module 8 cardiovascular Flashcards
Discuss the pathophysiology and clinical signs of cardiac failure
CANINE MYXOMATOUS MITRAL VALVE DISEASE; begins with defect in connective tissue, altering mitral valve, regurgitation of blood flow in left atrium, left ventricular enlargement, reduced stroke volume and decreased MAP, leading to activation of SNS(Sympathetic nervous system),RAAS(Renin angiotensin aldosterone system) and natriuretic peptide. Chronic activation of these systems leads to pulmonary oedema. Clinical signs of respiratory distress.
CANINE DILATED CARDIOMYOPATHY;medium to large breeds. Reduced cardiac contractility reduces SV, cardiac enlargement occurs, ascites and or pulmonary oedema occurs, also myocardial ischaemia and hen arrythmias. Clin signs may be resp distress but may also have signs of forward failure eg.lethargy, pale mm, weak pulses, often ventricular tachyarrythmia or atrial fibrillation.
FELINE HYPERTROPHIC CARDIOMYOPATHY;usually genetic basis esp maine coone, ragdoll & burmese but occurs in dsh also.Severe hypertrophy and fibrosis, reduced coronary arterial perfusion, myocardial ischaemia, neurohormonal activation as per previous, venous congestion, pulmonary oedema, tachycardia, and increased risk of clot forming in left atrium and high risk of systemic thromboembolism.
(Other much rarer feline heart dz’s include Restrictive cardiomyopathy, Arrythmogenic right ventricular cardiomyopathy, Dilated cardiomyopathy.)
Outline the diagnostic evaluation of cardiac system
PULSE OXIMETRY;hypoxaemia present (sPO2<94% and usually severe(<90%)
TFAST;rockets indicate pulmonary oedema.Might see pleural effusion, might see pericardial effusion if have had arterial tear. May see mild pericardial effusion before fulminat congestive heart failure.
ECG;
Left ventricular enlargement can appear as tall R waves and sometimes a widening of the QRS complex.
Left atrial enlargement may lead to the widening of P waves (longer time to depolarise)
Atrial fibrillation: often associated with DCM or occasionally with severe left atrial enlargement from MMVD
Ventricular tachycardia – associated with DCM or can result in DCM if it is sustained
THORACIC RADIOLOGY;
Typically, shows an enlarged cardiac silhouette in canine patients but may not be obvious in felines. Atrial enlargement is visible in patients with left sided heart failure.
Pulmonary oedema is the most common manifestation of pulmonary congestion
Interstitial and/or alveolar pattern with often a peri-hilar appearance. Though rare, lobar manifestations have been described
In cats the pattern can be patchy and distributed irregularly
Pleural effusion may be visualised (cats mainly), as well as if right sided heart failure if present (dogs mainly)
Pulmonary venous congestion may be visible where the vein appears more prominent than the artery and is greater than the width of the 9th rib where it intersects on a VD/DV view. Arteries and veins can both be distended at times.
Other radiographic findings include: a distended caudal vena cava, hepatomegaly and ascites
BLOOD GAS & ELECTROLYTE;
A decrease in venous blood carbon dioxide (PvCO2) indicating hyperventilation.Hyponatraemia may be present, secondary to water retention (activation of RAAS) and carries poor px. Monitor for hypokalaemia esp with diuretic tx.
BIOCHEM;monitor kidneys might have issues due to reduced cardiac output or poor perfusion.
URINE;for kidney checks
BP;indicated for those with signs of poor forward flow, only if does not induce further stress.
ECHOCARDIOGRAPHY;required for dz dx and further planning.
Outline the medical treatments and procedures used in management of cardiac
emergencies
O2 supplementation.
Warmth as req.
Anxiolytic eg BUTORPHANOL 0.1 - 0.4mg/kg IV/IM/SC.
Diuretic eg FRUSEMIDE;Dog: Frusemide 2 - 6mg/kg IV/IM/SC initial dose
Cat: Frusemide 0.5 - 2mg/kg IV/IM/SC initial dose (cats are much more sensitive to Frusemide than dogs).Continue with Frusemide diuretic therapy:
Dogs: 2-4mg/kg IV q2hr vs 0.6-1mg/kg/hr CRI for 4-6hrs. Bolus administration can be given up to q4-6hr until respiratory rate and effort improves (maximum doses of 14-16mg/kg in initial 12-24hrs).
