Bedside Assessment of Hemodynamic Status - Emergency

Management
Related Summaries

● Major trauma - emergency management

● Trauma in pregnancy - emergency management

● Spinal trauma - emergency management

Overview

● Assessment of hemodynamics at the bedside is a necessary skill, especially for those who work with
critically ill patients

● Hemodynamic assessment methods include

⚬ Interpretation of physical examination ndings

⚬ Assessment and interpretation of laboratory results
⚬ Ultrasound imaging
⚬ Use of noninvasive monitoring
⚬ Use of minimally invasive procedures

● No single assessment method is su cient in isolation and must be considered in the context of other
available assessments and clinical information

General Information

● Hemodynamics refers to the interaction of various aspects of the heart and blood vessels to maintain
adequate perfusion to body organs

● Hemodynamic evaluation assesses

⚬ Preload- the amount of blood in the venous system and its capacitance
⚬ Cardiac contractility- the ability of the heart to pump blood systemically
⚬ Afterload- resistance of the arterial system blood vessels as created by the vascular tone against
which the heart must pump (see below)

● Hemodynamic assessment allows for

⚬ Early detection of impending cardiovascular decompensation

⚬ Identi cation of critical illness
⚬ Selection of appropriate treatment modalities
⚬ Monitoring of therapeutic interventions

● Hemodynamic assessment is performed in most clinical encounters

⚬ Degree of assessment usually correlates with the type and severity of the condition being
evaluated
⚬ Conditions in which hemodynamic evaluation is particularly important include

– Acute myocardial infarction

– Shock
 – Sepsis
– Heart failure
– Acute valvular pathology
– Hypertensive emergency
– Severe burns
– Acute renal failure
– Arrhythmia
– Major trauma
– Postoperative patients, especially postcardiac surgery
– Pulmonary hypertension

● Static vs. dynamic measurement

⚬ Static measurements include single data point evaluations which can be assessed over time (for
example, blood pressure cu measurements)
⚬ Dynamic measurements provide continuous data (for example, intra-arterial catheter for blood
pressure monitoring)

● Hemodynamic assessment considerations

⚬ No single assessment method is su cient in isolation and must be considered in the context of
other available assessments and clinical information
– Interpretation of the acquired parameters is contextual
– Trends are frequently more important than absolute values
– Hemodynamic reference ranges often vary based on multiple parameters such as age, sex,
weight, height

Definitions and Physiologic Concepts

● Shock

⚬ Circulatory insu ciency between tissue perfusion and oxygen supply and the metabolic demands
of the tissue, leading to cellular dysoxia
– Types of shock include

● Hypovolemic - due to depleted intravascular volume through rapid uid loss (for example,
blood loss or dehydration)
● Cardiogenic - characterized by persistent hypotension due to a reduced cardiac index and in
the presence of elevated pulmonary capillary wedge pressure (PCWP)
● Septic - vasodilatory hypotension below a mean arterial pressure of 65 mm Hg and lactate
level of > 2 mmol/L (18 mg/dL) despite adequate uid resuscitation

● Tissue oxygenation

⚬ A ected by several factors

– Cardiac output (de ned below)

– Oxygen content of the blood

● Most of the oxygen is bound to hemoglobin, with a small amount dissolved in the blood

– Hemoglobin level

● Hemoglobin binds most of the oxygen in the blood

⚬ Hemoglobin’s a nity to oxygen a ected by factors such as

– Partial pressure of oxygen
 – Acidosis

– Tissue oxygen demand

● Increased by 10%-40% by physiologic stresses such as

⚬ Fever
⚬ Severe infection
⚬ Massive trauma
⚬ Burns
⚬ Increased work of breathing
⚬ Pain
⚬ Agitation

● Tissue oxygen mismatch (dysoxia) compensatory mechanisms

⚬ When the tissue oxygen supply and demand are mismatched, the body employs certain
compensatory mechanisms to maintain adequate oxygen perfusion, but these mechanisms can be
insu cient
⚬ Stages of hemodynamic compensation

– Stage 1: increasing cardiac output by a ecting the heart rate (HR), blood pressure (BP), stroke
volume (SV), and other circulatory parameters
– Stage 2: increasing tissue oxygen extraction, subsequently a ecting the mixed venous oxygen
saturation (SvO2)
– Stage 3: increasing anaerobic metabolism which increases production of lactic acid

● Vascular tone (vascular resistance)

