Cardiology Flashcards
0
Q
What do differing colours of mucous membranes signify?
A
Pink - good forward output
Pale - poor forward output/ anaemia
Yellow - pre/intra/post hepatic icterus, beware of artificial light
Cyanosis - respiratory compronise
Capillary refil time should be <2s - good forward output
1
Q
What should you be examining in a cardio exam before you even touch the dog?
A
Demeanor, body ocndition, respiratory character - shallow eg pleural effusion, deep eg lower airway disease. Respiration rate - 15-30 minute in dogs, 15-40 min in cats. Resp rate is hypoxia driven.
2
Q
What can you tell from the jugular vein in a cardiopulmonary exam?
A
Distension - after occlusion, right atrial pressures
Pulsation - tricuspid regurgitation, pericardial effusion, pulmonic stenosis, 3rd degree AV block
hepatojugular reflex - when you squeeze abdomen with ascites does the jugular bulge
3
Q
What should you examine in the precordium?
A
Hands either side of cranial chest. Find apex beat on left side. Check heart rate, heart rhthmn, cardiac size, strength of apex beat, thrills from grade V or VI murmurs, check chest spring/compressibility.
4
Q
What should you check for in the abdomen?
A
Distension, fluid thrill - ascites, hepatomegaly, splenomegaly,
5
Q
What can you tell by taking the pulse?
A
Stroke volume, difference in systolic/diastolic, check femoral pulse, for pulse deficits, check both legs to see if symemtrical, check volume/strength, character.
6
Q
What do different pulses signify?
A
Weak - poor output
Bounding - high output, elevated metabolic rate, pregnancy, pyrexia, anaemia, PDA, aortic insufficiency
Brief - sub aortic stenosis
Brisk - mitral regurgitation
7
Q
What can you discover from checking the pulse?
A
Pulse deficits - arrythmia
Pulsus paradoxus - pericardial effusion - abnormally large decrease in systolic blood pressure during inspiration.
Pulsus alternans - myocardial failure - arterial pulse waveform showing alternating strong and weak beats. indicative of LV failure.
8
Q
How do you auscultate the heart?
A
animal should be standing. pay attention to individual heart valves. Use mainly diaphragm. Listen to audibility, heart rate, rhythm, pulse deficits, murmurs, gallops: use bell of stethoscope.
9
Q
What are the normal heart sounds?
A
AV valve closure - S1 LUB
S2 Dup - closure of aortic pulmonic valves - PMI left heart base
S3 - end of early ventricular filling
S4 - atrial contraction
10
Q
What are the different types of murmur sounds?
A
Plateau, Crescendo-decrescendo Pancystolic Holosystolic Diastolic Continuous
11
Q
What are the gradings Of murmurs?
A
Grade I - quiet difficult to hear with stethoscope
Grade II - VI - heard quickly but quieter than S1 and S2
Grade III - heard immediately, similar intensity to S1 and S2
Grade IV - louder than S1 and S2 but no precordial thrill
Grade V - precordial thrill but not heard if stethoscope lifted off chest wall
Gradee VI - precordial thrill and heard if stethoscope lifted off chest wall.
12
Q
Describe different lung sounds that can be heard?
A
Normal breath sounds
Stertor (grunting - from nasal passages)
rhonchi - low frequency, fast airflow
Stridor - upper airway, laryngeal paralysis
Fine crackles - high frequency, alveolar fluid
Coarse crackles - low frequency, pulmonary fibrosis
Wheezes - higher frequency, narrow larger lower airways
Squeaks - highest frequency, narrow smaller airways.
13
Q
What can you find out from percussing the thorax?
A
percussing assesses resonance. give a firm tap against middle finger. Dull over tissue - heart, consolidation lung, pleural effusion.
Resonant over air - normal lung, pneumothorax, pulmonary overinflation.
14
Q
What is congestive heart failure?
A
Inability to meet the demand of the body, oxygen, Co2, exercise, rest. Congestion - venous congestion, high capillary pressures, high filling pressures. Oedema - increased tissue fluid formation, lymphatic drainage overwhelmed.
15
Q
What are the presenting signs for CHF in dogs?
A
Coughing, breathlessness, abdominal distension - backward failure
Lethargy, excercise intolerance, syncope/collapse - forward failure.
Backward failure signs tend to proceed forward failure. Chronic coughing dogs tend to have more lethargy or excercise intolerance if the cough is due to cardiac disease. Cats with cardiac disease usually dont cough. Cats are either asymptomatic or dyspnoeic.
16
Q
Why does backward failure precede forward failure?
A
Fall in blood pressure, detected by baroreceptors, message to brain, sympathetic nervous system activated, vasoconstriiction, increased heart rate, increased contraction, sympathetic nerous system damages heart.
17
Q
What happens in chronic heart failure?
A
It is an alternative way of maintaining blood pressure. increased blood volume, activation of RAAS, activated by reduced renal filtration, activated by sympathetic nervous system, maintains blood pressure and cardiac outpu, counteracted by natriuretic peptides (atrial and ventricular stretch) ok for a while untill disease progresses, volume overload.
18
Q
How can you treat backward heart failure?
A
Diuretic - furosemide, counteract RAAS with an ACE inhibitor, or aldosterone antagonist, improve cardiac output with a positive inotrope (ppimobendan)
19
Q
What happens as CHF progresses?
A
Myocardial cell death, myocardial fibrosis, vasclar function reduced, cachexia, nitric oxide released, inflammatory cytokines TNFa, IL-1b, free radicals, necrosis, apoptosis, arrhythmias, myocardial remodelling
20
Q
Describe heart failure in cats
A
Diastolic failure, poor filling of usually left ventricle, atrial enlargement, there is a need for preload. Cats get pleural effusion due to L CHF as well as pulmonary oedema. Treat with furosemide, ace inhibitors, anti thrombotic agents, aldoesterone antagonists, positive inotropes.
21
Q
Name the key points of CHF
A
sympathetic tone is increased in CHF, dogs coughing due to CHF will usually have HR > 120 beats/min. Dogs coughing due to CHF will usually not have a sinus arrhythmia, feline CHF is not a true volume overload disease, medications don’t treat the underlying pathophysiology in cats as well as they do in dogs. Cats may need thoracocentesis with L CHF.
22
Q
Which methods of investigation can you use in cardiac disease?
A
Signalment/history, physical examination, thoracic radiography, ECG/24 hour ECG/event recorder, blood tests, echocardiography, blood pressure, catheterisation studies, phonocardiography, post mortem.
23
Q
What may the history be in cardiac failure?
A
Cough, dyspnoea, abdominal distension, Exercise intolerance/lethargy, syncope/collapse, inappetance, weight loss, stunting.
In canine cardiac cases commonly a cough is due to left atrial enlargement. Rare in cats with cardiac disease. Beware of concurrent cardiac & respiratory disease in dogs. Dyspnoea common in congestive heart failure in cats and dogs. Seen in left CHF due to pulmonary oedema. seen in right CHF due to pleural effusion. beware pleural effusion in cats due to left CHF. Exercise intolerance/lethargy - difficult to assess in cats, seen in many conditions affecting many systems. lethargy seen with severe CHF. Partial seizures may resemble syncope. Inappetanece more common in cats. Weight loss/cachexia - end stage CHF. Stunting - severe congenital disease.
24
What are common cardiac problems?
concurrent cardiac + respiratory - murmur + tracheal cllapse, murmur + asthma.
concurrent cardiac + endocrine/metabolic - aortic stenosis + insulinoma, DCM + hypothyroidism + laryngeal paralysis
25
What blood tests should be done for suspected cardiac failure?
Troponin-I, pro-BNP, hyperthyroidism, hypothryoidism, taurine deficiency, acromegaly, renal disease, hypadrenocorticism, insulinoma.
26
Which factors affect thoracic radiographic quality? What factors should you look at on the thoracic radiographs?
Phase of respiration, view, rotation, exposure factors, developing, obesity. Cardiac size, chamber size, great vessels, pulmonary vessels, lung pattern, pleural space changes.
27
What radiographic technique should be used in cardiac radiology?
Restraint for radiography is stressful for animals with minimal cardiac reserves. chemical restraint usually necessary but minimal doses should be used. to obtain good quality radiographs, the exposure time must be short. Best radiographs are obtained using low mAs, high kVP, use grid ( in large chests) only if short exposure time can be maintained. Dorso ventral and right lateral views should be obtained and accurate positioning is vital with minimum rotation.
28
What is the average cardiac size?
The length of the heart is measured on the lateral view against the number of vertebral bodies starting at the cranial edge of T4. the width of the heart is measured in vertebral bodies. The number of vertebral bodies from the length is added to the number of vertebral bodies from the width. The average number of vertebral bodies in dogs is 9.7 (8.5-10.5), and cats should not exceed 8 vertebral bodies. Cardiac size may also be evaluated using the number of intercostal spaces the heart occupies on the lateral view, 2.5-3.5 spaces is considered normal and the height should be less than 2/3rd o the height of the chest.
29
What is microcardia/cardiomegaly?
Microcardia is a decrease in cardiac size and is caused by hypovolaemia and hypoadrenocorticism. Cardiomegaly is an increase in cardiac size and generalised cardiomegaly is caused by pericardial effusion, peritoneo-pericardial diaphragmatic hernia and severe dilated cardiomyopathy.
30
Describe left atrial enlargement
Left atrial enlargement is one of the more reliable signs of cardiac disease. the angle between the terminal trachea and the caudal border of the heart becomes increasingly acute as the left atrium enlarges. the mainstem bronchi may become separated by a rounf soft tissue density on the DV view. A bulge caused by the left auricle may be evident at 2-3 oclock on the DV view. the cuadal vena cava may slope dorsally as it approaches the heart. left atrial enlargement is commonly seen with mitral insufficiency, dilated cariomyopathy, hypertrophic cardiomyopathy, patent ductus arteriosus.
31
Describe left ventricular enlargement
Left ventricular enlargement will result in straightening of the caudal border of the heart on the lateral view, and a rounding of the left border of the heart on the DV view at the 3-6 oclock position. there is often an increase in apico basilar length of the heart. in general if enlargement is due to dilatation then it is usually seen in association with left atrial enlargement. Left ventricular enlargement is commonly seen with mitral insufficiency, dilated cardiomyopathy, hypertrophic cariomyopathy, patent ductus arteriosus, ventricular septal defect.
32
Describe right atrial enlargement
Unless extreme, it appears as a cranial bulge on the lateral view. on the DV view a bulge may be seen in 9-11 oclock area. right atrial enlargement commonly seen with tricuspid insufficiency, pulmonic stenosis, dilated cardiomyopathy, restrictive/hypertrophic cardiomyopathy.
33
Describe right ventricular enlargement
Right ventricular enlargement results in increased sternal contact ont he lateral view and an increased rounding of the cardiac silhouette in the 6-9 oclock area on the DV view. right ventricular enlargement is commonly seen with tricuspic insufficiency, pulmonic stenosis, dilated cardiomyopathy, restrictive/hypertrophic cardiomyopathy.
34
Describe how the great vessels appear on cardiac radiology
Dilation of the aorta or pulmonary artery may occur due to turbulence frmo aortic or pulmonic stenosis, or from the patent ductus arteriosus. post stenotic dilation of the aorta may be visible as a prominent aortic arch on the lateral view, and as a bulge at the 12-1 oclock on the DV view. post stenotic dilation of the pulmonary artery may be seen as a bulge superimposed on the trachea on the lateral view and a bulge between 1-2 oclock on the DV. the caudal vena varies considerably in width with respiration but it may be persistently reduced in diameter in hypovolaemia or distended in right ventricular failure.
