Cardiac Arrhythmias

• Cardiac Arrhythmias involve an abnormal heart rhythm

Definition

• Abnormal heart rhythm due to disturbances in impulse formation or conduction

Etiology

• Primary cardiac diseases include DCM and myocarditis
• Electrolyte imbalances such as hyperkalemia, hypokalemia, and hypocalcemia
• Systemic diseases such as GDV and splenic masses
• Drug toxicities such as digoxin and anesthetics
• Hypoxia, pain, and trauma are additional factors

Signalment

• Primarily affects middle-aged to older dogs, especially those with degenerative conditions
• Dobermans with DCM
• Boxers with ARVC
• Labrador Retrievers
• Risk factors includes underlying heart disease, systemic illness, trauma, and high vagal tone

Key Clinical Signs

• Syncope or collapse
• Exercise intolerance
• Weakness and lethargy
• Pulse deficits
• Irregular heart rhythm or bradycardia/tachycardia

Pathophysiology

• Disruption in electrical conduction leads to poor cardiac output, resulting in reduced perfusion and clinical signs like syncope and weakness

Diagnostic Approach

• Auscultation reveals an irregular rhythm and pulse deficits
• ECG confirms arrhythmia type, such as VPCs or AV block
• Chest radiographs show the cardiac silhouette
• Echocardiogram shows structural heart disease
• Blood tests include electrolytes, cardiac troponin, and thyroid panel, especially in older dogs

Treatment

• Depends on the arrhythmia type
• For VPCs/Ventricular tachycardia, use Lidocaine IV bolus (2 mg/kg), then CRI if needed
• For Supraventricular tachycardia, use Diltiazem PO (0.5–1.5 mg/kg q8h)
• For Atrial fibrillation, use Digoxin (0.002 mg/kg PO q12h) ± diltiazem
• For 2nd/3rd degree AV block, a pacemaker is the treatment of choice
• Prevention involves monitoring at-risk breeds, early detection of underlying heart or systemic disease, and avoiding cardiotoxic drugs

Prognosis

• Varies with the arrhythmia type
• Benign VPCs has a good prognosis
• V-tach/3rd degree AV block without treatment has a guarded to poor prognosis
• Improved outcomes are seen with a pacemaker

Exam Traps/Differentials

• Rule out seizures in syncopal events
• Differentiate between physiologic arrhythmia like high vagal tone versus pathologic arrhythmia
• Avoid confusing artifact with arrhythmia on ECG
• GDV and splenic mass can cause VPCs without primary heart disease

Canine Heartworm Disease

• Parasitic disease caused by Dirofilaria immitis
• Leads to pulmonary artery and right heart disease

Etiology

• Transmitted by mosquito vectors
• Filarial nematode Dirofilaria Immitis

Signalment

• Dogs that spend a lot of time outdoors
• Affects dogs of any age, often found in dogs >1 YO
• Endemic in warm, humid climates such as SE USA

Key Clinical Signs

• Asymptomatic in early stages
• Symptoms when advanced: Cough, dyspnea, exercise intolerance and fatigue, weight loss
• Hemoptysis and syncope
• Caval Syndrome can have collapse and hematuria

Pathophysiology

• Worms in pulmonary arteries leads to inflammation & fibrosis causing pulmonary hypertension and right-sided heart failure

Diagnostic Approach

• Antigen testing (detects adult female worms): Gold standard screening
• Microfilaria test or test with Knott's test
• Thoracic rads show enlarged pulmonary arteries
• Echo visualizes worms
• CBC/UA may show proteinuria and eosinophilia

Treatment

• Must give strict cage rest to lower emboli risk
• Melarsomine dihydrochloride IM
• Macrocyclic lactones as microfilaricides
• Doxycycline: 10 mg/kg PO BID x 4 weeks which kills Wolbachia

Prevention

• Monthly treatments are preferred: moxidectin, selamectin, ivermectin, milbemycin
• Begin treatment in puppies at 6-8 weeks

Prognosis

• Early intervention: Good prognosis, mild to little pulmonary disease
• Advanced disease/ Cavel Syndrome: poor to guarded prognosis
• All-male infections may create negative results in heartworm tests
• Differentiate primary pulmonary problems from this disease; must extract in cavel syndrome

Canine Systemic Hypertension

• Persistently increased systemic arterial blood pressure
• Indicated by systolic reading above or around 160 mmHg

Etiology

• Most Common: Secondary hypertension from other diseases
• More Common: Kidney disease problems
• Hyperadrenocorticism(Cushings), Diabetes, Pheochromocytoma, Hypothyroidism
• Primary (idiopathic) is rare

Signalment

• Higher risk if prone to endocrine problems or kidney disease
• Most Common: Older or middle aged dogs
• Breeds are not predisposed

Key Clinical Signs

• Asymptomatic in early diseases
• Epistaxis, acute blindness, neurology signs
• TOD often occur, like retinal hemorrhage protein urea or left ventricular hypertrophy

Pathophysiology

• Organ damage and vascular resistance, RAAS activation leads to hypertension through underlying kidney problems and/ or fluid retention

Diagnostic Approach

• Indirect BP measurement: Hypertension = systolic >160 mmHg
• Repeat Measurements
• Fundic exam
• Rule out protein urea

Treatment

• Address any underlying health problems
• ACE inhibitors (enalapril, benazepril) are commonly utilized, especially in cases of proteinuria
• Check BP one to two weeks after starting therapy
• First in line meds, amiodipine (ca channel blocker)

