Cardiology

Describe the normal cardiac cycle (atrial contraction → diastole)

1. Atrial Contraction = End of ventricular diastole

   • Atria contract → pushes the final portion of blood into the ventricles.

   • AV valves open, semilunar valves closed

   • Completes ventricular filling = End-diastolic volume (EDV)

2. Isovolumetric Ventricular Contraction = Start of ventricular systole

   • Ventricles contract → ventricular pressure rises

   • AV valves close = S1

   • All valves are now closed

   • Ventricular volume stays constant, but pressure increases

3. Ventricular Ejection = Ventricular pressure > Ao/PA pressure

   • Semilunar valves open

   • Blood is ejected into the aorta/pulmonary artery

   • Ventricular volume decreases

4. Isovolumetric Ventricular Relaxation = End of systole → beginning of diastole

   • Ventricles relax → ventricular pressure falls

   • When ventricular pressure falls below aortic/PA pressure, semilunar valves close = S2

   • All valves are briefly closed

   • Ventricular volume remains constant at end-systolic volume (ESV) while pressure rapidly decreases

5. Ventricular Filling

   • When ventricular pressure falls below atrial pressure, AV valves open

   • Blood flows from atria → ventricles.

   • Rapid ventricular filling occurs first, followed by reduced filling (diastasis).

   • Then atrial contraction occurs again to complete filling

List 6 determinants of cardiac output (CO)

1. Heart rate

2. Stroke volume and preload

3. Contractility

4. Afterload

5. Distensibility

6. Synergy

Determinants of CO: #1 HR

• Control

• 3 Effects of increased HR

Control: Inherent automaticity of SA node

• PNS (vagal) stimulation → Decreases HR

• SNS → Increases HR

• Baroreceptors increase PNS and inhibit SNS

Effects of Tachycardia:

1. Increased CO (CO = HR x SV)

2. Increased myocardial O2 demand

3. Decreased time for ventricular filling and coronary perfusion during diastole → Myocardial ischaemia → Arrhythmia

Determinants of CO: #2 Stroke Volume and Preload

• Define preload

• 7 Determinants of preload

• 5 Factors increasing preload

• 3 Factors reducing preload

Preload: Amount of stretch of sarcomere at the end of diastole (eDV)

• eDV = Volume of blood in heart at end of diastole

• More blood → More stretch → More powerful contraction → Increased preload → Increased SV

Determinants of Preload:

1. Blood volume

2. Body position (recumbency increases VR)

3. Skeletal muscle activity (venous pump)

4. Intrathoracic pressure (increased pressure → decreased VR)

5. Atrial contraction (accounts of 20% of ventricular eDV)

6. Ejection fraction (less blood ejected → more volume in ventricle for next beat)

7. MAP

Factors Increasing Preload: Excessive preload → Venous congestion

1. Venoconstriction (SNS) → Forces blood into heart (less stored in veins)

2. Increased blood volume (eg. renal retention)

3. Reduced ventricular contractility → Reduced ejection of blood from ventricle (lower ejection fraction)

4. Venous congestion (eg. valvular insufficiency)

5. Decreased ventricular relaxation in diastole

Factors Decreasing Preload:

1. Venodilation

2. Reduced circulating blood volume

3. Increased volume of blood ejected at last contraction (higher ejection fraction)

Determinants of CO: #3 Contractility

• Define “shortening fraction”

• 3 Factors increasing contractility

• 3 Factors decreasing contractility

Shortening Fraction: % of blood volume ejected from ventricles of the total blood volume available to be pumped out at the end of diastole

• = SV ÷ eDV

  

• Fractional shortening = Change in internal ventricular diameter between diastole and systole

  • Reduced shortening indicates smaller difference between systole and diastole volume in ventricle due to volume overload

Factors Increasing Contractility:

1. Increased β-adrenergic stimulation (eg. dobutamine/pimobendan = positive inotropes)

2. Reduced vagal tone

3. Increased preload

Factors Decreasing Contractility:

1. Reduced SNS (eg. β-blockers = negative inotropes)

2. Reduced preload

3. Increased vagal tone (PNS)

Determinants of CO: #4 Afterload

• Definition

• Equation

• 3 Factors increasing afterload

Definition: Tension in myocardium during ejection (represents force opposing ejection of blood during systole)

Equation:

Factors Increasing Afterload:

1. Increased ventricular volume

2. Increased arterial vascular resistance

3. Decreased ventricular wall thickness

Determinants of CO: #5 Distensibility

• Definition

• Define lusitropy

• 4 Factors reducing distensibility

Definition: Ease of ventricular filling during diastole

• Reduced distensibility → Increased preload

Lusitropy: Ability to relax, distend and fill

Factors Decreasing Distensibility:

1. Pericardial disease (i.e. pericardial effusion)

2. Reduced SNS

3. Increased wall thickness

4. Increased collagen, scarring or cellular infiltration in ventricular wall

Determinants of CO: #6 Synergy

• Definition

• 2 Factors affecting synergy

Definition: Normal coordinated sequence of muscle activation

• Reduced synergy → Reduced SV

Factors:

1. Cardiac arrhythmia

2. Regional ventricular conduction abnormalities

Define congestive heart failure

Marks end of asymptomatic compensatory period of heart disease, characterised by retention of fluids in tissues/body cavities ± decreased perfusion of tissues

• Requires lifelong medication → Inevitable death with/of heart failure

• Often long asymptomatic period with heart murmur ONLY (no medication required)

• Forward failure = Inadequate perfusion of vital organs

• Backward failure = Venous congestion

  • eg. big spleen and liver OR pulmonary congestion

• Left OR right-sided

Clinical Signs of CHF

• 6 Historical findings

• 17 findings on PE

  • LCHF (3)

  • RCHF (4)

  • Both (10)

History: “Dogs With Cardiac Abnormalities Smoke Excessively”

1. Dyspnoea/wheeze/orthopnoea/tachypnoea (LCHF)

   • Pulmonary oedema/pleural effusion (backward failure)

   • Orthopnoea = Respiratory distress while recumbent

2. Weakness (LCHF)

   • Reduced tissue perfusion (forward failure)

3. Cough (uncommon) (LCHF)

   • LAE compresses L mainstem bronchus

   • Bronchial oedema (severe pulmonary oedema in dogs ONLY) = Wet and soft cough

4. Abdominal distension (RCHF)

   • Ascites ± hepatomegaly/splenomegaly (backward failure)

5. Syncope/lethargy (LCHF) = Temporary loss of consciousness due to insufficient glucose/O2 delivery to brain

   • Reduced cerebral perfusion (forward failure)

   • Commonly precedes excitement

6. Reduced Exercise Intolerance (LCHF/RCHF)

   • Low CO

Physical Examination:

LCHF

1. Increased RRR

2. Dyspnoea, cough, wheeze, crackles (pulmonary congestion)

3. Muffled heart sounds

RHCF

1. Jugular venous distension/jugular pulse (systemic congestion)

2. Hepatomegaly/splenomegaly

3. Abdominal effusion

4. SC oedema

BOTH = Low CO

1. Slow CRT (>2s)

2. Pale/cyanotic MM

3. No sinus arrhythmia

4. Dry/tacky MM

5. Cold extremities

6. Precordial thrill

7. Cardiomegaly on precordial percussion

8. Weak femoral pulses

9. Pulse deficits = Arrhythmia

10. Gallop/murmur

List 10 steps of the cardiac clinical examination (+ examples)

1. History and signalment

2. Distance examination

3. Peripheral circulation

   1. CRT

   2. MM

   3. Warmth of extremities

4. Jugular vein

5. Arterial pulse (femoral)

6. Precordial palpation

   1. Rate

   2. Rhythm

7. Abnormal fluid accumulation = Palpation and ballottement of dependent areas for ascites, SC oedema, pleural effusion and hepatomegaly/splenomegaly

8. Cardiac auscultation

   1. Heart sounds and murmurs

   2. HR

   3. Rhythm

9. Respiratory auscultation

   1. RR

   2. Pattern

   3. Sounds

   4. Cough

10. Additional tests

    1. Thoracic radiography

    2. Blood pressure

    3. ECG

    4. Echocardiography

    5. Blood tests

       1. proBNP

       2. Cardiac troponin-1

       3. Serum biochemistry

Jugular Vein Assessment

• Purpose

• 3 features to assess

  • Normal

  • Abnormal

• 8 DDx

Purpose: Assess for RCHF and systemic congestion (also thrombosis)

Features:

1. Jugular Distension (mild RCHF)

   • Normal: <1/3 up neck

   • Abnormal: >1/2 up neck (increased CVP and impaired right-sided filling)