35
Describe the pulmonary vessels on radiography
The pulmonary vessels give an indication of the state of pulmonary circulation. the normal width of the cranial lobe vessels on a lateral view is approximately the with of the 4th rib, just below the spine. usually the arteries and veins are similar in diameter. with raised left atrial pressures, the pulmonary veins may be wider than the corresponding arteries. In over circulation of the lungs, such as with left to right shunts and fluid overload, the pulmonary arterteries and veins are both distended and prominent. vascular markings can also be seen extending further into the periphery than normal. in pulmonary arterial hypertension the pulmonary arteries may be wider than the veins.
36
What does pleural effusion appear like on radiography?
Pleural effusion are sen particularly in cats with heart failure but also in dogs. scalloping or leafing of the lung lobes is evident on the lateral view and soft tissue density interlobar fissures are evident on the DV. the cardiac silhouette is obscured.
37
What can electrocardiography measure?
Electrocardiography is very useful tool in the investigation of cardiac disease. It can provide information on: heat rate, rhythmn, chamber enlargement in small animals, electrolyte imbalance. twenty four hour recordings of heart rhythm using a holter monitor can provide very useful information in the investigation of collapsing or excercise intolerant animals.
38
What is M mode in echocardiogarphy?
This is when a single ultrasound beam is directed to a very small portion of the heart and the structures interrogated by this beam are plotted against time. a simultaneous ECG allows accurate timing of events in systole or diastole. objective measurements of wall thickness, chamber dimensions and contractility are done from M -mode because of the greater accuracy of timing during the cardiac cycle.
39
Describe doppler echocardiography?
The change in frequency which occurs when an ultrasound beam hits a moving RBC is proportional to the speed and the direction of the RBC. This information can be converted into a visual display by the ultrasound machine and plotted against time. thus information may be gained about blood flow velocity, flow direction and flow character. Doppler echocardiography is a valuable tool in the diagnosis of congenital and acquired heart disease.
40
What equations can be used to determine how cardiac diseases affect overall cardiac performance and O2 delivery?
tissue O2 delivery (DO2) = cardiac output (Qt) x arterial oxygen content (CaO2). CaO2 = (SpO2 x Hb x 1.36) + (Pa02 X0.003)
Cardiac output Qt = stroke volume x heart rate
Stroke volume s influenced by preload, afterload and contractility
41
Describe the cardiovascular functional reserve?
Cardiovascular reserve is the capacity of the cardiovascular system to mete normal physiological challenges e.g pregnancy, excercise, extremes of temperature or volume. the cardiovascular reserve will allow the animal to meet the demands imposed by anaesthesia and surgery. when cardiovascular reserve is exhausted, oxygen delivery falls below oxygen consumption and obligatory anaerobiosis ensues. Cardiovascular reserve is eroded by disease but also by anaesthesia and surgery. The greater the reserve the greater the chance of a successful recovery. Cardiovascular reserve can be decreased by increasing resting effort or by reducing maximal effort.
42
Name the problems that in crease risks during anaesthesia
animals with cardiovascular disease are at increased risk during anaesthesia because: impaired cardiovascular function is the most important adverse side effect of anaesthetics. Cardiovascular disease adversely affects other organ systems in a way that increases risk. Cardiovascular disease alters drug disposition. The net results are unpredictable drug effects, both in magnitude and duration. the treatment of cardiovascular conditions involves drugs which may interact with anaesthetics.
43
How can you minimise the risks from surgery and anaesthesia?
Make an accurate diaggnosis i.e recognise the primary effects and assess the animals cardiovascular reserve capacity. recognise secondary complications. recruit cardiovascular reserve pre operatively by adequate preparation. use anaesthetics that offset, rather than aggravate the conditions haemodynamic effects (if the ideal drugs are not available, then use adjuncts to optimise cardiovascular function). Minimise the adverse haemodynamics effects of surgery. Recognise the problems of secondary complications, altered drug behaviour and drug interactions. Ensure adequate peri operative physiological monitoring NB peri operative includes the post operative period.
44
Describe the pre operative preparation needed before anaesthesia in cardiopulmonary disease patients?
this aims to lower risk by reversing the effects of pre existing disease. where possible treat the primary condition, many secondary complications (e.g related to decreased liver and renal perfusion) resolve as cardiovascular function improves. eliminate retained fluid with diuretics, sodium free diets and interventiosn like pericardiocentesis. reduce cardiac work with vasodilators, cage rest and anxiolytic drugs. control residual arrhythmias if necessary. aim to improve myocardial contractility if necessary. Properly performed, pre operative cardiological preparation purchases cardiac reserve and increases the chance of survival. Side effects of drugs may complicate anaestesia. Pre operative digitalisation can be a problem as digoxin causes arrhythmias and may confuse aetiology. Arrhythmias arising from digoxin toxicity are more likely to occur intra operatively due to changes in blood ph as a result of changes in PaCo2.
45
Describe local anaesthetic techniques
ajor surgery can be performed under sedation and local anaesthesia providing the surgical site is amenable to local techniques. high sedative doses may cause greater cardiovascular depression than a light general aanesthetic. in addition during sedation the airway and ventilation is often not supported. local anaesthetic injected into the spinal or extradural space can cause profound hypotension that may be catastrophic.
46
What anaesthetic technique should be used for minor procedures?
Pre anaesthetic medication with a neuroleptanalgesic combination, induction with an ultrashort acting injectable anaesthetic, light general anaesthesia produced with a volatile anaesthetic agent and possibly N2o providing adequate conditions for minor operations in animals with modest disease providing attention is paid to ventilation, temperature, circulating blood volume and peri operative analgesia.
47
What anaesthetic technique should be used for major proocedures?
Technique for minor procedures would be inadequate in cases wiith advanced disease undergoing major operations because it would not prevent the autonomic nervous responses to noxious stimulation. Balanced anaesthesia i more appropriate in such cases with consideration given to the use of neuromuscular blockade and multimodal analgesic techniques. choose the most apprpriate anaesthetic for a given case by choosing drugs that offset rather than aggravate the conditions haemodynamic effects int he same way you would choose therapeutic agents that is choose drugs with mimic effects of medical therapy e.g the use of acepromazine in cases with MR will reduce afterload, will reduce myocardial oxygen consumption and should reduce the regurgitant fraction.
48
What should you remember before anaesthesia?
Safe anaesthesia depends on good anaesthetic management, i.e patient position, ventilation, monitoring, fluid administration and temperature management, ogod monitoring will help improve management. adequate anaesthesia with unsafe drugs is safer than under dose or overdose with safer drugs. familiarity with a given technique often proves to be most appropriate. adjuncts may be used to redress imperfections in non ideal drugs. Eg if cardiac output is insufficient with halothane, dobutamine may be infused. nitrous oxide is frequently included because it has modest cardiovascular effects and reduces the delivered concentration of i nhalant dug requireed to produce a given level of anaesthesia.
49
How does myocardial hypoxia lead to cardiac arrest?
Tachycardia increases myocardial oxygen consumption, decreases the time available for ventricular filling, and in the anaesthetised animal will reduce preload and decrease stroke volume. be aware of conditions that increase resting myocardial oxygen consumption e.g HCM.
50
Which type of drugs should you choose in cardiopulmonary disease?
choose drugs that least affect ventricular contractility, choose drugs that least affect venomotor tone, choose drugs that reverse the 1st haemodynamic disorder i.e mimic the effects of medical therapy, choose drugs that are compatible with drugs used peri operatively, choose drugs that are suitable in the presence of secondary cerebral,myocardial, hepatic or renal complications. choose drugs that are minimally affected by altered pharmacokinetics. use adjuncts.
51
How should the cardiac disease patient be monitored?
Good monitoring will help improve anaesthetic management. be aware of limitations of the monitors chosen. ECG. blood pressure: direct or indirect methods. Oxygen: blood gases Pa O2, pulse oximetry, inspired gases. carbon dioxide: blood gases PaCo2, capnography, temperature.
52
What should the body position be in anaesthesia?
Severe head up body positions will impair venous return while steep head down positions impair breathing, reduce functional residual capacity and lower cerebral perfusion pressure. both positions must be avoided. excessive fore limb fixation with ropes may lower chest wall compliance and increase the work of breathing in spontaenously breathing animals.
53
What should you bear in mind in surgical manipulation of a cardiac patient?
during operations inolvng the thoracic viscera, unavoidable manulation of the heart and great vessels may limit cardiac output e.g rotating the heart kinks the great veins and impairs ventricular filling. accidental epicardial stimulation with surgical instruments produces ventricular ectopic b eats while the use of cold irrigation fluids impairs contractility.
54
Which ventilatory mode should be used in cardiiac patients?
Cardiovascular disease frequently affects pulmoonary function. the end results of ventilatory inadequacy - hypercapnia hypoxia or both are poorly tolerated by animals with cardiovascular disease. both are potent arrhythmogens because they simultaneously promote sympathetic nervous activity and increase cardiac work while impairing myocardial contractility. Spontaneously breathing animals normally hypoventilate and retain Co2, howeve the thoracolumbar pum is preserved. Elevated Co2 causes vasodilation which decreases after load and may improve Qt so providing respiratory depression is nto severe, cardiac output may not be unduly depressed. controlled ventilation raises mean intra thoracic pressure and inhibits the thoracolumbar pump causing hypotension. pulmonary vascular impedance increases during inspiration ad momentarily lowers RV stroke volume thus reducing pulmonary blood flow.
55
How should fluid balance be managed in the anaesthetised patient?
fluid loss, haemorrhage or venodilation are poorly tolerated in conditions which rely on ventricular filling pressures to maintain cardiac output e.g cardiac tamponade. in these, one large bore catheter should be dedicated to fluid adminitratio. Excess fluids are poorly tolerated in animals with increased left atrial pressures e.g hypertrophic cardiomyopathy. ideally fluids are replaced as they are lost, and on a like for like basis. monitoring of central venous pressure is an advantage.
56
Describe how body temperature should be controlled in the anaesthetised patient?
Hypothermia impairs cardiopulmonary funciton: it depresses ventilation, increases blood viscosity and left shifts the oxygen haemoglobin dissociation curve. arrhythmias may arise spontaneously in the chilled heart with fibrillation becoming increasingly likely as temperatures approach 28 degrees C. it also initiates shivering which increases whole body Vo2 Four fold.
57
How can neuromuscular blockage and cardiovascular adjunct drugs be used?
Neuromuscular blocking agents may be useful in animals with severe cardiovascular disease however their use may complicate management and may best be avoided by the inexperienced. rapid and short acting versions of drugs used for pre operative preparation can be used during surgery to offset adverse Haemodynamic events e.g antiarrythmics,
58
What are the elements of cardiovascular reserve?
Increased resting effort > surgical stimulation, anxiety, hypovolaemia, pyrexia, pain, abnormal position, hypoxia, hypercapnia
Limited maximal effort - Disease, anaesthetics, hypothermia, Myocardial disease, advanced age, haemorrhage, electrolyte derangement, sever arterial blood gas derangement.
59
What are the effects of cardiovascular disease on drug disposition?
Reduced volume of distribution - will decrease the required dose of IVAA. increased circulation time - will increase the time to effect of IV induction agents, reduced cardiac output - will decrease the induction time of inhaled anaesthetics,increased V/q discrepancy will increase induction time with these agents, reduced peripheral perfusion - will prolong redistribution and clearance. Reduced renal blood flow will prolong redistribution and clearance.
60
Describe depolarisation of the heart
Depolarisation usually begins in the sinoatrial node, which is situateed in the right atrium. Parasympathetic stimulation slows down the rate of discharge of these pacemaker cells, and sympathetic stimulation speeds up the rate. Depolarisation sreads from the SA node to the rest of the right and then left atrial myocardium and reaches the atrioventricular AV node. this corresponds to the Pwave on the ECG. Conduction is particularly slow through the AV node, to allow for time for atrial contraction to fill the ventricles before ventricular contraction occurs. conduction of the impulse from the AV node to the ventricles occurs through the specialised conduction fibres of the bundle of His.