Cats: 0.5-2mg/kg IV q2hr until respiratory rate and effort improves. Cats are more sensitive to Frusemide in this setting and only 1-2 doses may be necessary.
If the patient is not responsive to traditional diuretic therapy, consider SODIUM NITROPRUSSIDE (balanced arteriolar and venous dilator) at 2-10mcg/kg/min CRI. BP must be monitored as it has a potent hypotensive effect.
Thoracocentesis/Abdominocentesis as indicated.
PIMOBENDAN 0.25mg/kg PO q12hrs for dogs with MMVD or DCM, can be given IV in the emergency setting (0.15mg/kg IV)
Ventricular tachyarrhythmias
Perform the vagal manoeuvre by applying ocular or carotid pressure while monitoring the ECG to attempt to achieve conversion to sinus rhythm.
LIGNOCAINE is a class Ib antidysrhythmic agent. This can be administered at 1- 2mg/kg slow IV over 5 minutes with a maximum dose of 8mg/kg followed by a CRI of 20-80mcg/kg/min (1-4mg/kg/hr) constant rate infusion if no improvement is seen from the boluses.
Evaluate and monitor the patient for hypokalaemia if no response to lignocaine as this can perpetuate ventricular arrhythmias.
N.B.: IV lignocaine causes nausea and somnolence. High doses of lignocaine may cause vomiting, vasodilation and seizures.
Supraventricular tachycardias (Atrial fibrillation most common):
DILTIAZEM : calcium channel blocker inhibits the influx of extracellular calcium into myocardial cells and vascular smooth muscle. Its net effect is to slow AV node conduction and prolong refractory time. It is also a negative inotrope. Diltiazem can be administered at 0.5-4mg/kg PO q8hr, to be commenced at the lower dose and titrated upward.
DOBUTAMINE may be utilised if severe heart failure leading to severe hypotension is present. This is more commonly seen in DCM. CRI started at 2.5-5mcg/kg/min with a gradual increase in rate until blood pressure is adequate, to a maximum of 20mcg/kg/min.
Discuss the Renin-Angiotensin-Aldosterone System (RAAS) and blood pressure
maintenance
RAAS aims to preserve circulating blood volume.
RENIN released from granular cells of macula densa in juxtaglomerular complex in response to reduced bp detected in afferent arterioles in kidney. In plasma, renin causes Angiotensinogen to Angiotensin 1. For feedback, renin is inhibited by increased circulating blood volume and by angiotensin 2.
ANGIOTENSIN CONVERTING ENZYME (ACE) in pulmonary endothelium causes Angiotensin 1 to Angiotensin 2.
ANGIOTENSIN 2 causes arteriolar vasoconstriction (increased bp), increases sensitivity of vascular smooth muscle to catecholamines, facilitates noradrenalin and aldosterone (increased sodium and chloride resorbtion in renal tubules) release from adrenal gland and ADH from pituitary.
ANTIDIURETIC HORMONE (vasopressin) is released from posterior pituitary resulting in thirst, vasoconstriction and increased tubule resorbtion of water.
Describe the clinical signs of hypertension and hypotension
NORMAL BP
Dogs Cats
Systolic 110-180mmHg 110-170mmHg
Diastolic 55-110mmHg 70-120mmHg
Mean 80-130mmHg 60-130mmHg
HYPOTENSION;MAP<80 and concern for tissue perfusion at MAP <60. Clin signs often weak, pale, collapsed, mental dullness, tachycardia (cats may be bradycardic), weak pulses, cold extremities, prolonged crt. In early stages, may have compensated and have bounding pulse and injected mm, BEWARE of causing rapid decompensation if eg give vasodilatory med eg acp.
