1. Pathophysiology
1.1. Pump failure - inadequate stroke volume and fall in cardiac output
1.1.1. Dilated cardiomyopathy Coronary vascular diseae
1.2. Volume overload - increased output, overwork, eventual failure
1.2.1. Valvular insufficiencies (mitral, aortic) Shunting disease (ventricular septal defect, patent ductus arteriosus) Chronic anaemia
1.2.1.1. Eccentric Hypertrophy - inc lumen size, wall thickness same
1.3. Pressure overload
1.3.1. Hypertension (systemic, pulmonary) Narrow outflow tract (pulmonic stenosis, aortic stenosis)
1.3.1.1. Concentric Hypertrophy - inc wall thickening (greater resistance)
1.3.1.1.1. Hypertrophy - inc myocardial oxygen demand, fibrosis and hypoxia
1.4. Arrythmias
1.4.1. CO = HR x SV
1.5. Diastolic failure
1.5.1. Hypertrophic cardiomyopathy Dilated cardiomyopathy (myocardial fibrosis) Pericardial effusion
1.6. Body system equilibrium - maintained via homeostatic systems
1.6.1. Increased volume
1.6.1.1. RAAS (Ang II, Aldosterone) ADH (osmoregulation) Renal autoregulation of flow (dec. renal flow, inc. sodium retention
1.6.1.1.1. Inc. circulating volume, inc preload, inc. CO (Starling), inc systemic vascular resistance
1.6.1.1.2. RAAS - may lead to excessive fluid retention, excessive resistance to ventricular emptying, effects on myocardium (chronically)
1.6.1.1.3. ADH - retention of free water without sodium - hyponatraemia long term
1.6.2. Decreased volume
1.6.2.1. Natriuretic peptides (heart muscles, urinate sodium) Renal autoregulation (inc renal flow, dec. sodium retention)
1.6.3. Autonomic effects
1.6.3.1. Drop in CO, drop in arterial blood pressure (arterial underfilling) - baroreceptors, dec. parasympathetic activity, inc. sympathetic activity
1.6.3.1.1. Norepinephrine - alpha and beta receptors
1.6.3.1.2. Positive chronotrope = inc HR
1.6.3.1.3. Positive Inotrope = inc cardiac contraction force
1.6.3.1.4. Positive Luisitrope = improved cardiac relaxation
1.7. Heart failure
1.7.1. Tachycardia (symp tone) Poor peripheral perfusion (vasoconstriction) Fluid retention (RAAS, ADH) LCHF (elevated filling pressures on LHS, reteined fluid in pulmonary circulation) RCHF (retained fluid in systemic veins)