61
What is the bundle of his?
The bundle of his passes through the electrically insulated annulus fibrosus which separates the atria from the ventricles. this corresponds to the P-Q interval on the ECG. The bundle of his divides into left and right bundle branches which supply the left and right ventricles respectively. The left bundle further divides into anterior and posterior fasicles. The bundle branches divide into smaller and smaller fibres called purkinje fibres which extend into the myocardium. As the depolarisation wave spreads through the ventricles this corersponds to the QRS complex on the ECG. This is followed by repolarisation of the ventricle, which corresponds to the T wave on the ECG.
62
What is the SA node?
The SA node is the dominant pacemaker, but all of the specialised conduction tissue has innate automaticity i.e will spontaneously discharge. the SA node has the highest rate of discharge and the purkinje fibres have the slowest rate of discharge e.g if for some reason the SA node does not discharge, then the AV node will usually become the dominant pacemaker although the discharge rate will be lower. this is then called an escape rhythm and isolated beats originated from the AV node or more distally are called escape beats.
63
How can you obtain an ECG?
Patient gently restrained in a right lateral recumbency, avoid sedation if possible, ECG electrodes placed caudal and slightly proximal to the elbow and cranial and proximal to the stifle with gel or surgical spirit applied to increase electrical contact. held on an electrically insulated surface away from mains electrical equipment. Lead configurations - Red - right forelimb. Yellow - left forelimb, Green - left hindlimb, Black - right hindlimb.
64
What do the uses of ECG include?
The detection of abnormalities of cardiac rate and rhthmn, the detection of evidence of cardiac hypertrophy, the detection of metabolic abnormalities e.g hypoxia and electrolyte disturbances, providing evidence to suggest the presence of poor conduction b betwen the heart and skin surfaces.
65
Describe good ECG technique?
Clearly labelled, paper speed and vertical calibration, patient details, time and date, minimum of artefact, all 6 frontal plane leads if possible, record some of the trace at 50mm/sec.
66
What is the heart rate?
Brachycardia - may be sinus arrhythmia, sinus bradycardia, 2nd/4rd degree AV block, atrial standstill and sinus arrest.
Tachycardia - sinus tachycardia, atrial fibrillation, supraventricular tachycardias and some ventricular tachycardias.
67
What is the rhythm? is it regular or irregular?
Regular rhythmns - sinus rhthmn, sinus tachycardia, supraventricular tachycardias and sustained ventricular tachycardia. Regular irregular rhythm: sinus arrhthmia.
Irregular - irregular rhythm : atrial fibrillation and sinus rhythm interrupted by ectopics.
68
Is there a P wave for every QRS complex and a QRS complex for every P wave?
P waves without a QRS complex - This indicates atrial depolarization which has not been conducted through the atrioventricular node to the ventricles i.e atrioventricular block.
QRS complex without a p wave - these are either ectopic complexes, atrial fibrillation or sinoventricular complexes (atrial standstill).
69
Are the P waves and QRS complexes consistently and reasonably related?
Normal PQ interval which remains constant: sinus rhythm
Long PQ interval: first degree atrioventricular block
PQ interval is long and varies: vagal influence on SA node, wenckebach phenomenon.
No consistent relationship of any sort - third degree complete atrioventricular block.
70
Do all the complexes look the same?
QRS complexes ;
Sinus - normal narrow WRS complexes consistently associated with P wavves.
Supraventricular: normal, narrow QRS complexes
Ventricular: wide and bizarre QRS complexes
P wave complexes:
Suraventricular arryhthmia - different morphology P wave associate with single premature narrow QRS complexes or runs of tachycardia
Wandering pacemaker - high vagal tone can result in variable P waves, normal in dogs.
71
Do the P waves and QRS complexes measure within normal limits?
The waveforms should be measured in detail, selecting sinus complexes from a lead II recording ideally recorded at 50mm/sec.
72
What should the normal heart rate be?
```
70-160 min (adult dogs)
60--140 min (giant breeds)
70-189/ min (toy breeds)
Up to 220/ min (puppies)
Cat - 120-240 / min
```
73
What should the normal P duration be?
<0.04 secs in dogs and cats
74
What should the normal PQ interval be?
0. 06-0.13 in dogs
| 0. 05 - 0.09 in cats
75
What is congenital heart disease?
Congenital = any trait present at birth, whether the result of a genetic or non genetic factor significant cause of cardiovascular morbiditiy and mortality in small animal; most common congenital heart diseases of dog are in descending order > subaortic stenosis, PDA, mitral valve dysplasia, pulmonic stenosis and ventricular septal defecets, ventricular septal defects and atrioventricular valve dysplasias are most common in cats
76
What is aortic stenosis?
Varying degrees of obstruction to the left ventricular outflow tract; lesions may be subvalvular valvular or suprevalvular. seen in boxers, gsds, newfoundland, rottweiler and golden retrievers. Signs are excercise intolerance, syncope, left sided congestive heart failure, sudden death. Systolic ejection type murmur loudest over the left heart base, radiates up the carotid arteries in severe cases. murmur intensity correlates with severity of stenosis. electrocardiography shows left ventricular enlargement, myocardial hypoxia, ventricular arrhthmias. Radiography shows LV enlargement, post stenotic dilation of the aorta. Echocardiography: left ventricular wall thickening, abnormal valvular or subvalvular anatomy, increased outflow velocities on dopler echocardiography, velocities are used to grade the stenosis into mild, moderate and severe. Treatment is prophylaxis for bacterial endocarditis, exercise restriction and adrenergic blocking drugs indicated in moderate to severe cases, breed schemes in place.
77
What is a patent ductus arteriosus?
Ductus ateriosis connects the main pulmonary artery to the aorta in the foetus, diverts blood from the right heart into the systemic circulation, closure occurs within hours to days after whelpiing, incomplete closure allows continued shunting of blood. Reversed PDA: (right to left shunting) : dogs with large defects may develop severe pulmonary hypertension, causes shunting of un oxygenated blood from the pulmonary artery into systemic circulation. causes chronic hypoxia resulting in increased erythropoeitin release by the kidneys, increased red cell production by the bone marrow and development of polychthaemia. Cavalier King Charles, poodles, springer spaniels, collies, pomeraniens predisposed.
78
What are the clinical signs of PDA?
Signs of left sided congestive heart failure including coughing, dyspnoea and excercise intolerance, hing limb weakness exacerbated by excercise in cases of right to left shunting defects. A high grade continuous machinery heart murmur, audible loudest over the left heart base steep (water hammer) pulse; right to left shunting defects may have no audible murmur and animals may show differential hind quarter cyanosis. Left atrial enlargement (wide P waves), left ventricular enlargement (tall wide r waves) arrhthmias including atrial and ventricular premature complexes and atrial fibrillation. Left atrial and left ventricular enlargement, pulmonary over circulation, triple knuckle pattern on the dorso ventral view with bulges in the vicinity of the aorta, pulmonary artery and left auricle. pulmonary oedema and congestion. Left atrial and ventricular enlargement, ductus may be visible, doppler echocardiography demonstrates continuous blood flow in the main pulmonary artery. Occlusion of the ductus by surgical ligation or transvenously using ductal occluding devides, left sided congestive heartfailure may require management with use of diuretic and ACE inhibitor therapy.
79
What is Pulmonic Stenosis?
Obstruction to blood flow through the right ventricular outflow tract, obstruction may be either valvular, subvalvular or supra valvular. boxers, beagles, bull mastifs, bull dogs, cocker spaniels, miniiature schnauzers, terriers and chihuahuas. Clinical signs: excercise intolerance, syncope, ascites, acute death. Auscultation: harsh left heart base systolic murmur often radiates across to the right heart base. Right atrioventricular enlargement (deep S waves in leads I, II ad II, tall P waves). Radiography: right atrioventricular enlargement, post stenotic bulge of pulmonary artery. Right ventricular hypertrophy, structural abnormalities of pulmonic valves and right ventricular outflow tract, doppler echocardiography demonstrates increased velocities through the stenosis; velocities are used to grade the stenosis into mild, moderate, severe. Treat with adrenergic blocking drugs, balloon valvuloplasty and surgical procedures. Sever cases carry a more guarded prognosis and are at risk for a sudden death and right sided congestive failure.
80
What is mitral valve dysplasia?
Fairly common in dogs and cats, varying degrees of malformation of the mitral valve apparatus, leading to valvular insufficiency and in some cases stenosis. Seen in golden retrievers, english bull terriers and Great Danes. signs of left sided congestive heart failure - coughing, Exercise intolerance, dyspnooea. Auscultation: harsh pan systolic murmur audible loudest over the left apex. Electrocardioography: left AV enlargement pattern, various supraventricular arrythmias may also be noted. Radiography - Left AV enlargement, pulmonary venous congestion and pulmonary edema. Echocardiography: left atrial and ventricular enlargement, structural abnormalities of the mitral valve apparatus may be noted, valvular insufficiency and or stenosis. surgical repair or prosthetic replacement not currently available in the UK, treatment aimed at managing congestive heart failure with a combination of diuretics, angiotensin converting enzyme (ACE) inhibitors and positive inotropics as required.
81
What is tricuspid valve dysplasia?
Malformation of the tricuspid valve apparatus leading to valvular insufficiency; fairly common in dogs and cats, particularly prevalent in certain breeds of dog. Breed predisposition: labradors, golden retrievers, GSDs, irish setteers, Great Danes, right sided congestive heart failure with ascites and less commonly pleural effusion. Auscultation: harsh systolic murmur audible loudest over the right apex, jugular venous distension and pulsations may also be noted on clinical examination. Right AV enlargement pattern, supraventricular arrhthmias, association between tricuspid valve dysplasia and accessory pathway supraventricular tachycardias in labradors. Right AV enlargement; right atrium often being markedly enlarged. Right atrial and ventricular enlargement; structural abnormalities of the mitral valve appratus, doppler echocardiography demonstrates tricuspid valve insufficiency. Surgically repair or prosthetic replacement not currently available in the UK. treatment aimed at managing congestive heart failure with combination of diuretics, angiotensin converting enzyme inhibitors and positive ionotropics as required.
82
What are ventricular septal defects?
The most common congenital cardiac abnormality of cats, defect occurs as a result of incomplete separation of the ventricles during foetal development, results in a connection between the left and right ventricles and blood flow may either be from the left ventricle to the right or less commonly from the right to the left. predisposed - keeshonds, english bulldogs and english springer spaniels. left sided congestive heart failure most commonly seen, may also develop signs of right sided heart failure later in life. patients with large defects may present with right to left shunting, hypoxia and resultant polcythaemia.
83
How can you detect a ventricular septal defect?
There is a pansystolic murmur loudest over the right ventral thorax, murmur intensity not correlated with the size of the defect. Left atrioventricular enlargement (Tall R waves, increased QRS duration, wide P waves). Left atrioventricular enlargement; pulmonary over circulation; signs of left sided congestive heart failure. Echocardigraophy: left atrial and ventricular enlargement, septal defect may be visible, doppler demonstrates blood flow across the defect, high flow velocities suggest a less significant defect, lower velocity flow suggests equilibration of ventricular pressures and hence a more haemodynamically significant defect. Treatment is palliative and aimed at reducing the sign of congestive heart failure, palliative surgery procedures such as pulmonary artery banding may be employed. Poor prognosis if signs of congestive heart failure are present or if right to left shunting develops; small defects often well tolerated and of no clinical significance.
