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Cardiovascular monitoring under anesthesia (Proceedings)

Article

Cardiovascular monitoring of patients under anesthesia is necessary so that potentially harmful changes in the function of the cardiovascular system can be recognized and appropriate action can be taken.

Anesthesia can cause changes in the function of the cardiovascular system. Cardiovascular monitoring of patients under anesthesia is necessary so that potentially harmful changes in the function of the cardiovascular system can be recognized and appropriate action can be taken. The first step in successful monitoring is understanding how the cardiovascular system works. Methods of monitoring the cardiovascular system include use of an ECG to identify potential arrhythmias, determining heart rate and rhythm, measuring blood pressure and assessing volume status. Direct measurement of cardiac output in veterinary patients is rarely done except in research settings. It is invasive and requires the placement of a Swan-Ganz catheter that is passed from the jugular vein, through the right atrium into the pulmonary artery.

Anatomy and physiology of the heart

The heart is responsible for pumping blood around the body and consists of four chambers: the right atrium, the right ventricle, the left atrium and the left ventricle. Arteries are the vessels that carry blood from the heart and veins carry blood to the heart. Sodium, chloride, potassium and calcium are the electrolytes that are most important for normal cardiac function. Depolarization of the cell happens when sodium channels in the cell membrane open increasing sodium permeability. Resting membrane potential becomes less negative due to an influx of positive sodium ions. Cells begin repolarizing when the sodium gates close and negatively charged chloride ions begin to move into the cell. This causes calcium channels to open allowing an influx of these ions. Final repolarization happens when the calcium channels close and potassium permeability increases. Any alterations of normal plasma concentrations of these electrolytes can affect cardiac muscle function.

The sino-atrial node in the wall of the right atrium initiates the heartbeat. Impulses from this node transmit to the atrioventricular (AV) node. Other impulses in the heart are transmitted by the bundle of HIS, the bundle branches and the Purkinje fibers. Any damage to the cardiac muscle can result in unsynchronized impulse transmission, irregular heart contractions and reduced cardiac output. The sino-atrial (SA) node acts as an intrinsic pacemaker and controls the rate of contractions. Both parasympathetic and sympathetic nervous systems innervate the SA node. Acetylcholine and noradrenaline are nervous system mediators that affect sodium, calcium and potassium channels and can increase or decrease depolarization. Many drugs used for anesthesia purposes can affect heart rate and therefore monitoring is strongly indicated.

Cardiac cycle

The cardiac cycle is the complete series of events that happens in the heart during one heartbeat. Blood flows into the atria from the vena cava and pulmonary veins. The cycle starts with depolarization at the sinoatrial node leading to atrial contraction. The atrioventricular valves, called the mitral and tricuspid valves, open when atrial pressure exceeds ventricular pressure. While the atria contract, blood flows into the relaxed ventricles. This is diastole-when the ventricles are relaxed and filling. Next, the atria relax and the ventricles contract (systole) pushing blood out the aortic and pulmonary valves. Ventricular systole causes closure of the atrioventricular valves and this action is the first heart sound heard on auscultation. The second heart sound is generated when ventricular relaxation occurs and the pulmonic and aortic valves close.

Electrical activity

As the heart undergoes depolarization and repolarization, the electrical currents that are generated (as described above) spread not only within the heart, but also throughout the body. This electrical activity generated by the heart can be measured by electrodes placed on the body surface. The recorded tracing of this activity is called an electrocardiogram (ECG or EKG). The different waves that comprise the ECG represent the sequence of depolarization and repolarization of the atria and ventricles. The complete cardiac cycle that is portrayed on the ECG is represented by waves that are identified as P wave, QRS complex and T wave.

