Static hemodynamic monitoring variables
The usefulness of each variable as a single absolute value is questionable. Some individual hemodynamic values are primarily useful as threshold monitors. For example, since a primary determinant of organ perfusion is perfusion pressure, systemic hypotension below a certain threshold is clinically relevant. In addition, elevation in central venous pressure (CVP; i.e. > 10 mmHg) reflects right ventricular (RV) pressure overload, although this does not provide information on the exact etiology. Other hemodynamic values can only be interpreted relative to metabolic demand. For example, because blood flow varies to meet metabolic demands, which in turn can vary significantly, there is no specific level of cardiac output or oxygen delivery that can be defined as "normal." These characteristics of blood flow reflect either its ability or inability to meet the body's metabolic demands.
Arterial blood pressure is not a single pressure, but a series of systolic and diastolic pressure values. Mean arterial pressure corresponds best to organ perfusion pressure in non-cardiac tissues as long as venous or ambient pressure is not increased.
Because blood pressure is a regulated variable, normal blood pressure does not necessarily reflect hemodynamic stability. Organ systems also tend to self-regulate their blood flow, such that organ-specific blood flow remains constant over a wide range of blood pressure values when metabolic rate is unchanged, and varies with changes in local metabolic rate. Thus, there is no blood pressure threshold that defines adequate organ perfusion between organs, between patients, or within the same patient over time. However, since arterial pressure is a primary determinant of organ perfusion, hypotension (mean arterial pressure < 65 mmHg) is always pathological.
Pressure = Resistance x Flow: R x F or MAP = SVR x CO
Central venous pressure:
CVP is the back pressure to the systemic venous return. Normal is 0-8 and CVP is only increased with illness.
>1 mmHg decrease in CVP (or IVC diameter) during spontaneous inspiration suggests fluid reactivity.
Cardiac output (CO) is defined as the amount of blood ejected from the ventricles in one minute (in litres/minute). The normal cardiac output is between 4-8 l/min. However, there is no such thing as an absolutely normal cardiac output, only sufficient or insufficient.
Cardiac Output (CO) is calculated by multiplying Heart Rate (HR) by Stroke Volume (SV).
CO = HF X SV
The cardiac index (CI) is the cardiac output adjusted to the body surface area. The normal value for this is between 2.5 and 4.2 liters per minute and square meter of body surface. If the CI drops below 1.8 L/min/m2, the patient may be in cardiogenic shock.
Stroke volume (SV) is the amount of blood ejected from the left ventricle with each contraction of the ventricle. Stroke volume is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV). The normal stroke volume is between 60 and 120 ml/stroke.
When stroke volume is expressed as a percentage of end-diastolic volume, it is called ejection fraction (EF). A normal left ventricular EF is about 55-70%.
Arterial blood oxygen content:
Hemoglobin carries 97% of the oxygen and 2% is dissolved in plasma. Oxygen bound to hemoglobin and oxygen dissolved in plasma are collectively referred to as arterial oxygen content or CaO2 = (Hb x 1.34 x SaO2) + (0.003 x PaO2). Hemoglobin can carry 1.34 ml of oxygen per gram of hemoglobin.
The oxyhemoglobin dissociation curve shows the relationship between the oxygen saturation of hemoglobin and the oxygen partial pressure and how it delivers oxygen to the tissues or how it retains oxygen on the hemoglobin.
Because of the higher partial pressure of oxygen in saturated hemoglobin, oxygen can diffuse from the hemoglobin to the lower partial pressure of oxygen in the tissues.
Under normal circumstances, a PO2 of 50 mmHg saturates about 82% of hemoglobin. However, there are certain conditions that cause the curve to shift to the left, allowing for a hemoglobin saturation of 82% at a PO 2 of only 42 mmHg. This shift to the left (Bohr effect) increases oxygen's affinity for hemoglobin, but makes oxygen delivery to tissues more difficult, and is caused by increases in pH, hypothermia, and low 2,3-DPGs. 2,3-DPG or 2,3-diphosphoglycerate is an organophosphate that affects the affinity of oxygen for hemoglobin. A shift to the right decreases the affinity of oxygen for hemoglobin but facilitates the release of oxygen to tissues. This is caused by high 2,3-DPG, hyperthermia, and low pH. Therefore, in acidosis such as lactic acidosis, there is a decreased affinity of oxygen for hemoglobin and increased oxygen delivery to tissues.
