Cardiovascular system Flashcards
1
Q
Mammalian foetus
A
Foramen ovale connecting atria- becomes fossa ovalis
Ductus - vessel between the pulmonary trunk and aorta becomes the ligamentum arteriosum
2
Q
Normal blood pressures
A
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
3
Q
Atrioventricular valves
A
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
4
Q
Semilunar valves
A
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
5
Q
Cardiac sketeton
A
Structural integrity to the heart
Breaks up continuity between cardiac muscle cells of the atria and those of the ventricles
6
Q
Coronary circulation
A
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
7
Q
Large vessel structure
A
Internal elastic lamina -> endothelium -> tunica media (smooth muscle and collagen) -> tunica adventita (nerves) -> Vaso vasorum (arteries only)
8
Q
Starling forces
A
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
9
Q
Oedema
A
Excessive filtration
Defective resorption
Defective lymphatic drainage
10
Q
Cardiac action potentials
A
Pacemaker - SAN
Concentrations of important ions and the effect of opening a channel to create a current
Na+, K+, Ca2+
11
Q
Cardiac muscle
A
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)
12
Q
Conduction system
A
SAN -> Atria (via bundle of His)-> AV noda -> Purkinje system (modified myocytes) -> Ventricular muscle
13
Q
Ventricular action potentials
A
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
14
Q
Events of the cardiac cycle
A
-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
15
Q
ECG (electrocardium)
How it works
A
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
16
Q
ECG - provide information
A
Anatomical orientation of the heart Relative size of heart chambers HR, rhythm, origin of excitation Spread of impulse Decay of excitation
17
Q
ECG - phases
A
P wave - atrial depolarisation
QRS - ventricular depolarisation
T wave - ventricular repolarisation
PR interval - AV conduction time
18
Q
Increase heart rate
A
Sympathetic nerves - release noradrenaline, opens more channels for If
19
Q
Decrease heart rate
A
Parasympathetic nerves - release Ach, open fewer If channels
20
Q
Sinus rhythm
A
SAN acting as pacemaker
QRS complex follows each P wave, PR and QT complexes normal, RR interval regular
21
Q
Sinus arrhythmia
A
Normal QRS complex, PR and QT intervals but RR varies in set patterns
22
Q
Sinus tachycardia
A
Normal response to exercise (or fever, hyperthyroidism and reflex to low arterial pressure)
23
Q
Sinus bradycardia
A
May be abnormal (Addisionian crisis) but may be very fit individual
24
Q
Atrial myocytes
A
Respond to both sympathetic stimulation (beta1 receptors) and parasympathetic stimulations (M2 receptors)
25
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
26
Frank-Stirling relationship
Reservoir raised -> pressure causing ventricular filling increases -> more blood enters ventricle -> ventricular muscle stretches -> ventricular muscle responds with a stronger contraction
27
Afterload
The pressure at which the heart ejects
| Determined in vivo by the peripheral resistance which is proportional to arterial pressure
28
Preload
The filling pressure of the heart determined in vivo by the venous volume and rate of venous return
29
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
30
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
31
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
32
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
33
Short term regulation of blood pressure
Baroreceptor regulation - autonomic NS
| CVS system
34
Long term regulation of blood pressure
Control of fluid volume - vasopressin, renin-angiotensin-aldosterone, natruiretic peptides
Body fluid balance - renal system
35
Baroreceptors
Non-encapsulated nerve endings in adventitia of arteries - aortic arch and carotid sinus
Central axons terminate in nucleus trachus solitarius
Mechanoreceptors
36
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
37
Atrial receptors
Low pressure stretch receptors in the walls of the atria act as volume receptors
38
Atrial natruiretic peptide
Released into the circulation when the atrial walls are stretched by an increase in blood volume
1. Reduces blood volume b y stimulation excretion of salt and water by the kidney
2. Relaxes vascular smooth muscle (stimulate cGMP formation) vasodilator
3. Inhibits the renin-angiotensin-aldosterone system
Potent defence mechanism against voume overload
39
Mediastinum
