Cardiovascular system Flashcards
Mammalian foetus
Foramen ovale connecting atria- becomes fossa ovalis
Ductus - vessel between the pulmonary trunk and aorta becomes the ligamentum arteriosum
Normal blood pressures
Deoxygenated blood in the vena cava - 3mmHg
Oxygenated blood to body - 100mgHg
Oxygenated blood to the lungs - 12 mmHg
Oxygenated blood from lungs - 7 mmHg
Atrioventricular valves
Separate atria to ventricles - inlet valves to ventricles
When ventricles contact evasion of the cusps is prevented by the action of the papillary muscles through the chordae tendinae
Semilunar valves
Oulet valves of ventricles
Both valves have three cusps
Aortic and pulmonary valves prevent backflow at the end of systole into the LV and RV
Cardiac sketeton
Structural integrity to the heart
Breaks up continuity between cardiac muscle cells of the atria and those of the ventricles
Coronary circulation
Two coronary arteries just above the aortic valve
Little anastomosis between left and right arterial supply
Extensive capillarisation
Great cardiac vein empties into coronary sinus
Thebesian veins empty into ventricles
Large vessel structure
Internal elastic lamina -> endothelium -> tunica media (smooth muscle and collagen) -> tunica adventita (nerves) -> Vaso vasorum (arteries only)
Starling forces
OUT capillary hydrostatic pressure
IN interstitial hydrostatic pressure
OUT osmotic forces due to interstitial fluid protein concentration
IN osmotic force due to plasma protein concentration
ONCOTIC PRESSURE - pressure exerted by protein
BLOOD PRESSURE
Oedema
Excessive filtration
Defective resorption
Defective lymphatic drainage
Cardiac action potentials
Pacemaker - SAN
Concentrations of important ions and the effect of opening a channel to create a current
Na+, K+, Ca2+
Cardiac muscle
Functional synctium
Myocytes are electronically coupled together
INtercalated discs : contain gap junctions
Central nuclei (1/2) with perinuclear space, branched fibres, blood supply
Other autonomic foci (apart from SAN) - atrial, junctional, ventricular, SAN (80-100)
Conduction system
SAN -> Atria (via bundle of His)-> AV noda -> Purkinje system (modified myocytes) -> Ventricular muscle
Ventricular action potentials
Phase 0 - Rapid depolarisation, fast Na+ channels open
Phase 1 - ‘Notch’ fast Na+ channels close
Phase 2 - Plateau, Ca2+ enters, K+ permeability low
Phase 3 - Repolarisation
Phase 4 - Resting membrane potential
Events of the cardiac cycle
-Systole-
ATRIAL SYSTOLE atria contract, topping up mostly filled ventricles
ISOVOLUMETRIC CONTRACTION ventricles contract but all valves are closed
RAPID EJECTION semilunar valves open, ventricles expel blood
REDUCED EJECTION semilunar valves open and of ventricular contractions
-Diastole-
ISOVOLUMETRIC RELAXATION ventricles relax, all valves remain closed
RAPID VENTRICULAR FILLING AV valves open, blood begins to fill ventricles
DIASTASIS ventricles fill slowly as venous pressure > ventricular pressure
ECG (electrocardium)
How it works
Current only flows to surface of the body when cardiac muscle is partly polarised and partly depolarised
No changes are recorded when cardiac muscle is completely polarised/completely depolarised
ECG - provide information
Anatomical orientation of the heart Relative size of heart chambers HR, rhythm, origin of excitation Spread of impulse Decay of excitation
ECG - phases
P wave - atrial depolarisation
QRS - ventricular depolarisation
T wave - ventricular repolarisation
PR interval - AV conduction time
Increase heart rate
Sympathetic nerves - release noradrenaline, opens more channels for If
Decrease heart rate
Parasympathetic nerves - release Ach, open fewer If channels
Sinus rhythm
SAN acting as pacemaker
QRS complex follows each P wave, PR and QT complexes normal, RR interval regular
Sinus arrhythmia
Normal QRS complex, PR and QT intervals but RR varies in set patterns
Sinus tachycardia
Normal response to exercise (or fever, hyperthyroidism and reflex to low arterial pressure)
Sinus bradycardia
May be abnormal (Addisionian crisis) but may be very fit individual
Atrial myocytes
Respond to both sympathetic stimulation (beta1 receptors) and parasympathetic stimulations (M2 receptors)
Ventricular myocytes
Are not directly responsive to parasympathetic stimulation but have beta1 receptors
Effects of Ach on ventricular myocytes contractility are indirectly mediated via pre-synaptic inhibition of noradrenaline release
Frank-Stirling relationship
Reservoir raised -> pressure causing ventricular filling increases -> more blood enters ventricle -> ventricular muscle stretches -> ventricular muscle responds with a stronger contraction
Afterload
The pressure at which the heart ejects
Determined in vivo by the peripheral resistance which is proportional to arterial pressure
Preload
The filling pressure of the heart determined in vivo by the venous volume and rate of venous return
Alteration of preload
Increased venous return -> increase volume of blood entering the heart during diastole i.e increase end diastolic volume
Increase EDV increases strength of subsequent systole
Flow rate in and out of the heart equalise
Venous return
Venous reservoir holds about 2/3 total blood volume
Displacement of blood from the veins increases venous return to the heart and increases cardiac output
Pressure in RA is known as CVP (central venous pressure) - low but positive
Alteration of afterload
Increased resistance to flow from the left ventricle -> direct opposition to ejection
To maintain stroke volume at increased afterload, heart must contract more forcefully
Symp NS influence is required to maintain CO
Systemic arterial pressure
Major determinant of tissue perfusion pressure - controlled by negative feedback
Mean arterial pressure = DBP + (SBP-DBP)/3
R (resistance) = [viscosity (n) x L (length)]/radius (r) ^4
Short term regulation of blood pressure