2. Hepatojugular Reflux (moderate RCHF) = Gently compress cranial abdomen to increase venous return

   • Normal: Heart copes → No change in jugular distension

   • Abnormal: Jugular becomes more distended

3. Jugular Pulse (severe RCHF) = Do NOT mistake for carotid artery pulse

DDx:

1. Cardiac tamponade

2. Right atrial mass

3. DCM

4. Tricuspid valve regurgitation (TR)

5. Hypertrophic RV

6. Arrhythmia

7. Pulmonic stenosis (PS)

8. Hypertension

Systemic Arterial Pulse

• Definition

• Disadvantage

• 6 Abnormal characters of pulse pressure (+ DDx)

Definition: Difference between DAP and SAP → “Proxy” for MAP

• Usually due to ∆SAP (not DAP)

-ve: Can be near normal despite reduced CO due to compensatory arterial vasoconstriction

Abnormal Characters of Pulse Pressure:

1. Difference between R and L femoral pulse

   • DDx: Thromboembolism

2. Hyperkinetic = Strong/bounding due to large difference between DAP and SAP

   • DDx: HCM, PDA, bradycardia (increased diastolic filling → increased SAP)

3. Hypokinetic = Weak due to small difference between DAP and SAP

   • DDx: DCM, PS, AS, shock, dehydration, CHF (lower SAP and tachycardia reduces contractile strength)

4. Pulsus alternans = Alternating weak and strong pulse

   • DDx: Severe myocardial disease (LV systolic dysfunction)

5. Pulsus paradoxus = Weak pulse on inspiration

   • DDx: Cardiac tamponade

   • MoA: Inspiration → Increased intrathoracic pressure → Increased VR → Increased RV filling → Pushes on LV → Decreased LV filling → Decreased SAP

6. Pulse deficits = Heart beat without pulse (HR > PR)

   • DDx: Ventricular arrhythmia (often auscultated as premature heart beat with no pulse due to insufficient ventricular filling time)

Palpating the Apex Beat

• Location

• DDx for:

  • Caudal displacement (2)

  • Right displacement (2)

  • Hyperkinetic (1)

  • Hypokinetic (4)

Location: Left side, 5th ICS = Mitral valve at the level of the costochondral junction

DDx:

• Caudal Displacement

  1. Enlarged L-heart

  2. Space-occupying mass

• Right Displacement

  1. RVE

  2. Space-occupying mass

• Hyperkinetic = Volume overload

• Hypokinetic

  1. Obesity

  2. Reduced contractility

  3. Pleural/pericardial effusion

  4. Mass

Cardiac Auscultation

• 4 Ways to classify heart sounds

• Diaphragm vs. bell of stethoscope

• Approach

Classification:

1. Frequency (pitch)

2. Amplitude of vibrations (volume/intensity)

3. Duration

4. Quality (timbre) = Affected by heart structures hit by blood

Stethoscope:

• Diaphragm = Transmits high frequency and attenuates low frequency

• Bell = Transmits high AND low frequency → Ideal for gallop sounds or low-frequency murmurs

Approach:

1. Have patient standing (avoid displacement of heart) and ensure they are not panting/purring

2. Palpate for apex beat

3. Auscultate ALL valves

   • Cat: Mid-sternum → Cranially, caudally, left and right

Fill out the following table

Valve	Position	Sound Most Prominent
Mitral
Aortic
Pulmonic
Tricuspid

Valve	Position	Sound Most Prominent
Mitral	Left 4 - 6th ICS @ costochondral junction	S1
Aortic	Move dorsally and cranially from mitral valve (level of the point of the shoulder)	S2
Pulmonic	Left 3rd ICS @ sternal border (in axilla)	-
Tricuspid	Right 3rd - 4th ICS @ level of costochondral junction	-

Heart Rate and Rhythm

• Values for bradycardia/tachycardia of dogs vs. cats

• MoA of sinus arrhythmia

Species	Bradycardia	Tachycardia
Dog (Breed-dependent)	< 60 - 70	> 160
Cat	< 120	> 200 (true tachycardia >160 but stress-tachycardia common in consult)

Sinus Arrhythmia: Indicates no CHF (good CO and low sympathetic tone)

• Inspiration = Expansion of pulmonary vasculature → Decreased SVR

  • → Decreased vagal tone → Increased HR

• Expiration = Increased vagal tone → Decreased HR

S1 Heart Sound

• Definition

• Characteristics

• Location

• 4 Causes of increased S1 intensity

• 4 Causes of decreased S1 intensity

• Define split S1 (+ 3 causes)

Definition: “Lub” = Closure of AV valves (mitral and tricuspid)

• Coincides with onset of systole and QRS complex (S1 → systole → S2)

• Arterial pulse halfway between S1 and S2

Characteristics: Louder, longer and lower-pitched than S2

Location: Loudest over left apex (5th ICS) @ mitral valve

Increased S1 Intensity:

1. Thin chest wall

2. Tachycardia/increased SNS

3. Systemic hypertension

4. Anaemia

Decreased S1 Intensity:

1. Obesity/SC emphysema

2. Pleural/pericardial effusion/diaphragmatic hernia

3. DCM

4. Hypovolaemia

Split S1: Mitral and tricuspid valves close at different times (NOT simultaneous) due to

1. Large dog with slow HR (NORMAL)

   1. Larger heart = AV valves further apart than semilunar valves → Close at slightly different times

2. Electrical disturbances (eg. ectopic beats or bundle branch block)

3. Mechanical factors (eg. MV or TV stenosis)

S2 Heart Sound

• Definition

• Location

• Define split S2 (+ 5 causes)

Definition: “Dub” = Closure of semilunar valves (aortic and pulmonic)

• Coincides with end of systole and after T wave

Location: Loudest over left heart base

Split S2: Aortic and pulmonic valves close at different times due to

1. Physiological in healthy, large-breed dogs

   • Inspiration → increased RV filling → delayed closure of pulmonic valve

2. Heartworm and pulmonic hypertension

3. Delayed closure of pulmonic valve: ASD, PS, right bundle branch block, ectopic beats

4. Premature closure of aortic valve: MS or MR

5. Delayed closure of aortic valve: AS, left bundle branch block, ectopic beats, systemic hypertension

Gallop Sounds

• Define S3 (+ DDx)

• Define S4 (+ 3 DDx)

Gallop = Low frequency heart sounds during diastole

S3 = Ventricular gallop associated with rapid passive ventricular filling in early diastole

• DDx: NOT normal (indicates DCM)

S4 = Atrial contraction in late diastole

• DDx: Increased ventricular stiffness and hypertrophy

  1. HCM

  2. Anaemia

  3. Hyperthyroidism

Systolic Click

• Definition

• DDx

Definition: High frequency sound heard during systole (between S1 and S2)

DDx: Mitral valve disease (eg. dysplasia or MMVD)

Overview of Heart Murmurs

• Definition

• 3 Contributing factors

• 4 Ways to characterise murmurs

Definition: Caused by turbulent blood flow disrupting laminar flow

• Occurs at a high Reynolds number (Re)

  

Factors Increasing Turbulence:

1. Big radius change (enlarged chamber)

2. High velocity

3. Low blood viscosity (eg. anaemia → haemic murmur)

Characterising Murmurs:

1. Intensity (grade I - VI)

2. Character/quality

3. Timing in the cardiac cycle

4. Point of maximum intensity (PMI)

Define grade I - VI heart murmur

Grade I	Very soft murmur, barely audible (Takes several minutes to hear in perfect conditions and hence not often diagnosed due to sounds of consult room)
Grade II	Soft murmur, but easily heard in one location
Grade III	Murmur of moderate intensity heard over > 1 location
Gade IV	Loud murmur and radiates widely (eg. over whole thorax and opposite side)
Grade V	Loud murmur with precordial thrill Precordial thrill = Chest vibrates
Grade VI	VERY loud murmur which can be heard without a stethoscope Precordial thrill present

Provide DDx for the following murmur qualities/timing:

• Pansystolic, crescendo/decrescendo

• Pansystolic, plateau

• Diastolic, decrescendo

• Continuous, machinery-like

Pansystolic, crescendo/decrescendo = Ejection murmur due to obstruction of ventricular outflow

1. Subaortic stenosis (SAS)

2. Pulmonic stenosis (PS)

Pansystolic, Plateau = Holosystolic, regurgitant

1. Mitral regurgitation (eg. MMVD)

2. Tricuspid regurgitation

Diastolic, decrescendo

1. Aortic regurgitation (eg. infective endocarditis)

2. Pulmonic regurgitation (eg. infective endocarditis)

Continuous, machinery = Patent ductus arteriosus (PDA)

Provide DDx for the following systolic murmurs with PMI at:

• Left apex (4)

• Left base (4)

• Right hemithorax (2)

Left Apex:

1. MMVD

2. MV dysplasia

3. DCM

4. Endocarditis

Left Base:

1. SAS

2. PS

3. Hypertrophic obstructive cardiomyopathy

4. Physiological murmur

Right Hemithorax:

1. VSD

2. Tricuspid insufficiency

Cat Heart Murmurs

• Prevalence

• Location description

• 2 DDx

Prevalence: VERY common (up to 40% of adults)

Location: Left OR right parasternal OR sternal

DDx:

1. HCM (25%)

2. Functional/innocent/physiological (75%)

Respiratory Auscultation

• Characteristics of pleural effusion

• Characteristics of pulmonary oedema

• 4 Causes of cough with heart disease

Pleural Effusion: Inspiratory AND expiratory dyspnoea with dull respiratory sounds and percussion of fluid line

Pulmonary Oedema: Tachypnoea, dyspnoea and fine crackles at end of inspiration

Cough: Uncommon with heart disease (esp. cats) but caused by

1. LAE and compression of L mainstem bronchus

2. Bronchial wall oedema

   • Pulmonary oedema rarely causes coughing (no cough receptors) BUT severe pulmonary oedema → bronchial wall oedema → coughing

3. Pulmonary hypertension

4. Alveolar/bronchiolar fluid accumulation

Thoracic Radiography for Diagnosis of Heart Disease

• 4 Disadvantages

• 5 DDx for LAE

• 4 DDx for R cardiomegaly

• DDx for generalised cardiomegaly

-ve:

1. Patient must be stabilised first (DV superior)

2. Results affected by treatment

3. Radiographic signs may lag clinical improvement or deterioration

4. Cats with HCM have concentric hypertrophy → Normal cardiac silhouette

LAE:

1. HCM

2. Early DCM

3. MMVD

4. SAS

5. Systemic hypertension

R Cardiomegaly:

1. Heartworm

2. TR

3. PS

4. Pulmonary hypertension

Generalised Cardiomegaly:

1. DCM

2. Aortic insufficiency

3. Pericardial effusion

4. TV dysplasia

5. Septal defect

6. PDA

Importance of measuring BP for cardiac disease

• Measure baseline prior to ALL therapy

• Essential for signs of forward failure (weakness and syncope) → BP to ensure they are not hypotensive

ECG

• 2 Disadvantages

• 3 Types of ECG

• 7 Indications

-ve:

1. Crude assessment of heart size

2. Snapshot in time (may miss arrhythmia)

Types:

1. Conventional = Momentary evaluation of HR and rhythm

2. Continuous ambulatory Holter monitor = 24hr

3. Event monitoring = Assess after activation (eg. following collapse)

Indications:

1. Abnormal HR

2. Irregular rhythm

3. Pulse deficit

4. Variable intensity of heart sounds

5. Murmur

6. Split S1/S2

7. Syncope

3 Features to assess with echocardiography (+ examples)

1. Structure

   • Size of chambers and vessels (LA:Ao ratio)

   • Defects and masses

   • Pericardial fluid

   • Valve thickening or stenosis

2. Blood flow (colour doppler)

   • Regurgitation

   • Stenosis

   • Direction

   • Speed

3. Ventricular function

   • SV

   • Contractility

   • Preload

   • Distensibility

   • Synergy

   • CO

Overview of Blood Testing for Cardiac Disease

• 3 Functions

• 3 Tests

Functions:

1. Diagnose subclinical disease

2. Differentiate respiratory from cardiac disease

3. Monitor and prognosis

Tests:

1. NT-proBNP = N-terminal pro-B-type Natriuretic peptide

2. Cardiac troponin-1

3. Serum biochemistry

NT-proBNP

• Abnormal elevation

• Effect

• 2 Uses

Abnormal Elevation: Increased secretion from cardiomyocytes with subclinical/clinical heart disease due to wall stress, adrenergic, RAAS concentrations

Effect: Natriuresis (Na+ removal), diuresis and vasodilation

• Opposite effect of RAAS

Uses:

1. Determine likelihood of subclinical DCM or HCM

   • More specific for disease processes than troponin-1

2. Differentiating 1˚ respiratory from cardiac disease (when dog presents with respiratory signs)

   • proBNP low in pulmonary disease and high in cardiac disease

Cardiac Troponin-1

• Function

• 3 Uses

Function: Regulatory protein of contractile apparatus which leaks from myocytes after injury

Uses:

1. Breed-associated cardiomyopathies (eg. boxer arrhythmogenic right ventricular cardiomyopathy (ARVC)

   • Right side of heart becomes fatty and fibrotic

2. Detect myocardial injury (eg. doxorubicin chemotherapy)

3. With pericardial effusion present: Differentiates haemangiosarcoma (troponin-1 high) from idiopathic effusion

4 Features to assess on serum biochemistry with heart disease

1. Measures of GFR = Urea, creatinine and SDMA

   • More useful for LCHF (forward failure)

   • Crude indicator of renal perfusion (1st major organ supplied by aorta and extremely sensitive to blood flow)

   • CKD and cardiac disease commonly coexist

2. Lactate = Insensitive measure of peripheral perfusion

3. Electrolytes = Essential to measure before and during therapy for CHF

4. Liver parameters = RCHF monitoring (backward failure

List 9 congenital cardiac diseases

1. Patent ductus arteriosus (PDA)

2. Subaortic stenosis (SAS)

3. Pulmonary stenosis (PS)

4. Ventricular septal defect (VSD)

5. Atrial septal defect (ASD)

6. Tricuspid dysplasia (TD)

7. Mitral dysplasia (MD)

8. Tetralogy of fallot (ToF)

9. Persistent right aortic arch (PRAA)

List 4 compensatory mechanisms for CHF

1. Increase SNS activation

   • Increased HR, contractility and SVR

   • Initially maintains CO and BP

   • Chronic: Increased myocardial O2 demand, tachyarrhythmia, increased afterload

2. Activation of RAAS (due to decreased renal perfusion)

   • Angiotensin II → Vasoconstriction (increased afterload), stimulates aldosterone and ADH

   • Aldosterone → Increased Na+ and H2O resorption = Increased blood volume and preload

   • Chronic: Volume overload → Venous congestion and oedema

3. Release of vasoactive peptides and ADH

   • Increased water resorption in kidney, vasoconstriction → Increase BP

   • Chronic: Volume overload and congestion

4. Myocardial remodelling

   • Ventricular dilation and compensatory eccentric hypertrophy → Improves SV short-term

   • Chronic: Dilation prevents normal contraction

Describe the therapeutic approach to CHF (aims and DDx)

• Warm vs. col

• Dry vs. wet

Warm and Dry: Pre-disease (stage A - B)

Dry and Cold: Rare = Poor CO with no CHF

• Early DCM → Pimobendan to increase CO

Warm and Wet: Pulmonary oedema and effusion with good CO

• Early MMVD and early CHF

Cold and Wet:

• DCM and end-stage MMVD

COLD = Poor CO → Improve with pimobendan

WET = CHF → Relieve congestion with diuretics

Causes of Severe CHF

• 2 Causes of gradual deterioration

• 4 Causes of acute deterioration

• 2 Other causes

Gradual Deterioration:

1. Worsening regurgitation (dilation of annulus)

2. Myocardial failure due to overload

Acute Deterioration:

1. Ruptured chordae tendinae

2. Arrhythmia (supraventricular #1 due to atrial stretching)

3. LA rupture

4. Iatrogenic fluid overload

Other Causes:

1. Pulmonary hypertension

2. Owner misses doses

Stage A Heart Failure

• Definition

• 4 Treatments

Definition: At high risk for developing heart disease but currently has NO identifiable disorders of the heart (no murmur or structural change)

• aka. Pre-disease

• eg. Genetic predisposition due to breed (CKCS)

Treatment: Reduce hypertension

1. Encourage activity to avoid obesity

2. Avoid excessive salt (increases RAAS which is bad)

3. Revisit q6 - 12m and monitor SRR

   • Trend up of SRR → Book consult as may have progressed to CHF

4. Client education about CHF to reduce risk of developing

No benefit of medications (eg. β-blockers, spironolactone, ACE-i) until onset of CHF

Stage B Heart Failure

• Definition

• Treatments

Definition: Structural (valve) disease but NO clinical signs

• aka. subclinical disease

• B1 = No cardiac remodelling/enlargement on imaging (only regurgitation and valve structural changes → murmur)

• B2 = Imaging shows evidence of chamber enlargement

Treatments:

• B1 = As for stage A

• B2 = Pimobendan (must have evidence of cardiac remodelling) + as for stage A

  • ± Monitor with echo

Stage C Heart Failure

• Definition

• 5 Treatments

• 6 Other drugs to consider

• Monitoring

• Prognosis

Definition: Clinical signs of CHF with response to standard treatment

• Will NOT survive more than a few weeks without treatment

Treatment:

1. Avoid strenuous exercise

2. Pimobendan

3. Low dose frusemide (lowest effective dose)

4. ± ACE-i

5. Diet = Highly palatable and high energy (reduce weight loss), lower Na+ and increased n-3 PUFA

Drugs to Consider:

1. ± Amlodipine = Vasodilator

2. ± Digoxin = Anti-arrhythmogenic (atrial fibrillation)

3. Nitrates

4. Bronchodilators

5. Cough suppressants

6. Spironolactone

Monitoring:

• SRR, appetite, attitude, ensure drinking

• Assess for weakness of syncope

• Recheck after 7 - 14 days for urea, creatinine, lytes, Na+ , K+, Cl-

Prognosis: <1yr from onset of CHF with treatment

Stage D Heart Failure

• Definition

• 6 Treatments

Definition: End-stage heart failure, requiring advanced/specialised treatment to remain comfortable

• Refractory to treatment

Treatments: Do NOT give fluids (exacerbates pulmonary oedema)

1. Emergency respiratory distress stabilisation

   1. O2 supplementation

   2. Place IVC

   3. Butorphanol IV = Sedative/anxiolytic

   4. ± Thoraco-/abdominocentesis

2. Max dose frusemide IV until improved RR (4hr) → Stop pulmonary oedema

   • Refractory → CRI

   • IV until PO can be given (when RR < 30brpm)

   • Add ACE-i when no longer acute (not as effective as systemic vasodilation)

3. Pimobendan IV (when available)

4. ± Other vasodilators if necessary (amlodipine, nitrates, hydralazine)

5. ± Dobutamine with severe oedema

6. ± K+ supplementation (PO or IV) due to hypokalaemia from aggressive diuretic therapy

List 4 common types of presentations of patients with valvular disease

1. Puppy or kitten

   • Innocent/physiological murmur vs. congenital disease

   • Important to have early awareness to prevent disease progression

2. Annual health check

   • Asymptomatic detection of murmur or arrhythmia

3. Mild clinical signs

   • Cough (cardiac disease may NOT be cause)

   • Decreased exercise tolerance

4. Congestive heart failure or low output failure

   • Esp. large breed dogs

What is the difference between stenosis vs. insufficiency

Stenosis = Narrowing of valve orifice while valve is open

• Severity of stenosis is related to pressure gradient

  • Smaller orifice → Larger pressure gradient → Pressure overload

  • → Concentric hypertrophy

Insufficiency = Blood flowing through valve in WRONG direction (regurgitation) while valve is “closed”

• Severity of insufficiency/regurgitation is related to amount of regurgitant flow

  • Larger orifice → Greater regurgitant volume → Volume overload

  • Eccentric hypertrophy

Describe 4 factors which influence severity of valvular disease

1. Valve affected

   • R better than L

   • Tricuspid not as severe as aortic valve

2. Stenosis OR insufficiency/regurgitation

3. Severity of impairment

4. Other concurrent conditions which exacerbate the disease

   • Cardiomyopathy (eg. DCM → failing myocardium)

   • Pulmonary/systemic hypertension

   • CKD

   • Bacteria-associated disease

Overview of Myxomatous Mitral Valve Disease (aka. Endocardiosis)

• Prevalence

• Valves affected

• Signalment (breed, sex and age)

• Aetiology

• Pathogenesis

Prevalence: #1 heart disease of dogs (75%)

• Common incidental finding at necropsy

Valves: MV only = 60%, MV and TV = 30%, TV only = 10%

• Usually MV precedes TV due to larger circulatory bed

Signalment:

• Breed = Small - medium dogs

  • CKCS (>50% by 4yr and almost 100% by 10yr)

  • Dachshund, poodle, JRT, Yorkie, Chihuahua

  • Unusual in large breeds (but associated with more rapid CHF)

• Sex = Male > Female

• Age = Middle-aged to older

• Uncommon in cats

Aetiology: Non-inflammatory, degenerative process AND hereditary with complex inheritance pattern

Pathogenesis:

1. Abnormal collagen degeneration/remodelling (often associated with collapsing airways)

   • Loose fibroblastic tissue in spongiosa of valve

   • Deposition of HA and chondroitin sulphate

   • Collagen degeneration of valvular fibrosa and chordae tendinae

2. Valve laxity and prolapse

3. Valve becomes thickened and nodular due to scar tissue → Prevents valve from forming tight seal → Regurgitation

4. Chordae tendinae thicken and may rupture

5. Cardiac remodelling = Eccentric hypertrophy due to volume overload

6. Ventricle MAY split

Clinical Signs of MMVD

• 4 Presentations

• 4 DDx

Presentations: LCHF #1

1. Asymptomatic with holosystolic apical murmur on routine examination

2. Insidious onset of clinical signs

3. Acute respiratory distress (pulmonary oedema)

4. Acute decompensation (myocardial failure, tear in LA or ruptured chordae tendinae)

DDx:

1. Pulmonary disease (eg. chronic bronchitis or bronchopneumonia)

   • Differentiate with proBNP

   • If dog with mitral murmur and cough has NORMAL HR, it does NOT have CHF

2. Tracheobronchial malacia

3. Bacterial endocarditis

4. Congenital heart disease

Describe 7 diagnostic tools for MMVD

• Advantages

• Disavantages

• Results

1. Thoracic Radiography

   • +ve:

     1. Reliable method to evaluate LA size

     2. 2nd best method to monitor response to treatment

   • Results:

     • Mitral Regurgitation

       1. LAE = Dorsal displacement of trachea and divergence of mainstem bronchi

       2. LVE = No cardiac waist and bulge

       3. Pulmonary venous distension

       4. Pulmonary oedema = Interstitial → Alveolar

     • Tricuspid Regurgitation

       1. Right-sided enlargement = Reverse D and increased cardiosternal contact

       2. Distended CdVC

       3. Hepatomegaly/splenomegaly

       4. Loss of serosal detail due to ascites

2. Blood Pressure

3. Echocardiography

   • +ve:

     1. Assess anatomy of valves and size of chambers

     2. Confirm diagnosis and determine prognosis

   • Prognostic Indicators:

     1. LA:Ao > 1.6 = LAE

     2. End-systolic diameter/volume = #1 indicator of volume overload

        • Small dogs usually normal to increased LV function

          • FS > 50% due to increased diastolic diameter

        • Large dogs = Decreased in advanced cases (echo more indicated in large dogs)

          • FS 20 - 40%

4. ± Cardiac Biomarkers (NT-proBNP)

5. ± Airway Sampling

6. ± MDB

   • CBC = Rule out anaemia as exacerbating cause

   • Biochemistry = Kidney parameters and electrolytes

   • UA = Cardio-renal syndrome (difficult to manage as kidneys want to be wet and lungs want to be dry)

7. ± ECG

   • +ve: May be indicated when arrhythmia suspected (i.e. heavily disease ventricle or atrium)

   • -ve: Echo better to assess for atrial and ventricular enlargement

Overview of Endocarditis

• Dog vs. cat presentation

• Pathogenesis

• Risk of individual valve infection

• 4 Agents

• 2 Sources

• 7 Risks

Presentation: Rare and life-threatening disease

• Dog = Acute

• Cat = Chronic

Pathogenesis:

1. Bacteraemia results in colonisation of the free margins of the heart valves

2. Large friable/vegetative mass develops

3. Destruction of valves → Regurgitation

4. Destruction of adjacent endocardium

5. Thromboembolism in kidneys and spleen

Valves: Mitral > Aortic »» Tricuspid > Pulmonic

• Proportional to pressure on each valve

Agents: G+ aerobic #1

1. Staph. aureus

2. β-haemolytic Streptococci

3. E. coli (acute)

4. Bartonella (25% in USA)

Sources:

1. Discospondylitis

2. Dental disease

Risks:

1. Large dog

2. Immunosuppressive agents or disease

3. Inappropriate/inadequate antimicrobial therapy

4. Indwelling large IV or urinary catheter

5. Prior valvular disease (eg. subaortic stenosis due to jet lesions)

6. Bacteraemia

7. Periodontal disease?

Diagnosis of Endocarditis

• 5 Clinical signs

• 4 Diagnostic tools

Clinical Signs:

1. Fever

2. Vomiting

3. Lameness (IMPA and discospondylitis)

4. New heart murmur (74% systolic and 26% diastolic)

Diagnosis:

1. CBC and biochem (azotaemia/kidney failure)

2. Blood cultures

   • Treat based on most likely infection while awaiting cultures

3. Urine cultures

4. Echocardiography to differentiate between endocardiosis vs. endocarditis

   • Shows: Vegetative and destructive lesions

   • Difficult to distinguish with U/S but use younger signalment

Treatment of Endocarditis

• 2 Treatments

• Prognosis

Treatment:

1. AB q4 - 6hr for 4 - 6w until resolution of lesion

   • Parenteral → PO

   • Based on culture and sensitivity

2. CHF therapy

Prognosis: Poor (20%)

• G- infection worse than G+ infection

• Aortic valve worse than mitral valve

Overview of Subaortic Stenosis

• Prevalence

• Sites of stenosis

• Signalment (breed)

• Aetiology

• Pathogenesis

Prevalence: #1 congenital cardiac defect in NZ dogs

Sites: Subvalvular (>95%), valvular (5%), supravalvular (rare)

Signalment: Large breeds (boxer, GSD, GR, GSP, GD, Newfoundland, Rottweiler, bulldog, Labrador, bullmastiff, samoyed)

• Rare in cats

Aetiology: Congenital valvular disease

• Can by dynamic (narrowing changes overtime)

Pathogenesis:

1. Fibrous subaortic ring develops which reduces left ventricular outflow

2. LVE hypertrophy to pump blood through congenital narrowing stenotic region (pressure overload → concentric hypertrophy)

3. HR increases to maximise CO → Reduced myocardial perfusion with increased O2 demand

4. Underperfused myocardium → Ventricular arrhythmia

Diagnosis of Subaortic Stenosis

• 5 History findings

• 2 PE findings

• 3 Diagnostic tools (+ results)

History:

1. Progressive (silent < 3 months)

2. Exercise intolerance (low CO)

3. Syncope (low CO)

4. Sudden death (ventricular arrhythmias ~70% <3yr)

5. LCHF with MR = Dyspnoea (esp. cats)

PE:

1. Systolic crescendo-decrescendo left basilar murmur

2. Slow-rising hypokinetic pulse

Diagnosis:

1. Radiography = Aortic bulge and L-sided cardiomegaly

2. ECG = Exercise-precipitated ventricular arrhythmia

3. Echocardiography = Confirm diagnosis and determine severity of lesion

Treatment of Subaortic Stenosis

• 3 Treatments

• Prognosis

Treatments:

1. Balloon dilation of stenotic valve (NOT often successful vs. PS)

2. β-1 blockers (eg. atenolol)

   • Reduce HR in moderate to severe cases

   • Prevent arrhythmic effect of catecholamines in body and reduce myocardial O2 demand

   • Increased coronary perfusion

3. Exercise restriction

Prognosis: Poor if severe

Overview of Pulmonic Stenosis

• Prevalence

• Site of stenosis

• Signalment (breed)

• Pathogenesis

Prevalence: Common congenital valvular defect in dogs

Sites: Valvular #1 (> subvalvular > supravalvular)

Signalment: Small breed dogs (beagle, Newfoundland, samoyed, Chihuahua, English bulldog, GR, Chow Chow, mini schnauzer)

• Normally >1yr

Pathogenesis:

1. Congenital narrowing of pulmonic valve → Obstruction to RV outflow

2. Concentric hypertrophy of RV

3. ± RCHF

Diagnosis of Pulmonic Stenosis

• 3 History findings

• 5 PE findings

• 4 Diagnostic tools (+ results)

History:

1. Usually asymptomatic

2. Exercise intolerance and syncope

3. RCHF

PE:

1. Left basilar crescendo-decrescendo systolic murmur and precordial thrill

2. Jugular pulse

3. Arrhythmia and sudden death

4. Ascites and hepatomegaly

Diagnosis:

1. Radiograph = RVE, pulmonary artery bulge, hypoperfusion of lungs

2. ECG = Exercise-precipitated ventricular arrhythmia and R-sided cardiomegaly

3. Echocardiography = Confirm diagnosis and determine severity of lesion

Treatment of Pulmonic Stenosis

• 3 Treatments

• Prognosis

Treatments:

1. Balloon dilation OR surgery (good efficacy)

2. Exercise restriction

3. Treat CHF

Prognosis: Very good (even without treatment)

AV Valve Dysplasia

• 2 Types (+ signalment)

• Clinical signs

Types:

1. Mitral Dysplasia = #1 congenital defect in cats (also large dogs)

2. Tricuspid Dysplasia = Male large dogs

Clinical Signs: Related to valvular insufficiency/regurgitation

• Lesions tolerated for many years (acute or chronic)

Classification of Cardiomyopathies

• Aetiology

• 3 Types

Aetiology: 1˚ OR 2˚

Types:

1. Dilated cardiomyopathy (DCM) = Systolic pump failure

2. Hypertrophic cardiomyopathy (HCM) = Diastolic compliance failure

3. Restrictive cardiomyopathy (RCM) = Diastolic compliance failure with some systolic dysfunction

Overview of Dilated Cardiomyopathy (DCM)

• Definition

• 5 Aetiologies

• Pathogenesis

• Signalment (breed, age and sex)

• Side of heart affected

Definition: Eccentric hypertrophy of 2 OR 4 heart chambers (LV #1) → Myocardial dysfunction

• Characterised by SYSTOLIC dysfunction = Low %Fractional shortening (FS)

  

Aetiologies:

1. Idiopathic (90%)

   • Genetic predisposition

2. Taurine deficiency

   • MoA: Unknown, but concentrates inside excitable tissues eg. myocardium

   • Diets: Lamb meal, rice, grain-free diets, low S-amino acids (Met/Cys) necessary to synthesise Tau

     • Also carnitine deficiency in boxers → Poor mitochondrial function

3. Immune-mediated

4. Infectious agents (2˚ to myocardial damage)

5. Doxorubicin toxicity

Pathogenesis:

1. Progressive decrease in contractility → Decreased SV and increased eSV

2. Increased RAAS and SNS in attempts to maintain BP

3. Dysfunctional eccentric hypertrophic compensation due to volume overload → Increased wall stress ± mitral regurgitation (stretching of the LV damages the MV which causes insufficiency and exacerbates LCHF)

4. LCHF ± atrial arrhythmia due to reduced coronary filling AND cardiac remodelling (fibrosis)

Signalment:

• Breed = Giant

  • Doberman, boxer, Irish Wolfhound, Great Dane, St Bernard, Newfoundland, English sheepdog, Labrador, golden retriever, huntaway

  • X-linked in Great Danes

• Age = 6m - 14yr (~5yr)

• Sex = Male > Female

Side: L, R or biventricular failure

Clinical Signs of Dilated Cardiomyopathy

• 3 Presentations

• 5 PE findings

Presentations:

1. Long subclinical phase (due to compensation) → Short clinical phase

2. LCHF or RCHF (better prognosis)

3. Tachyarrhythmia (eg. a fib) → Syncope or sudden death

   • Often 1st clinical signs in boxers and dobermans

PE:

1. Irregularly irregular heart beat (atrial fibrillation #1)

   • VPC or VT for boxers and dobermans

2. Mitral valve murmur due to stretching of annulus (lower grade than MMVD)

3. Gallop rhythm (S3)

4. LCHF or RCHF

5. Low CO signs

Diagnosis of Dilated Cardiomyopathy

• 7 Diagnostic tools (+ results)

• 5 Major criteria for DCM

• 3 Minor criteria for DCM

• Prognosis

Diagnosis:

1. Radiography = Presumptive diagnosis of DCM (generalised cardiomegaly in young, large breed dog with NO prior clinical signs)

   • CHF mimics end-stage MMVD (BUT latter typical of older, small breed dogs and preceded by clinical signs)

   • Results:

     1. Generalised cardiomegaly

     2. Interstitial/alveolar lung pattern

     3. ± Pleural effusion/ascites

2. Echocardiography = Differentiate between DCM vs. MMVD as cause of MR

   • DCM = Annulus stretched and pulled away from septum vs. MMVD = Valve degeneration and thickening

   • Results:

     1. Increased LV eSD and eDD (heart stays large during systole due to failed contraction)

     2. FS% < 25% (reduced contractility)

     3. Increased LA:Ao ratio (2˚ to MR)

     4. Reduced wall thickness

3. Blood Pressure

4. ± ECG = Atrial fibrillation/ventricular arrhythmia

5. MDB = Monitoring for treatment

6. ± proBNP = Elevated

7. ± Taurine assay to seek for 1˚ cause (esp. with atypical breeds)

Major Criteria:

1. Increased LV eSD

2. Increased LV eDD

3. Reduced FS%

4. More spherical LV

5. Elevated NT-proBNP

Minor Criteria:

1. Left and bi-atrial enlargement

2. Increased mitral valve E point of septal separation (MV pulled apart)

3. Arrhythmia

Prognosis: <6m when CHF develops

Dobermans with DCM

• Age of onset of clinical signs

• 3 Diagnostic tools (+ results)

• Prognosis

Age: ~6.5yr

• Long pre-clinical phase (“occult DCM”)

