The critically ill patient is often in a clinical environment and changing physiological. The selection and interpretation of the parameters to be monitored, are useful only when associated with clinical reasoning of the patient's condition, based on the elements of history, physical examination and other diagnostic aids. It is essential to understand that monitors are treatment and should never separate the clinical side of patient.
Hemodynamic monitoring of critically ill patients has four basic purposes:
Alert: According to the patient's condition and level of monitoring, it alerts the clinician to any deterioration in the civil action.
Continuous Assessment: Allows observe behavior and changes in a patient's particular condition.
Forecast: The observation of trends in the observed patterns in evolution, helps to establish prognosis
therapeutic Guide: facilitates the evaluation and correction of the therapeutic measures implemented.
monitoring includes both noninvasive and invasive techniques, ranging from manual measurement of blood pressure and pulse rate until the measurement of cardiac output (CO) and intracardiac pressures by catheterization. In this chapter we describe the indications, hemodynamic variables and their interpretation, methods of monitoring and its complications.
Clinical Manifestations
Signs and symptoms associated with hemodynamic compromise are obvious and often vary from cardiac dysfunction that is expressed with tachycardia, the onset of lung sounds, jugular engorged, murmurs, rub, gallop and peripheral edema, to the profound shock and cardiovascular collapse with altered mental status, diminished or absent pulse, pale skin, cold and clammy, arrhythmias, and hypotension. It is important to state that there is a group of patients who self-regulatory mechanisms maintain all vital parameters until advanced stages of shock. It is in this group where clinical suspicion plays a proactive role, which can make a clear difference in the evolution and prognosis.
Some Hemodynamic Monitoring Indications
patients should be monitored by their clinical condition developed low cardiac output states. The magnitude and intensity of monitoring will vary depending on the disease, their medical history and risk factors.
A. Low cardiac output states.
Hypovolemia, dehydration, bleeding, burns, trauma.
Shock: septic, cardiogenic, neurogenic, or anaphylactic distributive. Alterations
cardiac function, congestive heart failure, cardiomyopathy or myocardial infarction.
B. Patients at risk of developing low cardiac output.
Patients with cardio-pulmonary history will be undergoing major surgery.
coronary bypass surgery or heart surgery.
major abdominal surgery.
Non-invasive monitoring
pulse oximetry
For many regarded today as the fifth vital sign, continuous monitoring is a simple method that measures functional saturation oxyhemoglobin. Also measures heart rate and can be applied depending on the type of sensor on a finger, hand or foot and ear. Reading may be affected in states of poor peripheral perfusion and give erroneous readings. To avoid this, if the oximeter allows, it is noted that the curve given on the screen, take the classic arterial pressure curve. Moreover, we note that the heart rate of the digital record of the oximeter, heart rate corresponds to the observed in the ECG monitor. As the principle of pulse oximetry is the difference in light absorption between oxyhemoglobin and reduced hemoglobin, any substance that colors the blood as methylene blue can give erroneous results.
Automated Blood Pressure Record
automated recording devices, measuring systolic, diastolic and mean, the latter being the most accurate. The accuracy of registration is affected in states of poor perfusion and arrhythmias. Remember that as in the manual registration, the pressure cuff should be appropriate to the circumference of the patient's limb. Do not use limb-threatening ischemia, and where there AV fistulas. The proper grip can be placed on the forearm, leg and thigh.
Invasive monitoring
Hemodynamic Variables and Interpretation
A-Preload: is the load or volume distending the left ventricle before contraction or systole. The preload is determined by the volume of blood at the end of ventricular filling. Its measurement is performed with the Swan Ganz catheter and corresponds to the pressure of pulmonary artery occlusion. Central venous pressure and right atrial pressure express the return of blood to the right of heart.
Some conditions in which the preload is decreased are:
- Hypovolemia due to hemorrhage, dehydration, vomiting, diarrhea, excessive diuretics.
- Tachycardia usually greater than 120 per minute, decreased ventricular filling time.
- vasodilation with consequent reduction in venous return as seen in the states of hyperthermia and endothelial permeability, with decreased effective circulating volume, as in sepsis or anaphylaxis.
Conditions or states in which the preload is increased are:
- vasoconstriction by endogenous or exogenous sympathetic stimulation and hypothermia.
- overload, volume overload or oliguric renal failure.
- Congestive Heart Failure.
B-Afterload: is the resistance to ventricular ejection. On the right side is expressed as the pulmonary vascular resistance (PVR) and on the left side as the peripheral vascular resistance (SVR). The greater the afterload lower cardiac output, just as the higher right atrial pressure. Some conditions that reduce afterload are vasodilation from sepsis, hyperthermia, hypertension and vasodilator drugs. While there is increased when vasoconstriction, hypovolemia, hypothermia, hypertension, aortic stenosis among others.
C-systemic arterial resistance: is obtained calculating the mean arterial pressure (MAP), central venous pressure (CVP) and cardiac output (CO).
Blood pressure is an indirect reflection of the afterload. But as mentioned often non-invasive methods in the critically ill, can not accurately estimate the true blood pressure. Under conditions of intense vasoconstriction, the PA is often lower than that obtained by invasive methods.
is important to note that the afterload is not fully estimated by the Vascular Resistance either pulmonary or systemic. The resistance is also influenced by the viscosity of blood and valvular resistance.
