1
Q
Draw the Heart with is anatomy and blood flow
A
2
Q
- Explain Stroke Volume
- How is Cardiac Output Calculated?
A
- Stroke Volume = The difference between the volume in the ventricle at the end of filling (End Diastolic Volume,EDV) and the volume in the ventricle immediately after contraction (End Systolic Volume, ESV)
SV = EDV - ESV
- Cardiac Output = Heart Rate x Stroke Volume
3
Q
- Explain the pressure differences during Systolie and Dyastolie.
- When does Isovolumetric Contraction occur?
- When does Isovolumetric Relaxation occur?
A
4
Q
What happens during Systole?
A
- Myocardial fibres shorten to 15-20% of their length
- Twisting of ventricles “Wringing function”
- the Ventricle is a stiff chamber which efficiently ejects blood into arteries at high pressure.
5
Q
- What is Systolic Dysfunction
A
- Systolic Dysfunction refers to impaired ventricular contraction (pump function) with reduced ejection fraction and an enlarged end-diastolic chamber volume (EDV)
- A reduction in myocardial contractility (loss of inotropy) results in decreased stroke volume and a resultant increase in ventricular volume and pressure due to incomplete ventricular emptying after systole
- Increase in EDV as the blood that normally fills the ventricle from the left atrium adds to the increased volume remaining after ineffective systolic emptying
- this causes increased pressure on the ventricular wall and eccentric dilation of the ventricle
6
Q
- What does an inotrope do/used for?
- Name the 2 types of inotropes used in vet medicine
A
- Inotropes increase myocardial contractility (usually used when you have Systolic Dysfunction
- Digoxin - Inhibitor of Cellular Na+/K+-ATPase increases intracellular Na- exits cell in exchange for Ca (NA-Ca exchanger) Ca++ binds to troponin-C modulates the polymerization of actin and myoson
- Pimobendan (Vetmedin, Boehringer-Ingelheim) Positive ionotrope: phosphodiesterase III and V inhibition, Increases intracellular {Ca++} Relaxes vascular smooth muscle (arterial Vasodiation “Inodilator”
7
Q
- What is Diastolic dysfunciton caracterised by?
- What are the 3 magor diastolic abnormalities?
- What are all of these features of?
A
- an increased resistance to filling with increased filling pressures.
- 3 major diastolic abnormalities
- Slowed or incomplete relaxation - due to increased myocyte calcium, decreased ATP, and activation of angiotensin II
- Reduced left ventricular filling
- Altered Passive elastic properties - wall stiffness due to endomyocardial fibrosis and altered collagen structure
- These are all features of Concentric hypertrophy secondary to hypertrophic cardiomyopathy (HCM) or chronic systemic hypertension
8
Q
Describe Systolic Dysfunction v’s Diastolic Dysfunction
A
Systolic Dysfunction -
Cardiac output (usually stroke volume) is decreased but diastolic filling of the ventricle is normal
Diastolic Dysfunction -
Abnormal cardiac filling with noirmal contractility (normal systolic function)
Often a combination of Systolic and diastolic dysfunction
9
Q
Define the distinction between Heart disease and Heart Failure
A
- Heart Disease = the presence of an abnormality in cardiac function or structure
- Heart Failure = the clinical manifestation of heart disease
10
Q
When does Primary heart failure occure?
A
Primary heart failure occures when the heart is disease, all compensatorymechanisms are exhausted, and characteristic clinical and pathological signs are present.
11
Q
What are some Clinical Signs of Heart Disease?
A
- Altered Heart Rate
- Altered Heart Rhythm
- Arrhythmia = a disturbance in the normal cardiac rhythym due to an abnormality in impulse initiation and or impulse propagation
- Pathalogic versus Physiologic
- Arrhythmia = a disturbance in the normal cardiac rhythym due to an abnormality in impulse initiation and or impulse propagation
- Altered audibility of heart sounds
- Presence of auditory vibrations
- Murmur = an auditory vibration of longer duration than the normal heart sounds created when laminar flow is distrupted (Grade 1-6)
- Pathologic versus Physiologic
- Murmur = an auditory vibration of longer duration than the normal heart sounds created when laminar flow is distrupted (Grade 1-6)
12
Q
Clinical signs of Heart Failure are attributable to?