1.8. Vascular disease
1.8.1. Underperfusion
1.8.1.1. Vascular obstruction, loss of function, ischaemia, ecrosis
1.8.1.1.1. Thrombosis, embolism
1.8.1.1.2. Increased hydrostatic pressures
1.8.2. Increased vascular permeability
1.8.2.1. Oedema, haemorrhage
1.8.2.2. Vasculitis
1.8.3. Abnormal flow and pressures
1.8.3.1. Decreased oncotic pressure
1.8.3.1.1. Hypoproteinaemia
1.8.3.2. Decreased lymphatic drainage
1.8.3.2.1. Lymphoedema
1.8.4. Degenerative, Inflammatory
1.8.4.1. Vasculitis
1.8.5. Malformations
1.8.5.1. Congenital and acquired
2. Physical exam
2.1. Pulse
2.1.1. Artery sites
2.1.1.1. External maxillary
2.1.1.2. Transverse facial
2.1.1.3. Median
2.1.1.4. Digital
2.1.1.5. Coccygeal artery (cattle)
2.1.2. Match with auscultation? Pulse deficit? Regularity? Quality?
2.2. Auscultation
2.2.1. Left side
2.2.1.1. Apex - Caudal, Mitral valve more audible (S1)
2.2.1.2. Base - cranial, Pulmonic and Aortic valve (S2)
2.2.2. Right side
2.2.2.1. Tricuspid valve, Maybe aortic valve, Ventricular septal defects
2.2.3. Heart sounds
2.2.3.1. Lub = S1 Dup = S2
2.2.3.1.1. Lup Dup = Systole
2.2.3.1.2. S2 to next S1 = Diastole
2.2.3.1.3. S1 = Closure of AV valve, systole beginning S2 = closure of outflow valve, end of systole
2.2.4. Heart murmurs
2.2.4.1. Left Heart base
2.2.4.1.1. Pulmonic and aortic valves, ribspaces 3/4
2.2.4.2. Left Heart apex
2.2.4.2.1. Mitral valve
2.2.4.3. Right side
2.2.4.3.1. Trcuspid, Ventricular septal defect loudest
2.2.4.4. Type
2.2.4.4.1. Systolic murmur
2.2.4.4.2. Diastolic murmur
2.2.4.4.3. Continuous murmur
2.2.4.4.4. Crescendo-Decrescendo
2.2.4.5. Grade
2.2.4.5.1. 1 = barely audible 2 = clearly audible, does not radiate, quieter than S1/S2 3 = as loud as S1/S2, may radiate 4 = louder than S1/S2 5 = Precordial thrill palpable 6 = audiible with stethoscope off thorax
2.2.4.6. Radiation
2.2.4.6.1. Aortic murmur radiate up carotid arteries
2.2.4.6.2. Mitral murmurs radiate dorsally
2.2.5. Gallop sound
2.2.5.1. Diastole, S3/S4 audible, poor diastolic relacation
2.2.6. Lung sounds
2.2.6.1. Crackles - pulmonary oedema
2.2.6.2. Wheezes or stretorous inspiratory noise = resp disease
3. Echocardiography
3.1. Best for defining type of heart disease, not heart failure
3.1.1. M-mode
3.1.1.1. Measure LV wall against time through systole and diastole
3.1.2. 2D
3.1.2.1. Whole heart, heart lesions
3.1.3. Colour flow Doppler
3.1.3.1. Blood towards transducer = red Away = blue Laminar flow = green
3.1.4. Spectral Doppler
3.1.4.1. Time with ECG Velocity/time graph
3.1.5. Anatomy
3.1.5.1. Right
3.1.5.1.1. Right parasternal long axis = 4 chambers 5 chamber - can see PA
3.1.5.1.2. Short axis papillary muscles - 90 degrees transverse towards tail Cut through aortic valve
3.1.5.1.3. Short axis mitral valve - fish mouth view
3.1.5.1.4. Short axis left atrium/aortic valve LA = comma, with L auricle
3.1.5.1.5. Short axis pulmonary artery - cranially
3.1.5.2. Left
3.1.5.2.1. Apical 4 chambers, long axis
3.1.6. Chambers
3.1.6.1. La:Ao diameter - see if LA enlarged Square shaped
3.1.6.2. M-mode LV systolic function (% change in LV diamter, fractional shortening) High = hyperdynamic ventricle Low = hypokinetic, e.g. DCM
3.1.7. Blood direction, velocity, turbulence
3.1.7.1. Valve stenosis, volume overload, shunts, endocarditis, pericardial effusion (echolucency)
4. Radiology
4.1. Heart failure
4.1.1. Right sided
4.1.1.1. Hepatomegaly Peritoneal effusion Pleural effusoin
4.1.2. Left sided
4.1.2.1. Pulmonary congestion Pulmonary oedema
4.2. Cats - oedema can affect any part of lung, and can be small part - common in cats Unusual to see pleural fluid in dogs
4.3. Cardiac size
4.3.1. Displacement of trachea
4.3.2. Shape of heart shadow, IC spaces, distance from diaphragm, vertebral heart score
4.3.2.1. Can see eccentric hypertrophy, but not concentric hypertrophy
4.4. Angiography
4.4.1. Contrast medium into vessels, can see chambers
4.5. Chamber
4.5.1. Lateral
4.5.1.1. Outward bend of cranial cardiac border - enlarged LA
4.5.2. Dorsoventral
4.5.2.1. Left atrial bulge
4.5.2.2. PDA - bump in aorta, dilation of PA, big LA, generalised cardiac enlargement
5. Therapeutic Principles
5.1. Preload
5.1.1. Venous reservoir Filling Tone (contracted state)
5.1.1.1. Venous tone and fluid volume
5.1.1.1.1. Diuretics - to remove fluid - too much persistent preload, full venous reservoir, congestive heart failure
5.1.1.1.2. Venodilators - decrease preload, doesnt improve afterload - forward AND backward failure?
5.1.1.1.3. Arteriodilators
5.2. Cardiac function
5.2.1. Inotropy Lusitropy Chronotropy (rate and rhythm)
5.2.1.1. Systolic function Diastolic function
5.2.1.1.1. Inotropes
5.2.1.1.2. Diastolic function e.g. HCM cats
5.3. Afterload
5.3.1. Arterial circulation Output Tone
5.3.1.1. Arterial tone
5.3.1.1.1. Arteriodilators, easier to eject Too much hypotension?
5.4. Anti-arrythmic therapies
5.4.1. Controversial, no licensed agents
5.4.2. Restore adequate peripheral perfusion, control rate/rhythm, prevent sudden death
5.4.2.1. Antidysrhythmic medication
5.4.2.1.1. Ventricular arrythmias
5.4.2.1.2. Supraventricular arrythmias
5.4.2.1.3. Bradyarrythmias