- Valvular Heart Disease — Kenneth Korr, M.D
- Blood pressure assessment in the hypovolemic shock patient
- Basic Principles of Noninvasive BP Measurement in Infants
- Physiology, Pulse Pressure
- Is Pulse Pressure Another Way to Measure Cardiac Risk?
- What Is Pulse Pressure?
- Matching Activity
- Patient Diagnosis Activity
- Patient Diagnosis Solution
- Pulse Pressure: What is it and how does it affect your heart health?
- What is pulse pressure?
- What influences the pulse pressure?
- How to measure your pulse pressure
- Normal pulse pressure
- Wide pulse pressure
- Narrow pulse pressure
- Isolated Elevation of Diastolic Blood Pressure
- Auscultated BP
- K2 BP
- Comparison by Clinical Subgroup
Valvular Heart Disease — Kenneth Korr, M.D
VALVULAR HEART DISEASE
Lecturer: Kenneth Korr, MD
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GENERAL PRINCIPLES OF VALVE MALFUNCTION:VALVULAR STENOSIS: Pressure in upstream chamber >> Pressure indownstream chamber during time of flow (when valve is normally open).
Hemodynamic Hallmark = “PRESSURE GRADIENT”
VALVULAR REGURGITATION: (Alsotermed “INSUFFICIENCY” or “INCOMPETENCE” )
Retrograde flow of blood “upstream” duringtime when valve is normally closed.
Hemodynamic Hallmark = “VOLUME OVERLOAD”
EXAMPLES OF VALVULAR HEART DISEASE
Obstruction of blood flow from LA toLV during diastole, causing increased pressure in the left atrium, pulmonarycapillaries and, eventually, the right side of the heart. (see fig1 and fig 1A)
As the valve area (i.e.
the cross-sectionalarea of the valve opening during diastole) becomes smaller, the pressuregradient increases.
The relationship between the mitral valve area, theforward cardiac output and the pressure gradient across the valve duringdiastole is complex, and is defined by this equation:
|CARDIAC OUTPUT (mI/min)|
|MITRAL VALVE AREA||=||DIASTOLIC FILLING PERIOD(sec/min)|
|SQ ROOT of PRESSURE GRADIENT(mm Hg)|
Examine the relationship between mitralvalve gradient and flow (cardiac output) for various valve areas.
(Fig2) As valve area gets smaller, conditions which increase valve flow(exercise, tachycardia) result in an increase in LA pressure (and henceworsening symptoms i.e. DYSPNEA).
Increased LA pressure -> Pulm HTN-> RV Pressure Overload -> RV failure & Tricuspid RegurgitationEtiology: Rheumatic HeartDisease
Symptoms:Dyspnea, Orthopnea, PND
Cough & Hemoptysis
Atrial Fibrillation, LA thrombus andsystemic Embolization
RV failure, TR and systemic congestionPhysical Signs:
Diastolic murmur (low-pitched rumble) & Opening Snap
Medical Rx:Digitalis — controls heart rateand maintains sinus rhythm
Anticoagulants — prevent systemicembolization
Diuretics — reduce pulmonary vascularcongestion Surgical Rx
Invasive Rx:Balloon mitral valvulotomy Surgical Rx:Mitral valve commissurotomy
Mitral valve replacement
LV ejects blood antegrade into theAorta and retrograde into the LA.COMPENSATORY MECHANISMS:
Frank-Starling: Increased preload–> LV Dilatation –> increased stroke volume
Initially — Increased LV EjectionFraction –> increased stroke volume
(Eventually — LV systolic functiondeteriorates and CHF ensues) The severity of MRand the ratio of forward cardiac flow (cardiac output) to backward floware determined by several, interacting factors:1) the size of the mitralorifice during regurgitation
2) the systemic vascular resistanceopposing forward flow from the ventricle
3) the compliance of the leftatrium
4) the systolic pressure gradientbetween the LV and the LA
5) the duration of regurgitationduring systole (not all regurgitation is holo-systolic)
Effect of MR on LA pressuredepends on LA Compliance (see Figure 3)
|ACUTE MR (non-compliantLA)||CHRONIC MR (compliant LA)|
|Normal LA size||Dilated LA|
|Increased LA pressure||LA pressure normal or sI inc|
|“V” waves on PCW tracing||Absence of V waves|
|Pulmonary Edema||Low output state|
Anatomic structures integralto MV competence: Posterior LA wall, Ant & Postvalve leaflets, chordae tendinae, papillary muscles and their attachmentto LV wall.Etiology:Myxomatous degeneration (MVprolapse) Coronary artery disease (ischemicpapillary muscle dysfunction)
Infectious endocarditis (acute andchronic)
Chronic rheumatic heart disease
Marked LV enlargement from any cause(e.g. dilated cardiomyopathy)
Ruptured papillary muscle &/orchordae tendinae
Hypertrophic Cardiomyopathy with obstruction
Mitral annular Ca++
Congenital cleft MV, etc.