A
- The accumulation of fluid (congestion) - dry to wet
- Tissue/organ ischemia (decreased cardiac output) - warm to cold
13
Q
Name some clinical signs of heart failure
A
Poor cardiac output:
- Weak pulses
- Pale mucous membranes
- Prolonged capillary refill time
- Tachycardia
- Cold extremities
14
Q
List the Clinical signs of Congestive Heart Failure
- Right Sided
- Left Sided
A
- Right Sided
- Ascites
- Pleural effusion
- Peripheral oedema (This is not painful and not warm)
- Jugular distention and pulses
- Hepatojugular reflux - small animals
- Left Sided
- Pulmonary oedema (Congestion of lungs)
- Adventitial sounds (Abnormal lung sounds)
- Cyanosis
- Tachypnoea (Sleeping respiratory rate increases)
15
Q
What drugs would be used as therapy for congestive heart failure? And how do they work?
A
- Furosemide(Frusemide)
- Loop diuretic
- inhibits sodium, chloride and water reabsorption by blocking the luminal Na-K-Cl cotransporter in the thichk ascending limb of the loop of Henle
- Spirinolactone
- Aldosterone antagonist
- Competitive binding of receptors at the aldosterone-dependent Na+-K+ exchange site in the distal convoluted renal tubule
- Hydroclorthiazide
- Blocks the Na+/Cl- co-transporter in the early segment of the distal convoluted tubule
16
Q
- What is Preload
- What does increased preload lead to?
A
- Preload is the load (volume) present before contraction has started (end of diastole)
- Preload reflects the venous filling pressure- the pressure that fills the left atrium and therefore left ventricle
- Increased Preload leads to left ventricular distention, which leads to increased stroke volume. Increased HR due to stimulation of atrial mechanoreceptors.
- The net effect is an increase of cardiac output. At a certain point cardiac performance plateaus, then declines. In systolic dysfunction (HF) the curve shifts downward, reflecting reduced cardiac performance at a given preload.
17
Q
- What is Afterload
- What is the responce to a sustained increase in afterload from arterial hypertension or aortic stenosis?
A
- Afterload is the systole load (pressure) on the left ventricle after it has started to contract (early systole) - inother words the pressure against which the heart must work to eject blood during systole
- the left ventrical will respond to a sustained increase in afterload by undergoing Concentric hypertrophy.
18
Q
What is Concentric Hypertrophy?
A
Concentric Hypertrophy is when a hollow organ undergoes hypertrohic changes but does not change the overall size of the organ hoever the walls will become much thicker, reducing the luminal volume. Usually the heart will undergo concentric hypertrophy in responce to increased afterload caused by hypertension of aortic stenosis.
19
Q
A fall in cardiac output is counteracted by:
A
- Frank-Starling mechanism -When there is increasd venous return ventricular filling increases (EDV) and therefore preload. This causes stretching of the myocytes increasing sarcomere lenght and resulting in an increased force of contraction (increased velocity of muscle fibre shortening) and therefore enhanced stroke colume.
- Activation of the sympathetic nervous system- increases inotropic (contractility) and chronotropic (heart rate) states
- Activation of the renin-angiotension-aldesterone system (RAAS)
20
Q
Sympathetic Nervous System
In relation to the heart:-
- What does activation of the SNS result in?
- What are the benificial effects?
- What are the Adverse effects?
A
- Activation results in :-
- Increased Heart Rate
- Increased contractility
- Neurogenic vasoconstriction
- Benifical effects:-
- Improved cardiac output
- Maintenance of blood pressure
- Adverse effects:-
- Increased afterload
- Reduced peripheral tissue prefusion
- Increased heart muscle oxygen requirements
- Enhanced potential for arrythmias
- Down-regulation of beta receptors
21
Q
- When there is a fall in cardiac output the RAAS will counteract the effects how?