Oxygen delivery: cardiac output x oxygen content. Its components are
Oxygen content: CaO2 = (SO2 x 1.36 x Hb ) + (0.0031 x PO2 )
Arterial oxygenation: CaO2 x CO x 10 = 20.1% by volume x 5 x 10 = 1005 ml/min
Venous oxygenation: CvO2 x CO x 10 = 15.5 vol% x 5 x 10 = 775 mL/min
Oxygen consumption can be measured by subtracting the volume of O 2 (arterial oxygen content) leaving the heart from the volume of O 2 (venous oxygen content) returning to the heart. Normal range 200 – 250 ml/min 25%. However, during a stress response, tissues are able to extract 80% of the oxygen.
Although SvO2 above 70% does not necessarily reflect adequate tissue oxygenation, persistently low SvO2 (>30%) is associated with tissue ischemia. A low SVO2 can indicate that either O 2 extraction is increased or O 2 delivery is decreased. This can be caused by anemia, decreased cardiac output, low arterial oxygen saturation, or increased oxygen consumption. Treatment of low SVO2 may include increasing cardiac output by increasing heart rate, optimizing preload, modulating afterload, increasing SaO2, giving positive inotropes, or improving oxygen-carrying capacity with blood transfusion. It is more difficult to lower the O 2 requirement. Sedatives and neuromuscular blockers can help decrease muscle activity and prevent tremors.
Mixed venous saturation and central venous oxygenation
Under normal circumstances, the body uses 25% of the oxygen supplied, resulting in a 75% return to the right side of the heart. Therefore, normal SVO 2 levels are between 60% and 80%, indicating a balance between DO 2 and VO 2 .
Low SVO2 may indicate a decrease in cardiac output (hypovolemia, myocardial infarction, increased intrathoracic pressure), oxygen saturation (pulmonary edema, ARDS, low FiO2), hemoglobin levels (anemia, hemorrhage, dysfunctional hemoglobin), or an increase in oxygen consumption (pain, anxiety , restlessness, tachycardia, chills, hyperthermia, burns).
It is the volume of blood that is pumped out of the heart with each heartbeat. When stroke volume decreases, the body compensates by increasing heart rate to maintain cardiac output. Pulse pressure is a poor man's stroke volume.
Stroke volume is affected by three factors: preload, afterload, and contractility.
subpoena: Preload is defined as the amount of stretch in the cardiac myofibril at the end of diastole. The amount of stretch is directly affected by the amount of fluid volume in the ventricle, therefore preload is directly related to fluid volume.
Preload is determined by the volume of blood filling the ventricle at the end of diastole. Essentially, the larger the fill volume, the greater the stretch in the myocardial muscle fibers. The more the myocardial muscle fibers are stretched, the greater the force of the myocardial contraction and possibly the greater the stroke volume, up to a physiological limit. As preload (fluid volume) increases, cardiac output also increases until cardiac output levels off. If additional fluid is added after this point, cardiac output begins to fall. (Frank-Starling mechanism).
How is preload measured? There is no practical method of measuring myofibril stretch in living subjects, nor is there a method of measuring ventricular end-diastolic volume. For this reason, pressures within the cardiovascular system are measured and used as a rough indicator of fluid volume. This correlation is only valid in a limited sense since the measured pressures are influenced by more than just the volume of liquid present. Preload pressures are also influenced by, for example, intrathoracic pressure, intra-abdominal pressure and myocardial compliance.The key to remember is that pressure does not equal volume.Pressure is displayed as an indicator of volume status. It is clinically acceptable to measure the pressure required to fill the ventricles as a measure of left ventricular end-diastolic volume (LVEDV).
Left ventricular preload can also be assessed clinically via the pulmonary artery (PA) catheter by measuring pulmonary artery wedge pressure (PAWP), also known as pulmonary artery occlusive pressure (PAOP) and more commonly referred to as "wedge pressure". Normal PAWP/PAOP can range from 6 to 12 mm Hg. Right ventricular preload is assessed by obtaining central venous pressure (CVP). A normal CVP can range from 0 to 8 mm Hg. Both the CVP and the PAWP reflect the right/left ventricular end-diastolic volumes.