HYPERTENSION;Hypertension is inappropriately high arterial blood pressure with or without concurrent increases in blood volume. May cause ocular signs (poor vision, unable to navigate, vocalisation, sudden blindness), renal issues, neuro issues (lethargy, seizures, altered mentation)
List the diagnostic tests used in the evaluation of blood pressure
INDIRECT;A)Doppler ultrasonography
* Sensitive in smaller patients (<10kg) or patients with severe hypotension
* Limitations: Only provides systolic blood pressure (best in cats). Accurate measurement affected by cuff size, skin thickness and fur, and requires a still patient
B)Oscillometric
* Advantage of being automated, no need for patient handling and provision of a mean arterial pressure (MAP) with systolic and diastolic pressures calculated
* Limitations: accurate measurement affected by cuff size, skin thickness and fur, insensitive in smaller patients or patients with severe hypotension and movement of the patient as
well as arrhythmias
DIRECT * Requires the use of an arterial catheter
* Gold standard of systolic blood pressure monitoring
* Minute to minute information
* Limitations: requires a still patient. Normally reserved for anaesthetised or heavily sedated patients.
Outline the medical treatment for hypotension and hypertension
HYPOTENSION;
a) Fluid as indicated.Boluses; Dogs: 10-20ml/kg bolus of an isotonic crystalloid over 15 minutes. Can be given twice (and more if necessary).
o Cats: 5-10ml/kg bolus of an isotonic crystalloid over 15 minutes. Can be given twice (and more if necessary).
o Consider a hypertonic solution. This is 2-5ml/kg of typically a 7% hypertonic
saline solution to temporarily expand intravascular volume. This is usually reserved for patients with severe acute haemorrhage.
* In cases of haemorrhage, whole blood or packed RBC may be required
b)Vasopressors;Used in patients with an inappropriate vasodilatory process such as sepsis or anaphylaxis, or if there is failure to respond to fluid resuscitation.
* Alpha receptors act on vascular smooth muscle causing vasoconstriction
* Beta receptors increases cardiac contractility and rate, as well as causes bronchial dilation.
Vasopressors commonly used:
Drug Alpha reception Beta reception
Adrenaline +++ +++
Noradrenaline +++ +
Dopamine ++ +++
Dobutamine + +++
Vasopressin (V1 receptors only) - -
Phenylephrine +++ -
(Vasopressin acts on the V1 receptors causing vascular smooth muscle contraction. This is unaffected by acidosis (pH <7.20) which causes a down regulation of catecholamine effectiveness.)
c)Positive inotropes;Should be used in cases of documented or suspected myocardial dysfunction, nonresponsive to fluid resuscitation AND vasopressor agents.
* Dobutamine is generally the preferred agent.
* Limitation: Increases myocardial oxygen demand and the potential to cause arrhythmia
HYPERTENSION;note emergency tx of hypertension is required for acute blindness, retinal detachment, hypertensive encephalopathy.Aim to significantly reduce hypertension so limit organ damage but may not get to normal.
a) ACE inhibitors; eg Benazepril, enalapril. Frequently used for cardiomyopathy. fairly safe. May cause weakness, azotaemia, hyperkalaemia.
b)BETA adrenergic blockers;eg Atenolol.Often used when 1st line anti-hypertensive fails. AVOID in asthmatic cats. May cause hyperkalaemia and or bradycardia.Often used in HCM.
c)CALCIUM channel blockers;eg amlodipine.1st choice for cats with chronic kidney dz. effect is gradual. May cause tachycardia, nausea, weakness,constipation. First choice for sudden onset blindness old cat with hypertension and detached retina
d)ARTERIOLAR vasodilators .eg.sodium nitroprusside. Is used rarely.acts rapidly and hihghly potent. should only be used when able to measure bp directly. Can cause shock and hypotension . Caution with renal/liver impairment.
Outline the aetiology, diagnosis and management of FATE (Feline Aortic
Thromboembolism)
FATE (Feline Aortic Thromboembolism) is a feline acute emergency presentation that results
from a thrombus/blood clot blocking a peripheral artery – most commonly the aortic
trifurcation, but may also occur in the lungs, kidneys or brain. Usually (80%) due to underlying heart dz.