- What drug would you use to stop this from happening
A
- See Picture
- Benazepril, Enalapril, Ramipril - blocks the Antiotensin Converting Enzyme (ACE)
22
Q
WHat are the Benificial and adverse effects of the Renin-Angiotensin-Aldosterone system?
A
Benifical Effects
- Improved cardiac output
- Increased preload (Frank Starling effect)
- Maintenance of blood pressure
Adverse effects
- Increased thirst, ADH, and aldosterone leads to water retention and congestion
- Vasoconstriction - increased afterload and decreased cardiac output
23
Q
Diseases of the heart that lead to decreased cardiac output may be associated with what mechanisms?
A
- Sustained volume overload (Preload)
- Sustained pressure overload (Afterload)
- Altered cardiac muscle contractility
- Altered cardiac muscle compliance
- Altered normal cardiac rate and rythym
24
Q
What are Haemodynamic disorders?
A
A group of diseases characterized by altered blood flow:
- An abnormal pattern of blood flow through the heart, or
- an impedance to chamber inflow or outflow
Results in altered preload or afterload.
25
What does systained Ventricular Preload (Volume overload) result in. Explain what it is.
Compensatory Hypertrophy (Eccentric)
26
What does sustained increased ventricular afterload (Pressure Overload) cause? How does it do this?
Concentric Hypertrophy
27
What are 5 mechanisms of Cardiac Failure?
1. Sustained pressure overload (afterload)
2. Sustained Volume overload (preload)
3. Altered Cardiac Muscle contractility (systolic dysfunction)
4. Altered Cardiac Mescle compliance (Diastolic Dysfunction)
5. Altered normal cardiac rate and rhythm
28
1. What does pathological changes does sustained pressure overload (increased afterload) cause.
2. Why causes pressure overload?
1. Concentric ventricular hypertrophy, Post-Stenotic vascular dilation
2. Sustained pressure overload can be due to an impedance to the chamber outflow, Stenosis or hypertension.
29
Explain what and Aortic Valve Stenosis is and what condition can it cause?
What is the most common Stenosis and what animals suffer from this predominately?
Where the Aortic valve becomes fibrotic and cannot open fully, it also will not close correctly.
Sub-valvular stenosis is the most common - it is a fibrous ring encircles the left ventricular outflow tract.
Pigs, Dogs (Golden Retriever, Boxer, Newfoundland.)
30
What is Post-stenotic vessel dilation and what does it cause?
The vessel after the stenosis is dilated due to blood turbulence, eddy currents and damage to the elastic elements within the vessel media. This is apparent on echocardiograph and thoracic radiograph.
31
What are some clinical signs of a SubAortic Stenosis. (SAS)
These are related to the degree of constriction and alterations in cardiac output.
* Initial signs of poor output
* weak pulse
* syncope
* sudden death
* Later signs of Left sided Chronic Heart Failure
32
1. What des Pulmonic Stenosis result in?
2. Where can Pulmonic Stenosis's be located?
3. The result can further cause what kind of dysfunciton and why?
1. Rusults in afterload of the right ventricle with progressive concentric right ventricular hypertrophy
2. Can be Subvalvular, valvular or supravalvular
3. The reduction in the RV leumn size causes diastolic dysfunction with increased filling pressure in the ventrical and the RA. Post-stenotic dilation.
33
1. What type of murmur is heard with a Pulmonic Stenosis?
1. Where would you find the Point of Maximum Impulse(PMI)
2. What type of murmur is heard with a SubAortic Stenosis?
1. Where would you find the Point of Maximum Impulse(PMI)
1. Systolic murmur
1. PMI over the heart base around the 3rd Intercostal Space
2. An ejection (systolic murmur)
1. PMI at the left heart base. There also would be low systolic blood pressure.
34
What are some non-cardiac causes of increased afterload?
