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Veterinary Medicine > Cardiovascular system > Flashcards

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

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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

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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

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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

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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

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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

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7
Q

Large vessel structure

A

Internal elastic lamina -> endothelium -> tunica media (smooth muscle and collagen) -> tunica adventita (nerves) -> Vaso vasorum (arteries only)

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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

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9
Q

Oedema

A

Excessive filtration
Defective resorption
Defective lymphatic drainage

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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+

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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)

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12
Q

Conduction system

A

SAN -> Atria (via bundle of His)-> AV noda -> Purkinje system (modified myocytes) -> Ventricular muscle

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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

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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

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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

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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
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17
Q

ECG - phases

A

P wave - atrial depolarisation
QRS - ventricular depolarisation
T wave - ventricular repolarisation
PR interval - AV conduction time

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18
Q

Increase heart rate

A

Sympathetic nerves - release noradrenaline, opens more channels for If

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19
Q

Decrease heart rate

A

Parasympathetic nerves - release Ach, open fewer If channels

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20
Q

Sinus rhythm

A

SAN acting as pacemaker

QRS complex follows each P wave, PR and QT complexes normal, RR interval regular

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21
Q

Sinus arrhythmia

A

Normal QRS complex, PR and QT intervals but RR varies in set patterns

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22
Q

Sinus tachycardia

A

Normal response to exercise (or fever, hyperthyroidism and reflex to low arterial pressure)

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23
Q

Sinus bradycardia

A

May be abnormal (Addisionian crisis) but may be very fit individual

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24
Q

Atrial myocytes

A

Respond to both sympathetic stimulation (beta1 receptors) and parasympathetic stimulations (M2 receptors)

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25
Q

Ventricular myocytes

A

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

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26
Q

Frank-Stirling relationship

A

Reservoir raised -> pressure causing ventricular filling increases -> more blood enters ventricle -> ventricular muscle stretches -> ventricular muscle responds with a stronger contraction

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27
Q

Afterload

A

The pressure at which the heart ejects

Determined in vivo by the peripheral resistance which is proportional to arterial pressure

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28
Q

Preload

A

The filling pressure of the heart determined in vivo by the venous volume and rate of venous return

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29
Q

Alteration of preload

A

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

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30
Q

Venous return

A

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

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31
Q

Alteration of afterload

A

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

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32
Q

Systemic arterial pressure

A

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

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33
Q

Short term regulation of blood pressure

A

Baroreceptor regulation - autonomic NS

CVS system

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34
Q

Long term regulation of blood pressure

A

Control of fluid volume - vasopressin, renin-angiotensin-aldosterone, natruiretic peptides
Body fluid balance - renal system

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35
Q

Baroreceptors

A

Non-encapsulated nerve endings in adventitia of arteries - aortic arch and carotid sinus
Central axons terminate in nucleus trachus solitarius
Mechanoreceptors

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36
Q

Renin-angiotensin-aldosterone system

A

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

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37
Q

Atrial receptors

A

Low pressure stretch receptors in the walls of the atria act as volume receptors

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38
Q

Atrial natruiretic peptide

A

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

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39
Q

Mediastinum

A

Midline partition within the thorax

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40
Q

Thymus

A

Found (large) in young animals
Cranial to heart
Connects two vessels - seals after puberty

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41
Q

Valves

A

Atrioventricular valves
RIGHT tricuspid
LEFT mitral

Semilunar valves
RV/PA pulmonary
LV/A aortic

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42
Q

Sympathetic NS - CVS

A

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

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43
Q

Parasympathetic NS - CVS

A

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

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44
Q

Local factors

A

Local vasodilation of blood vessels (NO, PGs, histamine released)
e.g. hypoxia
Increased CO2, H+ ions,

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45
Q

Adrenergic receptors

A

ALPHA 1 - smooth muscle, contraction -> blood vessels
BETA 1 - myocardium, excitatory -> HR increases
BETA 2 - smooth muscle, relaxation -> blood vessels

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46
Q

Body water content

A

60% of body
ICF - 40% (K, albumin)
ECF - 20% (Na, chloride)

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47
Q

Central regulation

A

CVS centre in medulla oblongata receives inputs from higher centres and baroceptors
Sympathetic and parasympathetic activity to the heart and blood vessels