⚬ Vascular resistance must be overcome by the ventricles to eject the blood into the circulation
⚬ Venous capacitance (preload) is a ected by

– Intravascular volume
– Venous tone

⚬ The systemic circulation is a high-resistance system and blood pressure is a clinical measure of
systemic vascular resistance
⚬ The pulmonary vascular resistance is normally lower than the systemic vascular resistance and can

be assessed by measuring the pulmonary artery pressure and pulmonary wedge pressure 1

● Volume status

⚬ The total amount of uid in the body. It may be adequate, high ( uid-overloaded), or low (volume-
depleted)
⚬ Total body uid is contained in 3 compartments

– Extravascular: which includes intracellular and extracellular

– Intravascular

⚬ A person can be overloaded in terms of total body uid but depleted intravascularly and assessing
the uid in the “right” compartment is necessary to optimize hemodynamics

● Stroke volume

⚬ Amount of blood ejected from the ventricles in each heartbeat

⚬ A ected by 3 factors

– Preload
– Afterload
– Cardiac contractility
 ● Ability of the heart to contract properly
● Measured through the left ventricular ejection fraction (LVEF)
● Normal LVEF in a healthy young individual is ≥ 55%

● Cardiac output

⚬ The volume of blood ejected by the heart each minute

⚬ Calculated as heart rate multiplied by stroke volume
⚬ Normal adult range- 4-8 L/minute
⚬ Can increase or decrease depending on the clinical situation

Table 1. Causes of Abnormal Cardiac Output

Causes of Elevated Cardiac Output Causes of Decreased Cardiac

Output

– Sympathetic nervous system – Severe tachycardia

stimulation – Bradycardia
– Positive inotropic simulation – Decreased myocardial contractility,
– Hyperthyroidism for example, cardiac ischemia
– Hypervolemia – Increased afterload
– Anemia

● Cardiac Index

⚬ Cardiac output divided by body surface area (BSA)

⚬ Normal adult range: 2.5-4 L/minute/m2
⚬ In cardiogenic shock, the cardiac index is < 2.2 L/minute/m2

● Central venous pressure (CVP)

⚬ The pressure in the vena cava, as a surrogate of right atrial pressure (RAP) and therefore right
ventricular preload
⚬ Normal adult value: 4-8 mm Hg

● Left ventricular end diastolic pressure

⚬ The pressure in the left ventricle at the end of diastole

⚬ Equal to the pulmonary artery occlusion pressure (pulmonary wedge pressure) - measured
indirectly using a pulmonary artery catheter (see below)
⚬ Normal adult value: 5-12 mm Hg

● Mixed venous oxygen saturation (SvO2)

⚬ The amount of hemoglobin saturated with oxygen in the venous circulation

⚬ Indicates the balance between oxygen supply and demand at the tissue level
⚬ Normal SvO2: 65%-75%
⚬ Lower values indicate increased extraction of oxygen from hemoglobin at the tissue level, which is
indicative of decreased tissue perfusion
 ⚬ Higher values indicate decreased extraction of oxygen from hemoglobin at the tissue level, which is
indicative of oversaturation with oxygen (hyperoxia) or decreased ability of the tissue to extract
oxygen, as in cyanide poisoning

History

● Clinical presentation

⚬ Clinical history provides important clues to the etiology of abnormal hemodynamics

⚬ Assess for

– Dehydration from decreased oral intake, severe diarrhea, or polyuria

– Trauma
– Gastrointestinal bleeding
– Anaphylaxis
– Noncompliance with diuretic prescriptions
– Acute myocardial infarction
– Infections

⚬ Nonspeci c symptoms (generalized weakness, lethargy, or altered mental status) may suggest
underlying hemodynamic compromise
⚬ Severe postural dizziness may suggest hypovolemia in patients with volume loss

● Age

⚬ A ects the normal parameters of certain hemodynamic measurements and the physiology of their
interactions

● Past medical history and medications

⚬ Underlying medical conditions and medications can a ect the accuracy of standard hemodynamic
monitoring and how di erent parameters are a ected with changes in physiology

Physical Examination

● No single measurement can be used to assess the adequacy of perfusion or resuscitation

● Vital signs

⚬ Blood pressure (BP)

– Blood pressure can be measured using

– Blood pressure cu over a large artery such as the brachial artery
– Intra-arterial line (see below)

⚬ Blood pressure cu s can use mercury (in manual cu s) or electronic oscillators

– Mean arterial pressure (MAP) is calculated from the systolic and diastolic blood pressure
measurements using the formula ⅓ (SBP-DBP) + DBP = MAP
⚬ Hypotension in an adult is de ned as

