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Cardiac emergencies

Sinus bradycardia regular P-QRS-T complexes are present on the ECG at the
heart rate of < 60 beats/min in dogs and <149 beats/min in cats.
Causes include increased vagal tone (gastrointestinal disease, respiratory tract
disease), hypothermia, medications (digoxin, beta blockers, calcium channel
blockers).
Atropine 0.04 mg/kg IV or 0.08 mg/kg intratracheal
Glycopyrrolate 0.005-0.01 mg/kg IV
Epinephrine 0.2 mg/kg IV for sinus bradycardia during cardiopulmonary arrest
Dopamine infusion 5-20 g/kg/min IV for sinus bradycardia detected when not
in cardiopulmonary arrest

1500:43=35

Sinus tachycardia regular P-QRS-T complexes are present on the ECG at the
rate of >160 beats/min in large breed dogs, >180 beats/min in small breed dogs,
and >240 beats/min in cats.
Causes include hypoxia, hypovolemia, hypotension, fever, fear, pain,
excitement,
and
some
drugs
(anticholinergics,
antihistamines,
sympathomimetics) .
Supportive and symptomatic treatment. Treatment of underlying disease.
Oxygen supplementation
Improved ventilation
Intravenous fluid therapy.
Analgesic, sedatives as indicated by the underlying etiology
Vagal maneuvers.

3000:12=250

Supraventricular tachycardia - repetitive supraventricular premature depolarizations that originate


from a site other than the sinus node, such as the atrial myocardium or atrioventricular nodal tissue.

Heart rate rapid, 150 to 350 beats per minute in dogs. The lower rate of SVT depends on the size of
the patient. Smaller dogs typically have higher sinus nodal rates than larger dogs.

Rhythm usually very regular (R - R interval is constant) and may be sustained, but there can be frequent
or infrequent short runs of SVT, so - called paroxysmal SVT.

Usually the QRS complexes are typical of normal sinus complexes, narrow with a normal mean
electrical axis.

P waves typically differ in configuration from the sinus P waves. P waves may be buried in the previous
T wave and therefore not visualized.

SVT may be primary (idiopathic) or secondary to other cardiac disease, generally those creating atrial
enlargement. May result from a reentrant mechanism or from abnormal automaticity in an ectopic focus.

3000:10=300

50 mm/s

Beta blockers

Calcium channel blockers: verapamil (0.05


mg/kg boluses IV over 3 5 minutes up to
three times) or diltiazem (0.05 0.25 mg/kg
IV over 5 15 min)

3000:20=150

50 mm/s

Ventricular tachycardia the QRS complexes have wide and bizarre pattern that is consisted for ventricular origin.

Causes include hypoxia, ischemia, CNS disease, splenic tumors, gastric dilatation and volvulus, pancreatitis,
electrolyte and acid base disturbances, valvular disease, myocarditis, cardiomyopathy and cardiac neoplasia.

After therapy

Lidocaine is indicated 2 mg/kg IV bolus or 4 mg/kg intratracheal, repeated until the


arrhythmia responds or until signs of toxicosis occurs (vomiting or seizures) or until a
maximal IV dose of 6 mg/kg is administered.

After the arrhythmia has responded, a continuous intravenous infusion of lidocaine may be
used 40-80 g/kg/min for continued control. To make a 1 mg/ml concentration, add 50 ml
of 2 % lidocaine to 1 l of fluids.

Calcium channel blockers, beta blockers, potassium channel blockers

Cats require a reduced dose of lidocaine 0.2 mg/kg IV bolus and a maximum dose of 0.5
mg/kg IV. As an alternative, use propranolol, 0.01-0.03 mg/kg IV.

Ventricular fibrillation a complete lack of unrecognizable P waves and QRS complexes.

This rhythm shows a complete disorganization of normal heart electric activity.

If available, immediate defibrillating shock is the treatment of choice. The initial setting for
external defibrillation should be:

2 J/kg for animals under 7 kg bw


5 J/kg for animals weighing 8-40 kg
5-10 J/kg for animals weighing over 40 kg.

A second dose at the same settings must be administered if the first discharge is ineffective
Increase the dose by 1.5 times for a third dose if the second discharge is ineffective.

The initial setting for internal defibrillation is 0.2 J/kg with a maximum of 50 J.
Chemical defibrillation:
Bretylium tosylate 5-10 mg/kg IV
Potassium chloride 1 mEq/kg IV and acetylcholine 6 mg/kg IV
Lidocaine is currently controversial so, should be avoided.