Midline partition within the thorax
40
Thymus
Found (large) in young animals
Cranial to heart
Connects two vessels - seals after puberty
41
Valves
Atrioventricular valves
RIGHT tricuspid
LEFT mitral
Semilunar valves
RV/PA pulmonary
LV/A aortic
42
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
43
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
44
Local factors
Local vasodilation of blood vessels (NO, PGs, histamine released)
e.g. hypoxia
Increased CO2, H+ ions,
45
Adrenergic receptors
ALPHA 1 - smooth muscle, contraction -> blood vessels
BETA 1 - myocardium, excitatory -> HR increases
BETA 2 - smooth muscle, relaxation -> blood vessels
46
Body water content
60% of body
ICF - 40% (K, albumin)
ECF - 20% (Na, chloride)
47
Central regulation
CVS centre in medulla oblongata receives inputs from higher centres and baroceptors
Sympathetic and parasympathetic activity to the heart and blood vessels
48
Volume overload
Disease which requires the heart muscle to increase its activity causing overwork -> heart failure
e.g. valve insufficiencies, PDA, septal defects
49
Preload
```
Degree of stretch of the ventricular myocardium at the end of diastole
When excessive:
- increased atrial pressure
- increases venous pressure
- signs of congestion
```
50
Dilated cardiomyopathy
```
Common in dogs
Ventricular and atrial dilation
Depressed systolic function
Weakened myocardium liable to further distension
Frank-Starling mechanism impaired
```
51
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
52
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
53
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
54
1st degree heart block
Prolonged PR intervals
| Contraction delayed due to increased time for AV conduction
55
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
56
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
57
First sound (S1)
'Lub'
Long, low frequency
Associated with closure of the AV valves
Occurs mainly during isometric ventricular contraction
58
Second sound (S2)
'Dub'
Shorted higher frequency than S1
Associated closure of the aortic and pulmonary valves at the onset of ventricular diastole
59
Third sound (S3)
Very faint ventricular sound caused for movement of blood from the atria into the ventricle during early ventricular diastole
60
Fourth sound (S4)
Associated with atrial systole
| Caused by rapid flow in ventricles
61
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.
62
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.
63
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+
64
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
65
Blood flow
Laminar: in arteries and veins
Turbulent: in ventricles
Bolus: in capillaries
66
Carotid sinus
Where internal carotid branches off from common carotid
| Receives bundle of baroreceptor nerve fibres (autonomic afferent) via carotid sinus nerve
67
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
68
Functional hyperaemia
Increase in blood flow in response to metabolic demand
| Especially in skeletal muscle, cardiac muscle, brain
69
Reactive hyperaemia
Increase in local blood flow in response to temporary ischaemia to facilitate to removal of accumulated metabolites
70
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)
71
Tetralogy of Fallot
4 defects
- Pulmonary artery narrowed
- VSD
- Aorta opens over top of atrial septum
- RV atrophies
72
Congenitial diaphragmatic hernia
3 types
1. Hole in postro-lateral corner
2. adjacent to zyphoid process
3. abnormal elevation
73
Persistent right aortic arch
Constrict oesophagus - regurges food at weaning
Increased appetite, loses weight, megaoesophagus, aspiration pneumonia
Cut ligament arteriosus
74
Portosystemic shunt
```
Liver shunt (ductus venosus doesn't shut down)
Unfiltered blood in circulation
```
75
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
76
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
77
ECG
| Is there a QRS for every P wave?
```
Failure of conduction of atrial depolarisation through AV node normally
AV block (3 types)
```
78
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
79
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
80
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
81
Radiographs - strengths
Multiple thoracic structures
| Demonstration of left sided failure
82
Radiographs - weaknesses
Cannot detect mild cardiac enlargement or which chambers are enlarged
Bad discrimination between fluid and soft tissue
83
Radiographs - what can you see?
