Hypotension and shock: The truth about blood pressure : Nursing2016

Hypotension & shock:
The truth about blood pressure
By Deborah Tuggle, RN, CCNS, MN
C
Consider these three hospitalized patients, all with BP readings of 92/60 mm
Hg:
• Elmer Smith, 84, was admitted to rule
out an ankle fracture from a minor fall.
He has a history of heart failure and
takes furosemide, lisinopril, and carvedilol. His skin is warm and dry and his
heart rate is 74 beats/minute.
• Brianna Jones, 32, has an infected
wound on her left hand. She has no
significant medical history and takes no
routine medications. Her skin is warm
and flushed, her heart rate is 118 beats/
minute, and she’s agitated and slightly
confused.
• Dexter Brown, 56, just had coronary
artery bypass graft surgery. During
the procedure, he had an episode of
severe hypotension and needed a liter
of 0.9% sodium chloride solution. He’s
now stable with a heart rate of 90 beats/
minute and is receiving I.V. infusions of
norepinephrine and vasopressin.
Although their BP readings are identical, these three patients differ greatly in their cardiovascular status. Mr. Smith’s BP is likely normal for him, reflecting his chronic cardiac dysfunction and the effects of
his heart failure medications. Ms. Jones’ tachycardia and
altered mental state point to hypoperfusion and sepsis.
Mr. Brown seems stable, but his BP is being maintained
by two potent vasopressors at doses that may actually
compromise blood flow and tissue oxygenation.
BP is a standard measurement in any routine cardiovascular assessment, but is it really a reliable reflection
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of cellular hypoperfusion and shock? These three patient
scenarios would suggest otherwise. This article focuses
on hypotensive states and attempts to clarify misconceptions about BP interpretation. I’ll also briefly review
basic hemodynamics and suggest measures of perfusion
beyond BP.
Causes of hypotension
Acute hypotension is the second leading cause of cardiac
arrest and sudden death, and is associated with tissue
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ischemia and progressive organ failure.1 Hypotensive
states are generally categorized into threats to one of
the three components of the cardiovascular system: the
heart, blood, or vessels. (For details, see Shocking causes.)
Cardiogenic shock occurs when the heart is unable to
pump enough blood to meet the body’s demand for oxygen. The number one cause of cardiogenic shock is acute
myocardial infarction (MI).2
Hypovolemic shock, the most prevalent form of hypoperfusion, occurs when the vascular system loses blood
or fluid either externally or internally, leading to a fall in
perfusion pressure.2
Vasogenic shock is when blood vessels dilate inappropriately, or more seriously, dilate and leak. Severe sepsis is
the predominant form of vasogenic shock.2
When a patient becomes hypotensive and shows signs
of hypoperfusion or shock, you’ll need to act quickly to
determine the underlying cause, so interventions can be
targeted to the source of the problem. To differentiate
among the three forms of shock, ask yourself questions
such as: Is the patient having chest discomfort or anginal
equivalent (pump)? Does he have ST-segment elevation
(pump)? What was today’s weight (volume)? Are his neck
veins distended or flat (volume)? Does he have a fever
(vessel/ sepsis)? Are there medications or pathologies that
could cause vasodilation (vessels)? The answers to these
questions will help determine the source of shock so that
targeted therapy can be initiated.
Building blocks of BP
Another way to assess hypotension and uncover its cause
is to consider the formula for BP, which is cardiac output
(CO) multiplied by systemic vascular resistance (SVR).
Systolic BP is primarily determined by CO and diastolic
BP by SVR. (See Breaking down BP.)
CO, in turn, is the product of heart rate and stroke
volume (SV, the amount of blood ejected with each beat).
And SV is determined by three parameters—preload,
afterload, and contractility. Let’s look at these three
building blocks.
Preload is the volume of blood in the ventricle waiting
to be ejected. This blood is brought to the heart by the
“preheart vessels” or veins, so any manipulation in volume or venous return affects preload and ultimately BP.
Afterload is the resistance to moving the preload, and
is primarily determined by the tone of the “after-heart
vessels” or arteries. Any manipulation in arterial radius
affects afterload and ultimately BP.
Contractility is the cardiac muscle’s strength for moving preload against afterload. This is a complex and
difficult parameter to pinpoint because it’s affected by
preload and afterload. Preload affects contractility via
the Frank-Starling mechanism (see Frank-Starling curve),
which states that greater ventricular stretch results in
greater cardiac contraction. This effect is limited, however, and reaches a plateau at the optimal level of preload
and best contractility.
Afterload can also affect contractility. Vasodilation
causes less resistance to flow, so less myocardial force is
needed to eject blood from the ventricles. Vasoconstriction causes greater resistance to blood flow and requires
more forceful myocardial contractions. Of course, this
too is limited: If the heart has diminished muscle reserves, for example, from chronic myopathy or ischemia,
it will resort to tachycardia as a means of maintaining
SV, CO, and BP.