Prevention

• Perform screenings in older dogs with kidney and or endocrine disease

Prognosis

• Good if properly recognized and managed
• Only guarded if severe or managed poorly
• Neurologic disease can mimic neurologic disease, or tachycardia which is hypoxia induced
• Must repeat blood pressure to discern hypertension from excited bp spikes

Canine Pericardial Disease

• Affects the pericardium, mainly pericardial effusion, ending in cardiac tamponade and impaired ventricular filling

Etiology

• Can be infectious, idiopathic, coagulation disorder, or trauma
• neoplasia is more common, especially hemangiosarcoma around the heart

Signalment

• More prevalent in goldens, and German Shepards with hemangiosarcoma

Key Clinical Signs

• Jugular Venous Distension, Weakness, exercise limitations
• Without pulmonary Edema: Ascites, Muffled Heart Sound, Tachypnea, collapse

Pathophysiology

• Pericardial fluid compression of the heart (mainly RA/RV) → reduces venous return and preload, and CO causing right side failure

Diagnostic Approach

• ECG may signify swinging heart
• Thoracic radiology signifies globoid heart
• Abdominocentesis for ascites to locate pure transducer
• Echo indicates effusion and masses

Treatment

• Pericardiectomy if relapse occurs
• Pericardiocentesis first line if tamponade becomes issue

Category

• Palliative or chemo dependent with neoplasic issues; diuretics may worsen the issue
• Neoplasia should be detected early for any hope

Prognosis

• Poor for neoplasia and good to fair for idiopatheic effusions
• Must differentiate with CHF where no pulmonary issues occur

Congenital Heart Abnormalities

• Altered flow and cardiac function can arise from structural problems upon birth
• errors and genetic
• early detection diagnose during youth
• Exercise limitations/stunted growth may indicate, asymtomatic early on

Etiology

• Genetic/developmental errors during embryogenesis
• Breed predispositions tend to be inherited

Signalment

• Diagnosed during childhood

General Notes

• Subaortic Stenosis: golden retrievers and new found lands
• VSD: Multiple Breeds
• Tetralogy: keeshond

Pathophysiology

• Valve defects arise causing preload, afterload, chamber hypertrophy

Diagnostic Approach

• ECG reads chamber enlargement
• Gold Standard is def Echo exam!!
• Auscultate Murmurs and locate issue from that

Treatments for Each

• PDA; coil and surgical
• Pulmonic Stenosis balloon Valvuloplasty
• Subaortic SAS: Atenolol for gradient reduction
• Often small VSD but will need surgery later
• Fallot requires medical management later on-prolong lifespan -pallitive only

Prognosis

• If a PDA is dealt eary on that creates excellent prognosis. If a tough complex defect occurs it is generally guarded
• Watch for heart flow and make sure grading is noted.
• Murmors, innocent mumur needs to be differentiated at all times, not congenital

Congestive Heart Failure

• Syndrome in which the heart falls to meet metabolic demands, and venous pressure leads to accumulation of fluid
• MMVD in small breeds, dilated cardiomyopathy (DCM) mainly in larger breeds

Etiology

• Disease and arrhythmias can cause

Key Clinical Sign

• Left- Cough dyspnea intolerance
• Right:pleural effusion ascites

Diagnostic Approach

• Rads to look for cardiomegaly
• echo is most specific for origin
• Nt Pro Bnp and arrhythmia's can be further checked

Treatment

• 1-4 mgs forosimide for treatment via multiple methodes.
• pimo.25 q12h
• check enalipril/ace inhibitors
• Oxygen cage rest
• Give abdo tap for right sided

Prevention

• Monitor breeds often, look for diastolic valve problems and treat

Progonsis

• can treat MVD, do not cure

Diabetes Mellitus

• Lack of insulin production causing hyperglycermia
• TYPE 1:destruction type 2: resistance Signalment females get more then males. schnauzers/dachsons
• Polyuria PU, polydipsia PD , weight reduction, cateracts, infections are key clinical signs Diagnostic Approach rule out UTI first. bg over 200 rules out diabetes
• reflects bg levels

Treament

Diet, fibre complex carb vetisulin, need insulin

8. Hypothyroidism

• When the thryroid stops and is slow, auto immune destorys function
• idopathic and latrogenis can relate golden retrieve, low activity, with dullness

Key Clinical signs

• hair loss and cool
• bradycardia, hair loss. rat line

Diagnostic Approach

• low T4, high TSH High cholosteral

Treatment

lethothyroxin .02

• treat 4-8 weeks

cushing disease

• high cortisol production

Etiology

1. PDH: Beniegn ACTH
2. ADH: Bad tumor on the kidney

Key Cinical Signs

• pot bellied weak dog +calcinosis cutis

Test

1. urine cortisol
2. Ldd suppression ###Treatment

• Trilotane for small problems
• mitotane

Hypodrenocorticism

• Addison disorder results from failure
• Immune mediated kills adrenal cortex

etiology

drug overdose, lack of failure

low sodium in blood

clin Signs

• slow with a great pretender addisons crisis= fluids

• gastro**

• parvo hemmorgia from diarrhea -

• hepatic*

• cirrhosis:long problems

• cholestrol, bile and albumim

• hemolymphatic**

• lymphomas:large glands

canine distemper virus is very complex with the neuro

tick bourne ricketsie

arthritous from joint disease