– Systolic blood pressure (SBP) < 90 mm Hg

– SBP decrease > 40 mm Hg from baseline
– MAP < 65 mm Hg

⚬ It is possible for a patient to have a normal blood pressure yet have hypoperfusion and be in shock
(see cryptic shock, below)
⚬ Pitfalls in measurement and interpretation
 – Inaccurate measures can be caused by a cu size/arm size mismatch
● More likely to happen in patients with obesity
● Strongly consider an intra-arterial line in critically ill patients with obesity

– Inability to use a cu because of the presence of a dialysis stula

– A normal blood pressure reading does not exclude shock

⚬ Hemodynamic compromise in older patients (> 65 years old) should be suspected at a higher

blood pressure than their younger counterparts (for example, SBP of 100 mm Hg) 2
⚬ Heart rate (HR)

– Heart rate normally increases when compensating for hypoperfusion to increase cardiac output
– Tachycardia (heart rate > 100 beats per minute [BPM] in adults), in the appropriate clinical
setting, is a speci c (96%) but not sensitive indicator of blood loss, even for volumes of more
than 1,000 mL
– Pitfalls in measurement and interpretation

● Young athletes usually have lower resting heart rates and will not manifest tachycardia until
late in their disease process
● Certain medications (for example, beta-blockers) decrease the tachycardic response to
volume loss
● Older patients have a blunted tachycardic response to volume loss

● Orthostatic (postural) vitals

⚬ Used to evaluate hypovolemia as the cause of dizziness

⚬ Intermittent measurement of blood pressure and heart rate while the patient is supine and then
after standing for 3 minutes
⚬ Orthostatic hypotension de ned as

– A ≥ 20-mm Hg decrease in systolic blood pressure or a ≥ 10-mm Hg decrease in diastolic blood

pressure within 3 minutes of standing compared to a supine position
– A decrease in systolic blood pressure ≥ 30 mm Hg in patients with hypertension (supine systolic
blood pressure ≥ 160 mm Hg)
⚬ Orthostatic tachycardia de ned as heart rate increase ≥ 30 beats/minute or persistent tachycardia
≥ 120 beats/minute
⚬ Orthostatic tachycardia of > 30 BPM is sensitive and speci c for a large blood loss (> 600 mL) but

not a moderate blood loss (≤ 500 mL) 3

⚬ Orthostatic hypotension (a decrease in the SBP of > 20 mm Hg after standing) is not sensitive for
volume loss. It occurs in 10% of normovolemic patients, 30% of patients > 65 years, and 30% of
patients with moderate blood loss (about 500 mL)
⚬ Shock Index (SI)

– De ned as heart rate divided by SBP (HR/SBP)

– Normal range: 0.5-0.7
– Values > 0.9 are an early sign of circulatory collapse and shock and have been linked to

hyperlactatemia and higher 28-day mortality rates 4

⚬ Respiratory rate

– Variation in breathing patterns and respiratory rate can indicate metabolic derangement
stemming from circulatory collapse but do not independently predict hemodynamic status
– Pitfalls in measurement and interpretation

● A ected by acid-base disorders

 ● Altered mental status and neurologic conditions may a ect respiratory drive independent of
hemodynamic status
⚬ Temperature

– Temperature measurement addresses 2 potential causes of hemodynamic collapse-

hypothermia and hyperthermia. Correction of these conditions is important in the management
of hemodynamically unstable patients 5
⚬ Pulse oximetry

– Uses the light wave spectrum to measure oxyhemoglobin saturation in the blood
– Normal oxygen saturation ranges between 96% and 98% in arterial blood (SaO2)
– Decreased cardiac output a ects saturation readings negatively
– Should not be used alone to assess hemodynamic status, as many factors a ect pulse oximetry

readings, including anemia and hemoglobinopathies 5

– Pitfalls in measurement and interpretation

● Pulse oximetry results < 75% do not correlate well with actual oxygen saturation 6

● Pulse oximetry can be falsely abnormal in patients with cold extremities, hypothermia, and
local tissue ischemia
⚬ End-tidal carbon dioxide (ETCO2) monitoring

