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 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 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 interventions. Let's look at how imbalances in heart rate, preload, afterload, or contractility affect BP.
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, minimally invasive systems that measure variations in BP across the respiratory cycle. Several devices are available to calculate systolic BP variation, pulse pressure variation, or 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.
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, 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.
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.
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 assessment 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 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.
* 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
* Infectious or inflammatory processes
* Traumatic chest contusion
* Exposure to cardiotoxic drugs
* Excessive doses of negative inotropes such as beta-blockers or calcium channel blockers
* Structural abnormalities such as valvular dysfunction or septal disruptions
* Obstructive pathologies including cardiac tamponade, pulmonary embolism, and tension pneumothorax
* External losses from decreased fluid intake, vomiting, diarrhea, diaphoresis, polyuria, hemorrhage, burns, and wound exudate
* Internal losses from bowel sequestration, internal hemorrhage, and ascites
* Systemic inflammation of multiple causes, such as pancreatitis or fulminant hepatitis
* Drug overdose
* Neurogenic insults such as a spinal cord injury or epidural drugs
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.