84
What is tetralogy of fallot?
an uncommon complex congenital cardiac defect, consist of four different abnormalities; ventricular septal defect, pulmonic stenosis, right ventricular hypertrophy and an overriding aorta, results in right to left shunting of blood and resultant chronic hypoxia. Breed predisposition in keeshonds. Clinical signs; stunted growth, poor exercise tolerance, cyanosis and dyspnoea. A murmur of pulmonic stenosis may be audible over the left heart base. right ventricular hypertrophy, right ventricular enlargement and pulmonary under perfusion. echocardiography confirms the presence of a complex cardiac abnormality, right ventricular hypertrophy, ventricular septal defect, pulmonic stenosis, overriding aorta. doppler echocardiography shows right to left shunting of across the ventricular septal defect. Palliative surgical procedures rarely carried out. management directed at Excercise restriction and managing resultant hypoxia and polycythaemia. guarded although some animals will survive for some time with these defects.
85
What is the normal PQ interval?
0. 06-0.13 sec in dogs
| 0. 05-0.09 in cats
86
What is the normal R amplitude?
3. 0mv in large breeds
2. 5 Mv in small breeds
0. 9mv (max) in cats
87
What is the normal S amplitude?
<0.5 mV in cats
88
What is the normal QRS duration?
0. 06 sec in large breeds (max)
0. 05 sex in small breeds (max)
0. 05 sec in cats (max)
89
What is the normal Qt interval
0. 15-0.25 sec depending on heart rate in dogs
| 0. 12-0.18 in cats
90
What is the normal T amplitude?
0.0-1.0mV (or < 1/4 R wave height,) positive, negative or biphasic
Cats - positive, negative or biphasic
91
What is the normal ST segmant?
<0.15 mV elevation in dogs
In cats - no depression, no elevation
92
What are the changes that may be noticed in P waves and QRS complexes and what do they signify?
Wide P wave - left atrial enlargement
Tall P wave - right atrial enlargement
Wide QRS - left ventricular enlargement or left bundle branch block
Tall R:left ventircular enlargement (dilation or hypertrophy)
small R: pericardial/pleural effusion/obesity/hypothyroidism
Alternate R waves different height: pericardial effusion
Deep S wave - right ventricular enlargement
Wide S wave - right bundle branch block
Long Q-t : hypocalcaemia, hypkalaemia, hypothermia
S-t segment elevation/depression: hypoxia, infarcts
S-t segment coving: left ventricular enlargement
93
What are the normal rhythms?
Sinus rhythm - regular rhythm, normal P waves, normal QRS complexes and rate: 70-160/min (dogs, 140-220 /min (cats.)
Sinus arrhthmia - heart rate varies with respiration, normal P waves, height may vary) and normal QRS complexes. not a normal rhythm in cats; often associated with respiratory disease in this species.
94
What is a sinus arrest and sinus block?
Sinus arrest is a period where there is no evidence of atrial activity for a period in excess of the two proceeding R-R intervals. If the period of block is an eact multiple of the proceeding R-R iintervals then sinus block is more likely. Both sinus block and sinus arrest are usually recognised in dogs with accentuated sinus arrhythmia, often those with high vagal tone such as brachycephalic dogs with underlying respiratory disease. Prolonged sinus arrest may result in syncope. ventricular escape beats may be recognised in an attempt to rescue the arrested heart. if these bradydysrhythmias are related to high vagal tone they should be easily abolished with atropine. other treatments include propantheline, terbutaline, pacemaker implant.
95
What is sick sinus syndrome?
The SSS describes a variety of electrocardiographic abnormalities in certain breeds of dogs, particularly miniature schauzers. there are periods of sinus arrest without appropriate escape beats. there is no response to atropine. in some cases periods of supraventricular tachycardia occur. the syndrome is known as the brady-tachy syndrome when this occurs. most cases present because of syncope.
96
What is sinus bradycardia?
This may be a normal rhthm. it may also be recognised in patients with hypothermia, hyperkalamia, CNS lesions, digoxin toxicity or high doses of calcium channel antagonists. If patients are symptomatic the underlying cause should be identified and treated.
97
What is atrial standstill?
This is a sino ventricular rhythm. There is no atrial activity and hence no p waves. the rate is slow. the WRS complexes may be wide and bizarre. this rhythm is associated with hyperkalaemia and certain muscular dystrophies. in the absence of hyperkalaemia treatment with atropine, propantheline, terbutaline or pacemaker should be considered.
98
What is a 1st degree AV block?
Conduction across the AV node is slowed. this is due to increased vagal tone. the P-q interval is prolonged. Digoxin and calcium channel antagonists will cause 1st degree AV block. there is no need to treat this condition.
99
What is a 2nd degree AV block?
Some of the P waves are not conducted across the AV node and do not result in a QRS complex. there are two types recognised. Im mobitz type 1 the Pr interval may be variable increasing prior to a block (wenckebach phenomenon) this is a manifestation of high vagal tone and will reverse with atropine. in Mobitz type II the P-r interval is constant , this is generally more serious and indicates disease of the conduction system. animals with this are not normally symptomatic but at high risk of developing 3rd degree AV block.
100
What is a 3rd degree AV block?
There is no conduction across the AV node. the P waves are not associated with the QRS complexes.. There tends to be a constant and regular P wave rate. The ventricles beat at a regular escape rate which is much lower than the p wave rate (usually 30-60 in a dog) the ventricular escape beats are bizarre in appearance. these cases tend to present with syncope due to the slow heart rate. On auscultation a constant ventricular rhythm is audible with sounds like metronome. with careful auscultation the atrial beats sometimes may be heard in the background. the atrial and ventricular pulses may be visible on careful inspection of the jugular veins. This condition may be idiopathic or due to fibrosis occurring in the AV node . the treatment of choice is pacemaker implantation.
101
What are bundle branch blocks?
The left bundle branch, right bundle branch, or anterior fascicle may become blocked resulting in abnormal depolarisation. RBBB produces a wide QRS complexes with Deep S waves, LBBB produces wide QRS complexes with tall R waves. Superficially the bundle branch blocks look bizarre and ventricular in origin however on close examination will reveal an associated P wave. No treatment is necessary.
102
What is supraventricular premature complex?
These complexes occur early. they resemble the sinus complexes in appearance. a P wave is associated with the premature complex but it is different in appearance to the normal sinus P waves and in some cases may not be visible because it is hidden in the preceeding T wave or in the premature complex. these are caused by atrial stretch of infiltration. The underlying cause should be treated.
103
What is supraventricular tachycardia?
If more than 4 premature supraventricular beats occur together this is called a run of supra ventricular tachycardia. it may be paraoxysmal or sustained. the rate may be very fast > 300bpm. It is caused by atrial stretch or infiltration. Beta blocking drugs, cardiac glycosides or calcium channel antagonists can be used to slow the rate.
104
What is atrial fibrrillation?
This is a chaotic rhthm where several foci are discharging at the same time in the atria. there is no recognisable P waves. the QRS complexes are of normal morphology as conduction is through the AV node. the rate is frequently rapid and irregular. this rhythm is caused by atrial stretch in small animals and is commonly seen with DCM or endocardiosis. In some large breed dogs have slow atrial fibrillation without atrial stretch thought to be related to an occult form of DCM, as most go on to develop DCM. on clinical exam there is a marked pulse deficit. on auscultation the heart rhythm is chaotic. the rhythm is rarely reversible in small animals and treatment is aimed at slowing the ventricular rate.
105
What are ventricular premature complexes?
These complexes occur early. they are wide and bizarre in appearance as they are ventricular in origin. there is no associated P wave. they may occur with primary cardiac disease due to stretch, hypoxia or infiltration of the ventricular wall. they are frequently associated with systemic disease e.g gastric dilatation volvulus, splenic mass, CNS disease, pancreatitis, pyometritis..
106
What are ventricular tachycardias?
More than 4 premature ventricular complexes occuring together are called ventricular tachycardia. the etiology is the same as for ventricular premature complexes. the ventricular tachycardia may be sustained or paroxysmal. the underlying disease should be identified and treated. sustained rapid ventricular tachycardia should be treated with lignocaine Intravenously and then followed with oral therapy of procainamide, mexiletine or in sympathetically mediated ventricular with beta blockers.
107
What are ventricular escape beats?
These occur late. they are wide and bizarre in apearance. there is no associated P wave. these are rescue beats and should not be suppressed.
108
How are bradyarrhythmias treated?
animals with Syncope, exercise intolerance should be carefully checked for electrolyte imbalances or systemic diseases causing high vagal tone. bradyarrhythmias due to high vagal tone may respond to medication. if there is no response to medication then pacemaker implantation is the only option. Vagolytic drugs: atropine, probantheline, glycopyrrolate. Sympathomimetic drugs: isoprenaline, terbutaline, methylxanthines. Other: pacemaker implantation.
109
How are supraventricular tachycardias treated?
In dogs - cardiac glycosides, beta blockers. calcium channel blockers.
In cats - calcium channel blockers, beta blockers.
Vagal maneuvers may disrupt sustained SVT. drugs may disrupt or just slow supra ventricular tachycardia.
110
How is atrial fibrillation treated?
Dogs - digoxin, beta blockers, calcium channel blockers. In dogs and cats the object of therapy is to slw the ventricular response rate not to convert to sinus rhythm. in cats - calcium channel blockers, beta blockers.
111
How is ventricular tachycardia treated?
Dogs - Iv lignocaine then oral Procainamide/tocainide/mexiletine/beta blocker.
Cats: beta blocker.
The aim of therapy is to convert to sinus rhythm.
112
What are pericardial effusions in dogs?
Idiopathic pericardial effusions are commonly seen in golden retrievers, st bernards, GSDs. GSDS and golden retrievers are also predisposed to right atrial haemangiosarcomas. heart base tumours are seen in boxer dogs. presenting signs - abdominal distension, weakness, lethargy and Exercise intolerace. hepatomegaly and ascites are commonly seen in small animals. the heart sounds are muffled and the jugular veins distended. The pulse is weak and pulsus paradoxus may be present.
113
What is present on radiography, electrocardiography and echocardiography in pericardial disease? what is the treatment?
Gross cardiomegaly with no distinguishable cardiac chambers. there is a static outline to the cardiac sillhouettte. the caudal vena cava is usually distened. concurrent pleural effusion may be present. on electrocardiography the QRS complexes are frequently small. the R waves may vary in height, this reflects the swinging of the heart in the pericardial fluid. on echocardiography - fluid may be seen surrounding the heart between the myocardium and the pericardium. Neoplastic masses can usually be seen if present. Pericardiocentesis is the treatment of choice for pericardial effusions on first presentation. recurrence is common and is best treated by sub total pericardectomy. diuretics should be avoided as they may lead to severe hypotension
114
Describe the technique of periocardiocentesis?
The animal is placed in left lateral recumbency. light sedation may be necessary. a large area is clipped on the right thorax. local anaesthetic is infiltrated at 5-6th intercostal space. prepare aseptically and drape. a sterile needle through jugular catheter or a dedicated pericardiocentesis catheter with stylet is used. a small incision is made aseptically in the skin and the catheter is passed through the skin and then through the intercostal muscles ino the pleural space. the catheter is then advanced until the pericardium can be felt and slowly advanced further into the pericardium. the needle /stylet is now retracted and the catheter left in the pericardium and effusion withdrawn using an extension set with three way tap and large syringe attached. An ECG is usually attached to the limbs and any contact with myocardium will result in ventricular arrythmias.
115
What are angiostrongylosis?
The adult worms, angiostrongylus vasorum, parasitise the pulmonary artery and right ventricle. eggs are laid in the pulmonary parenchyma and hatch to first stage larvae, enter the airways and are coughed up, swallowed and passed in the faeces. snails or slugs act as intermediate hosts, they ingest larvae from dog faeces. a dog becomes infected by eating infected snails or slugs. from the intestine the larvae migrate through the lymphatic system or hepatic portal vessels to the right heart, where they arrive as adults. the pre patent period is approximately 50-60 days. the fox lungworm crenosoma vulpis has a similar life cycle.
116
What are the clinical signs of angiostrongylosis?