– Also called capnography

– Expired CO2 is detected and displayed continuously in a waveform
– Some studies have shown that ETCO2 monitoring correlates logarithmically with cardiac output,

with lower values correlating with lower output 7 , but this relationship has not been
investigated thoroughly
– The ETCO2 value should not be used to determine a patient’s cardiac output or hemodynamic
stability in clinical practice
– ETCO2 values during cardiopulmonary resuscitation (CPR) may provide hemodynamic
information as a rise in ETCO2 values during CPR indicates return of spontaneous circulation
(ROSC) (an increase in cardiac output)

● Skin examination

⚬ Skin mottling and capillary re ll time (CRT) do not accurately or instantly re ect the hemodynamic
status of a patient, but they remain valuable tools for predicting postresuscitation mortality
⚬ Certain patient populations (for example, those with cirrhosis of the liver) have increased skin
perfusion and therefore can have falsely normal exam ndings, especially early in the course of
their disease
⚬ Skin mottling

– Patchy skin discoloration observed over the knee and on the anterior surface of the leg, thought
to be an indicator of poor perfusion in the absence of other thrombotic conditions in the leg
– Skin Mottling Score (SMS) is divided into 6 categories, from 0 to 5, with higher scores indicating

greater areas of skin mottling, and therefore worse perfusion 8 , 9 , 10

⚬ Limitations in interpretation

– Cannot be used on patients with dark skin

– Falsely normal in patients with cirrhosis

⚬ CRT

– Time required for blood ow (and color) to return to the distal capillaries after pinching and
releasing the nail beds or the knee (while at heart level)
 – In adult patients, the most common threshold used is 4 seconds on average
– Prolonged CRT (> 4-4.5 seconds) has been correlated with higher lactate levels, end-organ

dysfunction, and higher mortality rates 10 , 11

⚬ Limitations in measurement and interpretation

– CRT is a ected by many variables that can make the measurement inaccurate: 12 , 13

● Age: CRT increases with age 14

● Skin temperature
● Skin color
● Location of compression (CRT at the toes has not been studied)
● Amount of pressure applied
● Length of time
● Interrater variability in estimating the actual time

⚬ To improve the accuracy of measurement

– Use the same site of measurement for serial exams ( ngertip or knee)
– Use the same compression time and rmness
– Use a stopwatch
– Measure the CRT twice, allowing 1 minute between measurements and use the average

⚬ Skin temperature gradient

– The di erence in the temperature between a proximal and distal location is thought to increase
with worsening perfusion
– Examples

● Central-to-toe gradient (Tc-toe): > 7 degrees C is considered abnormal

● Forearm-to- ngertip gradient (Tskin-di ): > 4 degrees C is considered abnormal

– Limitations in measurement and interpretation

– Can be a ected by the ambient temperature, more so with the central-toe gradient 9

– Skin temperature probes might not be readily available

⚬ Extremity temperature

– The skin temperature of the extremities is tested using the examiner’s hands and classi ed as
either cool or warm
– It can be tested for all extremities or just the lower extremities
– Cold extremities correlate well with lower cardiac output in patients without peripheral vascular

disease 11 , 15
– Limitations in measurement and interpretation

● A ected by the ambient temperature

● A ected by the presence of peripheral vascular disease
● Less sensitive than the skin temperature gradient
● Subjective

⚬ Skin turgor

– Return of skin to its normal position after being pinched between the examiner’s thumb and
fore nger
– Decreased in patients with volume depletion
– Normal value is unclear, as is the e ect of age

⚬ Mucous membranes

– Moist mucous membranes and a tongue without furrows in the setting of vomiting, diarrhea, or
decreased oral intake make it less likely that the patient has hypovolemia (negative likelihood
 ratio of 0.3) 3
⚬ Axilla

– In patients with vomiting, diarrhea, or decreased oral intake, the presence of dry axilla makes it

more likely that the patient has hypovolemia. However, it is not sensitive (50%) 3

● Urine output

⚬ Total urine volume produced in 1 hour

⚬ Estimated normal value: 0.5 mL/kg/hour
⚬ Used as a surrogate of kidney perfusion
⚬ Decreased urine output is concerning for hypoperfusion of the kidneys
⚬ However, given that urine output depends on factors other than kidney perfusion, oliguria should

not be used independently as a marker of perfusion 5 , 16

● Passive leg raise (PLR) test (also called straight-leg lift)