Baroreceptor regulation - autonomic NS
CVS system
Long term regulation of blood pressure
Control of fluid volume - vasopressin, renin-angiotensin-aldosterone, natruiretic peptides
Body fluid balance - renal system
Baroreceptors
Non-encapsulated nerve endings in adventitia of arteries - aortic arch and carotid sinus
Central axons terminate in nucleus trachus solitarius
Mechanoreceptors
Renin-angiotensin-aldosterone system
Low blood pressure leads to decreased kidney perfusion which causes RENIN production
Renin converts angiotensinogen to angiotensin I
ACE converts angiotensin I to angiotensin II which goes to:
- Adrenal cortex
- Posterior pituitary
- Arterioles and venules
- Inactive peptides
Atrial receptors
Low pressure stretch receptors in the walls of the atria act as volume receptors
Atrial natruiretic peptide
Released into the circulation when the atrial walls are stretched by an increase in blood volume
- Reduces blood volume b y stimulation excretion of salt and water by the kidney
- Relaxes vascular smooth muscle (stimulate cGMP formation) vasodilator
- Inhibits the renin-angiotensin-aldosterone system
Potent defence mechanism against voume overload
Mediastinum
Midline partition within the thorax
Thymus
Found (large) in young animals
Cranial to heart
Connects two vessels - seals after puberty
Valves
Atrioventricular valves
RIGHT tricuspid
LEFT mitral
Semilunar valves
RV/PA pulmonary
LV/A aortic
Sympathetic NS - CVS
Norepinephrine and epinephrine (from adrenal medulla)
Increases rate of depolarisation of SAN so threshold is reached more rapidly - increase strength of contraction
Thoracolumbar
Neurotransmitters: Ach (preganglionic), Norepinephrine (post-ganglionic)
Innervates most areas of heart, blood vessels and airways
Parasympathetic NS - CVS
Vagus nerve - leaves brain, into thorax to heart, pass diaphragm to gut
Craniosacral
Innervates SAN -> decrease heart rate
Can be controlled with drugs that directly influence vagus
Decrease rate of depolarisation to threshold of SAN
Prolongs transmission of impulses to AV node
Local factors
Local vasodilation of blood vessels (NO, PGs, histamine released)
e.g. hypoxia
Increased CO2, H+ ions,
Adrenergic receptors
ALPHA 1 - smooth muscle, contraction -> blood vessels
BETA 1 - myocardium, excitatory -> HR increases
BETA 2 - smooth muscle, relaxation -> blood vessels
Body water content
60% of body
ICF - 40% (K, albumin)
ECF - 20% (Na, chloride)
Central regulation
CVS centre in medulla oblongata receives inputs from higher centres and baroceptors
Sympathetic and parasympathetic activity to the heart and blood vessels
Volume overload
Disease which requires the heart muscle to increase its activity causing overwork -> heart failure
e.g. valve insufficiencies, PDA, septal defects
Preload
Degree of stretch of the ventricular myocardium at the end of diastole When excessive: - increased atrial pressure - increases venous pressure - signs of congestion
Dilated cardiomyopathy
Common in dogs Ventricular and atrial dilation Depressed systolic function Weakened myocardium liable to further distension Frank-Starling mechanism impaired
Hyperthyroidism
Increased stimulation of beta-receptor by norepinephrine
Increases sympathetic NS
Activates G protein which will increase cAMP -> invcrease calcium release
More myosin being made by the isoenzyme, more crossbridge formation
Increase SV and/or HR -> increase blood pressure
Enlarges to cope from strain
Too much blood to lungs -> pulmonary hypertension -> oedema
Actions of norepinephrine and epinephrine on the heart
Sympathetic stimulation
Beta1 adrenoreceptors -> Gs -> adenylate cyclase -> increase [cAMP]
Sensitisation of troponin C to calcium
Stimulation of Ca uptake into the sarcoplasmic reticulum - muscle relaxes more quickly
Switches metabolism to less efficient fatty acid oxidation - needs more O2 per ATP metabolism
Positive chronotropic effects:
Phosphorylation of slow Ca2+ channels - conduct more calcium
Altered voltage gating of the inward current during phase 4 (resting membrane potential)
Faster repolarisation by earlier activation of potassium currents
Actions of acetylcholine on the heart
Vagal stimulation
Acts on muscarinic receptors on the SAN and AV node
Presynaptic muscarinic receptors can inhibit norepinephrine release from sympathetic nervous terminals
(Weak) Negative ionotropic effect:
Linked via an inhibitory G protein (Gi) to adenylate cyclase (inhibit cAMP formation)
Negative chronotropic effect:
Linked via a G protein to K+ ion channels
1st degree heart block
Prolonged PR intervals
Contraction delayed due to increased time for AV conduction
2nd degree heart block
AV node fails to transmit all atrial impulses (more p waves than QRS complexes
Atria beat more than once for each ventricular onctraction
3rd degree heart block
Transmission of impulse from atria to ventricles wrong
Atria and ventricles beat independently from each other
P waves and QRS complexes completely dissociated
First sound (S1)
‘Lub’
Long, low frequency
Associated with closure of the AV valves
Occurs mainly during isometric ventricular contraction
Second sound (S2)
‘Dub’
Shorted higher frequency than S1
Associated closure of the aortic and pulmonary valves at the onset of ventricular diastole
Third sound (S3)
Very faint ventricular sound caused for movement of blood from the atria into the ventricle during early ventricular diastole
Fourth sound (S4)
Associated with atrial systole
Caused by rapid flow in ventricles
Chronotropes
Change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the SAN.
Positive chronotropes increase heart rate
Negative chronotropes decrease heart rate.
Inotropes
Agent that alters the force or energy of muscular contractions.
Negatively inotropes weaken the force of muscular contractions.
Positively inotropes increase the strength of muscular contraction.