Whether your patient is hypertensive or hypotensive,
determining which parameter is out of balance and in
which direction is key to providing appropriate interven-
Shocking causes
Cardiogenic shock
• Acute coronary syndromes such as ST-segment elevation MI and non-ST-segment elevation MI
• Reperfusion injury states (stunned myocardium)
• Exacerbations of chronic heart failure
• Cardiomyopathy
• Infectious or inflammatory processes
• Traumatic chest contusion
• Exposure to cardiotoxic drugs
• Excessive doses of negative inotropes such as betablockers or calcium channel blockers
• Structural abnormalities such as valvular dysfunction
or septal disruptions
• Obstructive pathologies including cardiac tamponade,
pulmonary embolism, and tension pneumothorax
Hypovolemic shock
• External losses from decreased fluid intake, vomiting,
diarrhea, diaphoresis, polyuria, hemorrhage, burns,
and wound exudate
• Internal losses from bowel sequestration, internal
hemorrhage, and ascites
Vasogenic shock
• Sepsis
• Anaphylaxis
• Systemic inflammation of multiple causes, such as
pancreatitis or fulminant hepatitis
• Drug overdose
• Neurogenic insults such as a spinal cord injury or epidural drugs
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tions. Let’s look at how imbalances in heart rate, preload,
afterload, or contractility affect BP.
minimally invasive
Breaking down BP
systems that measure variations in BP
BP = CO x SVR
across the respiratory cycle. Several
Heart rate × SV
devices are available
to calculate systolic
Preload
BP variation, pulse
Afterload
pressure variation, or
Contractility
SV variation. Pressure changes during
respiration predict “fluid responsiveness” and the need
for preload augmentation to improve the patient’s hemodynamics.
Perhaps the best way to assess preload is simply to evaluate the patient’s response to fluid administration. Whenever a patient has symptomatic hypotension of uncertain
pathology, a fluid bolus should be the healthcare provider’s
first consideration. If the patient has a favorable response
to volume infusion, continue administering fluids until the
patient peaks and sustains hemodynamic stability.
Generally speaking, hypovolemic and vasogenic states
require preload augmentation to stimulate better cardiac
contractility and CO. Cardiogenic states, on the other
hand, respond better to fluid removal, to return the ventricle to optimal stretch for better pump function.
What can go wrong: Heart rate and preload
Hypotension and decreased perfusion could be caused by
a rapid heart rate (such as ventricular tachycardia at 160
beats/minute) or a low heart rate (such as third-degree
atrioventricular block at a rate of 30 beats/minute).
A preload imbalance creates another potential threat
to BP and tissue oxygenation. Whether preload is decreased or increased, myocardial workload and oxygen
demand increase. Decreased preload (hypovolemia)
forces the heart to pump faster to maintain BP, and in
severe situations, can lead to hypovolemic shock. However, increased preload also can cause hemodynamic
compromise, because an overstretched myocardium can’t
be an effective pump. Preload excesses can be systemic,
such as in hypervolemia, or isolated to the left ventricle,
as in early pump failure.
In an effort to reduce the myocardial workload caused
by a preload imbalance, clinicians sometimes say they
want to “keep the patient dry.” However, the reflex tachycardia and vasoconstriction stimulated by an underfilled
vascular system and decreased preload can sabotage this
strategy.
Many clinicians consider diuretics such as furosemide
as BP-lowering drugs. But a patient’s BP response to furosemide depends on his location on the Frank-Starling
curve: When patients are hypovolemic (understretched
myocardium) or even euvolemic (optimally stretched
myocardium), furosemide will generally lower BP. This
is why the drug works well for treating hypertension. But
in patients whose myocardium is overstretched (as in
hypervolemia or in heart failure), furosemide can reduce
ventricular volume, optimize stretch, maximize contractility, and even elevate BP.
Preload can be assessed clinically by considering the
patient’s medical history, baseline weight, intake and
output, neck vein status, and other physical findings, or
by the patient’s B-type natriuretic peptide (BNP) level.
BNP is secreted into the bloodstream by the ventricles
when they’re overly stretched, but levels also are sensitive
to other factors such as patient age, gender, weight, and
renal function. Serum BNP levels greater than the normal
upper limit of 100 pg/mL imply heart failure, but this is
considered reliable only in the absence of renal failure.3,4
Preload also can be evaluated by invasive monitoring of
central venous pressure and pulmonary artery (PA) occlusive pressure monitoring; however, these measurements
haven’t been shown to reliably reflect preload volume.