Airways - more obvious when disease
Pulmonary parenchyma
Vasculature
Cardiac silhouette
84
Echocardiography - strengths
Moving image - good differentiation between fluid and soft tissue
Can combine with ECG
85
Echocardiography - weaknesses
Cannot image lung
| Operator dependent
86
Haemostasis processes
Vascular spasm
Platelet adhesion and activation and coagulation (fibrin formation) (interaction)
Vasoconstriction
87
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
88
Clotting
```
Severed vessel - tissue factor, extrinsic clotting
> Collagen
> Platelet adhesion
> Platelet aggregation
> Temporary haemostatic plug
> Definitive haemostatic plug
> Fibrin
> Thrombin
> Intrinsic clotting
```
POSITIVE FEEDBACK
89
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
90
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
91
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)
92
Anti-platelet drugs
| Mechanisms
Inhibit TxA2 synthesis or block TxA2 receptors
Inhibit thrombin activity
Elevate platelet cAMP levels
Elevate platelet cGMP levels
93
Anti-platelet drugs
| Acetyl salicylic acid (aspirin)
Irreversible inhibitor of cyclo-oxygenase (COX) - infrequent and low dosing affects platelets more than endothelium
94
Anti-platelet drugs
| Epoprostenol (prostacyclin)
Elevates platelet cAMP and inhibits platelets aggregation
95
Anti-platelet drugs
| Nitrates
Raise platelet cGMP to inhibit adhesion and aggregation
96
Anti-platelet drugs
| Monoclonal antibodies to GP IIb/IIIa
And other compounds which block TxA2 synthesis/receptors are under investigation
97
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
```
98
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
99
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
100
Vitamin K
Post translational modification of some clotting factors
Oral (usaully)
Phytomenadium (natural), menadiol sodium phosphate (synthetic)
101
Warfarin
Structurally resembles vitamin K
| Prevents the reduction necessary for cofactor activity
102
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
103
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
104
Streptokinase
Streptococcal enzymes which activate plasminogen, increase the production of plasmin and cause generalised clot lysis
105
Urokinase
Activator of plasminogen extracted from human urine
106
Tissue plasminogen activator (tPA)
Act primarily on fibrin-bound plasminogen in the clot (clot selective)
Low affinity for circulating plasminogen
107
Congestion
Engorgement of vascular bed due to decreased outflow of blood
108
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
109
Congestion
| Damage to heart valves
Valves do not close efficiently - blood leaks back
Endocardiosis
Endocarditis - bacterial
110
Congestion
| Damage to heart muscle
```
Hypertrophic cardiomyopathy (cats)
Dilated cardiomyopathy (dogs)
```
111
Congestion
| Compression of heart from outside
Fluid in pericardial sac e.g. blood, pus, fibrin, fibrous tissue
Heart chamber are unable to fill adequately
112
PM change
| Hypostatic congestion
Before blood clots, it pools under gravity
| Distinguish from pathological congestion
113
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"
114
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
115
Haemorrhage
Escape of blood from blood vessels
| Can be distinguished from congestion microscopically
116
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
117
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
118
Haematome
Blood into tissue forming a clot
In spleen associated with hyperplastic lymphoid nodules and angiogenic tumours
Pinna of dogs
119
Bruise
Red for 48h
| Turns yellow due to macrophages converting haemoglobin into haemosiderin
120
Haemoglobinuria
Breakdown of product of RBCs appear in urine following intravascular haemolysis
121
Angiostrongylus vasorum
Worm that lives in pulmonary artery, RV and lungs of dogs and foxes
Secretes anticoagulant causing sporadic haemorrhage
122
Fibrocartiliginous emboli
Uncommon - probably arise from degenerate invetebral disc in dogs
Occlude spinal blood vessels and cause necrosis - sudden paralysis/paresis
123
Parasitic emboli
Dirofilariasis (heartworm)
124
Global infarction
Large or more proximal artery blockage causes more severe or extensive infarction
125
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
126
Neurogenic maldistributive shock
Trauma, electrocution, fear, emotional stress - profound autonomic stimulation - widespread vasodilation
127
Pump failure
Failure of systolic function of the myocardium results in inadequate SV and fall in CO
- Dilated cardiomyopathy
- Coronary vascular disease
128
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
129
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
130
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
131
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
132
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
133
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
134
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
135
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
136
Clinical signs of heart failure
```
Tachycardia
Poor peripheral perfusion
Fluid retention:
- Left sided - pulmonary circulation
- Right sided - abdominal fluid
```
137