* Pulmonary Hypertension
* effects right ventricle
* Systemic Hypertension
* Effects left ventricle
35
What are some causes of Pulmonary Hypertension?
* Pulmonary arterial hypertension
* Idiopathic: primary pulmonary hypertension (PPH)
* Congenital systemic to pulmonary shunts
* Pulmonary venous hypertension
* Left heart disease
* Left sided (mitral) valvue disease
* Hypoxic lung disease - Cor Pulmonale
* Chronic thromboembolic disease
* thromboembolism, dirofilariasis, neoplaia
* Miscellaneous
* Compression of pulmonary vessels eg neoplasia, granuloma
36
What are the clinical signs of Pulmonary Hypertension?
* Rapid Breathing, shallow thoracic wall excursions and syncope
* Split S2 heart sound (premature closure of the pulmonic valve relative to the aortic valve
* Acute signs of PH - pulmonary thromboembolism
* Chronic signs are associated with ling diseae and hypoxic pulmonary vasoconstriction
* If prolonged there would be hypertrophy of the right ventricle with secondary tricuspid regurgitation and right atrial enlargement.
* Cor Pulmonale - hypertrophy of the right heart resulting from disease that affect the structure of function of the lings. Initially the hypertrophy is concentric but then progresses to eccentric dialtion, often with tricuspid regurgitation.
37
1. What is the S1 sound of the heart related to?
2. What is S2 related to?
* S1 is the first and loudest heart sound and it is associated with the Mitral and tricuspid valve closure at the start of systole
* S2 is associated with the closure of the Aortic and Pulmonary Valves at the end of Systole
38
* What does Ionotrophic mean?
* What does Chronotrophic mean?
* Inotrophic = Beats harder
* Chronotropic = Beats Faster
39
* What is more common Primary or Secondary Systemic Hypertension.
* What are some causes for Secondary Systemic Hypertension
* Secondary is more common. Primary extreamly rare in dogs but may occur in cats.
* Secondary Systemic Hypertension
* Renal Disease
* Adrenal Causes
* Hyperaldosteronism
* Hyperadrenocorticism
* Phaeochromocytoma
* Diabetes mellitus
* Acromegaly (too much growth hormone)
* Polycythaemia
40
What are 2 reasons why Sustained Volume Overload (Preload) occurs?
* Valvular insufficiency
* Congenital defect (Shunt)
41
What are some pathological changes for Sustained Volume Overload (Preload)?
* Eccentric chamber dilation and hypertrophy
* Jet Lesions (endocardial fibrosis) damaged endothelium caused by high pressure jets of blood, typically on the distal side to an orifice between high pressure and low pressure chamber, eg on the left atrial side of the mitral valve in MR. Deposition of fibrin and platlets
42
What are some aeitologies for Mirtal Valve Disease?
* Infective
* Endocarditis
* Degenerative
* Myxomatous degeneration (Endocardiosis)
* Structral
* Dilation of the mitral annulus
* Rupture of the Chordae Tendinae
* Hypertrophic Cardiomyopathy
43
* What is Canine Endocardiosis?
* What Causes it? How do dogs get it?
* Where is the heart does it effect, what is involved?
* What other lesions are apparent?
* How prevalent is Canine Endocardiosis?
* What is the Therapy for it?
* Myxomatous Mitral Valve Disease (MMVD)
* Complex Inheritance pattern
* Atrial side of valve - subendothelial fibroblasts proliferate, thickening of spongiosa with myofibroblast proliferation, fibrosa (collagen) dissapears. Involvement and rupture of chords : Left atrial perforation.