PATHOPHYSIOLOGY;Usually due to heart dz, plus predisposing factors (Virchow’s triad) alterations of endothelium, blood flow and coagulation. Due to this, clot forms (usually in left atria) then travels and lodges.May break into small emboli. Clots lead to release of vasomediators, causing vasoconstriction and altered tissue perfusion.
CLIN SIGNS;Pain - acute distress, vocalising
* Hypothermia, lack of peripheral pulse, firm painful muscles
* Signs of poor perfusion and shock
* Systolic murmur/gallop arrhythmia may be present (absence does not preclude cardiac disease)
* Will depend on the site of clot embolization, how long the blockage has been in place and if collateral circulation is present
* Areas affected include hindlimbs (most common), bilateral forelimbs, pulmonary vasculature, renal and cerebral arteries.
If terminal aorta involved (saddle thrombus):
- Sudden onset of hind limb paralysis, marked pain, loss of femoral pulses, pallor/cyanosis of foot pads/nail beds and cool extremity of affected limb/s
- Sciatic neuropathy with absent ‘deep pain’ reflex/withdrawal and normal
patellar reflexes
- Rectal tone and urinary bladder function maintained
- Increased firmness to cranial tibial and gastrocnemius muscles - within 10-
12 hours
If emboli blocking renal, pulmonary, mesenteric or cerebral
arteries/capillaries:
- Tachypnoea and pain, which differs from congestive heart failure which is
not painful
- Pulmonary crackles vs normal on thoracic auscultation
- Heart murmurs or gallop rhythms
- Vomiting, abdominal pain, or CNS signs
TX;Provide analgesia minimum 48 hours eg Morphine, =/- fentanyl, +/-buprenorphine.
Treat underlying CHF eg frusemide (remember cats very sensitive to so usually max of 2 doses in 1st 12 hours).O2 therapy. (other meds eg.enalapril atenolol etc are commenced AFTER cardiac diagnosis via cardiac u/s.
Antithrombotic tx aims to prevent extension of current thrombus and prevent new thrombus formation. It does not break down existing thrombus. eg Clopidogrel 18.75mg/cat q24hr. or eg aspirin 5mg/kg q72hr. or Dalteparin 100-200 IU/kg SC q12hrs.
Thrombolytic therapy to break down existing therapy eg streptokinase IS NOT RECOMMENDED.(HIGH DEATH RATE DUE TO REPERFUSION INJURY).
Expect 2-5 days in hosp. Monitor for reperfusion injury. Supportive care as indicated. Success is touch and go. Some recur, some never regain nerve fn, some have large necrotic areas.
Describe the commonly seen cardiac arrhythmias and tx
BRADYARRHYTHMIA(<70bpm)
1. Sinus bradycardia; associated with resp, due to high vagal tone. Rare in cats.Regularly irregular or normal regular. Normal ecg complexes. More pronounced with some drugs, hypothermia and maybe head injury. Atropine will normalise in 20-30min.
2. Atrial standstill-no p waves. Sometimes with muscular dystrophy, or may occur transiently with hyperkalaemia.TX for transient atrial standstill:Calcium gluconate 10% - 0.5- 1.5 mL/kg slow IV over 10 minutes
* Insulin (regular short acting) 0.25-0.5 U/kg IV ALWAYS with 2gm of dextrose per unit of insulin = 4ml of 50% dextrose OR 40ml of 5% dextrose for each unit of insulin FOLLOWED
with CRI of 1.25-2.5% glucose at maintenance rates for 6 -8 hours
* Treat the underlying cause
3. AV block
o First degree AV block – P waves are associated with QRS complex, but there is a prolonged PR interval
▪ This can be found in young, healthy dogs due to high vagal tone
▪ It is also noted in Cocker spaniels and Dachshunds with degenerative
conduction system disease
o Second degree AV block – some of the P waves being blocked, while others are conducted with associated QRS complex
o Third degree AV block – complete dissociation between the atria and ventricle
(the atrial rate is independent of a junctional or ventricular escape rhythm)
▪ The most common cause of advanced AV block in dogs is progressive
fibrosis/degeneration of the AV node, but other causes include inflammation or infection of the heart muscle or the aortic valve (myocarditis and endocarditis), physical disruption of the AV node
secondary to other cardiomyopathy (disease of the heart muscle including neoplastic infiltration), electrolyte abnormalities, and exposure to certain toxins or medications.