Altering force of contraction
Alter the length-tension relationship of the heart muscle (preload)
Change the cytosolic free Ca2+ concentration
Change the sensitivity of the myocardial contractile proteins to Ca2+
Other effectors on contractility
Oxygen supply
Excess K+ (hyperpolarises excitable cells, weakens contractions, block conducting system, slows HR - heart flaccid and dilated)
Calcium - too much causes spastic contraction, too little causes flaccidity
Blood flow
Laminar: in arteries and veins
Turbulent: in ventricles
Bolus: in capillaries
Carotid sinus
Where internal carotid branches off from common carotid
Receives bundle of baroreceptor nerve fibres (autonomic afferent) via carotid sinus nerve
Peripheral arterial chemoreceptors
Located in carotid and aortic bodies and respond to hypoxia, acidosis (decrease in pH or increase in CO2), asphyxia
Also respond when arterial pressure
Functional hyperaemia
Increase in blood flow in response to metabolic demand
Especially in skeletal muscle, cardiac muscle, brain
Reactive hyperaemia
Increase in local blood flow in response to temporary ischaemia to facilitate to removal of accumulated metabolites
Endothelins
Family of peptides that have a series of differential actions depending on the organ/tissue
In the cvs, endothelins cause a biphasic reponse - initial vasodilation followed by a potent, sustained vasoconstriction
Positive inotropes and positive chronotropes (Rate and strength of contractions increased)
Tetralogy of Fallot
4 defects
- Pulmonary artery narrowed
- VSD
- Aorta opens over top of atrial septum
- RV atrophies
Congenitial diaphragmatic hernia
3 types
- Hole in postro-lateral corner
- adjacent to zyphoid process
- abnormal elevation
Persistent right aortic arch
Constrict oesophagus - regurges food at weaning
Increased appetite, loses weight, megaoesophagus, aspiration pneumonia
Cut ligament arteriosus
Portosystemic shunt
Liver shunt (ductus venosus doesn't shut down) Unfiltered blood in circulation
Patent foramen ovale
Retain hole in atrial septum
Usually no consequences as pressure keeps it shut
only treat if in conjunction with other heart defects
ECG
Is there a P wave for every QRS complex
Implies that:
- Atria did not depolarise normally before ventricular contraction
- Atria are unable to depolarise normally
- OR depolarisation giving rise to QRS complex arises in the wrong place
Possible causes: ventricular depolarisation, junctional depolarisation (AV node: bundle of His), atrial standstill, atrial fibrillation, sinus arrest with escape condition
ECG
Is there a QRS for every P wave?
Failure of conduction of atrial depolarisation through AV node normally AV block (3 types)
ECG
Are the P waves and QRS complexes consistently and reasonably related?
Show as inconsistent relationship between the two
Implies presence of separate ventricular and atrial rhythms
Atrioventricular dissocation
ECG
Are the QRS complexes and the P waves all the same?
Variation may imply that they have originated from a different site/been conducted differently
Abnormality of rhythm
However some variation in P wave can be normal in dogs and is described as a wondering pacemaker
ECG
Is the HR regular or irregular?
Normal rhythms tend to be regular or regularly irregular
Irregularly irregular always abnormal
Most common is atrial fibrillation - sounds chaotic
Auscultation is sensitive
Radiographs - strengths
Multiple thoracic structures
Demonstration of left sided failure
Radiographs - weaknesses
Cannot detect mild cardiac enlargement or which chambers are enlarged
Bad discrimination between fluid and soft tissue
Radiographs - what can you see?
Airways - more obvious when disease
Pulmonary parenchyma
Vasculature
Cardiac silhouette
Echocardiography - strengths
Moving image - good differentiation between fluid and soft tissue
Can combine with ECG
Echocardiography - weaknesses
Cannot image lung
Operator dependent
Haemostasis processes
Vascular spasm
Platelet adhesion and activation and coagulation (fibrin formation) (interaction)
Vasoconstriction
Thrombosis - an unwanted pathological process
Venous thrombosis - small number of platelets; large fibrin component
Arterial thrombosis - large platelet component
Inappropriate blood clotting (thrombosis) occludes blood vessels
Clotting
Severed vessel - tissue factor, extrinsic clotting > Collagen > Platelet adhesion > Platelet aggregation > Temporary haemostatic plug > Definitive haemostatic plug > Fibrin > Thrombin > Intrinsic clotting
POSITIVE FEEDBACK
Platelet adhesion and aggregations
> Vascular damage causes adhesion of platelets to exposed glycoproteins (requires von Willebrand factor)
Platelet activation (thombin and collagen)
Arachdonic acid generation from membrane phospholipids
Cyclooxygenase catalyses TxA2 synthesis
Expression of GP IIb/IIIa on platelet surface
Linkage of adjacent platelets by fibrinogen binding to GP IIb/IIIa
Release of 5HT and aggregation
These events can all be blocked by either cAMP or cGMP inside the platelets
Coagulation cascade
Proenzymes -> coagulation factors
Two pathways:
- Extrinsic coagulation: tissue factor binds to circulating factor VII
- Intrinsic coagulation: contact activation
Final pathway that generate thrombin (converts fibrinogen to fibrin, activates platelets and activates other coagulation factors [V, VIII and XIII])
Fibrinolytic cascade is initiated concomitantly with coagulation
Drugs that interfere with coagulation cascade
Modifying platelet adhesion and activation (prevent thrombosis)
Modifying the blood coagulation system (to correct and bleeding problem or prevent thrombosis)
Stimulating fibrinolysis (breakdown of fibrin - to clear unwanted blood clots)
Anti-platelet drugs
Mechanisms