* Jet Lesions - damage endothelium in left atrium with deposition of platelets and fibrin
* 75-80% of cardiac disease in small breed dogs
* Pimobendan was found to delay the onset of clinical congestive heart failure in dogs with increased heart size secondary to preclinical MMVD
44
1. What animal is Aortic Valve Regurgitation common?
2. How does it happen? and Where?
3. What type of Murmur would you hear if any and when would you here it?
4. What can it lead to?
1. Common in Older Horses
2. Degenerative changes in the aortic valve leaflets (Left Coronary Cusp) (nearly always)
3. Diastolic murmur (decresendo). You will hear leakage of aortic valve between S2 and S1
4. Can lead to secondary mitral valve regurgitation
45
* What is an Atrial Septal Defect?
* What animals is it common in?
* What does this cause?
* What is Decrescendo?
* Where there is a hole between the 2 atriums and the blood goes from LA to the RA for a second lap of the lungs.
* Cattle, Dogs (Boxer, Doberman, Samoyed)
* Increased preload (volume overload\_ of Right Atrium, Right Ventricle +/- LA
* Long Diastolic Murmur, blood comes back through the valve fast then slow.
46
* What is a patent Ductus Arteriosus
* How does this happen?
* What does it cause?
* What kind of murmur would you here and where?
* What would the animals pulse feel like?
* Shunt from Aorta to Pulmonary Artery's cause by failure to close as birth.
* Increased flow through the pulmonary circulation - Volume overload on the LA and LV Eccentric hypertrophy and increased afterload on the right ventricle - Concentric Hypertrophy.
* Continuous, machinery-like (rumbling) murmur over the left heart base
* Watson's water hammer pulse
47
* What is a Tetralogy of Fallot
* What are the Clinical Signs?
Complex of :-
* Pulmonic Stenosis
* VSD (Ventricular Septal Defect)
* Overriding Aorta
* RV Hypertrophy
Clinical Signs
* Polycythaemia
* Cyanosis
* Systolic Murmur
48
If the myocardium is unable to generate sufficient force to maintain cardiac output what kind of dysfunction is this?
Systolic Dysfunction. (Pump Failure)
49
What are the 3 types of Cardiomyopathy's, What is the most common cardiomyopathy.
* **Dilated Cardiomyopathy**
* Arrhythmogenic Right Ventricular Cardiomyopathy
* Hypertorphic Cardiomyopathy
50
* What animals/breeds are susceptable to Diated Cardiomyopathy?
* What could cause DCM in cats?
* When looking at a heart with DCM what would you see?
* Large Breed Dogs, Doberman, Boxer, Cocker Spaniels (Autosomal dominant in Dobermans, Irish Wolfhounds)
* Cats get it from a Taurine Deficiency
* Chamber dilation with a thin ventricular wall
* Reduced Contractility / Systolic Dysfunction
51
* What are some clinical signs of Dilated Cardiomyopathy?
* What test do you use to Diagnose?
* WHat is the Prognosis
* Lethargy, Weakness, Syncope, Pulmonary oedema, tachypnea (noted during sleep), Cardiac arrhythmias, Sudden Death.
* Echochardiography
* Prognosis is variable, breed dependent; worse in dobermans.
52
When we have the Mechanism of Cardiac Failure
* Altered Cardiac Muscle Compliance what kind of dysfunction is this?
* What are the 2 main disease within this?
* What are 2 acquired causes of Altered Compliance?
* Diastolic dysfunction
* Hypertrophic Cardiomyopathy (Cats)
* Restrictive Cardiomyopathy
* Pericarditis, Pericardial Effusion
53
Hypertrophic Cardiomyopathy (HCM)
* Describe HCM
* What is a potential danger and why does this happen?
* How is it caused?
* Ventricular muscle hypertrophy and fibrosis, Left ventricular outflow tract obstruction, reduced compliance of the left ventricle (cant relax and fill)
* Clot formation due to the Left Artial dilation (volume overload)
* Caused through increased afterload
54
Restrictive Cardiomyopathy
* Describe what RCM is
* What is the Systolic function of a heart with RCM?
* How does a heart get RCM?
* RCM is where the heart chambers are unable to fill properly due to stiffness of the heart. The heart is normal size but cannot relax normally during diastole (therefore Diastolic Dysfunction). Endocardial, sub-endocardial or mycardial fibrosis impede ventricular diastolic filling and so impair diastolic function.