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
138
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
139
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
```
140
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
141
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
142
Non-pathological murmurs
| horses
Grade 3/6 murmur near base of heart in foals
143
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)
144
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
145
Ultrasound measurements
Chamber size:
- Normal LA:Ao 55%)
- Hypokinetic (
146
Left atrial dilation
Mitral valve disease, L -> R shunts
DCM
Hypertrophy cardiomyopathy
147
Left ventricle dilation
MR, L-> R shunts, AR
| DCM, chronic volume overload
148
Left ventricle hypertrophy
Aortic stenosis, systemic hypertension
| HCM
149
Right ventricle hypertrophy
Pulmonic stenosis
| Pulmonary hypertension
150
Ventral heart shadow
Normal VHS = 8.7-10.7 - imprecise
| Many cardiac diseases do not change the VHS
151
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
152
```
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
153
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
154
```
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
155
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
156
Valve prolapse (horses)
Any valve, may cause murmur
Non-progressive regurgitation
Considered physiological rather than pathological
157
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
158
Right and left ventricular hypertrophy in atheletes (horses)
Usually mild and non progressive
Tricuspid
Could be considered physiological regurgitation
159
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]
160
Patent ductus arteriosus (horses)
After 1 month old
| 'Washing machine' murmur
161
Valvular dysplasia (horses)
Congenital, uncommon
| Rarely well-tolerated and usually part of complex cardiac disease
162
```
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)
163
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
164
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
165
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
166
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)
167
Cardiac troponin I
Cardiac isoenzymes: creatine kinase and lactate dehydrogenase
- Released into the circulation with myocardial call death
- Indicators of myocarditis/myocardial necrosis
168
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
169
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
170
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
171
Signs of heart failure (horses)
Resting tachycardia (60bpm)
Valve regurgitation especially mitral/tricuspid
Venous distension
Oedema
172
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
173
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
174
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
175
Lymphosarcoma in cattle
Bovine leukaemia virus (BLV) positive (notifiable)
Right atrial pressure, jugular distension
Pericardial effusion, right sided heat failure, cytology reveals neoplastic cells
176
Pericarditis in pigs
Haemophilus parasuis (Glasser's disease). Strep suis
Fever, depression, Fibrinous polyserositis, Synovia, Effusions in CNS, Pleural, Peritoneum
177
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)
178
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
179
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)
180
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
181
Therapeutics
| Poor systolic function
Dilated cardiomyopathy and latter stages of mitral valve disease
Ionotropic agents may improve output and signs
182
Therapeutics
| Poor diastolic function
Poor ventricular relaxation
| Drugs that hasten relaxation, slow HR or reduce fibrosis
183
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
184
Pre-load reduction
Diuretics
Spironolactone
Blocks aldosterone receptors
Oral
2nd line diuretic, may be beneficial in neurohormonal blockade
Risks: Hyperkalaemia
185
Pre-load reduction
Diuretics
Torasemide
Block Na absorption - ascending limb (loop of Henle)
Oral
Dogs refractory to furosemide
Risks: Electrolyte disturbances, hypovolaemia, azotaemia
186
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
187
Pre-load reduction
Venodilators
Glycerol trinitrate
Nitrates act like endogenous nitric oxide - relax smooth muscle
Percutaneous
Emergency management of acute heart failure
Risks: Hypotension
188
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
189
Afterload reduction
Arteriodilators or balanced dilators
ACE inhibitors
Block production of angiotensin II
Oral
Many indications in cats and dogs
Risks: Hypotension, renal underperfusion
190
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
191
Afterload reduction
Arteriodilators or balanced dilators
Amlodipine
Ca channel antagonist
Oral
Anti-hypertensive in cats and dogs
Risks: hypotension
192
Afterload reduction
Arteriodilators or balanced dilators
Hydralazine
Unknown mechanism
Oral
2nd/3rd line vasodilator
Risks: hypotension
193
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
194
Enhance diastolic function
Lusiotropes/negaive chronotropes
Diltiazem
Ca Channel antagonist
Oral
HCM in cats
Few risks
195
Enhance diastolic function
Lusiotropes/negaive chronotropes
Atenolol, propanolol etc.