Inhibit TxA2 synthesis or block TxA2 receptors
Inhibit thrombin activity
Elevate platelet cAMP levels
Elevate platelet cGMP levels
Anti-platelet drugs
Acetyl salicylic acid (aspirin)
Irreversible inhibitor of cyclo-oxygenase (COX) - infrequent and low dosing affects platelets more than endothelium
Anti-platelet drugs
Epoprostenol (prostacyclin)
Elevates platelet cAMP and inhibits platelets aggregation
Anti-platelet drugs
Nitrates
Raise platelet cGMP to inhibit adhesion and aggregation
Anti-platelet drugs
Monoclonal antibodies to GP IIb/IIIa
And other compounds which block TxA2 synthesis/receptors are under investigation
Calcium and coagulation
Co factor in both pathways Used to prevent clotting in vitro Diaminoethane tetra-acetic (EDTA) Sodium nitrate Sodium oxalate - precipitates calcium Acid citrate dextrose - store blood for transfusion
Heparin
Naturally in mast cells and endothelial cells
Large sulphated mucopolysaccharride that inhibits blood clot formation
Binds to anti-thrombin III and increases rate of inactivation of some clotting factors
Binds thrombin so some anti platelet action
Low molecular weight heparin-like molecules
Lower molecular weight and better pharmacokinetics than heparin
Enhance the inhibitory action of ATIII on factor Xa but not thrombin
Less anti-platelet activity than heparin since do not bind thrombin
Vitamin K
Post translational modification of some clotting factors
Oral (usaully)
Phytomenadium (natural), menadiol sodium phosphate (synthetic)
Warfarin
Structurally resembles vitamin K
Prevents the reduction necessary for cofactor activity
Thromboembolic disease
Aortic thromboembolism in cats with cardiomyopathy
Blood vascular parasites damage the lining of the blood vessels e.g. thromboembolic colic and iliac thrombosis (horse), pulmonary thromboembolism (dog)
Diseases that result in loss of antithrombin III e.g. nephrotic syndrome, Cushing’s disease
Navicular disease
Treating bleeding disorders
Targets:
Replace deficient clotting factors
Stimulate production of new clotting factors
Provide antidote to anticoagulant overdose or poisoning
Only fresh whole plasma or frozen fresh blood plasma contains active clotting factors
Vitamin K
Streptokinase
Streptococcal enzymes which activate plasminogen, increase the production of plasmin and cause generalised clot lysis
Urokinase
Activator of plasminogen extracted from human urine
Tissue plasminogen activator (tPA)
Act primarily on fibrin-bound plasminogen in the clot (clot selective)
Low affinity for circulating plasminogen
Congestion
Engorgement of vascular bed due to decreased outflow of blood
Congestive heart failure
Obstruction of blood flow through heart
Blood held back behind obstruction
Causes oedema
Left sided heart failure: pulmonary circulation congestion
Right sided heart failure: hepatic circulation congestion
Congestion
Damage to heart valves
Valves do not close efficiently - blood leaks back
Endocardiosis
Endocarditis - bacterial
Congestion
Damage to heart muscle
Hypertrophic cardiomyopathy (cats) Dilated cardiomyopathy (dogs)
Congestion
Compression of heart from outside
Fluid in pericardial sac e.g. blood, pus, fibrin, fibrous tissue
Heart chamber are unable to fill adequately
PM change
Hypostatic congestion
Before blood clots, it pools under gravity
Distinguish from pathological congestion
Congested lungs
Macroscopically: reddened (may have blue-ish tinge) and heavier
Microscopically: alveolar capillaries engorged with blood; if chronic haemosiderin form blood which has leak out of capillaries is phagocytosed by macrophages - “heart failure cells”
Congested liver
Enlarged, dark red, round edges
Nutmeg liver: dark congestion around central veins, pale yellow/brown non-congested appearance to portal veins
Distension of sinusoids around central veins and atrophy of the hepatocytic cords
Fatty change in hepatocytes surround the are which goes further out with time
Loss of hepatocytes and fibrosis may develop around central veins
Haemorrhage
Escape of blood from blood vessels
Can be distinguished from congestion microscopically
Rhexus
Haemorrhage from physical rupture of a vessel wall
Trauma, haemorrhagic enteritis, erosion of blood vessels by tumours, vascular tumours or abscesses, idiopathic rupture of arteries, intrapericardial rupture of the aorta (horses), arterial rupture associated with Cu deficiency (pigs), turkeys have ruptures of various vessels
Diapedesis
The escape of blood from vessels where it may be difficult to detect a disruption to the vessel wall
Septicaemia, toxaemia, poisoning
Strangles causes purpura haemorrhagica in horses - endothelial damage caused by accumulation immune complexes
Haematome
Blood into tissue forming a clot
In spleen associated with hyperplastic lymphoid nodules and angiogenic tumours
Pinna of dogs
Bruise
Red for 48h
Turns yellow due to macrophages converting haemoglobin into haemosiderin
Haemoglobinuria
Breakdown of product of RBCs appear in urine following intravascular haemolysis
Angiostrongylus vasorum
Worm that lives in pulmonary artery, RV and lungs of dogs and foxes
Secretes anticoagulant causing sporadic haemorrhage
Fibrocartiliginous emboli
Uncommon - probably arise from degenerate invetebral disc in dogs
Occlude spinal blood vessels and cause necrosis - sudden paralysis/paresis
Parasitic emboli
Dirofilariasis (heartworm)
Global infarction
Large or more proximal artery blockage causes more severe or extensive infarction
DIC (Disseminated intravascular coagulation)
Widespread intravascular coagulation esp capillaries caused by widespread generation of thrombin
Causes include: diffuse vascular damage, generation of tissue factor by endothelial cells (due to bacteraemia, systemic infections, toxaemia etc.)