Electromechanical dissociation little or no myocardial contractile activity with a normal heart rate on the ECG.
There is a lack of heart sounds on cardiac auscultation and a lack of palpable arterial pulses but P waves and/or
QRS complexes are present on the ECG.
Causes include hypovolemia, severe metabolic disease, severe cardiac disease, cardiac tamponade, severe pleural
effusion.
Treatment is controversial:
Epinephrine 0.2 mg/kg IV
Dexamethasone sodium phosphate 4 mg/kg IV
Correct abnormalities in circulation, oxygenation, ventilation and blood volume. Treat the underlying etiology.

Atrial standstill this occurs due to a failure of atrial muscle depolarization. SA node
discharges and stimulus is transmitted to ventricles by intermodal pathways.
Atrial standstill is related to hyperkalemia (Addisons disease, urethral obstruction, diabetic
ketoacidosis, and severe muscle damage).

P waves absent
Heart rate usually slow ( < 60 beats per minute)
Rhythm regular/iregular with supraventricular type QRS complexes
Heart rate does not increase with atropine administration.

Treat the underlying cause (e.g., oliguric renal failure, hypoadrenocorticism).

Aggressive fluid therapy with 0.9% saline and possibly sodium bicarbonate or insulin with
dextrose as will be discussed

Can administer sodium bicarbonate to patients with severe hyperkalemia to induce


translocation of potassium into cells; if blood pH and base deficit cannot be determined,
administer 1 to 2 mEq/kg slowly IV. Administer half of dose and reevaluate.

Can administer dextrose and regular insulin to patients with severe hyperkalemia to induce
translocation of potassium into cells (regular insulin, 0.5 U/kg IV with 50% dextrose, 1 g/kg IV);
dextrose can also be used without insulin; follow insulin and dextrose administration with 2.5%
dextrose as a CRI to prevent hypoglycemia.

For patients with life - threatening hyperkalemia, administer calcium gluconate 10% (0.5 1
ml/kg slowly IV over 10 minutes) while monitoring the ECG; calcium antagonizes
the effect of potassium

Asystole complete absence of QRS complexes, resulting in the flat line ECG.
Causes include end-stage cardiac or pulmonary disease, severe multisystemic disease, and increased vagal tone
(ocular surgery, dilation of the urinary bladder or stomach, oropharyngeal stimulation).

In patients with severe systemic disease, administer 1:1000 epinephrine 0.05-0.2 mg/kg IV, 0.1-0.4 mg/kg
intratracheal (diluted with 3-10 ml sterile water)

If asystole occurs in a previously healthy patient as a result of vagal stimulation, administer atropine 0.04 mg/kg
IV.

Pulmonary edema cardiogenic


Cardiogenic pulmonary edema is the accumulation of fluid in
the pulmonary interstitial space and alveoli subsequent to left sided cardiac dysfunction and elevations in pulmonary
venous and pulmonary capillary pressures.
.
Cardiogenic pulmonary edema impairs gas exchange and lung
mechanics and may ultimately lead to death.
Severe dyspnea, foam around nostrils, tachypnea, labored breath
with opened mouth.

Common congenital lesions that contribute to the development of pulmonary edema include:
left - to - right shunting PDA, left - to - right shunting ventricular septal defect, mitral valve dysplasia,
subaortic stenosis

Common acquired conditions that contribute to the development of pulmonary edema include:

chronic degenerative mitral valve disease (dogs), dilated cardiomyopathy (dogs), hypertrophic
cardiomyopathy (cats).

Therapy
Supplemental oxygen is readily administered to compromised animals by providing an
oxygen - enriched environment (i.e., oxygen cage) or via nasal insufflation.

Furosemide 2 to 4 mg/kg IV (dogs) and 1 to 2 mg/kg IV (cats). These large doses may need
to be repeated (initially every 1 to 2 hours) until the respiratory rate and dyspnea start to
decline (<30-35 /min). Once stable the dose should be reduced to 0.5 to 2 mg/kg every 8 to
12 hours, as dictated by clinical status.

Pimobendan 0.25 mg/kg PO twice a day

Long - term management of animals with a history of cardiogenic pulmonary edema often
includes diuretics, angiotensin - converting enzyme inhibitors, positive inotropes, blockers, calcium channel blockers, anti - arrhythmics, or other drug classes as dictated
by the underlying disease.

Pericardiocentesis
Pericardiocentesis is a relatively safe procedure when performed carefully
Depending on the clinical status and temperament of the animal, sedation may be helpful

ECG monitoring is recommended during the procedure. Needle or catheter contact with the
heart commonly induces ventricular arrhythmias.