Signs of insufficient preload include poor skin turgor, dry mucous membranes, low urine output, tachycardia, thirst, weak pulse, and shallow jugular veins. Signs of excessive preload in a patient with adequate cardiac function include distended veins in the neck, crackling in the lungs, and hopping pulses.
Inadequate preload is commonly referred to as hypovolemia or dehydration. When there is insufficient volume in the vascular tree, the sympathetic nervous system is stimulated to release the catecholamines, epinephrine and norepinephrine. These hormones cause increased heart rate and arterial vasoconstriction. When these patients are treated with catecholamine drugs instead of volume infusions, the tachycardia becomes very pronounced and the vasoconstriction can become severe enough to cause organ failure and distal extremity ischemic. The first step in treating any form of hemodynamic instability is to assess the patient for signs of inadequate preload (eg, volume or blood loss).
reload: Afterload is defined as the resistance that the ventricle must overcome in order to eject its volume of blood.
The most important determinant of afterload is vascular resistance. In the clinical setting, the most sensitive indicator of left ventricular afterload is systemic vascular resistance (SVR) and of right ventricular afterload is pulmonary vascular resistance (PVR). The normal value for the SVR is 800-1200 dynes/s/cm2. Normal PVR values are generally below 250 dynes/s/cm2.
High afterload increases myocardial work and decreases stroke volume. Patients with high afterload present with signs and symptoms of arterial vasoconstriction, including cool, clammy skin, capillary renewal lasting more than 5 seconds, and low pulse pressure. (Note: Low pulse pressure is an indicator of both decreased stroke volume and increased afterload.)
Low afterload reduces myocardial work and results in increased stroke volume. Patients with little afterload show symptoms of arterial dilatation such as warm, flushed skin, jumping pulses, and a broad pulse pressure.
Contractility & Compliance:Contractility refers to the heart muscle's inherent ability to contract regardless of preload or afterload status. Contractility is enhanced with exercise, catecholamines, and positive inotropic drugs. It is reduced by hypothermia, hypoxemia, acidosis, and negatively inotropic drugs.
Myocardial compliance refers to the ventricle's ability to expand to accommodate a given volume of blood. Normally, the ventricle is very compliant, so large changes in volume produce small changes in pressure. When compliance is low, small changes in volume lead to large changes in pressure in the ventricle.
The key to ensuring adequate cardiac output is to ensure that the patient has adequate tissue perfusion. Tissue perfusion is the transfer of oxygen and nutrients from the blood to the tissues. Performing procedures to improve hemodynamics is essentially about improving tissue perfusion.
Many of the signs of inadequate preload, afterload, and contractility also reflect poor tissue perfusion. These signs include: cool clammy skin, cyanosis, low urine output, decreased consciousness, metabolic acidosis, tachycardia, tachypnea, and hypoxemia.
Transducer is a device that converts the pressure waves generated by vascular blood flow into electrical signals that can be displayed on electronic monitoring devices.
Before the monitor can measure pressures, the transducer must be zeroed to atmospheric pressure. The purpose of this procedure is to ensure that the transducer reads zero when there is no pressure on it. To level the transducer, place the transducer at heart level. This position is in the 4th intercostal space, mid-axillary. If the transducer is too low (raising the bed and thereby the height of the heart above the transducer), the reading will be falsely high. Conversely, if the transducer is too high, the reading will be falsely low.
Square Wave Test:
The ideal square waveform consists of an initial sharp upstroke generated by the activation of the quick flush system, a flat line for the duration of the quick flush system activation and reflects the high pressure present in the flush bag. The sharp downward stroke represents the release of the quick flush device. The square wave should quickly return to baseline after a few rapid sharp waves called oscillations.
Over-damping causes an indistinct upstroke, missing dicrotic notch, and loss of fine detail.
If the oscillations are sluggish and far apart, i. H. no overshoot or undershoot, the system is said to be "overdamped". Overdamping results in reduced waveform size and loss of some waveform components, and consequently underestimation of systolic pressure and overestimation of diastolic pressure.
Possible causes of overdamping are:
Flexible tubing - Use only the semi-rigid tubing provided with the transducer assembly.