* Normal or near normal systolic function
* Congenital or acquired causes.
55
What are the hearts specialized conduction system parts?
* Sinoatrial (SA) node
* Interatrial conduction fibres
* Atrioventricular (AV) node
* Bundle of His
* Left and Right bundle branches
* Purkinje fibres
56
What is Automaticity?
Many myocytes have the ability to undergo spontaneous depolarisation without an external stimulus
57
* What is the hierarchy of automaticty?
* In a dog what is the rate of spontaneous depolarisation for SA, AV nodes and the Purkinje Fibres?
* SA node is dominant - fastest rate of spontaneous Action Potential generation. Therefore governs intrinsic rate of the healthy heart.
* The remaining portions of the conducting system are latent pacemakes (Fail-Safe System)
* Rate of Spontaneous depolarisation (Dog)
* SA node 60-180/minute
* AV node 40-60/minute
* Purkinje fibres 20-40/minute
58
* What does The Vagus Nerve do to the heart?
* What does Sympathetic NS do for the heart?
* What is Sinus Tachycardia?
* Slows the Heart
* Opposite to Vagus, so it speeds the heart
* Sinus rhythm with an elevated rate of impulses
59
There are 3 disorders of impulse formation, what are they and describe them
* Depressed normal Automaticity
* Slowing the normal rate of pacemaker cell discharge
* Disease, enhanced vagal tone, electrolyte disturbances
* Enhanced normal Automaticity
* Faster than the normal rate of pacemaker cell discharge
* Adrenergic stimulation of the SA node
* Abnormal Automaticity
* Damaged Cells that are not normally automatic become so
* Premature beats, tachyarrhythmias
* Cells that ahve a slow rate of automaticity become faster
* Purkinje fibres - tachyarrhythmias
60
Explain each of the phases shown in the graph.
* Phase 0
* Initial depolarization due to rapid influx of Na
* Phase 1
* Inactivation of the Na channels
* Phase 2
* Plateau due to inward slow Ca current and outward K current.
* Phase 3
* Repolarization due to outwerd K current
* Phase 4
* Resting membrane potential (-70 to -90 mV)
61
Explain what is hapening in these two triggered activity examples of Impulse formation.
* A = Early After-depolarization
* During phase 2 or 3 of the action potential
* After oscillations can reach the threashold potential and trigger a premature beat.
* B - Delayed after-depolarizations
* During phase 4 of the action potential
62
* What is Bradyarrhythmias?
* What could cause these and where?
* Slow Rhythm of the heart
* Conduction delays of Blocks
* SA node blockages
* AV node Blockages
63
* What is a Tachyarrhythmias?
* Describe what reentry is.
* What is it an important componant of?
* Fast Heart Rhythm
* Reentry - The restimulation of a cell by a nearby disease tissue after it has been depolarized. Does not occure normally due to the reftactory period after depolarization. Disease cardiac cells - impulse will travel more slowly in diseased tissue and a slowly conducted impulse from diseased tissue can re-erter the normal myocardium after those cells have undergone their refactory period - if before the next sinus impulse then a premature beat is formed.
* Important component of Atrial Fibrillation.
64
What is Atrioventricular Reentry Tachycardia
It is where the electical signal goes from SA node -\> AV node -\> Bundle of His -\> bundle fibres -\> Purjinke Fibres then through an accessory pathway back to start the atrial cell depolarisation again if they are not within their refractory period.
65
Label Where
* Isovolumic contraction
* Ejection
* isovolumic Relaxation
* Rapid Inflow
* Diastasis
* Atrial Systole
* Aortic Valve Opens
* Aortic Valve Closes
* P, Q, R, S and T Complexes
* 1st and 2nd Heart sounds
66
* When do you hear S4 in a horse?
* When do you hear S1 heart sound?
* When do you hear S2 heart sound?