⚬ Passive leg raise is the process of lowering the head and upper torso from a 45-degree angle to
lying supine while simultaneously raising the legs to a 45-degree angle for 4 minutes, which
increases the venous return to the heart and is akin to the administration of 250 mL of uid
bolus 17
⚬ It is referred to as “autotransfusion,” as a reversible uid challenge that is safe and simple
⚬ Hemodynamics are assessed before and after the PLR.; if cardiac output improves, the patient is
“ uid responsive” and administration of IV uids should improve hemodynamics
⚬ Provides a dynamic assessment of a patient’s preload and is accurate regardless of ventilation

mode and cardiac rhythm 18

⚬ Limitations in measurement and interpretation include 19

– A ected by

● Presence of abdominal ascites

● Deep venous thrombosis in the leg
● Lower extremity amputation
● Abdominal hypertension
● Pain induced by the test (causes sympathetic stimulation)

– Contraindication

● Traumatic brain injury as would increase intracranial pressure

Diagnostic Studies

Noninvasive hemodynamic monitoring techniques

● Bedside ultrasound

⚬ Used to diagnose causes of shock and guide therapy to optimize hemodynamic status
⚬ Used to evaluate cardiac function; to assess for the presence of hemorrhage, pulmonary edema, or
pneumothorax; and to evaluate the inferior vena cava (IVC) for uid tolerance and uid
responsiveness
⚬ Multiple protocols exist for bedside ultrasound assessment including the Rapid Ultrasound for
Shock and Hypotension (RUSH) exam
– Series of ultrasound examinations that are used to identify the cause of shock and to direct
management
 – HI-MAP mnemonic used to indicate focused exam locations

●
Organ Views Elements to Type of
Assess Shock

H Heart Subxiphoid, ⚬ Pericardial Cardiogenic

parasternal tamponad or
long and e obstructive
short views ⚬ Right
ventricular
size
⚬ Left
ventricular
function
and
ejection
fraction

I Inferior vena Longitudinal IVC collapse: Hypovolemic

cava view of the more than
subxiphoid 50%
area indicates
uid
tolerance
(see below)

M Morison Coronal view Hemorrhage Hypovolemic

pouch of the right in the space (hemorrhagi
ank between the c)
liver and
right kidney
(most
sensitive
area to
identify free
uid in the
abdomen)
 Organ Views Elements to Type of
Assess Shock

A Aorta Transverse ⚬ Aortic Hypovolemic

view of aneurysm (hemorrhagi
midabdomen ⚬ Aortic c)
in 3 locations dissection
(proximal,
mid, and
distal)

P Pulmonary Longitudinal Pneumothor Obstructive

bilateral ax
midclavicular
view of the
lungs

Abbreviation: IVC, inferior vena cava.

⚬ IVC ultrasound assessment

– IVC is a dynamic structure connecting the peripheral circulation directly to the right atrium
– Size and change in its diameter are measured while the patient is in a supine position, using a
curvilinear probe to obtain a longitudinal view of the subxiphoid area
– The optimal location of measurement is 2 cm from the IVC insertion into the right atrium
– Measurements are taken during inspiration and expiration in spontaneously breathing or
ventilated patients
● Variability in IVC diameter during the respiratory cycle is a better measure of uid
responsiveness than either alone
● Variability in IVC diameter is referred to as IVC Caval Index (IVCCI) in spontaneously breathing
patients and IVC Distensibility Index (IVCDI) in mechanically ventilated patients (see below)
– IVC diameter

● IVC diameter correlates with central venous pressure (CVP) and right atrial pressure (RAP) in
all respiratory phases
● In ventilated patients, positive end-expiratory pressure (PEEP) may increase IVC diameter

due to an increase in pulmonary pressures 20

– IVC Collapsibility Index (Caval Index) (IVCCI)

● Refers to the change in measurement of the IVC in spontaneously breathing patients

● During inspiration, the thoracic pressure decreases, leading to collapse in the IVC
● The IVC is measured during both inspiration and expiration, and the percentage of change is
calculated:
⚬ IVCCI = (IVCDe - IVCDi / IVCDe) × 100% (IVCDe, IVC diameter in expiration; IVCDi, IVC
diameter in inspiration)
● The IVCCI is inversely proportional to the CVP and RAP; the higher the IVCCI, the more likely
that the CVP is low, and the lower the IVCCI, the more likely that the CVP is high
 ● No uniformly accepted reference ranges

⚬ IVCCI values of < 20% to < 36.5% have been used as an indicator of high CVP
⚬ IVCCI values of > 60% have been used as an indicator for low CVP (< 8-10 mm

Hg) 20 , 21 , 22 , 23 , 24
⚬ Unclear correlation between IVCCI and uid responsiveness 21 , 25 , 26