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48
Q

Volume overload

A

Disease which requires the heart muscle to increase its activity causing overwork -> heart failure
e.g. valve insufficiencies, PDA, septal defects

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49
Q

Preload

A 
Degree of stretch of the ventricular myocardium at the end of diastole
When excessive:
- increased atrial pressure
- increases venous pressure
- signs of congestion
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50
Q

Dilated cardiomyopathy

A 
Common in dogs
Ventricular and atrial dilation
Depressed systolic function
Weakened myocardium liable to further distension
Frank-Starling mechanism impaired
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51
Q

Hyperthyroidism

A

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

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52
Q

Actions of norepinephrine and epinephrine on the heart

Sympathetic stimulation

A

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

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53
Q

Actions of acetylcholine on the heart

Vagal stimulation

A

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

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54
Q

1st degree heart block

A

Prolonged PR intervals

Contraction delayed due to increased time for AV conduction

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55
Q

2nd degree heart block

A

AV node fails to transmit all atrial impulses (more p waves than QRS complexes
Atria beat more than once for each ventricular onctraction

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56
Q

3rd degree heart block

A

Transmission of impulse from atria to ventricles wrong
Atria and ventricles beat independently from each other
P waves and QRS complexes completely dissociated

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57
Q

First sound (S1)

A

‘Lub’
Long, low frequency
Associated with closure of the AV valves
Occurs mainly during isometric ventricular contraction

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58
Q

Second sound (S2)

A

‘Dub’
Shorted higher frequency than S1
Associated closure of the aortic and pulmonary valves at the onset of ventricular diastole

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59
Q

Third sound (S3)

A

Very faint ventricular sound caused for movement of blood from the atria into the ventricle during early ventricular diastole

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60
Q

Fourth sound (S4)

A

Associated with atrial systole

Caused by rapid flow in ventricles

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61
Q

Chronotropes

A

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.

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62
Q

Inotropes

A

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.

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63
Q

Altering force of contraction

A

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+

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64
Q

Other effectors on contractility

A

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

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65
Q

Blood flow

A

Laminar: in arteries and veins
Turbulent: in ventricles
Bolus: in capillaries

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66
Q

Carotid sinus

A

Where internal carotid branches off from common carotid

Receives bundle of baroreceptor nerve fibres (autonomic afferent) via carotid sinus nerve

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67
Q

Peripheral arterial chemoreceptors

A

Located in carotid and aortic bodies and respond to hypoxia, acidosis (decrease in pH or increase in CO2), asphyxia
Also respond when arterial pressure

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68
Q

Functional hyperaemia

A

Increase in blood flow in response to metabolic demand

Especially in skeletal muscle, cardiac muscle, brain

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69
Q

Reactive hyperaemia

A

Increase in local blood flow in response to temporary ischaemia to facilitate to removal of accumulated metabolites

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70
Q

Endothelins

A

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)

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71
Q

Tetralogy of Fallot

A

4 defects

  • Pulmonary artery narrowed
  • VSD
  • Aorta opens over top of atrial septum
  • RV atrophies
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72
Q

Congenitial diaphragmatic hernia

A

3 types

  1. Hole in postro-lateral corner
  2. adjacent to zyphoid process
  3. abnormal elevation
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73
Q

Persistent right aortic arch

A

Constrict oesophagus - regurges food at weaning
Increased appetite, loses weight, megaoesophagus, aspiration pneumonia
Cut ligament arteriosus

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74
Q

Portosystemic shunt

A 
Liver shunt (ductus venosus doesn't shut down)
Unfiltered blood in circulation
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75
Q

Patent foramen ovale

A

Retain hole in atrial septum
Usually no consequences as pressure keeps it shut
only treat if in conjunction with other heart defects

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76
Q

ECG

Is there a P wave for every QRS complex

A

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

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77
Q

ECG

Is there a QRS for every P wave?

A 
Failure of conduction of atrial depolarisation through AV node normally
AV block (3 types)
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78
Q

ECG

Are the P waves and QRS complexes consistently and reasonably related?

A

Show as inconsistent relationship between the two
Implies presence of separate ventricular and atrial rhythms
Atrioventricular dissocation

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79
Q

ECG

Are the QRS complexes and the P waves all the same?

A

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

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80
Q

ECG

Is the HR regular or irregular?