Microthrombi can cause diffuse circulatory insufficiency
Leads to consumption of clotting factors, platelets and fibrinogen -> paradoxical bleeding disorder
Neurogenic maldistributive shock
Trauma, electrocution, fear, emotional stress - profound autonomic stimulation - widespread vasodilation
Pump failure
Failure of systolic function of the myocardium results in inadequate SV and fall in CO
- Dilated cardiomyopathy
- Coronary vascular disease
Volume overload
Necessity for a cardiac chamber to chronically increase output - can result in overwork and eventually failure
- Valvular insufficiencies (mitral, aortic)
- Chronic anaemia
- Shunting disease e.g. VSD, PDA
MITRAL INSUFFICIENCY
Total stroke volume = forward stroke volume + regurgitant stroke volume
Pressure overload
Chronically increase the pressure against which a ventricle has to pump blood can eventually result in failure of the myocardium
- Hypertension - systemic or pulmonary
- Narrowing of the outflow tract - pulmonary aortic stenosis
Arrythmias
Affect both cardiac filling and HR can compromise output
Low HR leads to a drop in CO
At very high HR, diastole is too short to allow adequate filling so SV and CO fall
Diastolic failure
Inability of the heart to relax normally can compromise filling and result in a fall in CO
- Hypertrophic cardiomyopathy
- Dilated cardiomyopathy (myocardial fibrosis)
- Pericardial effusion
Heart failure - autonomic
Results in a drop in arterial blood pressure - arterial underfilling - sensed by baroreceptors
Results in a decrease of parasympathetic activity mediated by alpha and beta receptors
EFFECTS
Positive chronotrope - increased HR
Positive ionotrope - increased force of cardiac contraction
Positive lusitrope - improved cardiac relaxation
Vasoconstriction
Stimulation of renin and RAAS
RAAS
Renin is a proteolytic enzyme secreted by specialised cells in the kidney (juxtaglomerular apparatus)
Stimuli for renin release:
- Renal sympathetic nerve stimulation (beta effect)
- Reduced pressure in afferent arteriole
- Reduced sodium chloride in distal tubules (macula dense)
(ACE is a non-specific carboxypeptidase which also bradykinin)
Advantages:
- Increase circulating fluid volume - increase preload
- Increase CO by Starling mechanism
- Increased systemic vascular resistance improves bp
Disadvantages:
- Long term stimulation results in excessive fluid retention
- Excessive resistance to ventricular emptying
Anti-diuretic hormone
Only relevant in serve heart failure
Increase vascular resistance to protect bp but ultimately deleterious
Increase fluid retention - retention of free water without sodium results in hyponatraemia
Hypertrophy
Structural adaptation of the ventricle which varies on the type of load exerted on the tissue Mediated by a number of factors : - Adrenergic stimuli - Angiotensin II - Aldosterone - Intracellular calcium
Consequences:
- Initially compensation
- Increase myocardial O2 demand and may result in fibrosis and hypoxia
Clinical signs of heart failure
Tachycardia Poor peripheral perfusion Fluid retention: - Left sided - pulmonary circulation - Right sided - abdominal fluid
Clinical signs of vascular disease
Under-perfusion - vascular obstruction (complete/partial, loss of function, ischaemia, necrosis)
Increased vascular permeability - vasculitis
Decreased oncotic pressure - hypoproteinaemia
Decreased lymphatic drainage - lymphoedema
Thromboembolism
Must be present:
- Disturbance of flow
- Endothelial integrity
- Haemostasis
- Fibrinolysis
Causes: Cardiac disease, Cushing’s, parasitic disease, protein-losing nephropathies, neoplasia, autoimmune haemolytic anaemia
Normal heart rates
Adult horse 28-42 Yearling horse >80 Neonatal foal >100 Adult sheep and goat 70-90 Cattle 55-80 Calves >100 Adult pigs 60-90
Auscultation
Left side:
Apex - caudal, mitral valve more audible, S1 loudest
Base - cranial, pulmonic and aortic valve more audible, S2 loudest
Right side:
Tricuspid valve, possible aortic valve, VSDs
Location of murmur
Left heart base - typically hear pulmonic and aortic valve (rib spaces 3/4 on the left)
Left heart apex - typical hear mitral valve
Right side - Typically hear tricuspid, VSD loudest on right
Gallop sounds - additional heart sounds, no murmur
Non-pathological murmurs
horses
Grade 3/6 murmur near base of heart in foals
Pathological murmurs
horses
Continuous murmur in anything old that 4 days
All murmurs with a thrill
Pansystolic (regurgitation) murmurs - mitral incompetence, tricuspid incompetence, VSD
All prolonged diastolic murmurs - aortic valve incompetence (less common - pulmonary valve)
Murmurs of doubtful significance
horses
Grade 2/6 systolic murmurs on the left thoracic wall in adult racing thoroughbreds and in hunters
Absence of CVS disease - reassess
Grade 3/6 systolic murmurs in sedated horses
Ultrasound measurements
Chamber size:
- Normal LA:Ao 55%)
- Hypokinetic (
Left atrial dilation
Mitral valve disease, L -> R shunts
DCM
Hypertrophy cardiomyopathy
Left ventricle dilation
MR, L-> R shunts, AR
DCM, chronic volume overload
Left ventricle hypertrophy
Aortic stenosis, systemic hypertension
HCM
Right ventricle hypertrophy
Pulmonic stenosis
Pulmonary hypertension
Ventral heart shadow
Normal VHS = 8.7-10.7 - imprecise
Many cardiac diseases do not change the VHS
Physiological ‘flow’ murmurs in horses
Mainly thoroughbred horses in training
Main mitral and tricuspid valves (sometimes aortic/pulmonary)
Differentiate from pathological
Around 30% horses in training
Mitral regurgitation (horses) (LA->LV)
Left 5th intercostal space
Severe: risk of collapse/sudden death due to pulmonary artery
Left atrium likely to become dilated
Left ventricle generates higher pressure impacts on peripheral perfusion - affects all organs
Significant if:
- Poor performance
- Resting tachycardia
- Abnormal pulse quality/slow CRT
- Signs of left sided failure
- Arrhythmias esp. atrial fibrillation
- > Grade 4, wide radiation
Aortic regurgitation (horses)
Often due to endocardiosis in older horses
Usually progressive but slowly
Aorta regurgitation -> LV overload -> LHS heart failure
Significant if:
- Poor performance
- Resting tachycardia
- Bounding, hyperkinetic arterial pulse - due to large systolic/diastolic pressure difference
- Slow CRT
- Signs of left sided failure
- Arrhythmias esp. atrial fibrillation
Tricuspid regurgitation (horses) (RA-RV)
Significant if:
- Poor performance
- Resting tachycardia
- Abnormal pulse quality/slow CRT
- Signs of right sided failure
- Arrhythmias esp. atrial fibrillation
- > Grade 4, wide radiation
Bacterial endocarditis
Ruminants:
- Liver abscess, traumatic reticulitis, metritis, mastitis, navel abscess, ‘joint ill’
- Enterococci, Streptoccoci, Actinomyces pyogenes
- Tricuspid and pulmonic valves, RV endocardium
Horses:
- Site of sepsis often not identified, septic jugular thrombophlebitis
- Pasteurella, Actinobacillus, Streptococci, Rhodococcus equi
- Mitral, aortic, can include aortic route, right sided associated with jugular thrombophlebitis
Pigs:
- Staphylococcus aureus, Actinobacillus suis, Erysipelothrix rhysiopathiae
- Mital aortic (usually PM finding)
Diagnosis: congestive heart failure, fever, cardiac murmur, tachycardia, tachypnoea
Treatment: prompt treatment with broad spectrum antibiotics (do a culture and sensitivity before)
Prognosis: guarded
Valve prolapse (horses)
Any valve, may cause murmur
Non-progressive regurgitation
Considered physiological rather than pathological
Ruptured chordae tendinae (horses)
Normally attaches valves and stops then from flipping
Rupture spontaneous or secondary to inflammation or degenerative changes in the chordae
More common for mitral valve
Severe regurgitation with a rapid change in haemodynamic status
Sudden death/signs of acute cardiac failure
Right and left ventricular hypertrophy in atheletes (horses)
Usually mild and non progressive
Tricuspid
Could be considered physiological regurgitation
Ventricular septal defect (horses)
Small VSD compatible with athletic life
Most common congenital defect in large animals
Defect is dorsal (membranous) part of the septum
2 murmurs producing ‘diagonal murmur’
- RHS murmur associated with LV-RV shunt
- LHS murmur assocaited with RV overload - functional pulmonary stenosis]
Patent ductus arteriosus (horses)
After 1 month old
‘Washing machine’ murmur
Valvular dysplasia (horses)
Congenital, uncommon
Rarely well-tolerated and usually part of complex cardiac disease
Primary myocarditis (large animals) Infectious
Viral: Equine Influenza, EHV, Equine Viral Arteritis, FMD, African Horse Sickness, Equine Infectious Anaemia
Bacterial: S. aureus, Clostridium chauvoei, Mycobacterium spp, Streptococcus equi equi, Actinobacillus spp., Rhodococcus equi
Parasitic: Strongyles, Onchocerca, Toxoplasma, Cysticerca, Sarcocysta, Borrelia burgdorfen (Lyme’s disease)
Nutritional myodegeneration - White muscle disease
Ruminants (and horses) grazing selenium deficient pastures
Cardiac form: neonates, acute/peracute, severe debilitation/sudden death, respiratory signs, arrhythmias
Skeletal muscle form: slightly older animal, weakness, stiffness and debilitation, signs precipitated by stress
Diagnosis: whole blood selenium concentrations, glutathione peroxidase concentrations
Treatment: Vitamin E and selenium IM
PM: pale streaky muscles, degeneration and fibrosis of muscles
Cardiomyopathies in large animals
Cattle: inherited, linked to red Holstein gene in Holstein-Fresians
Associated with curly hair coat in polled Herefords
Horses: occurs sporadically, causes unknown
Inflammatory lesions and fibrosis: focal or generalised, aetiology unknown, immune-mediate
Toxins: halothane, antibiotics (erythromycin)
Idiopathic
Cardiac neoplasia in large animals
Cattle: Right atrial lesions extending into the remainder of the heart and heart base area. Adult form - enzootic bovine leukosis
Horses: Lymphoma and others
Secondary myocardial disease and dysfunction
Most common causes:
- Endotoxaemia
- Hypoxia
- Electrolytes (K, Ca. Mg)
- Acidosis
- Catecholamines (horses - severe GIT disease and upper airway during obstruction)
Cardiac troponin I
Cardiac isoenzymes: creatine kinase and lactate dehydrogenase
- Released into the circulation with myocardial call death
- Indicators of myocarditis/myocardial necrosis
QRS complexes in large animals
Purkinje fibre system is extensive - branches from endocardium to epicardium
Depolarising wave is conducted mainly via Purkinje fibres with much less cell to cell spread through mycardium
Therefore, in contrast to small animals, the QRS size and duration does not accurately reflect the size and shape of the ventricular myocardium
Atrioventricular block (large animals)
First degree: delayed conduction through AV node, slow, slightly variable HR
Second degree: intermittent block of conduction, slow HR with pauses at regular intervals, isolated 4th heart sound before block, isolated normally-times P waves on ECG
Third degree: complete block of conduction - pathology of AV node, very slow ventricular rate, syncope, weakness
Atrial fibrillation (horses)
Large atrial mass, slow SA node rate, variable refractory periods
Only affects cardiac output during exercise
Irregularly-irregular cardiac rhythm, variable pulse quality, variability intensity of heart sounds, execise-induced pulmonary haemorrhage (EIPH)
Paroxysmal atrial fibrillation: May spon taneously resolve
ECG: no P waves, irregularly-irregular R-R interval, normal rate, F waves, random depolarisation of AV node
Signs of heart failure (horses)
Resting tachycardia (60bpm)
Valve regurgitation especially mitral/tricuspid
Venous distension
Oedema
Quinidine sulphate
Prolongs effective refractory period
Side effects:
- Vagolytic (ventricular tachycardia)
- Alpha adrenergic antagonist (hypotension)
- Negative ionotrope (decreases cardiac output)
- GI ulcers
Treatment protocol:
-By stomach tube 10g/450kg every 2h until conversion occurs of stop if:
- 6 doses and no conversion
- Signs of toxicity (tachycardia (25%
- Use digoxin (5mg/450kg) to slow conduction through AV node
Use magnesium sulphate. propanolol or lignocaine if arrhythmias
Ventricular premature complexes (VPC) and ventricular tachycardia (VT)
Horses
Idiopathic:
- Corticosteroids and rest
- Ventricular arrhythmias more likely to progress to fatal arrhythmias
Ventricular tachycardia:
- Likelihood that rhythm will destabilise to ventricular fibrillation
- Anti-arrhythmic therapy if ventricular rate
Traumatic pericarditis
Septic fluid in pericardial sac - fibrous ‘cheesy’ exudate and gas
Early signs: fever, anorexia, depression, cranial abdominal, reticular and thoracic pain, right sided heart failure, venous congestion, peripheral oedema
Lymphosarcoma in cattle
Bovine leukaemia virus (BLV) positive (notifiable)
Right atrial pressure, jugular distension
Pericardial effusion, right sided heat failure, cytology reveals neoplastic cells
Pericarditis in pigs
Haemophilus parasuis (Glasser’s disease). Strep suis
Fever, depression, Fibrinous polyserositis, Synovia, Effusions in CNS, Pleural, Peritoneum
Pericardial effusions (horses)
Mostly idiopathic
Minority are pericarditis:
- Equine viral arteritis, equine influenza,, Strep pneumonia, E. coli, Actinobacillus equii.