Symptoms:Acute MR: PulmonaryCongestion Chronic MR: weakness, fatigueand low output state
+ A. Fib., systemic emboli, RV failure (less common thanwith MS)NaturaI Hx => gradual LV dilatation andfailure
Physical findings:Holosystolic apical murmur
+ S3 gallop
+ laterally displacedapical impulseTreatment:Medical Rx: Digitalis for atrial arrhythmias(a. fib)
Anticoagulation to prevent systemicembolization
Diuretics to reduce pulmonary congestion
Vasodilators to reduce afterload (impedanceto LV ejection)
Surgical Rx: Mitralvalve replacement or repair
Obstruction to LV outflow during systole.
Pressure gradient across the aorticvalve (pressure higher in LV than aorta during systole), causes chronicLV “Pressure Overload”.
Compensatory concentric left ventricularhypertrophy –> reduced LV compliance.
Thus, LV is “stiff” (noncompliant)and LVEDP rises rapidly with increases in LV end-diastolic volume.
Classification:Valvular -> Rheumatic, Bicuspid,Degenerative Calcific
Subvalvular -> Fixed or Dynamic (ASH)
Supravalvular-> Congenital (rare) The relationship betweenthe aortic valve area, the forward cardiac output and the pressure gradientacross the valve is defined by this equation (similar to the equation formitral stenosis):
|CARDIAC OUTPUT ml/min|
|AORTIC VALVE AREA||=||SYSTOLIC EJECTION PERIOD sec/min|
|SQ ROOT OF SYSTOLIC PRESSURE GRADIENT|
Comparison with Mitral Stenosis:
Aortic valve area smaller than MVarea
Systolic Ejection Period
Blood pressure assessment in the hypovolemic shock patient
Updated January 18, 2016
Historically, EMS professionals relied on the vital signs, specifically blood pressure, in conjunction with other physical findings to determine if a patient was in hypovolemic shock.
Shock is a state of inadequate tissue perfusion.
However, it has become clearer that blood pressure and heart rate may not be a good early indicator of a hypovolemic shock state and may actually mislead the EMS practitioner when considering a differential diagnosis.
Alteration in vital signs primarily results from both a reduction in blood volume and a cascade of neural and hormonal responses in an attempt to increase the blood pressure and conserve body fluid. We have always looked for profound changes in the blood pressure to assist in making a differential diagnosis of shock.
Blood pressure may be the vital sign we measure the most and understand the least
For example, a drop in the systolic blood pressure to 90 mm Hg is an indication that the shock state deteriorated from a compensatory stage to a decompensatory, or progressive stage. This dramatic drop, which is a clear but late finding, represents approximately a 30 percent blood loss in a healthy individual.
The literature suggests that a patient could be in a true shock state and not initially present with a dramatic decrease in blood pressure or increase in heart rate [1,2].
Therefore, it is imperative to understand what the blood pressure is indicating and that the signs of poor perfusion can be assessed to identify early indicators of shock.
Blood pressure changes from fluid loss
Blood pressure is determined by the cardiac output (CO) and peripheral vascular resistance (PVR). The equation BP = CO × PVR represents the interaction of the two variables. Cardiac output is the amount of blood ejected from the left ventricle in one minute.
Peripheral vascular resistance is the resistance in the peripheral arteries and arterioles determined by the vessel size. A decrease in the vessel lumen will increase the resistance; whereas, a decrease in the vessel size will decrease the peripheral vascular resistance.
An increase in the cardiac output or peripheral vascular resistance will lead to an increase in the blood pressure; whereas, a decrease will cause a decrease in blood pressure.
Cardiac output is an interaction of heart rate (HR) and stroke volume (SV), which is reflected in the equation CO = HR × SV.
The stroke volume is defined as the amount of blood ejected from the left ventricle with each contraction and is determined by the preload, myocardial contractility and afterload.
In general, an increase in heart rate or stroke volume will lead to an increase in cardiac output. Inversely, a reduction in heart rate or stroke volume will lead to a decrease in cardiac output.
The loss of blood associated with hypovolemic shock causes a reduction in the venous volume, which in turn diminishes the preload, stroke volume and cardiac output.
A drop in cardiac output, which is reflected by a falling systolic blood pressure, results in a decrease in pressure in the carotid bodies and aortic arch, and triggers the baroreceptors (inhibitory stretch-sensitive receptors that constantly measure arterial pressure).
When the baroreceptors sense a decrease in the arterial pressure, the sympathetic nervous system is prompted to initiate a cascade of neural and hormonal responses in an attempt to restore the pressure back to a normal state.
The direct neural stimulation and hormonal influence will increase the heart rate, increase myocardial contractility and increase peripheral vascular resistance through systemic vasoconstriction.