A

Normal rhythms tend to be regular or regularly irregular
Irregularly irregular always abnormal
Most common is atrial fibrillation - sounds chaotic
Auscultation is sensitive

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81
Q

Radiographs - strengths

A

Multiple thoracic structures

Demonstration of left sided failure

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82
Q

Radiographs - weaknesses

A

Cannot detect mild cardiac enlargement or which chambers are enlarged
Bad discrimination between fluid and soft tissue

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83
Q

Radiographs - what can you see?

A

Airways - more obvious when disease
Pulmonary parenchyma
Vasculature
Cardiac silhouette

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84
Q

Echocardiography - strengths

A

Moving image - good differentiation between fluid and soft tissue
Can combine with ECG

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85
Q

Echocardiography - weaknesses

A

Cannot image lung

Operator dependent

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86
Q

Haemostasis processes

A

Vascular spasm
Platelet adhesion and activation and coagulation (fibrin formation) (interaction)
Vasoconstriction

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87
Q

Thrombosis - an unwanted pathological process

A

Venous thrombosis - small number of platelets; large fibrin component
Arterial thrombosis - large platelet component
Inappropriate blood clotting (thrombosis) occludes blood vessels

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88
Q

Clotting

A 
Severed vessel - tissue factor, extrinsic clotting
> Collagen
> Platelet adhesion
> Platelet aggregation
> Temporary haemostatic plug
> Definitive haemostatic plug
> Fibrin
> Thrombin
> Intrinsic clotting

POSITIVE FEEDBACK

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89
Q

Platelet adhesion and aggregations

A

> 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
Q

Coagulation cascade

A

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
Q

Drugs that interfere with coagulation cascade

A

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
Q

Anti-platelet drugs

Mechanisms

A

Inhibit TxA2 synthesis or block TxA2 receptors
Inhibit thrombin activity
Elevate platelet cAMP levels
Elevate platelet cGMP levels

93
Q

Anti-platelet drugs

Acetyl salicylic acid (aspirin)

A

Irreversible inhibitor of cyclo-oxygenase (COX) - infrequent and low dosing affects platelets more than endothelium

94
Q

Anti-platelet drugs

Epoprostenol (prostacyclin)

A

Elevates platelet cAMP and inhibits platelets aggregation

95
Q

Anti-platelet drugs

Nitrates

A

Raise platelet cGMP to inhibit adhesion and aggregation

96
Q

Anti-platelet drugs

Monoclonal antibodies to GP IIb/IIIa

A

And other compounds which block TxA2 synthesis/receptors are under investigation

97
Q

Calcium and coagulation

A 
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
Q

Heparin

A

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
Q

Low molecular weight heparin-like molecules

A

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
Q

Vitamin K

A

Post translational modification of some clotting factors
Oral (usaully)
Phytomenadium (natural), menadiol sodium phosphate (synthetic)

101
Q

Warfarin

A

Structurally resembles vitamin K

Prevents the reduction necessary for cofactor activity

102
Q

Thromboembolic disease

A

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
Q

Treating bleeding disorders

A

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
Q

Streptokinase

A

Streptococcal enzymes which activate plasminogen, increase the production of plasmin and cause generalised clot lysis

105
Q

Urokinase

A

Activator of plasminogen extracted from human urine

106
Q

Tissue plasminogen activator (tPA)

A

Act primarily on fibrin-bound plasminogen in the clot (clot selective)
Low affinity for circulating plasminogen

107
Q

Congestion

A

Engorgement of vascular bed due to decreased outflow of blood

108
Q

Congestive heart failure

A

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
Q

Congestion

Damage to heart valves

A

Valves do not close efficiently - blood leaks back
Endocardiosis
Endocarditis - bacterial

110
Q

Congestion

Damage to heart muscle

A 
Hypertrophic cardiomyopathy (cats)
Dilated cardiomyopathy (dogs)
111
Q

Congestion

Compression of heart from outside

A

Fluid in pericardial sac e.g. blood, pus, fibrin, fibrous tissue
Heart chamber are unable to fill adequately

112
Q

PM change

Hypostatic congestion

A

Before blood clots, it pools under gravity

Distinguish from pathological congestion

113
Q

Congested lungs

A

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
Q

Congested liver

A

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
Q

Haemorrhage

A

Escape of blood from blood vessels

Can be distinguished from congestion microscopically

116
Q

Rhexus

A

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
Q

Diapedesis

A

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
Q

Haematome

A

Blood into tissue forming a clot
In spleen associated with hyperplastic lymphoid nodules and angiogenic tumours
Pinna of dogs