The P wave represents the wave of depolarization that spreads from the SA node throughout the atria. The brief isoelectric period after the P wave represents the time in which the impulse is traveling within the AV node and the bundle of HIS. The period of time from the onset of the P wave to the beginning of the QRS complex is termed the P-R interval. This represents the time between the onset of atrial depolarization and the onset of ventricular depolarization. If the interval is prolonged or no QRS complex follows, (the impulse is unable to be conducted to the ventricles) there is an AV conduction block (first, second or third degree AV block).

The QRS complex represents the ventricular depolarization. The duration of the QRS complex is normally of relatively short duration which indicates that ventricular depolarization occurs very rapidly. If the QRS complex is prolonged, conduction is impaired within the ventricles. This can occur with bundle branch blocks or whenever an abnormal pacemaker site becomes the pacemaker driving the ventricle. Changes in the height and width of the QRS complex can indicate left heart enlargement. The shape of the QRS complex can also change depending on placement of the electrodes. The isoelectric period (ST segment) following the QRS is the time at which the entire ventricle is depolarized. The ST segment is important in the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated.

The T wave represents ventricular repolarization and is longer in duration than depolarization. The Q-T interval represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. At high heart rates, ventricular action potentials shorten in duration, which increase the Q-T interval. Prolonged Q-T intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias.

Heart rate can be determined by examining an ECG rhythm strip. The ventricular rate can be determined by measuring the time intervals between the QRS complexes, which is done by looking at the R-R intervals. Assuming a recording speed of 25 mm/sec and a lead II ECG, one method is to divide 1500 by the number of small squares between two R waves. Or one can divide 300 by the number of large squares between waves. If the heart rate is irregular, it is important to determine a time averaged rate over a longer interval. Changes in heart rate can affect the function of the heart. Very fast heart rates can reduce cardiac output by not allowing the ventricles to fill adequately. Bradycardia can also affect cardiac output. Troubleshooting heart rate abnormalities should include identifying and correcting the underlying cause if possible. Treatment with fluid therapy and/or additional analgesics may be necessary for tachycardic patients. Lightening anesthetic depth and/or treatment with an anticholinergic may be necessary for bradycardic patients. Arrhythmias should be identified and their effect on cardiovascular function needs be determined before treatment therapies can be decided on.

Contractility is the intrinsic ability of cardiac muscle to develop force for a given muscle length. It is also referred to as inotropism.

Preload is the force acting on a muscle just before contraction and it is dependant of ventricular filling (or end diastolic volume.) Preload is related to right atrial pressure. The most important determining factor for preload is venous return. Hypovolemia, vasodilation and venous occlusion decrease preload.

Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure, afterload for the right ventricle is determined by pulmonary artery pressure.

What exactly is blood pressure?

Blood pressure is the driving force for blood flow (perfusion) through capillaries that supply oxygen to organs and tissue beds of the body. Blood pressure is needed to propel blood through high resistance vascular beds, including those of the brain, heart, lungs and kidneys. Blood pressure values are expressed in millimeters of mercury (mm Hg) and as three measurements: systolic, mean and diastolic. Remember that the systolic pressure is the pressure generated when the left ventricle is fully contracted. Diastolic pressure is the pressure measured when the left ventricle relaxes. Mean arterial pressure (MAP) is calculated as one third the systolic pressure plus two thirds the diastolic pressure. Mean blood pressure determines the average rate at which blood flows through the systemic vessels. It is closer to diastolic then systolic because, during each pressure cycle, the pressure usually remains at systolic levels for a shorter time than at diastolic levels. Most times, under anesthesia, a patient's mean pressure is what the anesthetist focuses on. A mean arterial pressure of at least 60 mm Hg (70 in horses) is needed to properly perfuse the heart, brain and kidneys. Mean arterial blood pressures consistently below 60 mm Hg can lead to renal failure, decreased hepatic metabolism of drugs, worsening of hypoxemia, delayed recovery from anesthesia, neuromuscular complications and central nervous system abnormalities, including blindness after anesthesia. Prolonged hypotension (> than 15-30 minutes) can lead to nephron damage. Although the effects may not be immediately apparent since 65-75% of nephrons need to be damaged before renal disease becomes clinically observable, the effects may play a role in the onset of renal disease later in a pet's life. Severe untreated hypotension can lead to cardiac and respiratory arrest. Hypertension, or excessively high blood pressure, can lead to problems as well. Ideally, any animal under anesthesia should have should have regular blood pressure monitoring because most anesthetic drugs affect blood pressure in some way.