• Clinical phase = CHF (75%) and forward failure (25%) ± paradoxical bradycardia

Diagnosis:

1. Radiography = L-sided cardiomegaly

2. 24hr Holter monitoring = Ventricular arrhythmia (>100 VPCsin 24hr)

   • Atrial fibrillation = Worse prognosis

3. Echocardiography

Prognosis: <3m after onset

• Diastolic LVID (LV internal diameter) negatively correlates with prognosis

  • Larger the internal diameter of LV at diastole = worst prognosis

• Pimobendan improves survival (~ 1yr) prior to CHF

• Sudden death common due to arrhythmia

Cocker Spaniels with DCM

• Age

• Radiographic findings

• Prognosis

Age: 5 - 6yr

Radiography: Generalised cardiomegaly (often with concurrent MMVD)

Prognosis: Better than other breeds with DCM

• Often asymptomatic for long time

Cats with DCM

• Aetiology

• Pathogenesis

• 2 Treatments

Aetiology: Idiopathic OR taurine deficiency

• Potentially reversible with taurine supplementation

Pathogenesis: Systolic myocardial dysfunction of ALL heart chambers → Pleural and pericardial effusion (LCHF)

Treatments:

1. CHF management

2. Digoxin

Arrhythmogenic Right Ventricular Cardiomyopathy ARVC)

• Signalment

• 3 Diagnostic tools (+ results)

• 3 Categories (+ prognosis)

• Treatment of arrhythmia

Signalment: 1 - 11yr (~6yr) boxers

Diagnosis:

1. Radiography = NORMAL

   • RV becomes fibrotic and fatty

   • ± Mild eccentric hypertrophy of LV due to volume overload

2. 24hr Holter monitoring = Ventricular arrhythmia (>50 VPC in 24hr)

   • Positive trace on lead II indicates origin from R side of heart

3. Echocardiography = Mild eccentric LV hypertrophy

Categories:

		Survival
I (concealed)	Asymptomatic with arrhythmias ± Soft left apical systolic murmur ± Gallop	2yr
II (overt)	Arrhythmias with syncope and prone to sudden death	1 - 2 yr
III (myocardial failure)	Myocardial failure with CHF and arrhythmias	< 6 months

Treatment of Arrhythmia: Sotalol (β-blocker) → Treat ventricular arrhythmia

Feline Myocardial Diseases

• 2 1˚ disorders

• 5 2˚ disorders

1˚:

1. Feline HCM

2. Feline RCM

2˚: Restrict left ventricular function = pressure overload of ventricle = maladaptive concentric hypertrophy

1. Hyperthyoidism

2. Systemic arterial hypertension

3. Acromegaly

4. Aortic stenosis

5. Taurine deficiency

Overview of Feline Hypertrophic Cardiomyopathy (HCM)

• Definition

• Prevalence

• 5 Aetiologies (1˚)

• Signalment (breed, sex and age)

• 3 Gross pathology findings

• 3 Histological findings

Definition: 1˚ disease of the LV free wall and intraventricular septum → Diastolic failure due to concentric hypertrophy → Reduced ventricular compliance and myocardial relaxation

• ± Obstructive outflow from LV (associated with SAM)

  • MV becomes stuck

Prevalence: 15% of cats (increases with age)

• Very rare in dogs (except compensatory concentric hypertrophy 2˚ to SAS)

Aetiologies:

1. Genetic (breed disposition with mutation in myosin-binding protein C)

   • Autosomal dominant train in Maine Coons and American Shorthairs?

2. Idiopathic #1

3. Viral???

4. Immune-mediated???

5. Toxic???

Signalment:

• Breed = Maine Coon and American Shorthair (large cats)

• Sex = Male > Female

• Age = 5m - 17yr (~4.8 - 7yr)

PM:

1. Concentric hypertrophy of LV

2. Papillary muscle hypertrophy

3. Increased heart weight : BWT ratio

Histology:

1. Myocardial fibre disarray

2. Increased fibrous connective tissue

3. Arteriosclerosis and vascular dysplasia

Pathology of Feline Hypertrophic Cardiomyopathy (HCM)

• Pathogenesis

• Systemic anterior motion of the mitral valve (SAM)

  • Definition

  • 3 Causes

  • Diagnosis

  • Treatment

  • Prognosis

• Feline aortic thromboembolism (FATE)

  • Cause

  • 5 Clinical signs

Pathogenesis: Diastolic dysfunction

1. Abnormal concentric hypertrophy of LV → Thin lumen with reduced eDV → Small SV

2. Low CO

3. Tachycardia to increase CO (exacerbates issue due to reduced diastolic filling time)

4. RAAS activation → Increased end-diastolic pressure

5. Cardiac distortion causes MV leaflet prolapse → LVOT obstruction (exacerbates disease)

6. LAE → Thromboembolism

7. LCHF

SAM: MV pulled out of normal position and sucked into LVOT → Dynamic obstruction

• Causes:

  1. Position of papillary muscles

  2. Slack chordae tendinae not pulling valve closed

  3. “False/abberent” chordae

• Diagnosis: Echocardiography

• Treatment: β-blocker

• Prognosis: Same as no obstruction

  

FATE: Clots form in LAE (stagnant blood) and break off to lodge anywhere in body leading to

1. Paralysis (esp. HL due to lodging in caudal bifurcation fo Ao)

2. Pain

3. Pulselessness

4. Pallor

5. Poikilothermia

Clinical Signs of Feline Hypertrophic Cardiomyopathy (HCM)

• 2 Signs of subclinical disease

• 4 Signs of clinical disease

Subclinical Disease:

1. Left parasternal murmur (20 - 60%)

2. Gallop sounds (S4)

Clinical Disease: Often present very late in course of cardiac disease due to propensity for low activity

1. Non-specific clinical signs (depression, anorexia and inactivity)

2. LCHF

   • Can be peracute onset (silent periods with no clinical signs)

   • May be preceded by stressful event or IV fluid administration

   • Respiratory distress (cough rare)

3. Arterial thromboembolism = Posterior paresis (bifurcation of caudal aorta)

   1. Also: Haemorrhagic diarrhoea (GIT), azotaemia (kidney) and seizures (brain)

4. Arrhythmias

Diagnosis of Feline Hypertrophic Cardiomyopathy (HCM)

6 Diagnostic tools (+ results)

1. MDB = Rule out 2˚ HCM

   1. Hyperthyroidism (T4)

   2. Hypertension

   3. Aortic stenosis

   4. Acromegaly

2. NT-proBNP = Differentiate from 1˚ pulmonary disease when presenting in respiratory distress

3. Radiography

   1. Pulmonary oedema = Patchy, multifocal interstitial to alveolar lung pattern

   2. Pleural effusion (2˚ to pulmonary hypertension and biventricular failure)

   3. Valentine-shaped heart = Bi-atrial enlargement

   4. Distended pulmonary arteries and vein (pulmonary hypertension

4. ± ECG = Left anterior fascicular block, VPC or atrial fibrillation

5. Echocardiography = Diagnosis and assess LVOT

   1. LV hypertrophy (free wall and intraventricular septum = LVWd)

   2. LAE

   3. Normal to increased contractility (reduced diastolic measures)

   4. Narrowed LVOT

   5. SAM

6. Blood pressure

Treatment of Feline Hypertrophic Cardiomyopathy (HCM)

• 6 Treatments

• Follow-up

  • Cat with pulmonary oedema on frusemide

  • Cat with pleural effusion

  • Cat with FATE but no CHF

• 5 Principles of FATE treatment

• 4 Negative prognostic indicators

Treatment:

1. Frusemide (lower dose than dogs as cats more sensitivity)

2. ± Pimobendan if frusemide insufficient

   • -ve: Can make LVOT obstruction worse by increasing contractility of heart → Prolapse of mitral valve

3. ± Antiarrhythmic (β-blocker) to slow HR and reduce effect of SAM

4. ACE-i

5. ± Thoracocentesis (more predisposed to pleural effusion than dogs)

6. FATE treatment

Follow-Up:

• Pulmonary oedema on frusemide

  • Check bloods 1 - 2w after discharge → Adjust dose based on SAP, biochemistry and PE

  • Recheck q3m with ECG

  • Recheck q6 - 12m with radiography

• Pleural effusion = Check q3m

• FATE

  • Check q1m for 3m → q3m if stable

  • Consider annual echo and radiography q6 - 12m

FATE:

1. Analgesia = Opioids

2. Induce hypocoagulable state to reduce further thrombus formation

   • Clopidogrel = Inhibit platelet aggregation

   • ± Heparin, aspirin and vasodilators (no evidence of efficacy)

     • Heparin = Antithrombin III co-factor which neutralises clotting factors

   • Do NOT use thrombolytic therapy

     • eg. Plasminogen activator (rHU t-PA) which converts fibrin bound plasminogen to plasmin