The diastolic blood pressure is an indirect measure of peripheral vascular resistance; thus, as the vessels constrict and vascular resistance increases, the diastolic blood pressure is maintained or increases.
EMS provider assessment of blood pressure
Even though the patient is losing blood and the venous volume and pressure is decreasing, the blood pressure will look relatively stable as the heart rate, myocardial contractility and peripheral vascular resistance increase as a means to compensate. This could produce a blood pressure that is deceiving and may lead the EMS practitioner into a false sense of patient stability.
For example, a blood pressure of 102/88 mm Hg surely falls within a normal limit; however, it could also be a clear sign of hypovolemia when assessed closer.
It is important to not only look at the overall blood pressure, but also the pulse pressure, which can provide valuable information about the hemodynamic state.
The pulse pressure is the difference between the systolic blood pressure and the diastolic blood pressure.
For example, using the pressure discussed previously, the pulse pressure is calculated at 14 mm Hg (102 – 88 = 14 mm Hg). If the difference is less than 25 percent of the systolic blood pressure, the pulse pressure is considered to be narrow. A wide pulse pressure is considered to be greater than 50 percent of the systolic blood pressure.
A narrow pulse pressure in a hypovolemic shock patient indicates a decreasing cardiac output and an increasing peripheral vascular resistance. The decreasing venous volume from blood loss and the sympathetic nervous system attempt to increase or maintain the falling blood pressure through systemic vasoconstriction.
This increase in heart rate and myocardial contractility is reflected in the decreasing systolic BP, the increasing diastolic BP and the narrowing pulse pressure.
Thus, a blood pressure of 102/88 mm Hg no longer appears to be “normal” and requires further assessment of heart rate, respiratory rate and other signs of perfusion, such as the skin color, temperature, condition and the patient’s mental status.
Be careful when assigning a blood pressure assessment as “normal.” The pulse pressure may provide more valuable and important information than the actual blood pressure itself. Blood pressure should be considered in the “whole” assessment of the patient and not purely as an independent finding.
1. Edelman D.A., White M.T., Tyburski J.G., et al: Post-traumatic hypotension: should systolic blood pressure of 90–109 mm Hg be included?. Shock 27. (2): 134-138.2007.
2. Victorino G.P., Battistella F.D., Wisner D.H.: Does tachycardia correlate with hypotension after trauma?. J Am Coll Surg 196. (5): 679-684.2003.
Basic Principles of Noninvasive BP Measurement in Infants
Systolic, diastolic, and mean arterial pressures (MAP) are the 3 BP values typically reported; to interpret a BP reading, all 3 must be evaluated.
Systolic and diastolic BP are the pressures at the highest and lowest points, respectively, of the arterial waveform.
Mean arterial pressure is the average pressure during the entire cardiac cycle and integrates the area under the arterial pressure waveform. The value of MAP depends on the shape and size of the pressure-wave contour.
Although evaluating MAP alone is insufficient, MAP may provide an important indication of BP change because it represents the average perfusion pressure.
A single MAP value may be easier to trend; changes in MAP may also be easier to interpret than changes in systolic or diastolic pressures, which at times may move in different directions.
 In invasive, or intra-arterial BP (IABP), the measurement of MAP may be more reliable than systolic or diastolic pressures, because MAP is less prone to error caused by waveform damping.[8,9,10]
Most BP monitors report a MAP value. In any oscillometric BP monitor, the measurement of MAP is the principle that the oscillometric amplitude is a maximum at MAP.
 By definition, MAP is the average pressure during the entire cardiac cycle and can be calculated by integrating the area under the arterial pressure waveform.
Un systolic or diastolic pressure, MAP cannot be determined from a single point on IABP waveform.
If a MAP value is not available from a monitor, different formulas are available for estimating it.
[11,12,13,14,15] These formulas estimate MAP by making assumptions about the shape of the arterial pressure waveform (for example, adding one third of the pulse pressure value to the diastolic value).
There are some differences of opinion on whether or not estimates for MAP used in adults can be applied to neonates, primarily because of the different shape of neonatal and adult peripheral arterial pressure waves.
[14,15] Heart rate and peripheral amplification can affect the estimation of MAP because they affect the shape of the arterial pressure waveform. As seen in Fig 1, when heart rate or peripheral amplification alters the shape significantly, MAP estimated from a formula can differ significantly from the true time-averaged MAP.
Difference in mean arterial pressures (MAPs) differences in waveform shape. Courtesy of GE Healthcare Technologies.
Pulse pressure (PP), the numerical difference between systolic and diastolic values, is an indicator of cardiac status that is often not reported by standard BP monitors ( Table 1 ).
Pulse pressure may have a significant positive correlation with birthweight in infants weighing 610 to 4220 g; however, PP does not appear to change as much as systolic, diastolic, and mean pressures with increasing birthweight.
Before calculating PP (or reporting IABP values), evaluate the arterial waveform for overdamping.
