Draft horses, and nervous horses have a higher heart rate
• Heart sound intensity should be consistent unless there is an arrhythmia
• Muffled heart sounds indicate possibility of pericardial or pleural effusions
• Auscultation of all four heart sounds is normal in horses
• S1 is the closure of the A-V valves, and "split S1" is common
• S2 is the closure of the semilunar valves
• S3 is generated by ventricular filling
• S4 is caused by atrial contraction
• The order of heart sounds is S4-S1-S2-S3
• The left cardiac window includes pulmonic, aortic, and mitral valves
• The right cardiac window includes the tricuspid area

Cardiac Murmurs

• Murmurs result from turbulent blood flow that causes resonance in adjacent structures
• Turbulence increases with increased blood flow and decreased viscosity
• Anemia can result in a murmur, or make a soft murmur louder
• Describe murmurs by timing, duration, grade/intensity, quality/pitch, point of maximal intensity, and radiation
• Murmurs can be normal (functional) or abnormal (pathologic)

Functional Heart Murmurs

• Functional heart murmurs are caused by vibration from blood ejection through semilunar valves during systole or rapid ventricular filling during diastole
• Systolic ejection murmur is heard over the aortic and pulmonary valves, starts after S1, ends before S2, and is usually a soft grade murmur (2/6)

Pathologic Heart Murmurs

• Pathologic heart murmurs reasons include tricuspid regurgitation (TR), mitral regurgitation (MR), aortic regurgitation, and ventricular septal defect (VSD)
• Stenotic valves are rare in horses

Heart Rhythm

• Second-degree A-V block occurs in 15-18% of horses at rest, especially fit athletic racehorses, and is regularly irregular
• It is a common physiologic arrhythmia due to high vagal tone
• Heart rates can be low normal to bradycardic (24-28 bpm)
• Mobitz type I (Wenckenbach phenomenon) features progressive lengthening of the PR interval before the dropped beat
• S4 can often be auscultated during the dropped beat
• Second-degree A-V block is abolished by light exercise, but returns in 10-60 seconds

Cardiac Arrhythmias

• Causes of cardiac arrhythmias can be idiopathic such as with atrial fibrillation, autonomic imbalances, electrolyte abnormalities, and infectious or toxic agents causing myocardial inflammation or necrosis

Atrial Fibrillation

• Atrial fibrillation is the most common pathologic arrhythmia in horses
• It can be sustained or occur only during exercise (paroxysmal), with diagnosis being difficult if lasting 24-48 hours
• Often occurs without underlying cardiac disease, is more common in horses/cattle due to large atria size, and develops only with enlarged atria in small animals
• Common in racehorses, jumpers, and eventing horses
• Can result from underlying heart disease, viral myocarditis, strenuous exercise, and valvular cardiac disease
• Horses may present with poor exercise performance and epistaxis, often without reported clinical signs at rest
• Auscultation reveals irregularly irregular rhythm, firing cannons, and variable heart rhythm intensity, and normal resting heart rate without underlying heart disease
• Diagnosis via base-apex electrocardiogram showing no p waves, irregular R-R intervals with normal QRS configuration, and oscillating baseline termed little f waves
• The goal of atrial fibrillation treatment is to restore normal sinus rhythm
• Treatment in dogs focuses on controlling ventricular rate
• Do not restore normal sinus rhythm with underlying heart disease without confirming there is no other underlying reason
• Confirm with echocardiography and electrolytes

Atrial Fibrillation - Prognosis and Treatment

• Prognosis is good to convert with idiopathic atrial fibrillation if the heart rate is under 60 bpm and atrial fibrillation lasts less than 4 months
• Recurrences happen in about 25% of horses
• Transvenous electrical cardioversion has a good prognosis, but commonly relapses
• Quinidine is no longer available to convert horses
• ECG exercise test is recommended to determine if horses can be ridden post-conversion
• Horses with atrial fibrillation during exercise can develop elevated heart rates (>200), ventricular tachycardia, or V fib which can cause falls and injuries to the rider

Ventricular and Supraventricular Arrhythmias

• Ventricular tachycardia originates in the ventricles through abnormal pathways, resulting in wide and bizarre QRS complexes
• Supraventricular tachycardia originates above the ventricles, using normal conducting pathways and normal QRS
• Causes of Supraventricular tachycardia include sinus tachycardia, atrial tachycardia, atrial fibrillation, AV node and accessory pathways
• Etiology includes myocarditis from infectious agents (influenza), toxins (monensin), and other causes
• Cardiac Troponin I in cardiac muscle indicates myocardial injury
• Severe gastrointestinal disease, endotoxemia, persistent tachycardia (HR > 100 bpm insufficient diastolic time), electrolyte imbalance, and hypovolemia (horses with complicated GI disease), and endotoxemia/colic can increase Cardiac Troponin I for Ventricular arrhythmias
• Ventricular arrhythmias present with bizarre QRS complexes that are usually wide
• Treat the underlying disease, recommend rest and recheck, and avoid directly treating the arrhythmia unless life-threatening
• Use corticosteroids for myocarditis and treat gastrointestinal disease by fixing electrolytes, acid/base, and endotoxemia
• Treat ventricular arrhythmia with Lidocaine if the HR is very high, the VPC are frequent and multifocal , there is exercise intolerance, or there is an R on T phenomenon
• Magnesium salts are other anti-arrhythmic drugs
• Supraventricular tachycardia treatment depends on the cause (atrial fibrillation = TVE)
• There is no easy treatment for sustained atrial tachycardia, treat underlying disease if identified