       • -ve: Low efficacy and $

     • eg. streptokinase/urokinase which converts blood plasminogen to plasmin

       • -ve: Risk of hyperkalaemia, metabolic acidosis, haemorrhage and $

3. Improve blood flow to infarcted arterial bed by avoiding hypotension and dehydration

4. Treat concurrent CHF if present

5. Provide supportive care = Cage rest and nutritional support

Negative Prognostic Indicators:

1. CHF

2. Severe LAW

3. Thromboembolism

4. Older age

Describe the classifications of hypertension

Hypertension = Increased SAP (MAP superior assessment)

• Classification based on risk of target organ damage (TOD) and present TOD

• Use breed-specific RR (eg. sighthounds have normally higher BP)

SAP (mmHg)	Substage	Risk of TOD
<140	Normotensive	Minimal
140 - 159	Pre-hypertensive	Low
160 - 179	Hypertensive	Moderate
≥180	Severely hypertensive	High

• Hypertension SAP > 160mmHg (180mmHg in-clinic due to physiological hypertension)

3 Types of hypertension

1. Situational Hypertension (aka. “white coat” hypertension)

   • Normal patient with hypertension due to SNS stimulation caused by excitement/anxiety/pain

   • No treatment necessary as resolves with removal of stimulus

2. Idiopathic Hypertension (aka. “primary malignant hypertension” or “essential hypertension”)

   • Sustained hypertension with no identifiable cause

   • 20% of hypertensive cats

3. Secondary Hypertension

   • Treatment of 1˚ condition MAY resolve hypertension

List 9 causes of secondary hypertension (most to least common)

1. CKD (bidirectional)

2. Hyperthyroidism

3. Hyperadrenocorticism

4. Diabetes mellitus

5. Chronic hepatic disease

6. Pheochromocytoma (adrenal gland neoplasia → Secrete excess adrenaline/noradrenaline)

7. Chronic anaemia

8. Hyperaldosteronism

9. Polycythaemia

Cardiovascular disease does NOT cause hypertension (vs. humans)

4 Target organs damaged by hypertension (+ clinical signs)

EYES #1

1. Sudden blindness (often reversible)

2. Retinal oedema

3. Dilated and tortuous retinal vessels

4. Hyphaema

5. Retinal detachment

6. Dilated, hyper-reflective fundus

7. Scleral/conjunctival hyperaemia/iris aneurism

8. Slow PLR

9. Secondary glaucoma

KIDNEYS = CKD and proteinuria

BRAIN = High ICP

1. Cerebrovascular accidents (stroke)

2. Depression

3. Seizure

4. Ataxia

5. Focal brain and spinal cord lesions (aneurism)

HEART AND BLOOD VESSELS

1. Gallop sounds

2. Murmurs

3. LV concentric hypertrophy (pressure overload due to high systemic BP)

4. LCHF

5. Arrhythmia

6. Bleeding due to blood vessel changes (epistaxis, stroke, aortic rupture)

Vague Clinical Signs of Hypertension:

1. Restlessness

2. Anxiety

3. Panting

4. Behaviour changes

3 Indicators for blood pressure measurements

1. Dogs and cats ≥9yr

2. Diagnosis of condition associated with 2˚ hypertension

3. Evaluate patient with evidence of TOD

Label the following probe/doppler positions for measuring blood pressure

1. Forelimb

   • Digital artery (2) = Palmar metacarpals distal to carpal pad

   • Cuff between carpus and elbow (1)

2. Hindlimb

   • Dorsal pedal artery (6) = DM tarsus OR caudal branch of saphenous artery (5) = Plantar metatarsal proximal to metatarsal pad

   • Cuff just above or below tarsus (3 or 4)

3. Tail

   • Coccygeal artery (7) = Midline of tail

   • Cuff at base of tail

12 Standardised protocols for BP measurement (+ 3 things to avoid)

1. Quiet environment

2. Owner present (MAY make worse)

3. Allow 5 - 10 minutes for patient to acclimatise to environment

4. Gentle restraint in R lateral recumbency (cats can be in sternal to reduce stress)

5. Ensure cuff and probe are level with the heart

   • Cuff >10cm below RA → Falsely elevated BP

   • Formula to correct: Subtract 0.8mmHg for every 1cm cuff sits below the RA (when > 10cm)

6. Cuff width 30 - 40% limb/tail circumference

   • Too small/tight = False elevation of BP

   • Too large/loose = False lowering of BP

7. Always discharge 1st value

8. Record 5 - 7 consecutive and consistent values (<20% variability) → Take average

9. Record all parameters (position, site of measurement, environment, operator and cuff size)

10. Same operator each time

11. Use U/S gel to improve contact between Doppler probe and skin

12. Use headphones with doppler to reduced noise disturbance for patient AND ease of hearing

Avoid:

1. Avoid sedation (lower BP)

2. Do NOT clip hair to make detection of blood flow with Doppler easier

   • Consider noisy clippers = stress

   • Moisten hair with alcohol and liberally apply U/S gel instead (esp. cats)

3. Avoid taping cuff to secure in place

   • Taping can increase occlusion pressure (esp. when 360˚)

   • Use small pieces if necessary

When should hypertension treatment be initiated?

Begin Treatment When:

1. Single record of hypertension WITH EOD (end-organ damage = fundic examination)

2. Hypertension without EOD confirmed with ≥ 2 measurements on separate occasions (160 - 179mmHg) within 8 weeks

   • Two instances may be a few days apart

3. Hypertension without EOD confirmed with ≥ 2 measurements on separate occasions > 180mmHg within 14 days

7 Diagnostic tests to perform with a hypertensive patient

1. Fundic examination

2. MDB

3. Urine protein:creatinine ratio

4. Total T4 (hyperthyroidism)

5. Abdominal U/S

6. + Echocardiography

7. ± Brain MRI

Hypertension Treatment

• Aim of treatment

• 3 Management recommendations

• Dog treatment progression

• Cat treatment progression

Aim: SAP < 160mmHg (ideally 120 - 140mmHg)

• In-clinic values (avoid hypotension when home)

• ALSO no hypotensive signs (weakness and tachycardia)

• Do NOT start medication in unstable or dehydrated patients as it may drop GFR

Management:

1. Avoid excess Na+ in diet

2. Ensure stable and hydrated

3. Drugs to GRADUALLY reduce BP to avoid side effects

Dogs: Progress to next step when refractory

1. ACE-i (eg. Benazepril)

2. ACE-i x2

3. ACE-i + Amlodipine

4. ACE-i + Amlodipine + Telmisartan ± Hydralazine

Cat:

1. Amlodipine #1 OR Telmisartan

2. Increase Amlodipine

3. Amlodipine + Telmisartan

Short-term and long-term monitoring of hypertension treatment

Short-Term:

1. Monitor BP 7 - 10d after treatment (1 - 3d in emergency setting)

2. Monitor treatment with clinical signs and renal values (markers of GFR)

   • Increased potassium and creatinine with benazepril

   • Accept small increase in creatinine and SMDA due to medication

   • Hypotension with excessive amlodipine

Long-Term:

1. Recheck q3m for PE and eye exam

2. Recheck q6m for renal value assessment

Overview of Pericardial Effusion

• Define pericardial effusion vs. cardiac tamponade

• 3 Types of pericardial effusion (+ causes)

• Pathogenesis

Pericardial Effusion: Excessive/abnormal fluid accumulation in the pericardial sac

• Normal <2mL for lubrication

Cardiac Tamponade: Impaired ventricular filling due to increased intrapericardial pressure from

1. Pericardial effusion

2. Masses

3. Organs (eg. diaphragmatic hernia)

Types of Pericardial Effusion:

1. Blood

   1. Idiopathic #1 (up to 75%)

   2. Viral

   3. Immune-mediated

   4. Neoplasia (HSA, chemodectoma, lymphoma)

      • Chemodectoma = Pressure tumour of carotid body sinuses

   5. Ruptured LA (eg. MMVD)

   6. Trauma (eg. HCM)

   7. Coagulopathy (eg. rat bait toxicity)

2. Transudate

   1. RCHF

   2. Hypoalbuminaemia

3. Exudate

   1. Virus (eg. FIP = low cellularity exudate)

   2. Bacteria

Pathogenesis:

1. Pericardial effusion → Increased intrapericardial pressure

2. Results in diastolic collapse of RA

   • Right side before left side as RA = lowest pressure chamber

   • RV tamponade if severe

3. Impaired ventricular filling

4. Reduced CO (RV pumps less blood to left side of heart)

5. Hypotension

6. Increased venous pressure in vena cava

   • Blood backs up

Diagnosis of Pericardial Effusion

• 5 History findings

• 5 Clinical signs

• 4 Diagnostic tools (+ results)