Variable and many cases are subclinical. coughing may be he most common clinical presentation with a duration of a few to several months. additional clinical signs include weakness, subcutaneous swelling (haematoma), lameness, anaemia, pulmonary crepitation, right sided heart failure, collapse, dyspnoea and respiratory distress, emaciation, stunting and poor performance. there have been rare reports of lumbar pain and hindleg paresis - possibly associated with systemic embolisation of the worms.
117
What diagnostic tests should be done to diagnose angiostrongylosis?
Routine blood profile - will show eosinohphilia, thrombocytopenia, anaemia has been reported in some cases. The major lung parenchymal changes occur 7-9 weeks after infection and an be a mixed pattern with a patchy alveolar density and a diffuse interstitial pattern. Pulmonary congestion and right heart enlargement may also be noted on radiography. electrocardiography changes are non specific. echocardiography - visualisation of worms in the right ventricle or pulmonary artery in severe cases and signs of right ventricular dilation and hypertrophy may be evident, although in most cases echocardiography is likely to be unremarkable. Diagnosis - stage 1 larvae can be found in faeces. anthelmintics such as fenbendazole and moxidectin used to treat. the prognosis for subclinical and mildly affected cases are good. more severely affected cases may develop respiratory problems leading to death.
118
What is dirofilariasis?
Heartworm - the infestation of the pulmonary arteries and occasionally the right heart by the nematode dirofilaria immitis. the life cycle of D . immitis must pass through a female mosquito. the maturation time in the mosquito is 10-14 days in optimal conditions. once injected into the host the larvae migrate in tissues and moult this takes up to three months. The final maturation phase in the pulmonary arteries takes a further 3-4 months. female worms produce microfilaria that pass into the circulation. The presence of parasites in the pulmonary arteries leads to local changes in the blood vessels and can lead to pulmonary hypertension. pulmonary hypertension may result in right sided congestive heart failure. pulmonary parenchymal disease may occur as a local inflammatory response to the parasite and this may result in coughing and dyspnoea. immune complex glomerular disease may also be seen in heartworm disease.
119
What are the presenting signs of dirofilariasis?
Majority of cats and dogs are asymptomatic. coughing, tachypnoea and dyspnoea are most common clinical signs. excercise intolerance, syncope ,haemoptysis, ascites and hepatomegaly also reported. rarely dogs may present with caval syndrome; large number of worms in right ventricle causing poor cardia output and intravascular cell lysis. in cats the signs are very non specific and can mimic feline ashtma, lethargy, anorexia, vomiting, coughing, dyspnoea, syncope. On clinical exam - an easily elicited cough, weight loss, tachypnoea, dyspnoea, abnormal respiratory sounds, split second heart sound, fever, ascites. In caval syndrome: weakness, haemoglobinaemia, haemoglobinuria.
120
What will be present on blood profile, radiography, echocardiography in dilofilariasis?
routine blood profile - anaemia, neutrophilia, lymphopenia, eosinophilia, basophilia. Radiography - right heart enlargement and tortuosity of the pulmonary arteries with blunting. interstitial/alveolar infiltrates in the lungs and rarely large pulmonary granulomas may be seen. Electrocardiography - usually nomral, rarely evidence of right ventricular enlargemnet. Echocardiography - right ventricular enlargement, adult worms may be visualised in right ventricle or pulmonary artery. identification of microfilaria: wet blood smears, knott concentration test, filter test. Not all circulating microfilaria are D immitis, Dipetalonema reconditum is a harmless subcutaneous parasite that also produces microfilaria. Microfilaria antibody tests: indirect fluorescent antibody tests, enzyme linked immunosorbent antibody tests - non specific and insensitive. Female adult heartworm antigen tests: ELISA, immunochromatographic, haemagglutination based tests, high specificity and high sensitivity in dogs.
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What is thee treatment for dilofilariasis ?
AdulticideS: melarsomine, thiacetearsemide. both drugs ha elow safety margins. following adulticide therapy there is a high risk of worm debris causing pulmonary emboli and pneumonitis which is treated with corticosteroids, antibiotics and age rest, worms can be removed surgically. right heart failure is treated with frusemide and angiotensin converting enzyme inhibitors. Microfilaricidal therapy: avermectins, milbemycin oxime.
122
What is canine dilated cardiomyopathy?
This condition may be primary or secondary. it is esentially a biochemical lesion with minimal pathological or histopatholigcal cahnges. In most cases the aetiology is unknown. High prevalence in purebred dogs suggests hereditary predisposition. Doxorubicin may cause it. L carnitine myocardial deficiency a potentical cause of myocardial failure in boxer dogs. carnitine and taurine deficiency has been implicated in american cocker spaniels. Affects Great Dane, irish wolfwound, newfoundland, irish setter, doberman, boxer, springer spaniel, c ocker spaniel. Higher prevalence in males.
123
What is the usual history with DCM?
Boxers may present with collapse due to ventricular arrhthmias, dobermans may present with ventricular arrhthmias or acute onset coughing and dyspnoea due to left sided congestive heart failure. giant breeds may present just with atrial fibrillation. giant breeds may also present in biventricular failure with severe ascites. spaniels frequently present with coughing, excercise intolerance and dyspnoea.
124
What are the clinical signs of DCM?
Usually evidence of poor cardiac output with pallor and weak pulse. the precordial impulse may be weak. low grade apical murmurs are often present due to atrioventricular valve insufficiency. diastolic gallop sounds may be heart at the ape. a sinus tachycardia may be present. arrhythmias are common; atrial fibrillation in irish wolfhounds and Great Dane,s ventricular arrhythmias in dobermans and boxers.
125
What will be present on radiography, electrocardiopgrahy, and echocardiography in DCM?
Generalised cardiomegaly with marked left atrial enlargement. pulmonary venous congestion and pulmonary infiltrate consistent with pulmonary oedema will be present with left sided congestive heart failure. A pleural effusion may be present with right sided heart failure. Often evidence of left atrial enlargement (wide P waves) and left ventricular enlargement (tall R waves, wide QRS and ST coving). Supraventricular or ventricular arrhythmias may be present on electrocardiography. on echocardiography the left atrium and ventricle are usually dilated and there is poor contractility. the fractional shortening which is a measure of contractility based on the mode of the left ventricle is usually <20%.
126
What is the treatment of DCM?
Angiotensin converting enzyme (ACE) inhibitors have been shown in canine and huma studies to prolong life and improve quality of life in DCM patients. diuretics are indicated where there is evidence of congestive heart failure. digoxin is a negative chronotrope and a positive inotrope and is recommended in all cases where heart rate control and inotropic support is indicated. pimobendan is an inodilator (positive iontrope and vasodilator) and is used instead of digoxin where positive inotropic support is required and heart rate cntrol is not indicated. They can be used together. recent studies have shown that the use of pimobendan in the treatment of DCM can lead to increased survival and improved quality of life.
127
What is pre clinical (occult) dilated cardiomyopathy?
It is now well recognised that many dogs of breeds predisposed to DCM will have evidence of poor contractility on echocardiography for months - years before clinical symptoms typical of DCM appear. some may present with slow atrial fibrillation for several years which does not require therapy. some of these dogs will present with intermittent collapse due to ventricular arrhthmias. ACE inhibitors may slow the progression of disease in these cases.
128
What is feline dilated cardiomyopathy?
This used to be the most common form of myocardial disease in cats in the UK but is now rarely recognised. Plasma taurine levels were reduced in cats with DCM and supplementation of the diet with taurine has resolved the clinical signs. canning process was responsible for reduced availability of taurine, but this was overcome by increasing dietary levels. it is still seen sporadically in a form that is non responsive to taurine. the clinical findings are similar to DCM in dogs. both bradyarrhythmias and tachy arrhythmias have been seen in cats with DCM. Cats with DCM are prone to thrombo embolism.
129
What is idiopathic feline hypertrophic cardiomyopathy?
Common in cats. has a genetic basis. lethal mutation is present in a sarcomeric gene. causative mutations have been identified in the maine coon and ragdoll breeds. left ventricular hypertrpohy results in difficulty filling, thus diastolic failure occurs. the systolic function is normal. diastolic failure results in left atrial enlragement and increased left atrial pressures which may result in left sided congestive heart failure. This may be acute in onset or slowly progressive (gradual increase in exertional dyspnoea), severe septal hypertrophy may result in dynamic obstruction of the left or right ventricular outflow tract in systole. mitral insufficiency may occur due to the distortion of the mitral valve apparatus as the mitral valve leafleft gets sucked into ventricular outflow tract during systole. this is known as systolic anterior motion of the mitral valve or SAM. Left sided congestive heart failure in cats may result in pulmonary oedema, pleural effusion or both. it is a genuine emergency and requires prompt therapy, possibly before a definitive diagnosis is made. Cats may be asymptomatic and present with incidental acquired murmurs at vaccination.s ome cats may present with acute onset dyspnoea due to congestive heart failure whilst others may present with hindlimb paresis due to aortic thromboembolism.
130
What are the clinical findings in hypertrophic cardiomyopathy?
Usually good pulse, strong precordial impulse, pink mucous membranes, rapid capillary refill time, warm extremeties. systolic murmurs may be heard over the left or right mid heart / heart base due to dynamic obstruction of the outflow tracts caused by septal hypertrophy. a mitral insufficiency murmur may be present at the left apex. diastolic gallops maybe present at the right or left apex. brady or tachyarrhthmias may be present. the heart may be muffled on auscultation if a pleural effusion is present. pulmonary crackles may be audible if pulmonary oedema is presnet. painful stiff cyanotic hindlimbs with absence of femoral pulse is typical of aortic thromboembolism.
131
What may be present in diagnostic tests with hypertrophic cardiomyopathy?
radiography: early in the course of the disease the heart is unremarkable. hypertrophy may result in an elongated heart. as the disease progresses both atria enlarge resulting in a valentine shaped heart apperance on the DV view. plmonary venous congestion with evidence of pleural effusion/pulmonary oedema may be present. electrocardiography may be normal. there may be evidence of left atrial or biatrial enlargement. the left ventricle may be enlarged. AV conduction disturbances may occur eg 2nd or 3rd degree AV block. atrial or ventricular premature complexes may be present. Left anterior fascicular block commonly seen. Echocardiography: symmetrical or asymmetrical hypertrophy of the left ventricle can be visualised. left atrial or bi atrial dilation may be seen. doppler echocardiography will confirm the presence of mitral insufficiency or dynamic obstruction of outflow tract. Systemic blood pressure, renal function and thyroid function should be checked as hypertension and hyperthyroidism may result in hypertrophy.
132
What is the treatment of hypertrophic cardiomyopathy?
Beta blockers or calcium channel antagonists act as negative chronotropes and negative inotropes resulting in improved diastolic filling. the calcium channel antagonists also have a positive lusitropic effect resulting in improved relaxation. present recommendations suggest the use of beta blockers if dynamic obstruction is present and calcium channels antagonists otherwise. Good evidence that diuretics and ACE inhibitors are indicated and effective in the persence of congestive heart failure. Aspirin every 3rd day is recommended as long term therapy to prevent emboli formation.
133
What is secondary hypertrophy of the myocardium in cats?
Hypertension, hyperthyroidism and acromegaly all associated with secondary hypertrophy. very important that these conditions are ruled out before making a diagnosis of idiopathic HCM. the management of the cardiac disease is similar to idiopathic HCM however it is important that underlying disease is treated.
134
What is feline restrictive cardiomyopathy?
A poorly defined form of cardiomyopathy which is recognised clinically. the history, ECG and radiographic findings are similar to HCM, the main difference is the echocardiographic findings. there is no marked dilatation of the atria however the ventricular chambers appear normal and there is no or minimal hypertrophy of the left ventricular walls. the contractility is usually normal. Managed as for HCM.. may be a stage in the progression of HCM.