* Between the Pwave and the QRS complex
* During the QRS complex
* After the T wave
67
* What is a Sinus Arrhythymia?
* Why does it happen?
* What are the 2 forms?
* What treatment is required?
* Phasic variation in sinus cycle length.
* Respiratory Form
* P-P interval shortens during inspiration due to reflex inhibition of vagal tone and lengthens during expiration.
* Centrally mediated - Occurs without the influence of respiration
* Regularly irregular rhythm
* Should not require treatment
68
What drug would you use if an animal has **Sinus Bradycardia** through High vagal tone, drugs, hypothermia, intrinsic conduction diease?
Responds to Atropine (anti-cholinergic medication)
69
If you saw on an ECG QRST complexes but no associated P waves (and there was no atrial fibrillation) what could be the cause of this.
Atrial Standstill (Non Functioning SA Node)
70
* What could be the cause of this ECG?
* What treatment would you have?
* Sick sinus syndrome, Degenerative disease of the sinus node, Persistant brady cardia; paroxysms of rapid regular or irregular atrial tachycardia and SA block of arrest.
* Pacemaker Implant.
71
* What animal would this ECG belong to?
* Is this Bradydysrhythmias or Tachdysrhythmias?
* What would be your diagnosis?
* Explain this condition?
* What could be some causes for this?
* Horse
* Bradydysrhythmias
* Second-Degree Atrioventricular Block (Common in horses due to their high vagal tone)
* Some of the sinus depolarizations conduct through the AV node to depolarize the ventricles while others do not. P-Wave without following QRST complex, Regularly irregular rhythm.
* Elevated vagal tone, Xylazine (alpha2adrenoreceptor agonist [reduces norepinephrine], GI disease
72
What animal and arrhythmia is in this picture?
Horse Sinus arrhythymia
73
What animal and condition is seen in this ECG?
Horse with atrial fibrillation
74
* In this ECG what are your observations?
* What is the heart rate determined by and why?
* What is this conditon called?
* Treatment?
* None of the atrial pulses are conduted to the ventricles indicating a total blockage of the AV node. There is no relationship between P waves and QRS complexes indicating there is AV dissociation.
* Due to the AV blockage the heart rate is determined by the slower subsidiary pacemaker cells - ventricular escape rhythm.
* Third degree Atrioventricular Block
* Serious Condition requires a Pacemaker
75
* On an ECG how are tachydysrhythmias Differentiated?
* What location can the tachydysrhythmias occur?
* On the basis of the width of QRS complexes.
* Narmal (Narrow) or wide
* Normal width implies conduction through the AV node
* Location
* Supreventricular
* Ventricular (Wide because dont use specialized conduction system)
76
What can cause Sinus Tachycardia?
Higher than normal heart rate with regular rhythm
* Pain
* Anxiety
* Hypoxia
* Acidaemia
* Hyperthyroidism
* Drugs
77
* What is the arrow pointing at?
* What has happened to the AV node here?
* What treatment is required
* WHat may this condition predispose horses to?
* What is this condition called?
* Arrow is pointing at a monophasic P wave. This P-wave is premature and has a normal QRS complex.
* The AV node has been reset
* Single events do not require treatment
* May predispose to atrial fibrillation in horses
* Supraventricular premature depolarization.
78
* Without a history and looking at the animal what 2 conditions could this Tachyarrhythmia be?
* Sinus Tachycardia or Supraventricular (atrial, Junctional) Tachycardia
79
* With Atrial fibrillation (a form of Supreventricular tacharrhythmias) what are the 2 reasons for it?
* How would a Atrial Fibrillation animal heartbeat sound?
* What would you see on ECG?
* Atrial fibrillation
* Large atrial mass
* Horses can develop AF in absecnce of heart disase since their atrial mass is normally large (as can some large breed dogs)
* Atrial Enlargement
* Elevated Vagal Tone
* Coupled with increased sympathetic tone shortens the refactory period - predispose to AF
* Horses have a naturally high vagal tone.