Suspect overdamping when you see a slurred upstroke, absent or distorted dicrotic notch, and loss of overall fine detail.
 A severely overdamped arterial waveform has falsely decreased systolic values and falsely increased diastolic values, which, if used in calculations for PP, will result in an inaccurately narrowed PP.
There is a paucity of research involving PP changes in neonates. A definition of a narrow PP was not found. One study of very-low-birthweight (VLBW) infants with patent ductus arteriosus, a condition traditionally associated with wide PP, defined wide PP as a diastolic pressure less than half of the systolic pressure.
Pulse pressure and BP changes before the diagnosis of pneumothorax were examined in a small study (n = 7). Before the diagnosis of pneumothorax and subsequent thoracentesis, systolic BP and PP increased in 5 of 7 neonates and remained unchanged in 1.
Blood pressure decreased, and PP narrowed dramatically, in 1 infant with cardiac tamponade. Others suggest that PP increases when heart rate decreases during apnea in infants.
 The increased PP appeared to be related to increases in systolic pressure and occasionally decreases in diastolic pressure.
Adv Neonatal Care. 2005;5(5):252-261. © 2005 W.B. Saunders
Physiology, Pulse Pressure
Pulse pressure is the difference between the systolic and diastolic blood pressures.
Pulse Pressure = Systolic Blood Pressure – Diastolic Blood Pressure
The systolic blood pressure is defined as the maximum pressure experienced in the aorta when the heart contracts and ejects blood into the aorta from the left ventricle, usually approximately 120 mm Hg.
The diastolic blood pressure is defined as the minimum pressure experienced in the aorta when the heart is relaxing before ejecting blood into the aorta from the left ventricle, often approximately 80 mm Hg.
Normal pulse pressure is, therefore, approximately 40 mm Hg.
A change in pulse pressure (Delta Pp) is proportional to volume change (Delta V) but inversely proportional to arterial compliance (C):
Delta Pp = Delta V/C
Because the change in volume is due to the stroke volume of blood being ejected from the left ventricle (SV), we can approximate pulse pressure as:
Pp = SV/C
A normal young adult at rest has a stroke volume of approximately 80 mL. Arterial compliance is approximately 2 mL/mm Hg, which confirms that normal pulse pressure is approximately 40 mm Hg.
Arterial compliance is equal to the change in volume (Delta V) over a given change in pressure (Delta P):
C = Delta V/Delta P
Because the aorta is the most compliant portion of the human arterial system, pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again.
A pulse pressure that is less than 25% of the systolic pressure is inappropriately low or “narrowed,” whereas, a pulse pressure of greater than 100 is high or “widened.”
Arteries are efferent vessels that lead away from the heart. They are lined by endothelial cells and consist of 3 different layers, which can be seen in the figure below. The innermost layer, the tunica intima, consists primarily of an endothelial layer, subendothelial layer, and an internal elastic lamina.
The middle layer, also called the tunica media, has concentric layers of helically arranged smooth muscle cells, as well as varying amounts of elastic and reticular fibers and proteoglycans. Some of the larger arteries also contain an external elastic lamina.
Finally, the tunica adventitia also called the tunica externa, is the outermost layer made up of longitudinally oriented type-I collagen fibers.
There are 2 main types of arteries in the human body. The first, which is the more prominent of the 2, is the muscular artery. Muscular arteries have a thin intimal layer with a well-developed internal elastic lamina. They also have a muscular wall that can be up to forty layers thick.
The main function of these arteries is to regulate blood flow through adjustment of blood vessel caliber. The other main type of artery is the elastic artery. Elastic arteries are unique in that in the tunica media; they have elastic fibers interspersed in between the smooth muscle cells.
This allows elastic arteries to store kinetic energy to smooth out the surge in blood pressure that occurs during systole, known as the Windkessel effect.
An increase in pulse pressure can also be seen in a well-conditioned endurance runner. As he or she continues to exercise, the systolic pressure will progressively increase due to an increase in stroke volume and cardiac output.
Diastolic pressure, on the contrary, will continually decrease due to a decrease in the total peripheral resistance. This is due to the accumulation of red (slow twitch) muscle tissue in the arterioles instead of white (fast twitch) tissue. As a result, the pulse pressure is going to increase.
This can also be seen in individuals with larger amounts of muscle mass.
Aging impacts pulse pressure and arterial compliance. With aging, there is a decrease in the compliance of the large elastic arteries. This is due to structural molecular changes in the arterial wall, including decreased elastin content, increased collagen I deposition, and calcification which increases the stiffness of the wall. This process is often called “hardening of the arteries.
” As the left ventricle contracts against stiffer, less compliant arteries, systolic and diastolic pressures increase and can result in a widening of the pulse pressure. In response, the left ventricular tends to hypertrophy. When excessive pulse pressure is transmitted through the microcirculation of vital organs such as the brain and kidneys, extensive tissue damage tends to occur.