Extension hose too long
air bubbles in the circuit
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In an underdamped system, the square wave is followed by several large oscillations. An under-damped system overestimates systolic pressure and underestimates diastolic pressure.
Arterial blood pressure monitoring:
The arterial pressure wave can be described by its steady and pulsatile components. The stationary component is the MAP, which is considered constant from the aorta to the peripheral great arteries.
Although DAP is approximately constant from the aorta to the periphery, SAP and therefore PP increase from the aorta to the periphery in young, healthy individuals. Systolic blood pressure is lowest in the aorta and increases as the arteries get smaller. Mean arterial pressure (MAP) is the average driving force in the arterial system and is essentially the same in all parts of the body. Blood flow to all organs depends on MAP, not on systolic or diastolic pressure. Only coronary perfusion depends on diastolic pressure.
MAP = DBP + 1/3 x Pulsdruck
A normal arterial pressure waveform has five main components:
The anacrotic limb, oranacrotic rise, is a rapid upstroke that begins with the opening of the aortic valve in early systole. The steepness, rate of rise, and magnitude of this initial upswing depends on the contractility and stroke volume of the left ventricle.
The systolic peak represents the highest pressure generated by the left ventricle of the heart during myocardial contraction. This point marks the patient's actual systolic blood pressure.
The dicrotic limb begins during late systole when blood flow from the left ventricle begins to decrease.
The dicrotic notch marks the closure of the aortic valve and the beginning of diastole.
The end diastole landmark is the location where the patient's actual diastolic blood pressure is measured.
Central venous pressure (CVP) monitoring:
The CVP is the pressure of blood emptied into the right ventricle during diastole (the right ventricular end-diastolic pressure or RVEDP). The normal CVP is 0-8. This increases by about 3–5 cm H2O during mechanical ventilation.
Any condition that causes increased intrathoracic pressure, such as pneumothorax, increased intra-abdominal pressure, or mechanical ventilation, will cause the CVP to be fairly high while the end-diastolic volume is acutely low. Conditions that decrease elasticity or contractility and cause the right ventricle to become stiff, such as B. pericardial tamponade and myocardial ischemia or infarction, can also lead to high pressure with low blood volume.
Elevated CVP indicates that the pressure in the right ventricle has increased abnormally when the ventricle is full just before systole. This can be due to many factors including fluid overload, myocardial infarction, cardiogenic shock, congestive heart failure, pulmonary edema, COPD, pulmonary embolism, pneumothorax, pulmonary hypertension, pericardial effusion, or tamponade. Diseases of the right heart valve, such as tricuspid regurgitation and pulmonary stenosis, can also increase CVP.
Decreased CVP generally indicates a decreased volume of blood returning from the venous system to the right side of the heart.
- a wave: This wave is due to increased atrial pressure during right atrial contraction. It correlates with the P wave on an EKG.
- c wave: This wave is caused by a slight elevation of the tricuspid valve into the right atrium during early ventricular contraction. It correlates with the end of the QRS segment on an EKG.
- x descent: This wave is probably caused by the downward movement of the ventricle during systolic contraction. It occurs before the T wave on an EKG.
- v wave: This wave is caused by the pressure created when the blood filling the right atrium meets a closed tricuspid valve. It occurs when the T wave ends on an EKG.
- y descent: This wave is generated by the opening of the tricuspid valve in diastole when blood flows into the right ventricle. It occurs before the P wave on an EKG
The A wave occurs after the P wave of the ECG complex during the PR interval. It reflects the increased atrial pressure that occurs with atrial contraction during end-diastole. Note that the A wave is absent in patients who do not have a pronounced atrial contraction, such as B. in patients with atrial fibrillation. Since the CVP value should reflect the right ventricular end-diastolic pressure, the CVP value is taken in the last half of the A-wave at the midpoint of the X descent. Calculate the CVP by averaging the pressure measured at the peak of the A wave and the subsequent valley.
X descent reflects atrial relaxation.
The C wave occurs at the end of the QRS complex at the beginning of the ST segment in the ECG recording. It reflects the closure of the tricuspid valve between the right atrium and right ventricle and the slight protrusion of the tricuspid valve during isovolumetric ventricular contraction. The C wave is not always visible.
The V wave occurs at the end of the T wave in the ECG trace. It reflects the increased pressure during passive atrial filling by IVC.