135
What is feline unclassified cariomyopathy?
A form of cardiomyopathy recognised on echocardiography in which there are mixed findings eg the ventricle may be slightly dilated the walls mildly hypertrophied and the systolic function poor. these cases may represent end stage HCM.
136
What is feline thromboembolism?
A common sequel to myocardial disease in cats. cats have a high platelet mass/kg body weight and platelet aggregation occurs readily. blood stasis occurs in the left atrium and myocardial disease leading to thrombus formation. embolisation commonly occurs to the external iliacs and the renal arteries. clinical findings are hindlimb paresis, severe pain, spasm of the gastrocnemius muscles in particular, cyanotic nail beds, absence of femoral pulse.
137
What is the treatment for feline thromboembolism?
Analgesia - buprenorphine or morphine. sedation from opiods. ACP at low doses can be added in. Heparin prevents further embolization given for 2-3 days. aspirin or clopidogrel prevents platelet aggregation. i/v fluids but be careful if congestive heart failure is present. treat underlying disease. physiotherapy. Cats with this condition will require aggressive therapy and hospitalisation for atleast 3-5 days. the pain eases off after the first 3-4 days and limb function usually recurs within 14 days. prognosis very guarded. a high percentage will have recurrences later.
138
What is myocarditis?
Inflammation of the heart. animals with myocarditis typically have arrhthmias. they may present in congestive heart failure. ante mortem diagnosis is difficult and general prognosis is poor.
139
What is valvular endocardiosis?
The most commonly diagnosed cause of a heart murmur and hear failure in dogs. Myxomatous mitral/tricuspid valve disease. It is rarely diagnosed in cats. it is a myxomatous degeneration of the heart valves, affecting the mitral and tricuspid valves resulting in incompetence of the affected valves. CKCS, cocker spaniels, poodles, terriers, dachunds, irish setters predisposed. higher prevalence in males.
140
What are the clinical findings of valvular endoardiosis?
A systolic murmur over the mitral +/- tricuspid valves. the murmur starts off as a low grade left apical murmur in early systole and as the disease progresses the murmur grade increases and the murmur duration lengthens to become pansystolic. the mitral murmur radiates to the right side and can be impossible to distinguish a murmur of mitral insufficiency radiating to the right from a separate tricuspid murmur. coughing is a common presentation due to the large left atrium pressing on the mainstem bronchi. exercise intolerance is frequently noted. Many dogs will present at vaccination and the murmur is an incidental finding, other dogs will present in acute left sided or biventricular congestive heart failure.
141
What presents on radiographs with valvular endocardiosis?
Lateral and dorso ventral radiographs will show left atrial/left ventricular enlargement with significant mitral insufficiency and right atrial/right ventricular enlargement with significant tricuspid insufficiency. generalised cardiomegaly will occur with long standing disease. Thoracic radiograph is the most useful method of determining volume overload. the pulmonary veins and lung fields should be examined closely for evidence of congestion and oedema. radiographic changes may occur before there is clinical evidence of left sided congestive heart failure.
142
What may present on electrocardiography with valvular endocardiosis?
The P waves may be wide suggestive of left atrial enlargement or wide and tall indicating biatrial enlargement. The R waves are frequently tall and the QRS complexes wide indicating left ventricular enlargement. The presence of tall R waves, wide QRS complexes with deep Q waves is suggestive of biventricular enlargement. On echocardiography the thickened valves may be visualised confirming the diagnosis. dilated chambers may be present. doppler echocardiography allows confirmation and quantification of valvular insufficiency.
143
What is the treatment for valvular endocardiosis?
this depends on the class of failure on presentation. the majority of dogs are treated with furosemide, ACE inhibitors and pimobendan once congestive failure develops. advanced cases may require additional diuretics and digoxin/diltiazem if marked sinus tachycardia or atrial fibrillation develops. spironolactone is a weak diuretic that is often used in advanced cases. there is good evidence that it may be beneficial at a much earlier stage and is not routinely added in when congestive heart failure patients are first stabilized.
144
What is bacterial endocarditis?
Associated with systemic bacteraemia, the initial source of the infection may or may not be known. once established, septic emboli will seed to various parts of the body. in general valvular endocarditis it is initially associated with valvular incompetence. long standing lesions may eventually result in valvular stenosis. the sepsis usually more clinically significant to patient. Endocarditis most commonly affects the tricuspid valve in cattle. In horse dog and cat the left heart is most commonly affected. in cattle septic emboli are seeded to the lungs, in the horse dog and cat systemic emboli affect the joints and kidneys. in dogs periodontal disease may be a major source of infection.
145
What are the presenting signs of bacterial endocarditis and how is it diagnosed?
the presenting signs are variable and may include lethargy, fever, lameness, haematuria, dyspnoea. Pyrexia is the most common finding. shifting lameness may occur if there is septic arthritis. a new systolic or diastolic heart murmur may be present in some cases. the systolic murmur may be variable in nature. the diastolic murmur may reflect aortic insufficiency or mitral stenosis. the location of the murmur depends on the valve involed. Non specific findings on radiography and electrocardiography. Myocardial emboli or concurrent myocarditis may result in arrythmias. Vegetative lesions may be imaged and valvular lesions may result in valvular insufficiency or stenosis which can be shown with doppler echocardiography. haematology may be suggestive of bacterial infection. a positive blood culture is supportive of diagnosis. at least three samples should be taken over a 24 hour period. urine analysis and culture may aid in the diagnosis. Antibiotics needed for 4-6 weeks. initial therapy is frequently parenteral followed by oral therap. antibiotics are selected based on results of blood culture. the prognosis is guarded.
146
How should an animal be treated that presents in left sided congestive heart failure?
If stable - obtain a definitive diagnosis. if critical - stabilise first before tests, cage rest, oxygenate, preload reduction, after load reduciton, sedation if distressed eg buprenorphine or butorphanol. once stable obtain a definitive diagnosis (e.g chest radiography) and treat accordingly eg patent ductus Arteriosus stabilise congestive heart failure and then treat surgically. idiopathic dilated cardiomyopathy stabilise congestive heart failure and treat with positive inotropes.
147
How should an animal be treated that presents in right sided congestive heart failure?
If stable, obtain a definitive diagnosis. if large pleural effusion presenting causing severe dyspnoea then thoracocentesis. abdominocentesis is usually reserved for daignostic purposes. if severe ascites is interfering with ventilation then abdominal drainage may be indicated however unnecessary fluid removal deprives animals of protein. once stable obtain a definitive diagnosis and treat accordingly, pericardial effusions should be drained, in cases of severe pulmonic stenosis the congestive heart failure should be treated and referral for balloon valvuloplasty should be consideed, in idiopathic dilated cardiomyopathy and congestive heart failure should be stabilised and treatment with positive inotropes started.
148
What are the principles of long term management in heart failure?
identfy the cause of disease at an early stage, identify any surgically correctable conditions or secondary cardiac disease. treat the primary cause in cases of secondary cardiac disease e.g treat the hyperthyroidism in hyperthyroidism cat as well as the cardiac disease. arrange for treatment of any surgically correctable conditions. establish a treatment regime based on the need for preload reduction, need for afterload reduction, need for positive inotropic support, need for improved diastolic function, need for rhythmn management whether bradyarhthmic or tachyarrhythmic.
149
What are loop diuretics
used for pre load reduction.
Furosemide - cause a potent diuresis and natriuresis, rapidly acting, may cause dehydration, prerenal azotaemia, hypokalaemia, hyponatraemia and may stimulate the RAAS. It is best to give the minimum dose that will relieve clinical signs. NB furosemide administered intravenously also has venodilator efficacy and can be used to reduce to preload by this mechanismm.
150
What are thiazide diuretics?
Used for preload reduction. hydrochlorthiazide, chlorthiazie, cause moderate diuresis and natriuresis. associated with potassium depletion if combined with a loop diuretic.
151
What are potassium sparing diuretics?
Used for preload reduction.
Spironolactone, amiloride
They are weak diuretics, are potassium sparing. they have a slow onset of action but amy be effective in cases of refractory congestive heart failure when combined with other diuretics and ACE inhibitors.
152
What are venodilators?
Used for preload reduction. Glyceryl trinitrate - useful in acute cardiogenic pulmonary oedema. 2% ointment absorbed through skin. avoid contact with hands. also available as transdermal patches. short term therapy only as patients become refractory. Frusemide - given IV acts as a venodilator
153
What are Angiotensin converting enzyme inhibitors?
Enalapril, benazepril, ramipril, imidipril. licensed for use in dogs. Hyperkalaemia is theoretically possible and concurrent use of potassium sparing diuretics and potassium supplementation should be done with care. Enalapril is renally excreted and thus it is important to monitor renal function. benazepril is 50% viliary excretion and may have some advantages in dogs with combined renal failure and congestive heart failure. Ramipril has longer duration of action and better tissue penetration.
154
What are arteriodilators?
Used for afterload reduction.
Hydralazine - may be particularly beneficial in sever mitral insufficiency. may cause symptomatic hypotension and reflex tachycardia. large tablet size - difficult use.
Inodilators - such as pimobendan are positive inotropes, vasodilator/noeffect on heart rate.
155
How is systolic failure treated?
Calcium sensitisers/inodilators
Pimobendan - main indication is in systolic failure, proven benefit in dilated cardiomyopathy and myxomatous valve disease in dogs. increasingly used in cats.
156
What are the cardiac glycosides?
Eg digoxin - weak positive inotrope and mainly used now to control ventricular rate in atrial fibrillation. do not give loading dose - start on maintenance. steady state levels achieved within 5 days. check levels 6-8 hours post pill to check therapeutic lecels. always stop digoxin if anorexia, nausea, GIT signs or arrhythmias develop, reintroduce after 1-2 days at a lower dose. decrease dose proportionately for obese dogs, fluid retetion, renal failure, dobermanns, long half life in cats - can be used with caution
157
What are beta agonists used for?
Dobutamine
Only available as IV infusion
Main indication is severe myocardial failure
Some beneficial effects persist after cessation of infusion
158
How is diastolic failure treated?
Improving diastolic function will depend on the cause of dysfunction. pericardial effusions should be drained. in other causes of diastolic dysfunction drugs may be used to improve ventricular relaxation, slow heart rate and thus decrease diastolic filling time, decrease contractility and thus decrease myocardial O2 consumption.
159
What are the calcium channel antagonists?
Diltiazem, verapamil - diltiazem is the most widely used lusitropic drug in cats. some reports indicate very good clinical effects in cats with HCM, in comparison with verapamil and propanolol. Must be administered three times daily. mild negative inotropic effect may be beneficial in reducing myocardial oxygen consumption thereby improving relaxation by reducing subendocardial ischaemia the negative chronotropic effect improves diastolic filling by increasing length of diastole.
160
What are beta adrenergic blocking drugs?
Propanolol, atenolol - the main beneficial effect of beta blockers is to slow the heart rate, thus increasing the time spent in diastole, where filling is impaired and slow this effect alone may improve ventricular filling. by reducing heart rate, they also reduce cardiac work. they also have a negative inotropic effect and may be beneficiial in reducing myocardial oxygen consumption thereby improviing relaxation and reducing subendocardial ischaemia.
161
Describe the types of drugs used in cardiac disease?
Positive inotropes - inodilators, dobutamine, methylxanthines
Vasodilators - ACE inhibitors, inodilators, calcium channel blockers, nitric oxide donors.
Cardiac glycoside - digoxin
Diuretics
Antiarrhythmics - tachyarrthmias - VW classification, bradyarrythmias.
162
describe the pathophysiology of heart disease?
Cardiac disease > Cardiac dysfunction > decrease in cardiac output > decrease in blood pressure and peripheral perfusion> activation of the neurohumoral activation - sympathetic nervous ystem, RAAS, endothelin, vaospressin. > increase in cardiac hypertrophy and cardiac fibrosis
163
What is the main focus of cardiac treatment?