Valvular disease states such as aortic regurgitation and aortic stenosis result in changes in pulse pressure. In aortic regurgitation, the aortic valve insufficiency results in a backward, or regurgitant, flow of blood from the aorta back into the left ventricle, so that blood that was ejected during systole returns during diastole.
This leads to an increase in the systolic pressure and a decrease in the diastolic pressure, which results in an increase in pulse pressure.
In aortic stenosis, there is a narrowing of the aortic valve which interferes with the ejection of blood from the left ventricle into the aorta, which results in a decrease in stroke volume and subsequent decrease in pulse pressure.
Significant blood loss, such as seen in trauma or acute hemorrhage, leads to a decrease in both the preload and stroke volume and subsequently a decrease in pulse pressure.
The research done by Blacher et al. has shown that pulse pressure is a significant risk factor in the development of heart disease.
It has even been shown to be more of a determinant than the mean arterial pressure, which is the average blood pressure that a patient experiences in a single cardiac cycle.
In fact, as little as a 10-mm Hg increase in the pulse pressure increases the cardiovascular risk by as much as 20%. This finding was found to be consistent in both Caucasian and Asian populations.
Pulse pressure is also independently associated with an increased risk of developing atrial fibrillation. A study done by Mitchell et al. showed that patients with a pulse pressure of 40 mm Hg or less developed atrial fibrillation at a rate of 5.
6%, whereas patients with a pulse pressure greater than 61 mm Hg developed atrial fibrillation at a rate of 23.3%. In fact, for every 20-mm Hg increase in pulse pressure, the adjusted hazard ratio for developing atrial fibrillation is 1.28.
This risk is independent of mean arterial pressure.
Other research has focused on helping to maintain a normal pulse pressure. One of the most effective ways to do this is to increase arterial compliance. According to Thorin-Trescases et al.
, endurance aerobic exercise is the only intervention that has been shown to help mitigate age-related arterial stiffening by reducing age-related increases in collagen I and III and calcification.
These same benefits were not seen with resistance training, such as bench press, as this actually decreases the arterial compliance and increases the pulse pressure.
In addition to aerobic exercise training, Dart et al. demonstrated that one could also increase arterial compliance by increasing estrogen compounds (as in hormone replacement in post-menopausal women), increasing the consumption of n-3 fatty acids, and decreasing salt intake.
There has also been some evidence that supports the notion that ACE inhibitors have beneficial arterial wall effects and may be of use. Finally, research by Williams et al.
showed that folic acid supplementation (a 3-week treatment with 5 mg of folic acid per day) could decrease the plasma homocysteine concentrations, which improves endothelial dysfunction and causes a reduction in the stiffness of large arteries.
To access free multiple choice questions on this topic, click here.
1.Doherty TM, Salik I. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Mar 12, 2019. Physiology, Neonatal. [PubMed: 30969662]2.Campbell M, Pillarisetty LS. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Mar 31, 2019. Physiology, Korotkoff Sound. [PubMed: 30969600]3.Levanovich PE, Diaczok A, Rossi NF. Clinical and Molecular Perspectives of Monogenic Hypertension. Curr Hypertens Rev. 2019 Apr 09; [PubMed: 30963979]4.Iqbal AM, Jamal SF. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Dec 1, 2019. Essential Hypertension. [PubMed: 30969681]5.Taylor BN, Cassagnol M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Oct 11, 2019. Alpha Adrenergic Receptors. [PubMed: 30969652]6.Tackling G, Borhade MB. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): May 5, 2019. Hypertensive Heart Disease. [PubMed: 30969622]7.Rêgo ML, Cabral DA, Costa EC, Fontes EB. Physical Exercise for Individuals with Hypertension: It Is Time to Emphasize its Benefits on the Brain and Cognition. Clin Med Insights Cardiol. 2019;13:1179546819839411. [PMC free article: PMC6444761] [PubMed: 30967748]8.Anstey DE, Moise N, Kronish I, Abdalla M. Masked Hypertension: Whom and How to Screen? Curr. Hypertens. Rep. 2019 Apr 04;21(4):26. [PubMed: 30949843]
Is Pulse Pressure Another Way to Measure Cardiac Risk?
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When a nurse or doctor straps a blood pressure cuff around your arm, pumps it up to give your bicep a good squeeze and then watches where the needle lands on the dial, the two numbers that result are your systolic and diastolic blood pressure readings. They're taken at opposite ends of the cardiac cycle and represent the highest and lowest blood pressure levels at that particular time.
You may learn that your blood pressure is, say, 120/80, which is read as “120 over 80.
” The first number represents what's called systolic pressure, which indicates how much pressure your blood exerts against the walls of your arteries when your heart beats, according to the American Heart Association (AHA).
Your diastolic pressure, the second number, represents how much pressure is exerted between beats when the heart is at rest. (Incidentally, blood pressure is measured in units of mm Hg, which stands for millimeters of mercury.) A reading of 120/80, by the way, is considered healthy and normal by the AHA.