A better way to evaluate preload may be the newer,
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When afterload is out of balance
Afterload also has variable effects on BP. In states of
vasodilation such as sepsis and anaphylaxis, BP is difficult to maintain and the patient’s perfusion declines.
However, if the arterial beds are constricted to improve
BP, the patient can reach a critical point beyond which
the heart can no longer overcome resistance and can fail
to maintain CO. This is most likely to occur in patients
with depressed myocardial function and indicates the
need for a vasodilator, such as nitroglycerin. Although
nitroglycerin and other vasodilators often are thought
of as BP-lowering medications, and are appropriate for
treating hypertension, they also reduce vascular tone and
resistance to cardiac emptying.
As with the other hemodynamic variables, afterload
has an optimal level, and imbalances impair the patient’s
hemodynamics and effective tissue perfusion. Clinical
methods for evaluating afterload are limited to the patient’s skin characteristics, which can be subjective and
unreliable. Hypovolemic and cardiogenic problems can
cause stress-response-mediated vasoconstriction, the
classic cool and clammy skin of hypotension, and low
CO states. Vasogenic shock, on the other hand, evokes
vasodilation, so the patient’s skin generally is flushed,
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even warm, early in the physiologic process.
Unfortunately, better measurements of afterload can
only be obtained with invasive hemodynamic monitoring, and even then are mathematically calculated and
prone to error. In general, vasodilatory states benefit
from vasopressor agents to raise afterload back to its
optimal level. Cardiogenic states benefit from small and
careful additions of vasodilators to reduce cardiac workload and promote CO.
Frank-Starling curve
The relationship between myocardial contractility and
preload is shown in this curve. Under- and overstretching of the ventricle can lead to a drop in contractility, and
therefore a decrease in the patient’s BP.
LVED pressure (mm Hg)
0
Considering contractility
No matter what causes shock, myocardial contractility is
decreased. In cardiogenic shock, reduced contractility is
secondary to a direct myocardial insult. In hypovolemic
shock, reduced contractility is a consequence of poor
stretch and inadequate stimulation of Frank-Starling
mechanism, all of which are reversed once preload is
restored. In vasogenic shock, reduced contractility is the
result of vascular volume pooling in the periphery and
capillary leakage.
Vasogenic states also cause afterload to drop to levels
that may inadequately stimulate the heart to respond
with increased contractility. In the septic form of vasogenic shock, chemical mediators directly depress muscle
function.
Although increased contractility is rare, it can affect
BP. For example, patients with hypertrophic cardiomyopathy have adequate muscle strength, but due to
increased muscle mass, the ventricle has no room for
preload, and the patient can develop hypotension. In
some cases, surgical myectomy is performed to debulk
the muscle and create space for blood. Some centers perform catheter-based ablation procedures, infarcting the
ventricular septum to enlarge the outflow tract and augment CO.5
Treatment for contractility imbalances depends on
the type of shock. Patients with hypovolemic and vasogenic shock need fluid therapy to increase preload,
which then will improve contractility and BP. Patients
with vasogenic shock, particularly those who are septic,
also may benefit from inotropic support. Patients with
cardiogenic shock primarily need preload and afterload
reduction, but may also need inotropic support to maintain adequate perfusion.
20
Cardiac output (L/min)
30
40
50
A
10
8
B
6
4
2
Overlap
Optimal
Overstretched
ment of the patient.
So, what’s an acceptable BP? The BP level generally
equated with adequate perfusion and the absence of cellular hypoxia is a mean arterial pressure of greater than
65 mm Hg, or a systolic pressure of greater than 90 mm
Hg.6,7 Unfortunately, this target BP has never been scientifically scrutinized, and was merely proposed decades
ago based on the fact that the kidneys cease to produce
urine at pressures below 60 mm Hg.
Adding to these concerns, cuff pressures may not be
accurate for hypotensive patients. The most accurate BP
measurement is made invasively via an arterial line.8 Because an arterial catheter is inside the vessel, it eliminates
external variables that affect the accuracy of cuff readings,
such as disproportionate cuff size, misaligned cuff bladder, low-quality stethoscopes, and overall poor technique.
Also, the vasoconstriction common to both hypertension
and hypotension hampers vessel vibrations and reduces
Korotkoff sound transmission, making cuff pressures less
dependable when the patient’s BP is abnormal.
Accurate and trustworthy BP readings can be obtained by an arterial catheter placed in an appropriate
vessel, with the transducer stopcock properly leveled at
Getting back in balance
As the patients at the beginning of this article illustrate,
not every patient with a low BP is in shock and not all
hypoperfusing patients have dangerously diminished BP.