Historically used to focus on the heart, as the target. peripheral vasculature is now receiving far more interest as type of treatement.
164
Describe the inodilators (positive inotropes)
Main one - pimobendan;
Mechanism of action - inodilator.
Phosphodiesterase (PDE) III and partly V inhibitor and calcium sensitiser (sensitises myocardium). calcium sensitisation without increased myocardial oxygen consumption probably the most important for myocardial inotropic effect. Vasodilatory effects - PDE III and V inhibition. Modulation of pro-inflammatory cytokines demonstrated experimentallly.
165
Describe myocardial muscle contraction
When expenditure of energy - ionised calcium in the cytosol binds with troponin complex, shifts tropomyosin out of the way, so can get interaction of myosin with actin, and rowing action which moves the myosin across actin filaments which gives myocardial contraction. Oxygen involved in this process. Pimobendan makes the myosin more sensitive to the amount of calcium there already. Shoulnt require any additional oxygen for this to hapen.
166
How does pimobendan effect the vascular smooth muscle?
Calcium central to the whole mechanism of vascular smooth muscle contraction. Calcium through calcium channels and or being released from the SA in the smooth muscle cell. the mechanism involved i that calcium binds with calmodulin which activates the Myosin Light chain kinase, which allows phosphorylation of myosin light chain which then allows contraction to take place. Something that can inhibit MLCK - will prevent contraction - cause relaxation. Cyclic AMP and cyclic GMP will do this. Cyclic AMP is metabolised by Phosphodiesterase - so phosphodiesterase enzyme inhibitor blocks this, cyclic amp accumulates, inhibit Myosin light chain kinase - allows vasorelaxation to occur.
167
Describe the myocardial cell B1 receptor
The b1 adrenergic receptor interacts with G protein, positively couples to adenylate cyclase, and will increase cyclic amp levels in the cell. in the myocardial cell cyclic AMP increases levels of protein kinase A, which has the effect of increasing calcium in the myocardial cell. Pimobendan inhibits phosphodiesterase so increasing cyclic AMP, increasing PKA and Calcium, this will have a positive inotropic effect.
168
Describe the pharmacokinetics of pimobendan?
It is orally bioavailable, but is reduced in the presence of food, administered BID one hour prior to feeding. highly bound to plasma protein, eliminated in the bile, injectable form now available. Side effects- GI tract, some concerns with rupture of chordae in valvular disease? Not proved to be the case.
169
Describe dobutamine
A synthetic B1 a adrenergic agonist. reasonably selective - minimal affects on the B2 or A adrenergic effects. If it did have significant effects on these you would see - Increase in vasoconstriction, increased perippheral resistance.
170
What is the main indication for dobutamine?
Main indication is severe acute heart failure with poor left ventricular function. also used in horses during anaesthesia to maintain MAP. can induce arrythmias.
171
What are vasodilators used for?
aim to decrease the preload and afterload . results in reduced cardiac workload and congestion. several different classes - PDe inhibitors (pimobendan), angiotensin converting enzyme inhibitors , calcium channel aantagonists, nitric oxide donots, alpha 1 antagonists. Increasing relaxation in arterial side of circulation - decreasing the force at which diseased heart has to contract against.
172
Describe the RAAS system
RAAS system complex, Many knock on effects and interactions with other pathways. Angiotensin converted to angiotensin I> angiotensin II. also aldosterone release triggered - retention of water and sodium and loss of potassium. (not good for CHF). Can promote fibrosis and hypertrophy. Angiotensin II is a good vasoconstrictor, can have effects on baroreceptors (changing sensitivity), can affect adrenoceptors (making them more sensitive to adrenaline), can increase the release and activity of vasopressin and endothelin. (vasoconstrictor).
173
How do the angiotensin converting enzyme inhibitors work?
Angiotensin II has numerous effects. ACE inhibitors block these actions and are beneficial in heart failure. revolutionised the treatment of cardiac disease. they increase quality of life and longevity. enalapril, benazepril, ramipril and imidapril.
174
Describe enalapril?
A prodrug converted to enalaprilat by serum esteerase. good oral bioavailability. long duration of action (once daily dosing), excreted by the kidney, hypotension possible side effect, care to avoid hyperkalaemia if used wit potassium sparing diuretics.
175
Describe benazepril
Also a prodrug converted to benazeprilat. metabolised by both the liver and the kidney in the dog. may be better in dogs with renal disease. dosing once daily. several months before benefits with ACE inhibitors.
176
What is amlodipine? (calcium channel antagonists)
This is now the drug of choice for treatment of feline hypertension. greater effect on calcium channel of vascular smooth muscle compared to cardiac effect. slowly absorbed and prolonged duration of effect. can be administered once daily.
177
What are the nitric oxide donors?
Glyceryl trinitrate - a pure venodilator. applied topically because of extensive first pass metabolism. refractoriness after several days. acute management of pulmonary oedema and heart failure. cant be given orally - first pass hepatic metabolism. induces the intracellular production of nitric oxide. Nitric oxide - activates guanylyl cyclase > converts GTP to cGMP - smooth muscle relaxation. cyclic GMP and AMP cause relaxaation in vascular smooth muscle.
178
What is sodium nitroprusside?
Nitric oxide formation in vascular smooth muscle. given as an intravenous infusion, can be useful in severe fulminant pulmonary oedema. hypotension is a side effect as well as cyanide poisoning. rapidly metabolised light sensitive. reconstituted in 5% dextrose solution.
179
What are the cardiac glycosides?
Low therapeutic index. beneficial effects of digitalis purpurea (foxglove) in the treatment of dropsy. several important features - negative chronotropy, modulating effects on autonomic nervous system effects, positive inotropy.
180
Describe the effects of the digitalis glycosides
Parasympathomimetic activity - they decrease the discharge of the sinoatrial node, decrease the rate of conduction through the atrioventricular junction. They are frequently used to slow down the ventricular response to atrial fibrillation. They reduce the release of sympathetic neurotransmitter and reduce the release of renin from the juxtaglomerular apparatus. Digitalis glycosides block the Na/K+ ATPase and the cell becomes transiently hypernatraemic. This reduces the activity of the Na/Ca2+ exchanger and more calcium stays in the cell. Within limits Ca2+ number of cross bridges = forces of contraction.
181
Describe the pharmacokinetics of digoxin
Oral bioavailability - 75%, 25% plasma protein bound, renal excretion and some hepatic metabolism, long half life >30 hours > in general it takes 5 plasma half lives to attain a steady state therefore about one week required for digoxin. large volume of distribution. skeletal muscle acts as a reservoir not fat. low doses are best especially in dobermans, generally BID. Calculate on body surface area if possible or at least an estimation of lean body weight.
182
What are the special considerations with digoxin?
Hypoproteinaemia, cardiac cachexia ( lose muscle mass - animal losing muscle mass - losing reservoir and increasing amount of ,free drug available) obesity and ascites > overdosing. hypothyroidism > increases half life. Hypokalaemia > toxicity (same binding sites on Na/K+ ATPase) Renal dysfunction > decreased excretion. Reduce dose if calcium channel blockers used as well since both protein bound (30% reduction), mainly used in dogs, in the cat the half life is longer therefore the dose only every 24-48 hours. bioavailability of digoxin can vary with the proprietary brand. Toxic side effects - very low therapeutic index, anorexia, nausea,vomiting, depression, arrhthmias. TDM - take a blood sample, plasma levels hsould be assayed after one wek, withdraw the drug, check electrolytes and kidney parameters, may be necessary to use lidocaine.
183
What are the antiarrhythmics used for?
Important to eliminate easily rectifiable cause of the rhythmn disturbance. many of the drugs are toxic and pro arrhthmic. recent years less inclination to rush into the treatment of rhythm abnormalities. Rational approach; diagnose rhythm disturbance, eliminate electrolyte disturbances, assess if requires treatment or not, if yes select a drug. Antiarrhthmics in the vaughan williams classification used to treat tachyarrhthmias.
184
Describe the class I antiarrhythmics
Membrane stabilising drugs. they inhibit Na+ influx by blocking sodium channels - local anaesthetic properties. normal potassium levels important for activity. three subdivisions - class 1A, 1B, 1C. Use dependent block
185
What is the effective refractoy period?
The shortest interval at which a premature stimulus results in a propagated response. Drugs can manipulate and prolong the refractory period making it less likely that the cardiomyocyte can be triggered into an action potential
186
How do Class 1A drugs work?
Decrease automaticity, increase action potential threshold, increase action potential duration, this may be due to effects on other ions, decrease conduction, increase effective refractory period, slow the rate of respiration.
187
What are the ways in which drugs can alter the ERP?
They can make the ERP take up more of the action potential AP as in A. they AP duration stays the same . they can prolong the action potential duration so effectively the ERP is also longer.
188
Describe Quinidine a class 1A antiarrythmic
It has all the Class 1A effects.
It has slow recovery from ion channel block. at low doses Vagolytic activity > increase SA node discharge and conduction, extensively protein bound, large volume of distribution, metabolised in the liver and eliminated by the kidney, good oral bioavailability and half life of 6 hours.
189
What are the indications for quinidine use?
Atrial fibrillation in the horse, ventricular tachycardia in the horse, administered orally (i/v formulation for V tach. in horses)
190
What are the side effects and toxicity of quinidine?
Hypotension through a-adrenoceptor blockade, gastrointestinal upset, heart block can precipitate digoxin toxicity, QT interval prolongation of 25% indicates toxicity. sodium bicarbonate administration increases protein binding and lowers potassium to aid in toxicity treatment.
191
Describe the class 1B antiarrythmics
They are membrane stabilising and have their effect mainly through sodium channels. they have an effect on action potential panel A - this is the more usual effect of the class 1 drugs.
192
Describe Lidocaine - Class 1B
TIt increases the ratio of ERP to AP duration, accelerates repolarisation, decreases the automaticity and conduction velocity primarily in diseased tissue, recovery from block is generally rapid. extensive first pass hepatic metabolism > given i/v only, very short half life (20-30 min). Drug of choice for emergency treatment of life threatening ventricular arrhythmias given as a bolus followed by infusion. can cause convulsions.
193
Describe mexiletine (also 1B)
Similar properties and effects to lidocaine since it is structural analogue. recovery from ion channel block is rapid. orally bioavailable due to reduced first pass metabolism. essentially an oral form of lidocaine. hepatic metabolism, generally indicated for ventricular arrythmias.
194
Describe Class II the B blockers (antagonists)
Effect mediated through blockade of B adrenoceptors. they slow the heart rate and speed of conduction. little effect on the action potential of the nodal tissue. EADS and DADS well managed with these (early and delayed afterdepolarisations)
195
Describe the effects of atenolol and esmolol (class II)
B1 selective (cardioselective). esmolol is ultrashort acting for acute treatment of for example SVT and is administered i/v. it is metabolised by RBC esterases. selective for B1 adrenergic receptors in the heart so minimal vasodilatory or bronchoconstrictive effects. tachyarrhythmias or in HCM in cats.
196
What are the side effects of the B blockers
Can all cause hypotension and bradycardia - transient hypertension (unopposed a adrenergic stim) may be reported at the start of treatment. B2 effect can cause bronchospasm. enhance hypoglycaemic effect of insulin. start and stop treatment gradually. beta adrenoceptor downregulation.
197
What are the pharmacokinetics of the B blcokers?
Atenolol can be administered orally tablet and syrup generally every 12-24 hours. hepatic metabolism, urinary elimination.
198
Describe the class III - K+ channel blockers
Examples include sotalol. Sotalol has beta blocker and K+ channel blocker effects. prolongs action potential duration, decreases automaticity, slows AV conduction and refractoriness, eliminated through the kidney unchanged.