There's another measurement of heart health, however, that you may not be familiar with: pulse pressure. Pulse pressure is calculated by taking the difference between systolic blood pressure and diastolic pressure. The pulse pressure reading for a person whose blood pressure is 120/80, therefore, would be 40.
There's some evidence that pulse pressure is a better predictor of a person's heart health than systolic or diastolic blood pressure alone. However, using pulse pressure to diagnose cardiac problems is complicated.
Because it's determined using systolic and diastolic readings it really doesn’t provide unique information.
In other words, saying that someone has an “elevated pulse pressure” is usually the same as saying that they have an “elevated systolic blood pressure,” which will already have been determined.
What's more, a person with a normal blood pressure reading of 120/80 will have a pulse pressure of 40. But a person with a pulse pressure of 40 won't necessarily have normal blood pressure.
For instance, someone whose blood pressure reading is 140/100 also has a pulse pressure of 40 (the difference between 140 and 100 is 40), but that person's blood pressure would be considered elevated.
Sometimes pulse pressure does provide important information. There's research showing that pulse pressure can be valuable when looking at a patient’s overall risk profile. Several studies have identified that high pulse pressure:
- Causes more artery damage compared to high blood pressure with normal pulse pressure
- Indicates elevated stress on a part of the heart called the left ventricle
- Is affected differently by different high blood pressure medicines
So if you're diagnosed with high blood pressure, your doctor may consider it when designing your overall treatment plan.
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American Heart Association. Understanding Blood Pressure Readings.
Vaccarino V, Berger AK, Abramson J, et al. Pulse pressure and risk of cardiovascular events in the systolic hypertension in the elderly program. Am J Cardiol. 2001;88(9):980-6. doi:10.1016/s0002-9149(01)01974-9
Dart AM. Should pulse pressure influence prescribing?. Aust Prescr. 2017;40(1):26-29. doi:10.18773/austprescr.2017.006
Homan TD, Cichowski E. Physiology, Pulse Pressure. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2019 Jan-.
- American Heart Association. “Understanding Blood Pressure Readings.”
- Vaccarino, V, et al. “Pulse Pressure and Risk of Cardiac Events in the Systolic Hypertension in the Elderly (SHE) program.” American Journal of Cardiology, 2001 Nov 1; 88(9):980-6.
What Is Pulse Pressure?
As you learned in the lesson, pulse pressure is the difference between an individual's systolic and diastolic blood pressure. Normal pulse pressure ranges between 30 and 50 mm Hg. In people over age 60, an increase or decrease in pulse pressure outside of the healthy range can be an indicator of heart disease or poor heart function.
Match each of the health conditions/risks listed below to the correct column in the accompanying table.
- ascites (excess fluid in the peritoneal cavity)
- atherosclerosis (fat deposits in the aorta)
- bradycardia (decreased heart rate)
- excess medication to reduce blood pressure
- hyperthyroidism (overactive thyroid gland)
- hypovolemia (low blood volume)
- pericardial effusion (fluid around the heart)
- sustained tachycardia (increased heart rate)
Patient Diagnosis Activity
A 61 year old woman checks in at an urgent care clinic complaining of dizziness, especially when she gets up in the morning. On her intake form, she lists all the medications she is currently taking, which includes ibuprofen for joint pain and propranolol as treatment for migraine headaches and essential tremor.
Ibuprophen is a nonsteroidal anti-inflammatory drug (NSAID) often used for treatment of arthritis pain and inflammation. Propranolol is a general beta-blocker used to treat chest pain, high blood pressure, heart rhythm disorders, and tremors, as well as to reduce the severity and frequency of migraine headaches.
When you take the patient's pulse and blood pressure, she has pulse rate of 48 and BP of 104/56. She reports these as the lower end of normal for her.
Is the patient's pulse pressure outside of the normal range? Is her dizziness ly a result of taking either medication?
Patient Diagnosis Solution
The female patient's pulse pressure is 104 – 56 = 48, so it is within the normal range. Her pulse is lower than typical. Most healthy adults have a resting heart rate of 60-100 beats per minute. A resting pulse rate of 48 is not unusual for healthy athletic individuals, though.
A variety of conditions can result in a low heart rate, or bradycardia.
These include aging, infection of heart tissue (myocarditis), hypothyroidism, calcium or potassium imbalance in the blood, chronic inflammatory diseases, and long term use of medications for other heart rhythm disorders, high blood pressure and tremor.
Propranolol belongs to a class of drugs known as beta adrenergic blockers or beta blockers. Propranolol affects the activity of epinephrine receptors of cardiac cells, slowing the heart rate of individuals taking it.
For individuals over 60 who have taken it a long time, there is risk of the heart beat becoming too low. NSAIDs, ibuprofen, may decrease the blood pressure-lowering capabilities of propranolol.