History:

1. Sudden onset

2. Signs of RCHF (slow onset)

3. Generalised weakness

4. Collapse

5. Sudden death

Clinical Signs:

1. Jugular vein: Distension, jugular pulses and hepatojugular reflux

2. Muffled heart sounds with normal lung sounds

   • Cannot detect apex beat

3. Tachycardia

4. Hypokinetic pulse or pulsus paradoxus

   • ALSO bounding hyperkinetic pulse due to increased difference between SAP and DAP

5. Poor peripheral perfusion

   • Cold extremities

   • Extended CRT and pale MM

Diagnosis:

1. T-fast

2. Radiography → Globose heart

3. ± ECG → Electrical alternans = Variation in QRS height due to heart swinging in fluid of pericardium = different position in relation to leads

4. Echocardiography = Definitive diagnosis

5 Differences between pericardial effusion and DCM

Feature	Pericardial Effusion	DCM
Heart sounds	Muffled (effusion)	Loud
ECG	Electric alternans	NO electrical alternans
Cardiac silhouette	Globose and sharp edged	Blurred edges due to movement with heart beat
Pulmonary oedema	Less/absent	Prominent feature
Pulsus paradoxus	Common	Rare

List 2 treatments of pericardial effusion

1. Pericardiocentesis = Drain fluid

2. Pericardiectomy = Removal of part of pericardium to allow bleeding into pleural space

Pericardiocentesis

• Patient positioning

• Surgical preparation

• 3 Pieces of equipment

• Location of catheter placement

• Monitoring

• 4 Laboratory features to evaluate

Positioning: LEFT lateral recumbency

Surgical Preparation: Ribs 3 - 8 on right side from sternum to mid thorax

• Apply local anaesthetic (lignocaine) from skin to pleural surface

Equipment:

1. 12 - 16G catheter with added side holes

   • Side holes prevent occlusion of catheter

   • Too many = weaker catheter and allows air to enter space

2. Extension set + 3-way tap

   • Stops movements

3. 50mL syringe

Location: RIGHT side with large cardiac notch

• Cardiac notch = Area where heart touches chest wall without touching lung

• 4th - 6th ICS

Monitoring: Ventricular tachycardia on ECG = Hit ventricle

Laboratory Assessment:

1. Assess clotting of fluid

   • Blood from pericardial space should NOT clot (defibringinated blood via normal fibrinolysis cascade)

   • Clot = Accidental aspiration from RV or actively bleeding into pericardium

2. HCT usually lower than peripheral blood BUT can be much higher

3. Cytology

4. pH of fluid? NOT useful

Pericardiectomy

• 2 Advantages

• 4 Indications

• 3 Methods

+ve:

1. Blood resorbed by lymphatics

2. Larger space → Less pressure build up than pericardial space

Indications:

1. Idiopathic haemorrhagic pericardial effusion

   • 50% recur after pericardiocentesis

   • ≥ 3 pericardiocentesis → Pericardectomy

   • Curative!

2. Septic pericarditis

3. Left atrial tear

4. Neoplasia (palliative and NOT curative)

Methods:

1. Open thoracotomy

2. Fluoroscopy to remove bottom half

3. Pericardial window (make space in pericardial tissue)

7 Principles for treating sick cardiac patients

“SOCROTH”

1. Minimise chronic STRETCH

   • Increases O2 demand

   • Myocyte injury and arrhythmia

2. Remove pulmonary OEDEMA

   • Lung heavy, wet and stiff → V:Q mismatch

   • Fatigue on respiratory muscles

   • Increases O2 demand

3. Improve CO

   • Increase HR or contractility

   • Reduce regurgitation

4. Normalise heart RATE and RHYTHM

   • Tachycardia → Reduces myocardial perfusion and increases demand

   • bradycardia → MAY reduce CO

   • Arrhythmia → MAY be fatal

5. Improve OXYGENATION of blood

6. Minimise THROMBOEMBOLISM

   • Ischaemic infarct and organ damage

   • Esp. kidneys, brain, heart and saddle embolism

7. Treat HEARTWORM

   • Occludes pulmonary arteries

Cardiology Drugs

• 5 Diuretics

• 5 Vasodilators

• 3 Positive inotropes

• 2 Negative inotropes (reduce CO for severe LVOT obstruction)

• 3 Antithrombotics

Diuretics:

1. Frusemide

2. Thiazide

3. Spironolactone

4. Amiloride

5. ACE-i

Vasodilators:

1. Pimobendan

2. Nitroglycerine

3. Sodium nitroprusside

4. Amlodipine

5. Hydralazine (arterial)

Positive Inotropes:

1. Pimobendan

2. Digoxin

3. Dobutamine

Negative Inotropes:

1. Diltiazem

2. β-blocker (atenolol, sotalol, propanolol)

Antithrombotics:

1. Aspirin

2. Heparin

3. Clopidogrel

Anti-Arrhythmogenic Drugs/Treatments

• AV block (2)

• Sinus arrest (2)

• Atrial standstill (2)

• Atrial fibrillation (3)

• Supraventricular tachycardia (3)

• Ventricular tachycardia (2)

AV Block:

1. Atropine

2. Pacemaker

Sinus Arrest:

1. Atropine

2. Pacemaker

Atrial Standstill:

1. Treat 1˚ cause of hyperkalaemia

2. Pacemaker

Atrial Fibrillation:

1. Digoxin

2. Diltiazem

3. β-blocker (atenolol, sotalol, propanolol)

Supraventricular Tachycardia:

1. Diltiazem

2. β-blocker (atenolol, sotalol, propanolol)

3. Digoxin

Ventricular Tachycardia:

1. Acute = Lignocaine

2. Chronic = Sotalol

Frusemide

• Indication

• MoA

• Onset

• Peak

• Duration

• Routes

• 4 Side effects

• Dosing protocol

Indication: Acute, fulminant CHF with pulmonary oedema

• Fastest way to turn ECF into urine → Reduce volume overload

• Vasodilator when IV

MoA: Loop diuretic

• Inhibits active absorption of Cl- in ascending loop of Henle → Reduced resorption of Na+, K+ and Cl- in the DCT → Increased water loss in DCT

Onset: 5 minutes (60 minutes PO)

Peak: 30 minutes (1 - 2hr PO)

Duration: 2 - 3hr (6hr PO)

Route: IV (lowest effective dose PO at home for management)

• Do NOT use with digoxin → Exacerbates toxicity

Side Effects:

1. Hypokalaemia #1 and electrolyte depletion

2. Hypotension

3. Pre-renal azotaemia

4. Antitussive (BAD if productive cough)

Dosing: Proportional to severity of CHF

• IV bolus q1 - 2hr → CRI if refractory

• Monitor RR q15 - 20 minutes

• Maximum effective dose = 12mg/kg/d

Thiazides

• 2 Examples

• 2 Indications

• MoA

• Advantage

Examples:

1. Hydrochlorothiazide

2. Chlorothiazide

Indications:

1. Combined with frusemide if refractory and severe CHF

2. Long-term diuretic to manage CHF alone

MoA: Decrease membrane permeability to Na+ and Cl- in the DCT

+ve: Less K+ washout than frusemide but more potent diuretic than spironolactone

Spironolactone

• Indication

• Advantage

• MoA

Indication:

1. Combined with frusemide if refractory and severe CHF

2. Long-term management of CHF (mild diuretic)

+ve: No K+ washout

MoA: Competitive aldosterone antagonist → Prevents binding in collecting duct → Increased Na+ elimination (and Cl-)

ACE-i

• 3 Examples

• Indication

• MoA (+ 2 effects)

• Caution

Examples:

1. Benazepril

2. Enalapril

3. Ramipril

Indication: #1 long-term management of mild CHF (stage C)

• NOT for acute CHF (slow onset of action)

• No benefit during pre-clinical stage

MoA: Inhibits function of angiotensin converting enzyme (ACE) which converts ATI → ATII

1. Vasodilation (ATII = Vasoconstrictor)

2. Moderate diuresis (ATII stimulates aldosterone secretion)

Caution: Ensure well-hydrated, normal renal parameters and no emesis

Telmisartan

• Indication

• MoA

Indication: Hypertension treatment

• 3rd line therapy for dogs and 1st line therapy for cats

MoA: Angiotensin receptor blocker

• Inhibits angiotensin II from binding receptor in vascular smooth muscle → Vasodilation

Digoxin

• Indication

• 2 Effects

• Disadvantage

Indication: Atrial fibrillation ± other supraventricular tachyarrhythmias (eg. dogs with DCM)

• Aim to get HR < 140bpm

Effects:

1. Positive inotrope = Increase myocardial contractility

2. Negative chronotrope = Decrease HR

-ve: Narrow TI (must use with good awareness of drug)