Resuscitation Part 2 - Evaluation of Cardiovascular Status

See drug doses on the inside covers and Cardiopulmonary-Cerebral Resuscitation (CPCR) & Kit Suggestions.
In evaluating cardiovascular status, ask five questions:

1. Is the heart beating? If not, go directly to cardiac arrest protocol.
2. If the heart is beating, is the heart beating too slow, too fast or is there an arrhythmia present? If so, go directly to discussion of bradycardia, tachycardia, or arrhythmias.
3. If the heart is beating, is it mechanically effective (auscultable amplitude, palpable pulse quality, arterial blood pressure and its proper waveform). If not, go to discussion on shock (See Shock (SIRS)).
4. If the heart is beating, are the peripheral and visceral tissues being perfused? If there is evidence of peripheral vasoconstriction see Shock (SIRS) 
5. In the newborn is there a loud murmur and cyanosis suggesting a congenital heart defect? (See Congenital Cardiac Anomalies)

I. Cardiac Arrest

1. If the heart cannot be auscultated or palpated, if peripheral pulses cannot be palpated, and if there is an absence of breathing attempts, the foal should be considered to have a cardiac arrest.

1. Endotracheally intubate the foal and commence positive pressure ventilation at an airway pressure of 20-30 cm of HO (just enough to elevate rib cage) at a rate of 20 times per minute.
2. Commence external chest compression over the heart with a strong pressure at a rate of about 60-80 times per minute.

1. Compression technique must be continued without interruption.
2. Evaluate effectiveness of compression technique by the generation of a palpable pulse with each compression and an improvement in mucous membrane color. If compression technique is not effective, change technique and proceed with pharmaceutical intervention.

3. Insert an intravenous catheter and rapidly administer a bolus of fluids (lactated Ringer's): 20 ml/kg (about 1 liter for a 50 kg foal), and then reassess the cardiovascular status.
4. Administer epinephrine:

1. 0.01-0.02 ml/kg of 1:1000 dilution IV or intraosseally (0.5-1 ml/50 kg)
2. 0.1-0.2 ml/kg of 1:10,000 dilution intratracheally or IV (5-10 ml/50 kg)
3. Can be repeated every 2-5 minutes

5. Attach ECG electrodes and evaluate electrical activity of heart.

1. Flat line (asystole): Administer epinephrine.
2. Chaotic activity (ventricular fibrillation):
   Lidocaine (1-2 mg/kg)
   Amiodarone (5 mg/kg)
   Defibrillation
3. Normal activity (cardiovascular collapse): Administer a second bolus of replacement crystalloids (10-20 ml/kg).

6. Vasopressin (ADH)

1. Vasopressin indicated after 2-3 attempts of failed epinephrine administration.
2. Long half-life, use only once
3. Dose: 0.2-0.6 U/kg (10-30 U/foal)

7. Other drugs-limited indications

1. Parasympatholytics in bradyarrhythmias, bronchoconstriction

1. Atropine (0.01-0.02 mg/kg)
2. Glycopyrrolate (0.001-0.002 mg/kg)

2. Electrolytes 

1. Calcium (1-10 mg/kg) to improve cardiac contractility
2. Sodium-bicarbonate (1-2 mEq/kg) if severe acidosis present
3. Magnesium-sulfate (14-28 mg/kg) can be useful in cases of ventricular or junctional tachyarrhythmias

3. Glucose (3-5 mg/kg/min) if severe hypoglycemia (<50 mg/dl; <2.8 mmol/l) present.
4. Corticosteroids - Not useful in septic, anaphylactic shock, maybe in suspected adrenal insufficiency of prematurity

1. Prednisolone Na-succinate 1.3 mg/kg/d (see Chapter 12).

5. Class III antiarrythmic drugs if severe ventricular tachyarrhythmias unresponsive to lidocaine and magnesium sulfate

1. Amiodarone 5 mg/kg
2. Bretylium 5 mg/kg

2. If external compression technique is not judged to be effective try one of the following:

1. Change the compression technique:

1. Faster or slower.
2. Harder or softer.
3. Hold compression a little longer.
4. Place a sand bag under chest.

2. Administer IV:

1. Epinephrine 0.01 mg/kg (1:1000) about 1 ml for a 50 kg foal or
2. Norepinephrine 0.4 mg/kg or
3. Neosynephrine® 0.2 mg/kg (phenylephrine) and/or
4. A bolus dose of replacement crystalloids: 20 ml/kg of lactated Ringer's (about 1 liter for a 50 kg foal) and/ or a bolus of colloids at a dose of 2-10 ml/kg (about 100-500 ml for a 50 kg foal).