More information is needed about the patient's health history to determine the exact cause of her dizziness and if it might be due to impaired heart function.
Pulse Pressure: What is it and how does it affect your heart health?
Your pulse pressure (also known as blood pressure amplitude) represents the force generated by your heart every time it contracts. It can easily be calculated as the difference between systolic and diastolic blood pressure.
What is pulse pressure?
The pulse pressure is the difference between your systolic and diastolic blood pressure. Just as your blood pressure it is measured in millimeters of mercury (mmHg).
Example: Your blood pressure reads 130 over 85 mmHg. This means that your pulse pressure is 45 mmHg.
|130 mmHg||–||85 mmHg||=||45 mmHg|
Pulse pressure can be an indicator for cardiovascular risks. It is, therefore, advisable to regularly monitor your pulse pressure.
What influences the pulse pressure?
There are several factors which influence the pulse pressure. In general, the blood pressure amplitude is primarily an indicator for the elasticity of your blood vessels which decreases with increasing age.
However, the blood pressure amplitude is also dependent on the amount of blood ejected from the heart (the so called stroke volume) and the time between two heart beats (the so called diastole).
How to measure your pulse pressure
The pulse pressure can be measured by reading your blood pressure.
Learn more: How to measure read your blood pressure
The blood pressure app Cora Health is ideal for analyzing your pulse pressure. When reading your blood pressure you can either import your values automatically via Bluetooth and Apple Health into Cora (with these blood pressure monitors) or log your values manually to get a graphical evaluation of your pulse pressure in the app’s dashboard.
Normal pulse pressure
Contrary to blood pressure – where there are defined values of healthy blood pressure – there are no generally recognized norms for pulse pressure values.
Nonetheless, there are benchmarks for your orientation: A blood pressure amplitude between 25 mmHg and 50 mmHg is often referred to as normal pulse pressure.
Values above 50 mmHg are commonly referred to as wide pulse pressure, whereas values below 25 mmHg are referred to as narrow pulse pressure.
Wide pulse pressure
High pulse pressure affects the circulation of coronary vessels and causes a reduction in oxygen supply in the heart muscle.
As a result, wide pulse pressure can cause cardiovascular diseases. A study showed that an increase in pulse pressure by 10 mmHg raised the risk of stroke and heart attack by about 20 percent.
Furthermore, the study demonstrated that a high blood pressure amplitude is a better predictor for cardiovascular diseases than systolic and diastolic blood pressure.
Moreover, Harvard Medical School found out that high pulse pressure poses the risk for atrial fibrillation.
Increased pulse pressure can be triggered by a variety of factors.
Illnesses that can affect your pulse pressure include aortic insufficiency (valvular heart defect), hyperthyroidism (overactive thyroid gland), and arteriosclerosis (a pathological storage of cholesterol in the wall layer of the arteries which reduces the elasticity of the blood vessels). Arteriosclerosis is particularly prevalent in people over the age of 60 and should be monitored by older people. Arteriosclerosis can also lead to isolated systolic hypertension (high blood pressure).
Narrow pulse pressure
Even though there are no commonly accepted values for narrow pulse pressure, low pulse pressure values can be an indication for heart conditions such as cardiac insufficiency (also known as congestive heart failure).
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Isolated Elevation of Diastolic Blood Pressure
Elevated blood pressure (BP) has been widely documented as an important risk factor for stroke and a major risk factor for coronary heart disease.
1 Physicians have tended to regard elevation of diastolic blood pressure (DBP) as more important than elevation of systolic blood pressure (SBP) on the grounds that it is more closely related to end-organ damage.
2 However, epidemiological studies have shown that SBP may be at least as important a risk factor as DBP, with many studies showing it to be more important with regard to cardiovascular morbidity and mortality.345
Patients with elevation of both SBP and DBP67 and patients with isolated systolic hypertension89 have been shown to benefit from drug treatment. Thus, when SBP is significantly elevated, the argument for treatment can be made independent of a small degree of inaccuracy or variation in DBP.
Not infrequently, patients present with elevation of DBP only. This could be regarded as “isolated diastolic hypertension.
” In the National Health Examination Survey (NHES) and National Health and Nutrition Examination Survey (NHANES) studies, 6% to 9% of subjects with elevated BP readings had (isolated) elevation of DBP with a normal SBP.
1011 According to the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure, as many as 58 million people in the United States may have high BP.1 Thus, a considerable number of individuals have isolated elevation of DBP.
current widely accepted guidelines, a person with such a BP, for example, 125/100 mm Hg, may be treated pharmacologically, perhaps for life. However, in this example the pulse pressure (the numerical difference between SBP and DBP) is smaller than expected for this level of mean arterial pressure,12 raising concern about the accuracy of the BP measurement.
Either underestimation of SBP or overestimation of DBP could contribute to such a reading. The existence of an auscultatory gap is widely known to affect SBP measurements. However, the accuracy of DBP measurements in such patients has not been adequately studied.