* First degree and some of second-degree AV block are vagal mediated – check with
Atropine test
o Atropine 0.04mg/kg SC
o Complete response in 20-30 minutes with resultant sinus tachycardia (heart rate
>160 bpm)
* Pacemaker is indicated for definitive therapy for severe second-degree AV block and
third-degree AV block
o Some might respond transiently to Theophylline
4. Sick sinus syndrome;
* In this condition, the SA node intermittently fails to send electrical impulses. Escape beat can be seen from other part of the conduction system.
* The majority has structural cardiac disease and certain breeds of dogs are overrepresented (e.g. Miniature Schnauzer, West highland white terriers, Cocker spaniels, Dachshund).
* This condition results in a variety of ECG abnormality including sinus bradycardia,
sinus arrest with no escape rhythm, AV block and paroxysmal episodes of supraventricular tachyarrhythmias.
* Medical treatment: Theophylline 10mg/kg PO q12h or Propantheline 0.25-0.5 mg/kg PO q8-12h.
* Pacemaker is required if medical management fails.
TACHYARRHYTHMIA
1.Sinus tachycardia;
* Often a compensatory response to various stressors, however it can be secondary to
primary cardiac disease
* Fast heart rate, normal complexes and tall P wave. There may be superimposition of
the T and P wave.
* Vagal manoeuvres (carotid sinus massage /gentle eyeball pressure) can slow but do not
normally break the rhythm.
* Rule out the following causes:
o Physiologic – exercise, pain, fear, excitement, anxiety
o Pathologic – fever, shock, hypoxia, anaemia, hypotension, infection/sepsis, hypovolaemia, neoplasia
* Treat the underlying cause.
2. Atrial fibrillation;
This is caused by multiple re-entrant circuits in the atria that can fire up to 500 to 600
bpm.
* More commonly associated with significant cardiac disease and atrial enlargement.
* Giant breed dog (e.g. Irish wolfhound) can develop atrial fibrillation without structural
heart disease
* Lack of P waves (or fibrillation waves on baseline) and irregularly irregular
supraventricular rhythm with or without tachycardiac (HR >160bpm)
* Treatment:
o Aim to slow the ventricular rate to 140-160bpm
o Digoxin 0.005-0.011mg/kg PO q12h – can cause cardiotoxicity. Not for cats.
o Diltiazem 1-2mg/kg PO q8h or Diltiazem CD 3-5mg/kg PO q12h
3.Ventricular tachycardia;
* Potentially life threatening arrythmias
* Can occur in patients with primary cardiac disease (arrhythmogenic right ventricular
cardiomyopathy in boxers or dilated cardiomyopathy)
* Can occur in patients with structurally normal heart
* Wide and bizarre QRS complexes unassociated with P waves in addition to
tachycardia (HR >180bpm)
* Treatment:
o Lignocaine 2mg/kg IV bolus; followed by 25-75mcg/kg/min CRI – toxic if
>8mg/kg IV in 1 hour. Not for cats.
o Mexiletine 4-8mg/kg PO q8h
o Sotalol 1-3mg/kg PO q12h
* Accelerated idioventricular rhythm – heart rate often <180bpm
o Seen in patients with systemic disease (GDV, pancreatitis, haemangiosarcoma)
rather than primary cardiac disease
o Anti-arrhythmic is required if HR >180bpm
4. Ventricular fibrillation;
* Erratic, patternless waves of electrical activity in all leads
* Must rule out poor ECG electrode contact artifact
* Patients are unconscious due to lack of adequate cardiac output and cerebral perfusion
– cardiopulmonary arrest is imminent
* Treatment:
o Lignocaine 2mg/kg IV bolus; followed by 25-75mcg/kg/min CRI – toxic if
>8mg/kg IV in 1 hour. Not for cats.