– IVC Distensibility Index (IVCDI)

● Refers to the change in measurement of the IVC in mechanically ventilated patients

● During inspiration, thoracic pressure increases, causing distension of the right atrium and
subsequently the IVC
● IVC is measured during both inspiration and expiration, and the percentage of change is
calculated:
⚬ IVCDI = (IVCDmax - IVCDmin / IVCDmax) x 100%

● IVCDI predicts uid responsiveness similarly to the IVCCI

● Accuracy limited by variable pressure exerted from adjacent organs or increased
intraabdominal pressure which is common in ventilated patients undergoing abdominal
surgeries 21 , 27 , 28 , 29
⚬ Transthoracic Echocardiography

– Used in the assessment of stroke volume and cardiac output

– Accuracy of results is operator-dependent
– Phased-array probe used to obtain an apical 5-chamber view of the heart to determine the
Doppler velocity of blood moving through the left ventricular outlet tract (LVOT)
– Aortic outlet diameter and velocity time integral (VTI), a measure which quanti es blood ow

across the aortic valve during systole, are used to calculate stroke volume and cardiac output 30

● Peripheral perfusion index (PFI) (using a pulse oximeter)

⚬ PFI is measured by pulse oximeter, which calculates the ratio between pulsatile blood ow and
nonpulsatile blood ow in the peripheral circulation which reaches the oximeter’s photosensor
⚬ Changes in PFI correlate with changes in core-to-toe temperature, which can provide a noninvasive

estimation of peripheral perfusion in critically ill patients 31 , 32

● Thoracic electrical bioimpedance (TEB)

⚬ Bioimpedance measures the resistance of electrical current through di erent body tissue and
uids, and can quantify the amount of tissue and uid in the body
⚬ Can calculate the di erence in uid content between areas in the body to calculate stroke volume
and cardiac output
⚬ Small electrodes are placed on the upper and the lower parts of the thoracic area
⚬ TEB is inversely related to total uid conductivity (TFC)
⚬ Many factors a ect the accuracy of this study (for example, the presence of uid in the thorax, as
in pulmonary edema or pericardial e usion) and can make the result inaccurate if used in these
clinical conditions 30 , 33

Minimally Invasive and Invasive Hemodynamic Monitoring Techniques

● Arterial lines

⚬ Blood pressure can be obtained directly from an intra-arterial cannula inserted into the radial,
brachial, axillary, or femoral artery
 ⚬ Arterial line insertion carries the risk of damage to surrounding structures, thrombosis, or stula

formation at the site of insertion 5

⚬ Provides more accurate measurement than blood pressure cu , especially in patients with obesity
and those with severe atherosclerosis
⚬ Useful in patients on vasoactive drugs who require continuous dynamic monitoring of their blood
pressure
⚬ Because they do not account for vascular resistance, they are poor measures of cardiac output

● Central venous catheters

⚬ Central venous catheters (through the internal jugular or subclavian vein) can be used to measure
central venous pressure (CVP) (see above), which is a surrogate for right atrial pressure (RAP)
⚬ A measurement between 4 and 8 mm Hg is considered normal
⚬ CVP is often used to guide uid therapy, although recent studies have shown poor correlation with
uid status or cardiac output as it is a ected by many factors such as obstructive cardiopulmonary
pathologies and increased intra-abdominal pressure
⚬ Central venous catheters can also be used to determine mixed venous oxygen saturation (see
below)

● Pulmonary artery catheterization (Swan-Ganz Catheter):

⚬ In this procedure, a multi-lumen catheter is inserted through the internal jugular vein, through the
subclavian vein, right atrium and ventricle to end in the pulmonary artery
– Proximal lumen (usually blue): measures the RAP, which is similar to the CVP (see above). Can
also be used to obtain the mixed venous oxygen saturation (see below)
– Distal lumen (usually yellow): measures the pulmonary artery pressure
– Balloon in ation port (usually red): the balloon is in ated to “wedge” the catheter in the
pulmonary artery and obtain the pulmonary artery opening pressure (PAOP), which accurately
correlates with the left atrial pressure
⚬ Not used routinely due to invasive nature and the lack of evidence that it improves mortality in

patients with undi erentiated shock 34

⚬ Commonly used in the management of postoperative cardiac patients and those with complex
physiology such as severe pulmonary hypertension
⚬ Can be used to measure cardiac output using the pulmonary thermodilution technique, which
speci cally looks at right cardiac output, which can be used as a surrogate for left cardiac output