- Penicillin, pericardial drainage and lavage
- Venous distension, Ventral oedema, muffled heart signs. pericardial friction ruts, pleural effusion)
Cor pulmonale (farm)
Secondary to pulmonary hypertension
- hypertrophy, dilation and ultimately failure of the right ventricle
Causes: chronic pulmonary disease, pulmonary vascular disease, high altitude causing vasoconstriction - brisket disease
Exercise Induced Pulmonary Haemorrhage
Volume varies, horses, dogs and humans atheletes
From pulmonary rather than bronchial vessels
Typically (horses) on caudo-dorsal lung:
- Higher blood flow
- Displacement of diaphragm causes transient transient falls in alveolar pressure
Mechanical forces transmitted to lung are greater in caudodorsal lobes
Capillary stress failure:
- Mechanical pressures generated in pulmonary capillaries during exercise exceed their stress failure point
- Failure point of equine pulmonary capillaries - 75-100mmHg
Predisposing:
- Young
- Lower respiratory tract disease especially RAO
- Upper respiratory tract obstruction especially RLN (recurrent laryngeal neuropathy)
- Cardiac disease (atrial fibrillation, mitral valve disease)
Dust free environment, furosemide, vasodilators (NO, arginine)
Therapeutics
Increased afterload
Signs of poor output due to vasoconstriction - decrease afterload
Increases myocardial work and diminishes perfusion
Pale or cold e.g. mitral regurgitation
Therapeutics
Poor systolic function
Dilated cardiomyopathy and latter stages of mitral valve disease
Ionotropic agents may improve output and signs
Therapeutics
Poor diastolic function
Poor ventricular relaxation
Drugs that hasten relaxation, slow HR or reduce fibrosis
Pre-load reduction
Diuretics
Furosemide
Block Na absorption - ascending limb (loop of Henle)
Oral/IV/SC/CRI
Congestive heart failure
Risks: Electrolyte disturbances, hypovolaemia, azotaemia
Pre-load reduction
Diuretics
Spironolactone
Blocks aldosterone receptors
Oral
2nd line diuretic, may be beneficial in neurohormonal blockade
Risks: Hyperkalaemia
Pre-load reduction
Diuretics
Torasemide
Block Na absorption - ascending limb (loop of Henle)
Oral
Dogs refractory to furosemide
Risks: Electrolyte disturbances, hypovolaemia, azotaemia
Pre-load reduction
Diuretics
Thiazides
Block Na reabsorption in distal convoluted tubule
Oral
2nd/3rd line diuretic in end stage heart failure
Risks: electrolyte disturbances, hypovolaemia, azotaemia
Pre-load reduction
Venodilators
Glycerol trinitrate
Nitrates act like endogenous nitric oxide - relax smooth muscle
Percutaneous
Emergency management of acute heart failure
Risks: Hypotension
Pre-load reduction
Venodilators
Nitroprusside
Nitrates act like endogenous nitric oxide - relax smooth muscle
CRI
Emergency management of acute heart failure
Risks: Hypotension and cyanide toxicity
Afterload reduction
Arteriodilators or balanced dilators
ACE inhibitors
Block production of angiotensin II
Oral
Many indications in cats and dogs
Risks: Hypotension, renal underperfusion
Afterload reduction AND Enhance systolic function
Ionotrope AND Arteriodilators or balanced dilators
Pimobendan
Phosphodiesterase inhibitor (also Ca sensitiser)
Oral
Pre-clinical DCM. Heart failure secondary to DCM and mitral valve disease
Risks: Effects of HR and rhythm
Afterload reduction
Arteriodilators or balanced dilators
Amlodipine
Ca channel antagonist
Oral
Anti-hypertensive in cats and dogs
Risks: hypotension
Afterload reduction
Arteriodilators or balanced dilators
Hydralazine
Unknown mechanism
Oral
2nd/3rd line vasodilator
Risks: hypotension
Enhance systolic function ANDOptimise cardiac rate and rhythm
Ionotrope AND Anti-arrhythmias
Digoxin
Blocks Na/K ATPase increase intracellular Ca and increased vagal tone
Oral, IV
Advanced heart failure, supra-ventricular arrhythmias
Risks: Narrow therapeutic ration, proarrhythmia, GI side effects
Enhance diastolic function
Lusiotropes/negaive chronotropes
Diltiazem
Ca Channel antagonist
Oral
HCM in cats
Few risks
Enhance diastolic function
Lusiotropes/negaive chronotropes
Atenolol, propanolol etc.