* Irregularly irregular rhythm (tennis shoes in a dryer)
* No P=waves; fibrillation waves, no fourth heart sound (as there is no atrial contraction)
80
What is the Atrial Kick?
What does it contribute to?
* Atrial Kick = Atrial contaction which contributes to about 20% of Cardiac Output (CO)
81
What can you see in this ECG?
Atrial Fibrillation - Equine
82
* What do you see in the two circled areas of thise ECG?
* What is the cause of this?
* Name the condition?
* Premature, wide and bizarre QRS Complexes
* Premature Ventricular depolarizations, originate below the bundle of His, depolarizes muscle cell rather than through specialized conduction system **Slow Conduction**.
* There is no related P wave, large bizarre T wave
* Can occur in patterns
* Ventricular bigeminy (every other beat)
* Ventricular trigeminy (every third beat)
* Premature Ventricular Contractions
83
* What is it?
* What is abnormal about this ECG?
* Ventricular Tachycardia - Idioventricular Rhythm
* 3 or more successive PVC's,
* Sustained if \>30 seconds
* Non-sustained \<30seconds (paroxysmal)
* ECG
* Wide QRS complex
* Monomorphic and polymorphic
* Most are regular
84
What would the clinical signs for Ventricular Tachycardia be?
* If VT is slow - no signs
* If VT is rapid - poor cardiac output, syncope
85
* What is happening in this ECG?
* What treatment?
* WHat happens if not treated?
* Ventricular Fibrillation
* Make sure electrodes are properly connected, Use a Difibulator
* Pre-terminal event - Fatal if not treated.
86
Name some Inflammatory diseases that cause Altered Heart Rate and Rhythm
* Myocarditis and Vasculitis
* Immune mediated non-infectious
* Infectious
* Viruses - Influenza, Bluetongue, Parvo, FMD, EMC
* Bacteria - Erysipelas, Streptococci, Clostridium Chauvoei
* Fungi - Aspergillus
* Parasites - Toxoplasmosis, Strongylus, Neospora
87
What is Mulberry Heart Disease?
What animals does it Effect?
What organs does it effect
Vitamin E / Selinium dificiency in pigs
Affects many pig deaths over a short period
Multifocal areas of Necrosis in heart +/- Liver
Arrhythmias of ventricular origin - cause of death.
88
* What are the pathophysiological mechanisms associated with Haemorrhage?
* Give an example and explain the clinical signs associated?
Haemorrhage
* Hemostasis
* Controlled by platelets, coagulation factors, vascular integrity
* Haemorrhage
* Large vessel rupture
* Endothelial damage
* Hog Cholera, Sepsis
* Coagulopthy
* Primary
* Secondary (Consumptive) (DIC)
89
* What are the pathophysiological mechanisms associated with Haemorrhage?
* Give an example and explain the clinical signs associated?
Ischemia
* Reduction of cessation of blood flow
* Reduced oxygen dlivery
* Arteries/Arterioles:
* Vasoconstriction
* Vasoconstricting agents (ergot alkaloids)
* Arterial Thrombosis (eg Saddle Thrombus)
* Clinical Signs
* Size and location of Vessel
* Degree of Collateral Circulation
* Organ affected.
90
* What is Aortic Thromboembolism common in?
* What is it also called?
* Where is it located?
* What does it do?
* Common complication of feline Hypertrophic Cardiomyopathy
* Increased risk with left atrial enlargement
* Poor blood flow - Coagulation
* As for atrial fibrillation
* Thrombus lodges in distal aorta
* Obstructs flow to belvic limbs - acute posterior pareses
* Intense pain
* Nailbed cyanosis
* Cold Limbs
91
What are the 4 causes of Oedema
* Decreased colloidal osmotic pressure
* Increased hydrostatic pressure
* Increased vascular permeability
* Decreased Lymphatic Drainage.
92
What are some causes of Vasculitis?
* Infectious :MCF, Equine Viral Arteritis, Hendra Virus
* Sterile : Drugs (antibiotics)
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