● Transpulmonary thermodilution (for example, PiCCO, VolumeView)

⚬ This procedure requires the use of a central line and an arterial line
⚬ A cold uid bolus is introduced through the central line and the di erence in temperature
(thermodilution) is measured before and after introduction of the cold sample through a sensor in
an arterial line
⚬ The di erence in temperature is used to calculate left cardiac output
⚬ This is slightly di erent from the pulmonary thermodilution technique, which uses the same
principles but requires the use of a pulmonary artery catheter (Swan-Ganz)
⚬ In most patients, the results of these techniques correlate well (the transpulmonary method is less
invasive)
⚬ In some patients (for example, those on positive pressure ventilation), the results of the 2 methods
do not correlate as well because transpulmonary thermodilution measures left cardiac output and
the pulmonary thermodilution measures right cardiac output 30 , 33
● Transpulmonary dye dilution (for example, LiDCO)

⚬ Similar to the thermodilution method, this method uses a central line and an arterial line to
introduce a bolus of lithium and measure its concentration at the central venous and the arterial
level
⚬ Measurements of concentration di erence provide an estimate of cardiac output 30

● Ultrasound ow dilution (for example, COstatus)

⚬ The use of this device requires an arteriovenous primer (a connection between a central line and
an arterial line)
⚬ The device sends continuous ultrasound waves that are conducted through the blood
⚬ The conduction of ultrasound waves is repeated after administering a cold uid bolus, which will
then help calculate the cardiac output
⚬ Limitation: the requirement for invasive measures, along with a primer

● Pulse contour and pulse pressure analysis (for example, FloTrac/Vigileo)

⚬ Pulse contour and pulse pressure analysis devices use the data obtained from an existing arterial
line along with data collected about vascular tone to calculate volume ow and cardiac output
⚬ Accuracy of method is not uniformly accepted compared with other invasive measures 35

⚬ Predicts uid responsiveness with good sensitivity and speci city that reaches up to 82%-88% and

87%-88% respectively 36

● Transesophageal echocardiogram/Doppler

⚬ In both techniques, a transducer is inserted into the esophagus to obtain accurate measures of
stroke volume and cardiac output
⚬ Transesophageal echocardiogram is used to diagnose conditions that a ect cardiac output, such
as pericardial e usion
⚬ This method is considered safe but requires trained personnel and the patient must be intubated

– Accuracy of measurements is operator dependent

⚬ Device may be kept in place for continuous monitoring but carries risk of dislodgement while

moving patient or performing other procedures 30

Laboratory Tests

● Laboratory tests should not be used alone to assess hemodynamics

● Metabolic acidosis should raise suspicion of hypoperfusion due to hemodynamic compromise

● Elevated blood urea nitrogen (BUN) and creatinine may indicate acute kidney injury due to
hypoperfusion

● Identi cation of acidosis

⚬ Hypoperfusion leads to anaerobic metabolism with production of lactate and resultant metabolic
acidosis
⚬ Acidosis may be caused by medical conditions not related to hypoperfusion, such as renal disease,
ketoacidosis, toxic ingestions, and respiratory acidosis due to CO2 retention
⚬ Blood gas analysis can be used to detect acidosis and includes
 – pH- direct measurement re ecting oxygen debt, metabolic bu ering, and compensatory
respiration
– Bicarbonate (HCO3-) - the primary bu er in the body

● Decreases in response to acid load

● Normal value 24 mEq/L

– Base excess (BE)

● The calculated amount of base (in mmol) that is required to titrate 1 liter of whole blood to
normal pH, assuming normal arterial partial pressure of oxygen (PaO2), partial pressure of
carbon dioxide (PaCO2) and temperature
● Base excess = (0.93 × [HCO3-]) + (14.84 × [pH - 7.4]) - 24.4
● Base excess < - 2 mmol/L is considered metabolic base de cit (acidosis); > + 2 mmol/L is
considered metabolic base excess (alkalosis)
● A ected by the concentration of hemoglobin and albumin

⚬ Lactate:

– Biomarker often used to diagnose hypoperfusion and assess for signs of hemodynamic
compromise
– Normal product of anaerobic cell metabolism and is metabolized by the liver; increased blood
lactate concentration can be caused by:
● Anaerobic glycolysis related to inadequate oxygen delivery, as in shock or mesenteric
ischemia, referred to as type A lactic acidosis
● Other causes not related to tissue hypoperfusion, such as cancer and liver failure, referred to
as type B lactic acidosis