Beta-blockers
Oral
HCM in cats
Risks: Bradycardia and induction of heart failure
Optimise cardiac rate and rhythm
Anti-arrhythmias
Quinidine
Class IA anti-arrhythmic
Oral, injectable
Conversion of atrial fibrillation
Risks: GI effects, tachycardia
Optimise cardiac rate and rhythm
Anti-arrhythmias
Lignocaine
Class IB anti-arrhythmic
IV
Ventricular arrhythmias
Risks: GI and neuro side effects, Pro-A
Optimise cardiac rate and rhythm
Anti-arrhythmias
Maxilitine
Class IB anti-arrhythmic
Oral
Chronic oral management of ventricular arrhythmia
Risks: GI and neuro side effects, Pro-A
Optimise cardiac rate and rhythm
Anti-arrhythmias
Sotalol
Class III anti-arrhythmic
Oral
Chronic oral management of ventricular arrhythmia
Risks: Pro-arrhythmia
Optimise cardiac rate and rhythm
Anti-arrhythmias
Verapamil
Ca Channel antagonist
Oral, IV
Supraventricular tachycardia
Risks: bradycardia
Optimise cardiac rate and rhythm
Anti-arrhythmias
Dilitiazem
Ca Channel antagonist
Oral
Slow atrial fibrillation
Risks: bradycardia
Degenerative Mitral Valve disease
CKCS, spaniels, terriers, poodles (older small breed dogs)
Left apical systolic murmur - intensity increases with disease progress
May have elevated heart and lose sinus arrhythmia
Signs of heart failure, lose BCS, breathlessness, crackles
Diagnosis:
Doppler echocardiogram
Progressive left sided cardiac enlargement
Heart failure can be diagnosed on xray - pulmonary congestion and oedema
Therapy:
Furosemide and pimobendan (maybe ACEI and spironolactone)
Dilated cardiomyopathy
Large breed dogs (Dobermans, Boxers, Great Danes and Cocker spaniels)
Arrhythmia, soft left apical systolic murmur due to heart dilation
Signs associated with heart failure
Diagnosis:
Echo, ECG, xray (cardiomegaly, heart failure)
Treatment:
Pimonedan - Dobermans delay onset of clinical signs
ACEI - benefits prior to onset of clinical signs
Pericardial effusion
Older dogs, acquired - Labradors, GSD, St Bernards
Secondary to neoplas or idiopathic
- Inadequate output (forward failure) - weakness, collapse
OR
- Signs of congestion (backward failure)
- Signs of right sided heart failure (ascites, pleural effusion and increase respiratory effort), jugular venous distension
Muffled heart sounds, pulsus paradoxus - intensity of the femoral pulse decreases during inspiration
Diagnosis:
Echo, xrays
Treatment:
Pericardiocentesis, local analgesia/sedation
Right side of thorax, u/s guidance
Hypertrophic cardiomyopathy
Cats
Idiopathic left ventricle hypertrophy
Maine Coons and Ragdolls - myosin binding protein C mutation
Impaired ventricular relaxation/increased ventricular stiffness
Dynamic left ventricular outflow tract obstruction
Mostly young adult male cats
Asymptomatic, congestive heart failure, aortic thromboembolism, sudden deat
Systolic murmur/prominent apical impulse/gallop/tachypnoea/crackles
Xray: LV hypertrophy - long cardiac silhouette, pulmonary oedema/pleural effusion
Echo
Prognosis: poor
Dilated cardiomyopathy
Cats
All 4 chambers, thinning of ventricle wall and hypokinesis Middle aged - older cats Taurine-deficient cats Hypotension, hypothermia, bradycardia Murmur quite/absent +/- gallop Thromboembolic disease is common
Diagnosis: through echo
Prognosis: Grave
Restrictive cardiomyopathy
Cats
Severely impaired diastolic filling, still LV
Endomyocardial form: severe endomyocardial scarring
Myocardial: normal lv dimensions, sever atrial enlargement in both forms
Older cats, dyspnoea (pleural effusion) +/- low output signs +/- aortic thromboembolism
Arrhythmia common
Echo: bilateral arial enlargement
Arrhythmogenic RV cardiomyopathy
Cats
Fibrofatly infiltration of the RV
Right heart enlargement
Asymptomatic/syncopal/right-sided heart failure
Echo: Severe RV and RA dilation tricuspid regurgitation
Feline heart disease treatment
ACE inhibitors - if LA dilated
Diltiazem - licensed, no evidence of benefit
Beta-Blocker (atenolol) - control of LVOTO, long term benefit?
Feline post/past heart failure treatment
Oxygen
Sedation (butorphanol 0.25mg/kg IM)
Thoracocentesis
IV furosemide to effect
Mild-moderate feline heart failure
Treat at home
- Eliminate abnormal fluid retention
- Furosemide (1-4mg/kg q12-24h PO)
- ACE inhibitor - benazepril 0.5mg/kg q24h - Modulate neurohormonal activation
- ACE inhibitor - benazepril (Imidapril - tasteless liquid) - Optimise haemodynamic function
- Decreased heart rate?
- Beta blocker such as atenolol
- Ca channel such as diltiazem - Negative ionotropes for dynamic obstruction
Chronic Refractory heart failure (cats)
Increase dose of furosemide
Spironolactone: (not license for cats) 1mg/kg every 24h PO
Thiazides: Moduret
For cats with systolic dysfunction:
Pimobendan can be added 0.625-1.25mg q12-24h
Acute aortic thromboembolism - management
Analgesia: fentanyl, methadone
Manage electrolyte of acid-base abnormalities
Heparin: Prevention of thrombus extension
Prevent with aspirin:
High dose - 40mg/cat q72h
Low dose - 5 mg/cat q72h
Ventricular septal defect
Most common (except dogs)
Failure of normal formation of the inter-ventricular septum
Intense systolic murmur usually loudest on the right
Prognosis depends on size of shunt
PDA
L->R shunt Continuous left base murmur and bounding pulses Can see with Doppler Surgical ligation/interventional closure Good prognosis of closed
Aortic stenosis
Narrowing of left ventricle outflow tract - pressure overload of left ventricle
Left base systolic murmur, poor pulse
Concentrically hypertrophied LV - Doppler
Pulmonic stenosis
Narrowing of right ventricle outflow tract - RV pressure overload
Left base systolic murmur - less affected pulse
Right ventricular hypertrophy, pulmonary artery dilation, increased pulmonary outflow ventricle with Doppler
Balloon valvuloplasty and surgical patch grafting
Vascular ring anomaly
Malformation of great vessels e.g. PRAA Obstruction of thoracic oesophagus No murmur, regurgitation Dilate oesophagus cranial to heart Surgical reliefs
Atrial septic defects
Failure of formation of atrial septum (L -> R shunt) - may have no significance
Normal or soft murmur over pulmonic valave
Mitral and tricuspid dysplasia
Malformation of one or both AV valves - stenosis and/or insufficiency of valve leading to volume overload
Murmurs over mitral valve or tricuspid valve
Enlargement of left/right side
Definitive repair can be attempted surgically