199
Describe the effects of the Class IV calcium channel blockers
They block the slow calcium channels. they have a profound effect on nodal tissue (unlike the class I drugs). they are more reliant on calcium for its AP. Slow sinus rate, speed of conduction, they induce vasodilation, three classes examples of each class include, verapamil, dilitiazem and amlodipine, Diltiazem - well absorbed but has first pass metabolism is extensive. extensively protein bound. Has a short half life -1.5-5 hours. Downside is it requires TID dosing. metabolites are weakly active. intermediate in terms of selectivity for cardiac and vascular smooth muscle.
200
Describe the drugs used to manage bradyarrhthmias
Abnormally slow rhythmn - abnormality of sinus node impulse formation, abnormality of AV nodal impulse conduction, often associated with escape complexes. Condition may be due to something which may be rectified e.g hyperkalaemia, anaesthesia. More long term abnormalities due to disease within the heart tend to respond poorly to the medical management but pacemaker is the treatment of choice. Muscarinic antagonists like atropine/propantheline/glycopyrronium - Muscarinic antagonist - parasympatholytic effect, sinus block, sinus arrest, AV block and sick sinus syndrome may respond. Refer to autonomic pharm. Terbutaline - a B2 agonist, may have beneficial dromotropic effects, oral bioavailability is low, half life 14 hours, 50% renal excretion.
201
Describe renal physiology
Kidneys receive about 25% of the C.O. 99% of the glomerular filtrate is reabsorbed under normal circimstances. this involves the active transport of electrolytes and other solutes from the lumen into the tubule cell and into the extracellular fluid. Sodium is very important. throughout the length of the tubule the Na+/K+ ATPase is important for the movement of sodium from the cell into the extracellular fluid. five different mechanisms exist for moving sodium from the lumen into the cell.
202
What is the mechanism for transport of sodium into the cell
Na+ entry along an electrochemical gradient. Na+ entry coupled to an organic solute or phosphate. Na+ entry in exchange for a positive ion e.g H+ or K+. Na ion entry with K+ and 2 Cl-, Na Ion entry with Cl-.
203
Describe the proximal convoluted tubule
No osmotic gradient is created here, water and Na+ are both reabsorbed. the osmolarity of the fluid in the lumen does not alter. sodium reabsorption accompanies a Cl- ion. HCo3 is also reabsorbed.
204
What occurs in the descending loop of henle
The medulla is hypertonic, this causes water to move out of the tubule into the medulla. Na+ may move back into the tubule because of the osmotic gradient created by the hypertonic medulla.
205
Describe the ascending loop of henle
Impermeable to water. sodium actively removed with one K+ and @cl- ions. this contributes to the hypertonicity of the medulla.
206
Describe the distal convuluted tubule
Urine in this part of the tubule is hypotonic in relation to the plasma . due to the active transport of sodium out in the ascending loop. sodium is still removed in this region together with a Cl- ion. potassium and hydrogen ions are added to the filtrate. sodium can be reabsorbed in exchange for potassium. this is influenced by aldosterone. aldosterone can also alter the number of sodium pumps in the basolateral membrane of the tubular cells.
207
What happens in the collecting tubule?
ADH can control the amount of water reabsorption by altering the permeability in this region of the neprhon. H+ and K+ are excreted into the lumen.
208
What are diuretics?
Diuretics are agents which increase the production of urine. most of the clinically useful diuretics have a direct action on the kidney. main use is in the management of cardiac failure to control oedema and congestion. Several types exist; thiazides, high ceiling loop diuretics, aldosterone antagonists, potassium sparing diuretics, carbonic anhydrase inhibitors, osmotic diuretics.
209
How do thiazide diuretics work?
The main site of action is the DCT. excreted into the PCT and need to be in the tubule to exert an effect. moderate diuretics due to site of aciton. much sodium has already been reabsorbed by this time. inhibit the Na+/Cl= co transport system by binding to it. they prevent sodium and chloride ion reabsorption and reduce the loss of Ca2+. They increase the loss of K+ since more sodium presented in the collecting tubule and more urine flow due to increased volume.
210
When are thiazides used?
Chlorothiazide, hydrochlorothiazide, bendroflumethiazide, trichlormethiazide. uses: mlld cardiac failure to manage oedema, combined with other diuretics e.g furosemide, oedema secondary to hypoproteinaemic disorders, diabetes insipidus, side effects: generally quite safe, main side effect is hypokalaemia, decrease effect of insulin. may potentiate anaesthetics, cardiac glycosides.
211
How do the thiazide diuretics work in relation to diabetes insipidus?
Works in some animals but do not really know why. the mechanism of the thiazides is nclear. D insipidus can be central or nephrogenic. central form vasopressin treatment of choice. the thiazides - loss of sodium and water int he DT leads to hypovolaemia. more sodium and water reabsorbed in the PCT. less urine in the loop of henle > less urine presented to the collecting tubule.
212
What are the pharmacokinetics of the thiazides?
Administered orally, oral bioavailability variable between different agents. chlorothiazide 10% oral bioavailability, hydrohclorothiazide 70% oral bioavailability. half life between 1.5-2 hours. rapid effects within 1 hour of administration
213
Describe the loop diuretics
The mechanism of action - site of action is the thick ascending loop of henle. they are powerful diuretic agents. they inhibit the cotrasnport of Na+/K+/2Cl- from the lumen into the tubule cell. this reduces the hypertonicity of the medulla responsible for the reabsorption of water from the collecting tubule and the descending loop of henle. they result in a dramatic increase in water loss by the kidney. potassium also lost due to decreased reabsorption in the ascending loop and also increased sodium presentation in the collecting tubule. Ca2+ loss is increased also. intravenously have a vasodilatory effect. Oral bioavailability is generally good - furosemide 60%. Furosemide main example used in V med. highly protein bound. secreted into the PCT. Non secreted metabolised in the liver by cytochrome p450 pathways. furosemide undergoes glucuronidation. Rapid onset of action (1 hour or 30 mins if I/v). half life of about 90 minutes and duration of action 3-6 hours.
214
What are the uses and side effects of the loop diuretics?
Heart failure for the management of oedema. given i/v vasodilation can help to reduce preload and increase renal perfusion. treatment of hypercalcaemia since promote calcium loss (lymphosarcoma). side effects - mainly hypovolaemia and hypokalaemia. ototoxicity (care with aminoglycosides)
215
Describe the aldosterone antagonists?
Spironolactone is an aldosterone antagonist - since it inhibits the effect of aldosterone the effect is a loss of sodium and water and the retention of potassium. pharamcokinetics - 70% oral bioavailability, highly protein bound, first pass hepatic metabolism. canrenone is an active metabolite, canrenoate is an active metabolite but can be converted to canrenone. half life only about 1- minutes but half life of canrenone is about 16 hours. onset of action takes several days. side effects - hyperkalaemia is a risk especially (ACE inhibitors).
216
What are the aldosterone antagonists and other potassium sparing diuretics?
Effects of aldosterone on the kidney in the DCT - at the end of the DCT aldosterone increeases the number of na+ K+ atpase sites on the basolateral membrane of the tubular cell. aldosterone enhances the activation of Na+ channels on the apical aspect of the tubular cell through directing synthesis of a mediator protein. it stumulates the membrane Na+/H+ exchanger.
217
Describe amiloride and triamterene (other potassium sparing diuretics)
They prevent the reabsorption of sodium through the luminal sodium channels. they reduce the loss of potassium and increase the loss of sodium. they are moderate diuretics. potassium sparing effect is greater where potassium loss is elevated. They have moderate oral bioavailability.. triamterene 60% plasma bound much less binding with amiloride. triamterine metabolised in the liver and some excreted unchanged in the urine. amiloride mostly excreted unchanged in the urine. Duration of action for triamterine about 12 hours and for amiloride about 24 hours. side effets; hyperkalaemia. the main use is in conjunction with other diuretic agents in the management of severe cardiac failure. used with furosemide since it compliments the potassium loosing effect of this diuretic. Preparations containing both a potassium sparing and a thiazide diuretic e.g co flumactone (hydroflumethiazide and spironolactone)
218
Describe the osmotic diuretics
Several important features - freely filtered by the glomerulus, reabsorption is limited, Pharmacologically inert. mannitol is the classical osmotic diuretic.
219
What is the mode of action of mannitol?
As Na+ and water are removed in the PCt the mannitol becomes progressively concentrated. it reduces the reabsorption of water int he PCT. Na+ removal then declines. prostaglandin release enhances the renal medullary blood flow reducing the hypertonicity of the medulla. less water is reabsorbed in the descending loop of henle. Mannitol is used in the management of acute renal failure to restore urine production, used to reduce CSF pressure, used to reduce Intraocular pressure in glaucoma. Toxicity - transient elevation in extracellular fluid volume can lead to decompensation in some animals e.g underlying cardiac disease. mannitol is administered by slow intravenous infusion after a test dose.
220
What are carbonic anhydrase inhibitors?
Carbonic anhydrase is an enzyme responsible for HCo3 + H+ > H2o + Co2. This occurs both in the lumen and tubular cell in the PCT. in the lumen HCo2 is converted to H2o and Co2 on the addition of H+. The H2o and Co2 are absorbed into the tubular cell and carbonic anhydrase allows the reformation of HCO2- and H+. The Hco3- is absorbed back into the plasma and the H+ transported back into the lumen. the net effect is the reabsorption of Hco3 from the PCT. when carbonic anhydrase is inhibited, bicarbonate stays in the lumen together with Na+ and K+. This causes a rise in urine volume and an increase in urinary pH. Metabolic acidosis ensues due to the reduced HCO3- which in turn reduces the actions of the diuretic.
221
Describe Acetazolamide (diamox) (a carbonic anhydrase inhibitor)
Acetazolamide is the classical thiazide diuretic - administered orally, not really used as a diuretic, used to treat glaucoma since carbonic anhydrase of the ciliary epithelia is involved in the formation of the aqeous humour. oral absorption is good. It is excreted by the kidney, possibly teratogenic, calculus formation possibly due to altered urinary pH. gastrointestinal upset may be a feature, hypokalaemia.
222
What are the clinical signs of pericardial effusion and how would you investigate a suspected case?
Weakness, exercise intolerance, lethargic, abdominal distension (Ascites), poor cardiac output, pale mm, prolonged CRT, tachycardic. Physical signs - hepatomegaly, heart sounds muffled, jugular veins distended. Radiogrpahy shows gross cardiomegaly and no distinguishable chambers (static cadiac silhouette and CVC distended, ecg shows low QRS complexes and variable R wave peaks, EKG shows fluid surrounding the heart. treatment with pericardiocentesis and find underlying condition.
223
Describe the fundic appearance that might be present in a cat with a systolic blood pressure of 240mmhg. list two commonly occuring causes of hypertension in the cat. name the class of anti hypertensive agent that is currently the drug of choice for hypertension in the cat.
The fundus looks red due to retinal and vitreal haemorrhage. retinal vessels look tortuous and large. retinal detachment most likely will happen or has happened and of course sudden visual loss. causes - hyperthyroidism, hypertrophic cardiomyopathy, chronic renal failure, amlodipine bysalate (calcium channel blocker).
224
What are the clinical signs of a cat with hypertrophic cardiomyopathy?
very warm extremities, pink MM, quick CRT, high cardiac output, strong pulses, tachycardic dyspnoea, may present with hindlimb paresis if there is an aortic iliac thromboembolism or even asymptomatic.
225
In the diagnosis of dilated cardiomyoopathy, what information can you gain from EEG, Echocardiography?
EEG - wide p wave, wide QRS complex, tall R waves, maybe deep S wave suggesting left atrial enlargement and biventricular enlargement. Echocardiography Shows biventricular enlargement, atrial enlargement, poor blood flow velocity through chambers and poor contractility of the ventricular chambers (systolic dysfunction).