Because the decision to treat is often DBP rather than SBP, overestimation of DBP by as little as 5 mm Hg may frequently affect the treatment decision.
Confirmation of the accuracy of auscultated measurements has traditionally required invasive intra-arterial measurement, which is not practical in the clinical setting. Recently, we have described an objective noninvasive method of BP measurement that uses analysis of the brachial wideband external pulse recorded during BP cuff deflation.
131415 Wideband external pulse recording is the ability of a pressure sensor to record inaudible frequencies (down to 0.1 Hz) during cuff deflation. Three distinct components of the wideband external pulse signal can be detected (called K1, K2, and K3), one of which, K2, appears and disappears at SBP and DBP, respectively.
Fig 1 demonstrates the disappearance of K2 as cuff pressure is reduced from above intra-arterial DBP to below. The visible appearance and disappearance of the K2 signal are not subject to the vagaries of auscultation. It should be noted that K1, K2, and K3 are not related to the five phases of the Korotkoff sound.
We have previously shown that BP measured by K2 analysis is closer to intra-arterial pressure than auscultatory measurements13 and that no statistically significant differences of BP determination occurred between K2 and intra-arterial measurements with the use of a solid-state Millar catheter.
Thus, K2 analysis offers an alternative to invasive intra-arterial measurement in assessing the accuracy of indirect cuff measurements.
The purpose of this study was to compare BP measurement by auscultation with K2 analysis in a wide range of subjects, including those with isolated elevation of DBP.
BP was measured simultaneously by the auscultatory method and by K2 analysis in 175 nonobese subjects (109 men, 66 women); 132 were from a larger waveform analysis study, and 43 were specifically recruited because their seated clinic BP, auscultated by a physician, was characterized by a narrow pulse pressure (defined below).
Twenty-eight of the 175 subjects also underwent auscultation simultaneously by two observers using a dual stethoscope (S.G.B. and one of the trained Cardiovascular Center staff, ie, nurse, technician, or physician).
The second observer was unaware of the hypothesis of the study.
Auscultation by two rather than one examiner was the availability of personnel but was emphasized when the referred subject was believed to have a narrow pulse pressure.
The wideband external pulse was recorded with a specially designed Foil Electret Sensor that is similar in principle to conventional electret microphones used for airborne sound reception.
The Foil Electret Sensor amplifier system has a flat frequency response from below 0.1 Hz to above 2000 Hz.
Detailed characteristics of this sensor1617 and sensor-amplifier system18 have been described.
Recordings were obtained in a quiet room, with the subject in the supine position.
The wideband external pulse was recorded during cuff deflation with the sensor positioned over the brachial artery and under the distal portion of a BP cuff.
The cuff bladder (width) size (12- to 14-cm width×40-cm length) was selected to match the circumference of the subject’s arm as recommended by the American Heart Association.19 An electrocardiogram was also recorded.
The cuff was rapidly inflated to a pressure that was visually confirmed to be above the SBP by examination of the wideband external pulse recording, as previously described.
18 The cuff pressure was controlled by a cuff pressure inflator/regulator (E-10, DE Hokanson) and was read by both a mercury column and pressure sensor coupled to a VR6 physiological recording system (Electronics for Medicine).
Cuff pressure was manually deflated, with the use of the E-10 rotary pressure regulator handle, at a rate of 2 to 3 mm Hg/s.
The cuff inflation/deflation procedure enabled BP measurement simultaneously by the auscultatory and K2 methods. Inflation/deflation was performed three times on each subject.
Auscultation was performed with the use of a switch to mark the onset and disappearance of sound (Korotkoff phase V). The stethoscope was positioned distal to the cuff and held firmly in position without excessive pressure with the use of an elastic strap.
This eliminated extraneous noise caused by human touch and ensured that the surface of the stethoscope was maintained flush against the skin.
Each channel of the VR6 physiological recorder was sampled at 500 Hz by a 12-bit analog-to-digital convertor for storage into an IBM PC/AT computer using the codas (Dataq) data acquisition software.
SBP was identified as the cuff pressure at the electrocardiographic QRS complex immediately preceding the listener’s mark for the onset of Korotkoff sounds.
DBP was identified as the cuff pressure two QRS complexes before the mark identifying the disappearance of sound.
This procedure, which allows for the expected lag time before the appearance or disappearance of sound can be marked, is exactly analogous to extrapolation backward to the last auscultated sound during standard sphygmomanometry.
Identification of SBP and DBP from the K2 analysis has been previously described.13 Briefly, SBP was identified by the cuff pressure at the cardiac cycle in which the K2 signal initially appears and DBP by the cuff pressure at the last cardiac cycle before the K2 signal disappears.
Comparison by Clinical Subgroup
the auscultated BP, subjects were categorized into four clinical subgroups characterized by normal BP (NT: systolic