Table 2. Causes of Elevated Lactate

Tissue Hypoperfusion (Type A) Absence of Tissue Hypoperfusion

(Type B)

⚬ Mesenteric ischemia ⚬ Malignancy (usually hematologic

⚬ Sepsis such as leukemia, lymphoma,
⚬ Shock and multiple myeloma)
⚬ Hyperthermia ⚬ Renal failure
⚬ Seizure ⚬ Liver failure
⚬ Drug or toxic ingestion
(metformin, salbutamol,
albuterol, epinephrine, cocaine,
INH, linezolid, Valproic acid, HIV
drugs [zidovudine, didanosine,
lamivudine], propofol)
⚬ Congenital enzyme de ciencies
(for example, G6PD)

● Lactic acidosis can be due to overproduction or decreased clearance

 – No single cuto value identi ed but 2 to 2.5 mmol/L considered the upper limit of normal, with
4 mmol/L used as cuto by the Surviving Sepsis Campaign and other critical care organizations
– Some studies have shown that pH and lactate are better predictors of tissue hypoperfusion

than base excess (or de cit) 37 , 38 , 39

⚬ Limitations in measurement and interpretation 40

– Elevated lactate has about 100% sensitivity for hypoperfusion, but speci city as low as 40% as
lactate levels are frequently elevated without tissue hypoperfusion
– Tissue hypoperfusion can exist in the setting of normal blood pressure as in cryptic shock

where there is an elevated lactate level and end-organ dysfunction 41

– Arterial and venous lactate levels are highly correlated (0.94) in most patients, except in cases of
local venous stasis (for example, prolonged tourniquet placement)
– Lactate in lactated Ringer solution does not signi cantly a ect serum lactate levels and does not
cause lactic acidosis

● Anion gap

⚬ Anion gap (AG) is the di erence between serum sodium (Na+) (measured cation) and measured
anions
⚬ AG = [Na+] - {[Cl-] + [HCO3-]}

⚬ Elevated anion gap in the presence of acidosis should raise suspicion for hyperlactatemia in the
correct setting
⚬ Di erential diagnosis for patients with anion gap metabolic acidosis includes toxic ingestions and
ketoacidosis

● Mixed and Central Venous Oxygen Saturation (SvO2 and ScvO2)

⚬ Measurement is obtained through a central venous catheter (mixed venous oxygen saturation,
SvO2) or a pulmonary artery catheter (central venous oxygen saturation, ScvO2)
⚬ Devices allow samples to be taken from their distal end to measure mixed venous oxygen
saturation (which is a marker of tissue perfusion when compared to arterial blood gas [ABG]
oxygen saturation results)
⚬ Normal SvO2 is 65%-75%. Lower values indicate increased tissue extraction of oxygen, which is a
marker of tissue hypoperfusion (see above)
⚬ SvO2 can be used to calculate cardiac output using Fick principle when combined with the arterial
O2 saturation and hemoglobin values

– Method is not accurate in its correlation with CO or tissue perfusion

– However, results above 70% during resuscitation, along with other measures, correlate with

decreased mortality in patients with sepsis 5

Special Populations

● Pediatric patients

⚬ Hemodynamic parameters are a ected by 1 or more of age, sex, and height

⚬ Pathophysiology of shock is di erent in children and adults
⚬ Pediatric patients have decreased cardiac output and increased systemic vascular resistance when
they present in septic shock, unlike their adult counterparts
⚬ Skin turgor is used commonly in the assessment of pediatric patients and is part of the
recommended assessment for those presenting with vomiting, diarrhea, or other causes of volume
 loss

● Geriatric patients

⚬ Older patients (> 65 years old) have a decreased catecholamine response to intravascular volume
depletion,
– Unable to mount su cient tachycardic response to hypoperfusion patients causing heart rate
to be relatively low despite intravascular volume depletion
⚬ decreased elasticity and the increased prevalence of hypertension in older patients

– Systolic blood pressure tends to be higher at baseline

– Must consider baseline systolic blood pressure (SBP) to determine if there is a change
– Consider higher SBP threshold of 100-110 mm Hg for hypotension instead of 90 mm Hg 2

– Capillary re ll time prolonged at baseline, with average time being 4.5 seconds (as opposed to

2-3 seconds in younger adults) 14

– Skin turgor, moist mucous membranes, and axillary moisture are not reliable measures in

geriatric population 42

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