Beta-blockers
Oral
HCM in cats
Risks: Bradycardia and induction of heart failure
196
Optimise cardiac rate and rhythm
Anti-arrhythmias
Quinidine
Class IA anti-arrhythmic
Oral, injectable
Conversion of atrial fibrillation
Risks: GI effects, tachycardia
197
Optimise cardiac rate and rhythm
Anti-arrhythmias
Lignocaine
Class IB anti-arrhythmic
IV
Ventricular arrhythmias
Risks: GI and neuro side effects, Pro-A
198
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
199
Optimise cardiac rate and rhythm
Anti-arrhythmias
Sotalol
Class III anti-arrhythmic
Oral
Chronic oral management of ventricular arrhythmia
Risks: Pro-arrhythmia
200
Optimise cardiac rate and rhythm
Anti-arrhythmias
Verapamil
Ca Channel antagonist
Oral, IV
Supraventricular tachycardia
Risks: bradycardia
201
Optimise cardiac rate and rhythm
Anti-arrhythmias
Dilitiazem
Ca Channel antagonist
Oral
Slow atrial fibrillation
Risks: bradycardia
202
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)
203
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
204
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
205
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
206
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
207
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
208
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
209
Feline heart disease treatment
ACE inhibitors - if LA dilated
Diltiazem - licensed, no evidence of benefit
Beta-Blocker (atenolol) - control of LVOTO, long term benefit?
210
Feline post/past heart failure treatment
Oxygen
Sedation (butorphanol 0.25mg/kg IM)
Thoracocentesis
IV furosemide to effect
211
Mild-moderate feline heart failure
Treat at home
1. Eliminate abnormal fluid retention
- Furosemide (1-4mg/kg q12-24h PO)
- ACE inhibitor - benazepril 0.5mg/kg q24h
2. Modulate neurohormonal activation
- ACE inhibitor - benazepril (Imidapril - tasteless liquid)
3. Optimise haemodynamic function
4. Decreased heart rate?
- Beta blocker such as atenolol
- Ca channel such as diltiazem
5. Negative ionotropes for dynamic obstruction
212
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
213
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
214
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
215
PDA
```
L->R shunt
Continuous left base murmur and bounding pulses
Can see with Doppler
Surgical ligation/interventional closure
Good prognosis of closed
```
216
Aortic stenosis
Narrowing of left ventricle outflow tract - pressure overload of left ventricle
Left base systolic murmur, poor pulse
Concentrically hypertrophied LV - Doppler
217
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
218
Vascular ring anomaly
```
Malformation of great vessels e.g. PRAA
Obstruction of thoracic oesophagus
No murmur, regurgitation
Dilate oesophagus cranial to heart
Surgical reliefs
```
219
Atrial septic defects
Failure of formation of atrial septum (L -> R shunt) - may have no significance
Normal or soft murmur over pulmonic valave
220
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