The presence of hypotension, however, should alert you
to a possible problem and spur a thorough clinical assessED Insider
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the phlebostatic axis, and the system’s dynamic response
deemed adequate by square wave testing. Because arterial
line pressures and cuff pressures aren’t expected to be the
same, comparing the two is unnecessary. With the move
from mercury to aneroid devices, cuff BP will become
more questionable, differing from arterial line readings
even in normal pressure ranges.9,10
With all the concerns about accurate BP readings, the
lack of an evidence-based BP target, and variable tolerance of hypotension, BP appears to be an unreliable measure of perfusion at best. One better reflection of cellular
oxygenation and the absence of shock is a serum lactate
level. Serum lactate levels above 2 mmol/L are abnormal;
levels above 4 mmol/L indicate lactic acidosis, anaerobic
metabolism, and poor cellular perfusion.11 Fluid and
medications to improve perfusion can be titrated to BP,
but efficacy may be better confirmed by tracking changes
in lactate levels as well.
Another measure of perfusion adequacy is venous
oxygen saturation. Traditionally, mixed venous oxygen
saturations are used with PA blood sampling, requiring
insertion of a PA catheter. However, central venous oxygen saturation (SCVO2) has been shown to parallel mixed
venous readings and can be obtained from a central venous access.
SCVO2 reflects the balance between oxygen delivery and
consumption. Oxygen delivery is determined by arterial
oxygen saturation (SaO2, a measure of the lungs’ ability
to bring in oxygen), hemoglobin (the blood’s ability to
carry oxygen), and CO (the heart’s ability to transport
oxygen). Oxygen consumption is determined by cellular
extraction. To stabilize a hypotensive and hypoperfusing patient, the SaO2, hemoglobin, and CO can be manipulated to reach an SCVO2 range of 70% to 75%, the
level deemed to represent oxygen balance at the cellular
level. For example, the prescriber might order ventilator
adjustments to improve SaO2, a blood transfusion to augment hemoglobin, I.V. dobutamine to increase CO, or
sedatives to reduce myocardial oxygen demands.
The truth about BP is that it’s not as reliable as we
would like to think, and that it’s an imperfect assessment
for something as complex as perfusion. The true assessment of cellular hypoxia is made clinically and chemically. By looking for signs and symptoms of hypoperfusion
and measuring byproducts of anaerobic metabolism and
oxygen imbalance, you can better determine a patient’s
true cardiovascular status and the efficacy of your interventions. Although BP is still an important parameter to
monitor, it’s better viewed as a warning for the need to
further investigate rather than the definitive marker of
shock and the primary target for supportive therapy. ■
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REFERENCES
1. Buist M, Bernard S, Nguyen TV, Moore G, Anderson J, et al. Association between clinically abnormal observations and subsequent in-hospital mortality: a prospective study.
Resuscitation. 2004;62(2):137-141.
2. Tuggle D. Optimizing hemodynamics: strategies for fluid and medication titration in
shock. In: Carlson K, ed. AACN Advanced Critical Care Nursing. Elsevier Inc; 2008.
3. Cowie MR, Jourdain P, Maisel A, et al. Clinical applications of B-type natriuretic
peptide (BNP) testing. Eur Heart J. 2003;24(19):1710-1718.
4. McKie PM, Burnett JC Jr. B-type natriuretic peptide as a biomarker beyond heart
failure: speculations and opportunities. Mayo Clin Proc. 2005;80(8):1029-1036.
5. Kimmelstiel CD, Maron BJ. Role of percutaneous septal ablation in hypertrophic
obstructive cardiomyopathy. Circulation. 2004;109(4):452-456.
6. Kellum JA, Pinsky MR. Use of vasopressor agents in critically ill patients. Curr Opin
Crit Care. 2002;8(3):236-241.
7. Pinsky MR, Vincent JL. Let us use the pulmonary artery catheter correctly and only
when we need it. Crit Care Med. 2005;33(5):1119-1122.
8. Pittman JA, Ping JS, Mark JB. Arterial and central venous pressure monitoring. Int
Anesthesiol Clin. 2004;42(1):13-30.
9. O’Brien E. Demise of the mercury sphygmomanometer and the dawning of a new era
in blood pressure measurement. Blood Press Monit. 2003;8(1):19-21.
10. Valler-Jones T, Wedgbury K. Measuring blood pressure using the mercury sphygmomanometer. Br J Nurs. 2005;14(3):145-150.
11. Rivers EP, Ander DS, Powell D. Central venous oxygen saturation monitoring in the
critically ill patient. Curr Opin Crit Care. 2001;7(3):204-211.
Deborah Tuggle is a critical care clinical nurse specialist at Jewish Hospital & St. Mary’s
HealthCare in Louisville, Ky. Adapted and updated from Tuggle D. Hypotension and
shock: the truth about blood pressure. Nursing Critical Care. 2009;4(6):29-35.
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