Basic physiology of blood pressure

Mean arterial blood pressure = cardiac output (CO) x systemic vascular resistance (SVR). Cardiac output is defined as the amount of blood pumped by the heart in a unit period of time. CO = Heart rate (HR) x stroke volume (SV = contractility). Systemic vascular resistance is the amount of resistance to flow through the vessels. Some vessels may be dilated, and therefore allow more flow at less resistance. Constriction of vessels may limit blood flow and require more pressure to get blood through. It's important to know that many of the drugs we use for anesthesia affect one or more of these systems in some way.

Methods of measuring blood pressure

Pulse palpation: If no monitor is available, the manual palpation of an arterial pulse can give some indication of the state of the blood pressure. A palpable pulse pressure is the difference between the systolic and diastolic pressures. A difference of at least 30 mm Hg is necessary to palpate a strong pulse. Peripheral pulse palpation sites include the lingual, dorsal metatarsal, carpal, auricular and coccygeal. It is best to monitor the peripheral arteries because these pulses are lost at a much higher mean than the central (femoral) arteries. Potential cardiovascular abnormalities may be detected by regular palpation. Pulses should be assessed for strength, rate, and regularity and palpation should begin prior to induction so that differences in these can be tracked (monitor trends) from the very onset of anesthesia through recovery.

Capillary refill time

Blanching the mucous membranes with direct pressure should result in a refill time of less than 2 seconds. Delays in refill time can indicate intense vasoconstriction or hypotension.

Indirect blood pressure monitoring

Oscillometric devices work by picking up pulsation under an occlusion cuff placed over an artery. The cuff is connected to a monitor that can be programmed to measure blood pressure at specific intervals of time. These devices deliver systolic, mean and diastolic readings as well as the heart rate. Most have alarms that can be set to alert when readings are out of the accepted range. The cuff size should be approximately 40% of the circumference of the limb (or tail) around which it will be placed. Cuffs that are too large will lead to artificially low readings and too small a cuff will give false high readings. Ideally, cuffs should be placed on a limb that is close to heart level (the level of the right atrium is the zero mark for blood pressure). Limbs well above the heart may give artificially low readings. Legs hanging well below the heart will give false highs. The cuffs are usually marked with the proper placement over the artery. They must not be applied too tightly as this may occlude flow and cause inaccurate readings as well as swelling distal to the cuff. Poor pulse signals from poor flow (the rear limbs during a severe GDV or large abdominal mass), or any movement of the limb during a reading will interfere with the device and may cause it to fail or deliver an inaccurate reading. These devices do not usually work consistently or at all on very small patients, although there are some newer, veterinary specific monitors out that claim to work accurately on small dogs and cats.

Doppler ultrasonic flow detector

Doppler flow detectors involve the placement of an ultrasonic probe (crystal) over an artery. The frequency of the sound reflected from the moving arterial blood differs from that of the sound from the crystal and the shift in frequency is converted into an audible sound. Doppler probes may be placed over any artery, but the most useful for measuring blood pressure are the palmer arterial arches of the forelimb and hindlimb. The area should be shaved and a generous amount of ultrasonic or lubricating gel applied to the area or the crystal. The crystal is secured in place snugly (but not too tightly) with tape. A properly sized occlusion cuff is placed above the crystal. The cuff is inflated using a sphygmomanometer. The cuff is allowed to deflate slowly until the flow returns. The first audible sound heard is the systolic blood pressure. In some patients it may be possible to detect a second sound, this is said to be the diastolic pressure. There are some controversies over what the first audible sound heard in cats is. Some suggest that the first audible sound heard correlates most closely with MAP in feline patients. In the absence of a mean arterial pressure, systolic pressure should be maintained above 80-90 mm Hg. Doppler flow detectors are very useful monitors, with one of the biggest advantages to them being the audible sound of blood flow. Changes in flow can be heard as well as changes in the regularity of the pulse. These monitors have the advantage of being useful in all sizes of patients, from the tiny exotic species to large equine and zoo animals. Another advantage is that they are relatively inexpensive. Disadvantages of this method of blood pressure monitoring include inaccuracies at low pressures, systolic only readings and the importance of proper cuff size on accuracy.