D-Debit or cardiac output is the product of heart rate (HR) and systolic ejection volume (VS) in liters per minute.
DC = FC x VS
Unless there is an intracardiac shunt, the left and right cardiac output is basically the same. To measure the debit is necessary to insert a Swan Ganz catheter (see below) The decision to measure the DC is given by the suspicion of a deficit in tissue oxygenation alterations in cardiac function. It is important to remember that DC changes are often a symptom of the problem rather than the problem itself.
Conditions that decrease cardiac output:
- Mal fill ventricular hypovolemia.
- Mal emptying alterations in ventricular contractility or valvular disease (tricuspid or aortic)
- Increase SVR for hypertension, vasoconstriction, mitral regurgitation, septal defects among others.
- conditions that increase cardiac output.
- increased oxygen demand such as exercise.
- Liver disease and thyrotoxicosis.
- Mbarazo.
- pain, fear, anxiety. (Eye)
- Response to early systemic inflammation with a decrease in SVR.
- Mal emptying alterations in ventricular contractility or valvular disease (tricuspid or aortic)
- Increase SVR for hypertension, vasoconstriction, mitral regurgitation, septal defects among others.
- conditions that increase cardiac output.
- increased oxygen demand such as exercise.
- Liver disease and thyrotoxicosis.
- Mbarazo.
- pain, fear, anxiety. (Eye)
- Response to early systemic inflammation with a decrease in SVR.
E-systolic ejection volume (VS) (Stroke Volume) and Index Systolic Ejection (IS): corresponds to the volume of blood ejected with each heartbeat. In a dysfunctional heart first in fall is the stroke volume or stroke index (SI) or (Stroke Index). Initially can be maintained within normal parameters or unchanged by compensatory mechanisms. It is one of the most important parameters in monitoring invasive.
Factors determining systolic ejection volume (remember that any factor affecting stroke volume Cardiac amended).
1. Preload.
2. Afterload.
3. Contractility.
F - Contractility: not more than the ability of the heart muscle to contract. The more muscle fibers lengthen the greater the force of contraction and blood volume ejected (Ley de Frank - Starling). As is evident there is a direct relation between contractility and cardiac output. Contractility is increased by sympathetic stimulation or endogenous catecholamines exogenous dobutamine, adrenaline and dopamine. At the same time is decreased in diseases affecting the heart muscle, hypoxia, acidosis and action of drugs with negative inotropic effect. Contractility can not be measured but inferred from the volume or stroke index.
Direct Blood Pressure (blood line)
The installation of an arterial line is indicated as mentioned in states where invasive monitoring is inaccurate. Also meets the goal of continuous monitoring and allows for repeated arterial blood samples without resorting to multiple punctures. According to some authors an arterial line should be installed in any patient who is going to analyze arterial blood gases> 4 times in 24 hours, reducing the risk of complications. The arteries of choice are the radial, axillary or femoral. Some authors promote the election of central arteries such as the axillary and femoral some circulatory conditions of intense vasoconstriction. This is due to the severe constriction of the muscular arteries generate up to 50 mmHg gradient between radial artery and the axillary and femoral arteries. Among the complications with the installation of LA described hematomas, arterial thrombosis, distal ischemia, arterial pseudoaneurysm, AV fistula and infection. Most of these complications can be obviated with the selection of a punctured artery, proper technique and subsequent management of nursing. Cardiac output is directly proportional to the area under the curve of pressure. Negative oscillations of the curve, particularly in patients ventilated with positive pressure are a good indicator of intravascular volume deficit.
Central venous pressure in patients with suspected volume loss CVP monitoring is a useful guide to volume replacement. The PVC by itself is not an indicator of hypovolemia and may be normal or even elevated in patients with poor left ventricular function. The PVC therefore does not reflect the current volume, but rather indicates the relationship between the volume entering the heart and the effectiveness with which the ejecta it. While measurement alone can not have any value, serial measurements in patients with good left ventricular function can guide fluid replacement. Diagnostic utility in clinical situations such as tension pneumothorax and cardiac tamponade Kussmaul's sign is most evident in the records of the curve.
placement of central venous catheters not only complies with built-in monitoring (central venous pressure) if it also allows us depending on the diameter and length of it, provide volume, administer drugs by either irritant osmolarity or pH, parenteral nutrition, hemodialysis, or the insertion of catheters for its lumen as the Swan Ganz catheter or pacemaker endocavitary. The routes of choice are the internal and external jugular, sub-clavicular approach of the subclavian and femoral veins. The catheter tip should be housed in the superior vena cava, confirming its position by CXR. Among the complications that can occur is the arterial puncture and hematoma formation in the case of the neck can cause airway obstruction. Training of hematomas by tearing of the subclavian vein or artery puncture, obviously are not compressible, forming extrapleural hematomas visible on chest radiograph control. Pneumothorax is the most frequent complication even in experienced hands and is only produced in the internal jugular and subclavian puncture. The collision left internal jugular and subclavian can injure the thoracic duct resulting in a chylothorax. Finally catheter infection is common when not respected sterile technique.
Swan Ganz Catheter
As mentioned, the Swan Ganz catheter allows us to analyze the hemodynamic profile a patient and characterize the etiology of hypotension and / or hypoperfusion. This must be inserted by a doctor who knows both the technique, complications and the interpretation of parameters derived from the installation.
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