Although cardiac tamponade is uncommonly caused by coagulopathy, verifying that


coagulation parameters are normal is helpful, if patient status allows time for this

Low QRS amplitude


Electric alternans

is performed from the right side of the chest. This minimizes the risk of
trauma to the lung and major coronary vessels, most of which are located
on the left
sometimes sternal recumbency is used if the dog is cooperative
alternatively, other option is represented by an elevated echocardiography
table with a large cut-out; the animal is placed in right lateral recumbency
and the tap is performed from underneath
sometimes pericardiocentesis can be performed successfully on the
standing animal, but the risk of injury is increased if the patient moves
suddenly

Over the needle catheter

Butterfly needle

Three way clock stop

Pericardiocentesis Procedure
The skin is shaved and surgically prepared over the
right precordium, from about the third to seventh
intercostal spaces and from sternum to
costochondral junction or higher
Sterile gloves and aseptic technique should be used.

If echo machines is available the puncture site is


found where fluid width is largest.

If echo machines is not available, the puncture site


is identified by palpating for the cardiac impulse
(usually between the fourth and sixth ribs just
lateral to the sternum); the optimal site must be
estimated if no precordial impulse is felt.

local anesthesia is recommended and is essential


with use of a larger catheter. Two percent
lidocaine is infiltrated (with sterile technique) at
the skin puncture site underlying intercostal
muscle and into the pleura
A small stab incision is made in the skin when
using a larger catheter system.
The puncture site should be just cranial to a rib
to avoid the intercostal vessels located caudal
to each rib.
Once the needle has penetrated the skin, an
assistant should apply gentle negative pressure to
the attached syringe (with three-way stopcock
and extension tubing) as the operator slowly
advances the needle toward the heart
In this way, any fluid will be detected as soon as
it is encountered.
It is helpful to aim the needle tip toward the
patient's opposite shoulder.

the needle is advanced with gentle pressure through the


pericardium

a loss of resistance may be noted with needle penetration, and


pericardial fluid (usually dark red) will appear in the tubing

after the catheter is advanced into the pericardial space and the
stylet removed the extension tubing is attached to the catheter.

initial pericardial fluid samples are saved in sterile EDTA and clot
tubes for evaluation; then as much fluid as possible is drained.

A scratching or tapping sensation usually is felt if the needle or catheter contacts the heart;
also, the device may move with the heartbeat, and ventricular premature complexes are
often provoked.

If this occurs the needle and catheter should be retracted slightly to avoid cardiac trauma.
If it is unclear whether pericardial fluid or intracardiac blood (from cardiac
penetration) is being aspirated, a few drops can be placed on the table or into a clot tube
and a sample spun in a hematocrit tube.
Pericardial fluid does not clot (unless associated with very recent hemorrhage).
The packed cell volume is usually lower than that of peripheral blood, and the supernatant
appears yellow-tinged (xanthochromic).
Furthermore, as pericardial fluid is drained, the patient's ECG complexes usually increase
in amplitude, tachycardia diminishes, and the animal often breathes more deeply and
appears more comfortable.

Complications of Pericardiocentesis
Ventricular premature beats occur commonly from direct myocardial injury or
puncture. These are usually selflimited, resolving when the needle is withdrawn.

Coronary artery laceration with myocardial infarction or further bleeding into


the pericardial space can occur but is uncommon, especially when
pericardiocentesis is done from the right side.

Lung laceration causing pneumothorax or hemorrhage or both is also a potential


complication during the procedure.
In some cases, dissemination of infection or neoplastic cells into the pleural
space may result.

Arterial thromboembolism

ATE is most commonly associated with myocardial disease in cats, including hypertrophic,
restrictive, and dilated cardiomyopathy
exact etiology of ATE has not been determined, it is theorized that abnormal blood flow (stasis)
and a hypercoagulable state contribute to the formation of the thrombus within the left atrium.

the blood clot is then embolized distally to the aorta

the most common site of embolization is the caudal aortic trifurcation causing ischemic injury
to both hind legs.

other less common sites include the front leg, kidneys, gastrointestinal tract, or cerebrum.
the exact prevalence of ATE is not known in the general population of cats.
in one study of cats with hypertrophic cardiomyopathy, approximately 17 percent presented with
signs of ATE
although clear risk factors have not been defined, it is theorized that an enlarged left atrium or
spontaneous echo contrast of the red blood cells or smoke observed on an echocardiographic
examination may be risk factors.

Clinical features
acute onset of paralysis/paresis and pain are the most common
owner complaints
typically both rear legs are affected equally but occasionally one
leg is worse than the other.
less commonly, monoparesis of a front leg; pain upon palpation
of the affected legs; absent or diminished femoral pulses

cyanotic or pale nail beds and footpads

affected limbs will be cooler than unaffected limbs upon


palpation.