Direct method

Direct blood pressure measuring is the gold standard for blood pressure measurements. It involves placing a catheter into an artery and attaching the catheter to a transducer. The transducer (placed at heart level) is connected to an oscilloscope that gives systolic, mean and diastolic readings continuously. In addition, most monitors also display a wave form that corresponds with the pulse. This provides important information about the patient and the blood pressure. The arterial wave form should match the ECG complexes. Catheters may be placed in any artery. The most common sites are the same as listed above, but the femoral and auricular arteries may also be used in some patients. The possible complications of arterial catheter placement should be considered when choosing a site. Hematomas, air embolism, thrombosis and infection are the most common, yet rare, complications. Sterile technique should be considered when placing these catheters to reduce complications. Arterial catheters should be clearly marked so that nothing but heparinized saline is ever injected into them. The catheter needs to be flushed at regular intervals with heparinized saline to prevent clotting. Drugs should never be given through an arterial catheter. Unfortunately, direct arterial blood pressure measuring technology can add $1,000 or more to the price of a monitor making cost a big factor when choosing blood pressure measuring components on a monitor.

If a transducer system is not available, blood pressure can be measured through the arterial catheter using the same method as for measuring central venous pressure. Centimeters of water pressure can be converted to millimeters of mercury by dividing the number by 1.36. This measurement will roughly give mean arterial pressure.

Volume status

Central venous pressure is the blood pressure within the intrathoracic portion of the caudal or cranial vena cava. It can be measured to gain information about intravascular blood volume and cardiac function. CVP correlates with the volume reaching the right atrium during diastole. A single measurement of CVP yields little information, but serial measurements are useful. Measuring CVP can be helpful in determining hypovolemia or fluid overload. Normal CVP should be 4-8 cm H2O.

Urine output can also be measured to determine volume status. Normal urine output should be 1-2 mls/kg/hr.

References

Muir, W.W. & Hubbell, J., (1995) Handbook of Veterinary Anesthesia. Mosby-Year Book, Inc., 236-257

Smith, Lesley, "Hypotension" in Veterinary Anesthesia and Pain Management Secrets, (Greene, Stephen, Ed.). Philadelphia: Hanley & Belfus, Inc., 2002, 135-140, 23

Clark, Louise. "Monitoring the Anaesthetised Patient" in Anaesthesia for Veterinary Nurses, (Welsh, Elizabeth, Ed.), Ames, Iowa: Blackwell Publishing, 2003. 227-233, 9

Forsyth, Sandra. "Monitoring the Anesthetized Patient" Veterinary Information Network, 2003, 25 Feb. 2007, http://www.vin.com/proceedings/Proceedings.plx?CID=WSAVA2003&PID=6680&0=Generic

Battaglia, Andrea, M., Small Animal Emergency and Critical Care. Ithaca, NY: W. B. Saunders Co., 2001

Abbott, Jonathan, A., Small Animal Cardiology Secrets. Philadelphia, PA: Hanley & Belfus, Inc., 2000

Lumb and Jones Veterinary Anesthesia and Analgesia. (Tranquilli, William, J., Thurmon, John, C., Grimm, Kurt, A., Ed.) Ames, Iowa: Blackwell Publishing, 2007.

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