The Y descent occurs before the P wave in the ECG recording. It reflects the opening of the tricuspid valve and passive blood flow from the right atrium into the right ventricle prior to atrial contraction.
There are three parts of the waveform that are systolic events (c, x, v). There are two parts of the waveform that are diastolic events (a, y). The terms systole and diastole refer to VENTRICULAR events only
Mnemonic for the CVP wave
- "a" wave due to atrial contraction
- "c" wave due to tricuspid closure and ventricular contraction
- "v" wave due to venous filling of the atrium
Tachycardia shortens the time spent in diastole and causes a short "y" descent. This can cause the "v" and "a" waves to appear to merge.
In spontaneous breathing, there is a drop in pleural and pericardial pressure during inspiration - these are pressures that are passed on to the right atrium. This results in a decrease in measured CVP (but transmural pressure may actually increase). Mechanical ventilation produces the opposite effect with forced inhalation
Pleural and pericardial pressures are almost equal to atmospheric pressure at the end of expiration. This applies to both spontaneous and mechanical ventilation
Pericardial constriction: Restricted venous return to the heart, increased CVP, end-diastolic pressure equalization in all ventricles. Striking "a" and "v" waves, steep "x" and "y" descents.
All hemodynamic measurements are taken at the end of exhalation. The most accurate method is to obtain an actual printout of the CVP waveform and ECG trace and average the A wave at the end of exhalation. The CVP is calculated by averaging the peak and trough of A wave. The CVP value is recorded at the midpoint of the X descent. In spontaneously breathing patients, the CVP baseline falls during inspiration and rises during expiration. Take the reading just before the inspiration baseline drops. Patients receiving positive pressure ventilation show a rise in baseline during inspiration and a fall in baseline during expiration. For these patients, take the measurement just before the inspiration rises.
The A wave is absent in patients without pronounced atrial contractions, such as B. in patients with atrial fibrillation or in patients with ventricular pacemakers and no atrial activity. How is CVP determined in patients without an A wave? In these cases, a reading can be taken on the CVP waveform where it coincides with the end of the QRS complex on the ECG trace.
The brachial artery has no collateral circulation, but the radial and femoral arteries do.
Although expiration is usually passive, active expiration is very common in critically ill patients. When expiration is active, contraction of the abdominal and pectoral muscles increases pleural pressure during expiration, and there may not be a phase during the respiratory cycle when the pressure, measured by a transducer referenced to atmospheric pressure, gives a good approximation of the atrial transmural pressure
If the central venous pressure falls by > 1 mmHg during inspiration and this is not due to relaxation of the expiratory muscles, the patient is usually responsive to fluids
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PAWP is accurate when in a zone III area of the lung where Pa > Pv > PA (alveoli). On the x-ray, the median line should be no more than 3-5 cm. Wedge pressure should always be less than diastolic pulmonary pressure except in mitral regurgitation.
The insertion length of PA catheter (cm) to reach different chambers:
- RV25 cm
- PCWP45 cm
- In a study by PaulMarik, there was no correlation between CVP and blood volume, or CVP and fluid response, or ΔCVP (change in CVP with inspiration) and fluid response. Therefore, he says CVP should not be used to predict response to liquids. Even if the CVP is 0, it does not mean the patient is fluid responsive. Volume overload may occur in patients with low CVP and volume depletion in patients with high CVP.
- The CVP is a measure of right atrial pressure alone, not right ventricular volume.
- In mechanically ventilated patients, right ventricular filling depends on transmural right atrial pressure and not CVP.
- Blood pressure is directly related to CO and stroke volume (BP = COxSVR = SVxHRxSVR). However, in one study, blood pressure changes after a fluid challenge did not always correlate well with changes in cardiac output. Some patients had an increase in CO from a fluid bolus but no change in blood pressure, or there was an improvement in blood pressure but no change in CO or pulse pressure. However, in individuals who responded to a fluid challenge, there was an overall increase in blood pressure, CO, and pulse pressure.
- An IVC less than 2 cm has an 87% chance of a CVP less than 10.
- EtCO2 depends on CO2 production in the tissues, blood flow to the lungs, i. H. the cardiac output, and the ability of the lungs to absorb the returned CO2, i. H. the ventilation, to eliminate.