Congenital Heart Disease - Ventricular Septal Defect (VSD)

• VSD is the most common congenital heart lesion with a genetic basis in Arabian Horses
• It can be solitary or occur with other cardiac lesions, and the clinical signs range from none to poor performance/heart failure
• A harsh holosystolic murmur is loudest just below the tricuspid valve
• Horses with small VSDs can be used as performance horses
• Diagnose with 2-D or Color Flow

Acquired Valvular Heart Disease

• Stenotic valvular lesions are rare, and regurgitant valvular lesions are common
• Causes of valvular lesions include degenerative changes, bacterial endocarditis, ruptured chordae tendinae, and inflammatory valvulitis
• Mitral and Tricuspid Regurgitation are common murmurs
• Tricuspid regurgitation is the most frequent murmur recognized
• These are common in athletic horses as incidental findings and older horses may also have mitral regurgitation
• Degenerative changes are the most common cause and bacterial endocarditis and ruptured chordae tendinae also occur
• The clinical presentation varies with an incidental finding or poor performance
• There is a grade 2 out of 6 holosystolic murmur with the PMI over the affected valve
• Echocardiography is needed to confirm
• Degenerative valve changes usually have mild regurgitation and bacterial endocarditis causes severe regurgitation

Acquired Valvular Heart Disease - Prognosis

• Prognosis depends on the severity and cause of regurgitation
• Use echocardiography to check valve morphology, chamber size, and contractility
• It can lead to congestive heart failure if the regurgitation is severe
• Mild regurgitation has no clinical significance
• Aortic Regurgitation is a common murmur in older horses with degenerative valve changes and is detected incidentally
• Aortic Regurgitation may be pathologic if detected in a young horse
• The murmur is a holodiastolic murmur loudest over the aortic valve, is harsh, and of decrescendo with a blowing nature

Myocardial Diseases

• Myocardial injury is due to drugs, toxins, ischemia, hypoxia, infectious agents, parasitic migration, prolonged tachycardia, metabolic diseases, or nutritional imbalances
• Myocardial disease can result in reduced myocardial contractility, reduced diastolic dysfunction and impaired ventricular filling, mitral or tricuspid valve insufficiency, and arrhythmias
• The amount of damage ranges from little to severe
• Clinical signs vary but include poor performance, arrhythmias, and cardiac murmurs which are exacerbated by exercise
• Serum troponin I can be increased
• Treat myocardial disease with supportive care and rest and anti-arrhythmic therapy for life-threatening arrhythmias only
• Digoxin and furosemide are indicated if there is congestive heart failure unless there is monensin toxicity which is contraindicated
• Corticosteroids can be used for active myocarditis

Specific Causes of Myocardial Disease

• Myocarditis, or myocardial inflammation, is difficult to diagnose especially to figure out the exact cause
• Prior infections such as influenza, Streptococcus equi infections, and immune-mediated diseases can cause myocarditis
• Monensin toxicosis is a toxic-induced myocardial injury
• Horses are the most sensitive species, but salinomycin and lasalocid have also been reported
• Monensin toxicosis is caused by accidental contamination of equine feeds at a feedmill or delivery of cattle or poultry feeds to horses
• Ingesting > 2-3 mg/kg body weight of monensin can result in monensin toxicity
• Ionophores react with polar cations to form lipid-soluble complexes, leading to cation transport across myocardial cell membranes
• Clinical signs vary, depending on the amount ingested and type of ionophore and can involve multiple body systems
• Clinical signs include weakness, lethargy, ataxia, colic, diarrhea, and death which can occur in 12-36 hours
• Myocardial damage can result in heart failure if there is no acute death
• The bloodwork shows decreased electrolytes, increased muscle enzymes, increased troponin I, and azotemia
• Diagnosis involves detection of ionophores in feed or stomach contents
• If acute, treat with mineral oil, maybe Vitamin E, intravenous fluids, and electrolyte supplementation without calcium
• Antiarrhythmic drugs are used for life-threatening arrhythmias
• Digoxin and calcium channel blockers are contraindicated
• Stall rest is needed for 1-3 months, with echocardiograms to check myocardial function
• Glycosides from plants like Japanese yew, oleander, and foxglove inhibit the Na K ATPase
• Blister beetles produce Cantharidin, which has a direct toxic effect, transporting excess calcium into myocardial cells
• Rattlesnake venom has been associated with cardiac injury and arrhythmias
• Additional causes of myocardial disease/dysfunction include idiopathic dilated cardiomyopathy and nutritional deficiencies like vitamin and selenium deficiency in young growing foals

Heart Failure

• Clinical signs include exercise intolerance, cachexia, tachycardia, and poor peripheral perfusion
• Right heart failure presents with jugular pulse, engorged veins, and edema, with ascites being less common
• Left heart failure presents with cough, increased respiratory rate, and pulmonary edema
• A murmur with palpable thrill
• Arrhythmia
• Etiology can be valvular degenerative with ruptured chordea, which leads to chamber enlargement and arrhythmia
• Etiology can be Congenital VSD, tetralogy of Fallot, patent ductus arteriosus
• Etiology can be Infectious vegetative endocarditis, or pericarditis
• Etiology can be Toxic, such as monensin or Taxus
• Diagnosis is based on clinical signs and echocardiography to find the underlying cause
• Treat if can identify disease and cardiac failure with furosemide, digoxin, vasodilators and ACE inhibitors
• Poor prognosis with low usage as a pasture or breeding horse, owners should not ride the horse due to sudden death and falls