119
Q

Bruise

A

Red for 48h

Turns yellow due to macrophages converting haemoglobin into haemosiderin

120
Q

Haemoglobinuria

A

Breakdown of product of RBCs appear in urine following intravascular haemolysis

121
Q

Angiostrongylus vasorum

A

Worm that lives in pulmonary artery, RV and lungs of dogs and foxes
Secretes anticoagulant causing sporadic haemorrhage

122
Q

Fibrocartiliginous emboli

A

Uncommon - probably arise from degenerate invetebral disc in dogs
Occlude spinal blood vessels and cause necrosis - sudden paralysis/paresis

123
Q

Parasitic emboli

A

Dirofilariasis (heartworm)

124
Q

Global infarction

A

Large or more proximal artery blockage causes more severe or extensive infarction

125
Q

DIC (Disseminated intravascular coagulation)

A

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
Q

Neurogenic maldistributive shock

A

Trauma, electrocution, fear, emotional stress - profound autonomic stimulation - widespread vasodilation

127
Q

Pump failure

A

Failure of systolic function of the myocardium results in inadequate SV and fall in CO

  • Dilated cardiomyopathy
  • Coronary vascular disease
128
Q

Volume overload

A

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
Q

Pressure overload

A

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
Q

Arrythmias

A

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
Q

Diastolic failure

A

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
Q

Heart failure - autonomic

A

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
Q

RAAS

A

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
Q

Anti-diuretic hormone

A

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
Q

Hypertrophy

A 
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
Q

Clinical signs of heart failure

A 
Tachycardia 
Poor peripheral perfusion
Fluid retention:
- Left sided - pulmonary circulation
- Right sided - abdominal fluid
137
Q

Clinical signs of vascular disease

A

Under-perfusion - vascular obstruction (complete/partial, loss of function, ischaemia, necrosis)
Increased vascular permeability - vasculitis
Decreased oncotic pressure - hypoproteinaemia
Decreased lymphatic drainage - lymphoedema

138
Q

Thromboembolism

A

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
Q

Normal heart rates

A 
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
Q

Auscultation

A

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
Q

Location of murmur

A

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
Q

Non-pathological murmurs

horses

A

Grade 3/6 murmur near base of heart in foals

143
Q

Pathological murmurs

horses

A

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
Q

Murmurs of doubtful significance

horses

A

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
Q

Ultrasound measurements

A

Chamber size:

  • Normal LA:Ao 55%)
  • Hypokinetic (
146
Q

Left atrial dilation

A

Mitral valve disease, L -> R shunts
DCM
Hypertrophy cardiomyopathy

147
Q

Left ventricle dilation

A

MR, L-> R shunts, AR

DCM, chronic volume overload

148
Q

Left ventricle hypertrophy

A

Aortic stenosis, systemic hypertension

HCM

149
Q

Right ventricle hypertrophy

A

Pulmonic stenosis

Pulmonary hypertension

150
Q

Ventral heart shadow

A

Normal VHS = 8.7-10.7 - imprecise

Many cardiac diseases do not change the VHS

151
Q

Physiological ‘flow’ murmurs in horses

A

Mainly thoroughbred horses in training
Main mitral and tricuspid valves (sometimes aortic/pulmonary)
Differentiate from pathological
Around 30% horses in training

152
Q 
Mitral regurgitation (horses)
(LA->LV)
A

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
Q

Aortic regurgitation (horses)

A

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
Q 
Tricuspid regurgitation (horses)
(RA-RV)
A

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
Q

Bacterial endocarditis

A

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
Q

Valve prolapse (horses)

A

Any valve, may cause murmur
Non-progressive regurgitation
Considered physiological rather than pathological

157
Q

Ruptured chordae tendinae (horses)

A

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
Q

Right and left ventricular hypertrophy in atheletes (horses)

A

Usually mild and non progressive
Tricuspid
Could be considered physiological regurgitation

159
Q

Ventricular septal defect (horses)

A

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
Q

Patent ductus arteriosus (horses)

A

After 1 month old

‘Washing machine’ murmur

161
Q

Valvular dysplasia (horses)