II. Bradycardia

1. If the heart is beating at a rate below 60 per minute, administer epinephrine 0.01-0.02 mg/kg. (0.5-1 ml/ 50 kg foal 1:1000)
   Editor's Comment - This presumes you are ventilating the foal. Providing oxygen and breaths may allow heart rate to increase.
2. If the heart rate remains below 60, administer dobutamine (5-10 ug/kg/min) by mixing 250 mg dobutamine to 500 ml D5W, 0.9% saline, or LRS (0.5 mg/ml). Administer via minidrip (60 drops/ml) at a rate of 6-60 drops/min (for a 50 kg foal) or with infusion pump at a rate of 6-60 ml/hour using this dilution).
3. If heart rate remains below 60 or MAP<60 mmHg, increase infusion rate gradually every 15 minutes.
4. If heart rate remains below 60 or MAP<60 mmHg after a near maximum dose of dobutamine CRI, start norepinephrine at a rate of 0.1 ug/kg/min up to 1.5 ug/kg/min gradually or vasopressin at a rate of 0.25-1.5 mU/kg/min.
5. Once stabilized, monitor vitals, urine output, blood gas parameters, blood pressure frequently (every 2-4 hours).

III. Tachycardia

1. Tachycardia is a response to an underlying stress and therapy is usually directed towards alleviating the underlying abnormality rather than the tachycardia, per se. Treat the hypovolemia, hypotension, hypoxia, hypercapnia, hyperthermia, or sympathomimetic therapy.

IV. Arrhythmias

Abnormal electrical activity is a well-known phenomenon immediately after birth. Arrhythmias should not be treated in the first few hours of life, unless they manifest in clinical signs (cyanosis, respiratory distress, pulmonary edema, fatigue).

1. Atrial fibrillation in newborn foals [1].

1. Irregular heart rate without pulse deficits.
2. Pale or cyanotic mucous membrane.
3. Detected at birth and lasting more than 3 hours.
4. Foals are depressed, unable to rise, respiratory distress.
5. May spontaneously disappear.
6. Treatment with 300 mg Procainamide IV [1].

2. Although there is a wide variety of arrhythmias which may manifest themselves, aside from sinus bradycardia and tachycardia, and atrioventricular conduction block (same causes and treatment as bradycardia), premature atrial (PAC) and ventricular (PVC) pacemaker activity and bundle branch blocks (BBB) [2] are the most common. In general, they should be considered to be a sign of an underlying disease process and should not be treated specifically. Premature ventricular contractions may progress in severity (frequency, multifocal) and predispose to ventricular tachycardia and fibrillation, and may at some point require specific therapy. The salient questions to answer from the electrocardiogram are:

1. Is the rate too slow or too fast?
2. Is the rhythm regular or irregular?
3. Is the PQRST waveform consistently present and/or approximately normal in size and shape?
4. Is there synchrony between the ECG and the palpated pulse? Are all of the pulses of equal quality?
   Pulse deficits may be caused by:

1. Premature atrial contractions.
2. Premature ventricular contractions.
3. Variable diastolic ventricular filling, especially with high heart rates.
4. Electromechanical dissociation (correct fluid and electrolyte abnormalities; calcium, magnesium and glucocorticosteroids may be beneficial).

5. Is there a P wave prior to each QRS or is the P-R interval shortened? Absence of a P wave differentiates VPCs from right BBB and right ventricular hypertrophy.
6. Is there a compensatory pause after the PQRST waveform in question? (Premature atrial and ventricular contractions are usually followed by a pause.)
7. Is the S-T segment in the isoelectric line? S-T segment depression is usually attributed to myocardial hypoxia or potassium or calcium abnormalities but may commonly occur with no other demonstrable cardiopulmonary problems.
8. Are the T waves abnormally large? (Normally less than 25% of the height of the R waves; be sure to measure the actual height since small R waves may make the T wave appear to be tall).

1. T waves may normally be a positive or a negative deflection or may be biphasic.
2. Abnormally tall-tented T waves may be due to hyperkalemia, hypoxia or atrial dilatation (excessive venous return) and tachycardia.

9. Is there any artifact or unexpected wave on ECG? Poor quality electrocardiograms will result if the electrode-patient contact has high impedance. Usually this is minimized by using an electrolyte gel such as commercial ECG paste, Phisohex® soap, ultrasound coupling gel or alcohol (which dries fast and is not recommended). Skin resistance can be reduced by defatting the skin with acetone and deepithelializing it by scrubbing.