Diagnostics
the diagnosis of ATE is made by physical exam alone.
Thoracic Radiography
Cardiomegaly is common and radiographic signs of congestive heart failure (i.e., pulmonary edema and/or
pleural effusion) is seen in approximately 50 66 percent of cats. The presence of a pulmonary mass in the
absence of heart disease in a cat with ATE is concerning for pulmonary carcinoma associated embolus.
Echocardiography
The majority of cats will have hypertrophic cardiomyopathy characterized by left ventricular hypertrophy, nondilated left
ventricular lumen, and enlarged left atrium.
Abdominal Ultrasonography
An experienced sonographer may be able to identify the thrombus in the caudal aorta.

The main objectives of treatment are:

First, immediate treatment of the pain associated with ischemic injury of the
legs, typically with injectable opioids.

Treatment directed at resolving the actual thrombus with anticoagulants or


possibly thrombolytic agents.

Treatment of the cats heart disease and possible congestive heart failure.

Pain Management
intravenous opioid administration is preferred because of its rapid onset of action,
bioavailability, and safety profile
bupremorphine at 0.005 to 0.01 mg/kg IV every 6 to 8 hours as needed is an initial
good choice. Buprenorphine can also be given SQ if intravenous access is not obtained.
hydromorphone (0.025 0.1 mg/kg IV or SQ every 4 6 hours)
hutorphanol (0.05 0.3 mg/kg IV or SQ every 2 6 hours as needed) has fewer
analgesic effects than buprenorphine but is a good sedative

Antithrombotic Management
thrombolytic therapy with drugs such as streptokinase and tissue plasminogen activator is
used extensively in human and infrequently in cats
these drugs are expensive, carry a significant risk for bleeding complications,

unfractionated heparin is the preferred drug in most clinical practices


heparin actually has no effect on the established clot; however, it prevents further activation of the
coagulation cascade and allows the bodys endogenous fibrinolytic system to break down the clot.

the initial dose typically is given IV then followed with subcutaneous administrations every 6 to 8
hours
the initial intravenous dose is 100 to 200 units/kg and the subsequent subcutaneous dose is 200 to
300 units/kg

in addition to heparin, the concurrent use of an antiplatelet agent is also advised.


the two antiplatelet options are aspirin (5 81 mg PO every 3 days) or clopidogrel
18.75 mg (1/4 of a 75 - mg tablet) PO every 24 hours)
the higher dose of aspirin may be associated with more gastrointestinal adverse
effects. The theoretical benefit of clopidogrel is less gastrointestinal adverse effects
and possible enhanced efficacy.
once signs of clinical improvement are seen, heparin therapy is gradually weaned over
1 to 2 days and long - term therapy is continued.

Long term therapy


Commonly used long - term anticoagulant therapies include aspirin, clopidogrel, or a
low molecular weight heparin
aspirin (5 to 81 mg every 3 days) is the least expensive option and is dosed every 3 days
but carries a higher risk of gastrointestinal and renal adverse effects.
clopidogrel (18.75 mg every 24 hours) is moderately expensive and is dosed daily but
may have enhanced long - term efficacy
Low molecular weight heparins have also been used in the long - term management of
cats surviving an ATE.
Dalteparin (100 200 unit/kg SQ every 12 24 hours) or enoxaparin (1.5 mg/kg SQ
every 12 24 hours) are two commonly used low molecular weight heparins.

Possible Complications

Death is unfortunately a common outcome either due to progression of


disease or complication of therapy.

Bleeding complications may arise with the anticoagulant therapy.

Permanent neurological deficits or muscular abnormalities in the hind


limbs may arise in some cats ( 15 percent) with severe and prolonged
ischemia.

If a cat survives initial episode of ATE, recurrence of ATE and congestive


heart failure is common.

Expected Course and Prognosis

Both short - term and long - term prognosis are generally poor. Most cats ( >50 percent)
are euthanized or die during their initial ATE event regardless of therapy utilized.

Admitting rectal temperature of >37 C, fast heart rate, only one limb affected and
presence of motor function are all associated with better short - term prognosis.

Concurrent congestive heart failure is associated with a worse long - term prognosis. In
one study, cats with concurrent congestive heart failure had a median survival time of 77
days verus those without congestive heart failure of 233 days.

Refractory congestive heart failure or recurrence of ATE is typical terminal issues if a cat
survives an initial ATE event.

Expected course of recovery is generally days but can be weeks for return of function to
the legs.

Most cats that survive an initial episode will recover completely but approximately 15
percent of cats may suffer permanent neuromuscular deficits or ischemic injuries such as
loss of digits or tip of tail.