A

Congenital, uncommon

Rarely well-tolerated and usually part of complex cardiac disease

162
Q 
Primary myocarditis (large animals)
Infectious
A

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
Q

Nutritional myodegeneration - White muscle disease

A

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
Q

Cardiomyopathies in large animals

A

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
Q

Cardiac neoplasia in large animals

A

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
Q

Secondary myocardial disease and dysfunction

A

Most common causes:

  • Endotoxaemia
  • Hypoxia
  • Electrolytes (K, Ca. Mg)
  • Acidosis
  • Catecholamines (horses - severe GIT disease and upper airway during obstruction)
167
Q

Cardiac troponin I

A

Cardiac isoenzymes: creatine kinase and lactate dehydrogenase

  • Released into the circulation with myocardial call death
  • Indicators of myocarditis/myocardial necrosis
168
Q

QRS complexes in large animals

A

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
Q

Atrioventricular block (large animals)

A

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
Q

Atrial fibrillation (horses)

A

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
Q

Signs of heart failure (horses)

A

Resting tachycardia (60bpm)
Valve regurgitation especially mitral/tricuspid
Venous distension
Oedema

172
Q

Quinidine sulphate

A

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
Q

Ventricular premature complexes (VPC) and ventricular tachycardia (VT)
Horses

A

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
Q

Traumatic pericarditis

A

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
Q

Lymphosarcoma in cattle

A

Bovine leukaemia virus (BLV) positive (notifiable)
Right atrial pressure, jugular distension
Pericardial effusion, right sided heat failure, cytology reveals neoplastic cells

176
Q

Pericarditis in pigs

A

Haemophilus parasuis (Glasser’s disease). Strep suis

Fever, depression, Fibrinous polyserositis, Synovia, Effusions in CNS, Pleural, Peritoneum

177
Q

Pericardial effusions (horses)

A

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
Q

Cor pulmonale (farm)

A

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
Q

Exercise Induced Pulmonary Haemorrhage

A

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
Q

Therapeutics

Increased afterload

A

Signs of poor output due to vasoconstriction - decrease afterload
Increases myocardial work and diminishes perfusion
Pale or cold e.g. mitral regurgitation

181
Q

Therapeutics

Poor systolic function

A

Dilated cardiomyopathy and latter stages of mitral valve disease
Ionotropic agents may improve output and signs

182
Q

Therapeutics

Poor diastolic function

A

Poor ventricular relaxation

Drugs that hasten relaxation, slow HR or reduce fibrosis

183
Q

Pre-load reduction
Diuretics
Furosemide

A

Block Na absorption - ascending limb (loop of Henle)
Oral/IV/SC/CRI
Congestive heart failure
Risks: Electrolyte disturbances, hypovolaemia, azotaemia

184
Q

Pre-load reduction
Diuretics
Spironolactone

A

Blocks aldosterone receptors
Oral
2nd line diuretic, may be beneficial in neurohormonal blockade
Risks: Hyperkalaemia

185
Q

Pre-load reduction
Diuretics
Torasemide

A

Block Na absorption - ascending limb (loop of Henle)
Oral
Dogs refractory to furosemide
Risks: Electrolyte disturbances, hypovolaemia, azotaemia

186
Q

Pre-load reduction
Diuretics
Thiazides

A

Block Na reabsorption in distal convoluted tubule
Oral
2nd/3rd line diuretic in end stage heart failure
Risks: electrolyte disturbances, hypovolaemia, azotaemia

187
Q

Pre-load reduction
Venodilators
Glycerol trinitrate

A

Nitrates act like endogenous nitric oxide - relax smooth muscle
Percutaneous
Emergency management of acute heart failure
Risks: Hypotension

188
Q

Pre-load reduction
Venodilators
Nitroprusside

A

Nitrates act like endogenous nitric oxide - relax smooth muscle
CRI
Emergency management of acute heart failure
Risks: Hypotension and cyanide toxicity

189
Q

Afterload reduction
Arteriodilators or balanced dilators
ACE inhibitors

A

Block production of angiotensin II
Oral
Many indications in cats and dogs
Risks: Hypotension, renal underperfusion

190
Q

Afterload reduction AND Enhance systolic function
Ionotrope AND Arteriodilators or balanced dilators
Pimobendan

A

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
Q

Afterload reduction
Arteriodilators or balanced dilators
Amlodipine

A

Ca channel antagonist
Oral
Anti-hypertensive in cats and dogs
Risks: hypotension

192
Q

Afterload reduction
Arteriodilators or balanced dilators
Hydralazine

A

Unknown mechanism
Oral
2nd/3rd line vasodilator
Risks: hypotension

193
Q

Enhance systolic function ANDOptimise cardiac rate and rhythm
Ionotrope AND Anti-arrhythmias
Digoxin

A

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
Q

Enhance diastolic function
Lusiotropes/negaive chronotropes
Diltiazem

A

Ca Channel antagonist
Oral
HCM in cats
Few risks

195
Q

Enhance diastolic function
Lusiotropes/negaive chronotropes
Atenolol, propanolol etc.

A

Beta-blockers
Oral
HCM in cats
Risks: Bradycardia and induction of heart failure

196
Q

Optimise cardiac rate and rhythm
Anti-arrhythmias
Quinidine

A

Class IA anti-arrhythmic
Oral, injectable
Conversion of atrial fibrillation
Risks: GI effects, tachycardia

197
Q

Optimise cardiac rate and rhythm
Anti-arrhythmias
Lignocaine

A

Class IB anti-arrhythmic
IV
Ventricular arrhythmias
Risks: GI and neuro side effects, Pro-A

198
Q

Optimise cardiac rate and rhythm
Anti-arrhythmias
Maxilitine

A

Class IB anti-arrhythmic
Oral
Chronic oral management of ventricular arrhythmia
Risks: GI and neuro side effects, Pro-A

199
Q

Optimise cardiac rate and rhythm
Anti-arrhythmias
Sotalol

A

Class III anti-arrhythmic
Oral
Chronic oral management of ventricular arrhythmia
Risks: Pro-arrhythmia

200
Q

Optimise cardiac rate and rhythm
Anti-arrhythmias
Verapamil

A

Ca Channel antagonist
Oral, IV
Supraventricular tachycardia
Risks: bradycardia

201
Q

Optimise cardiac rate and rhythm
Anti-arrhythmias
Dilitiazem

A

Ca Channel antagonist
Oral
Slow atrial fibrillation
Risks: bradycardia

202
Q

Degenerative Mitral Valve disease

A

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
Q

Dilated cardiomyopathy

A

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
Q

Pericardial effusion

A

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
Q

Hypertrophic cardiomyopathy

Cats

A

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
Q

Dilated cardiomyopathy

Cats

A 
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
Q

Restrictive cardiomyopathy

Cats

A

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
Q

Arrhythmogenic RV cardiomyopathy

Cats

A

Fibrofatly infiltration of the RV
Right heart enlargement
Asymptomatic/syncopal/right-sided heart failure

Echo: Severe RV and RA dilation tricuspid regurgitation

209
Q

Feline heart disease treatment

A

ACE inhibitors - if LA dilated
Diltiazem - licensed, no evidence of benefit
Beta-Blocker (atenolol) - control of LVOTO, long term benefit?

210
Q

Feline post/past heart failure treatment

A

Oxygen
Sedation (butorphanol 0.25mg/kg IM)
Thoracocentesis
IV furosemide to effect

211
Q

Mild-moderate feline heart failure

A

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
Q

Chronic Refractory heart failure (cats)

A

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
Q

Acute aortic thromboembolism - management

A

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
Q

Ventricular septal defect

A

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
Q

PDA

A 
L->R shunt
Continuous left base murmur and bounding pulses
Can see with Doppler
Surgical ligation/interventional closure
Good prognosis of closed
216
Q

Aortic stenosis

A

Narrowing of left ventricle outflow tract - pressure overload of left ventricle
Left base systolic murmur, poor pulse
Concentrically hypertrophied LV - Doppler

217
Q

Pulmonic stenosis

A

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
Q

Vascular ring anomaly

A 
Malformation of great vessels e.g. PRAA
Obstruction of thoracic oesophagus
No murmur, regurgitation
Dilate oesophagus cranial to heart
Surgical reliefs
219
Q

Atrial septic defects

A

Failure of formation of atrial septum (L -> R shunt) - may have no significance
Normal or soft murmur over pulmonic valave

220
Q

Mitral and tricuspid dysplasia

A

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

Veterinary Medicine (15 decks)

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