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ANTHROPOMETRICS:
BLOOD PRESSURE
Companion Guide
nsight.org
Version 14
Table of Contents
Patient Positioning...........................3
Order of Exam..................................3
Orthostatic Hypotension................11
Functional Medicine
Matrix Model..................................13
Conclusion.....................................13
Acknowledgements.......................14
Additional Resources.....................15
Equipment Needed
n Stethoscope with diaphragm and bell
n Blood pressure cuffs: pediatric, small, regular, and large adult, as well as thigh sizes
n Aneroid blood pressure gauge and cuffs
n Oscillatory blood pressure device and cuffs
n Vascular doppler
Patient Positioning
Arm Blood Pressures: The patient should be seated in a chair with their feet on the ground and their back
supported. The clinician needs to have access to both arms. Blood pressure is taken with the arm forward, parallel
to the floor, and at the level of the heart, with the arm resting comfortably on a table. It is preferable to take two
readings, 1-2 minutes apart and then average the measurements to obtain the blood pressure.2,3
Leg Blood Pressures: The patient is prone, lying on the exam table with the legs supported (not hanging past
the end of the table) to check popliteal pressures, and then rotates to supine to check pressures of the lower leg by
auscultating the dorsalis pedis or the posterior tibial artery using the bell of the stethoscope or a vascular doppler.
Standing, Sitting, and Lying Blood Pressures and Pulse (Orthostatic Blood Pressure determination):
It may be necessary to obtain standing blood pressures to check for postural effects in older adults or those with
diabetes, autonomic dysfunction, or on antihypertensive medications.
Patient lies supine for at least 2 minutes before the blood pressure and pulse is recorded. Patient then transitions
to a seated position; after 2 minutes, blood pressure and pulse is taken. Patient then transitions to a standing
position; after 2 minutes the blood pressure and pulse is taken again. Any symptoms of dizziness, lightheadedness, or
palpitations should be noted.
Order of Exam
Exam Techniques and Methods
n Note that blood pressures can be affected by the patient drinking caffeine or alcohol, smoking or using smokeless
tobacco, and taking over the counter medications within 12 hours prior to taking the blood pressure.
n Before taking the reading, have patient sit for 5 minutes in a quiet comfortable environment, with the arms
(20% wider than the diameter of the extremity). A new patient should have pressures checked in both arms
and both legs.
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Lying, Sitting, and Standing Bilateral Arm Pressures
n Determine the blood pressures in first the left arm then the right arm.
n Discrepancies in the systolic pressures should be no greater than 5 mm Hg.
Arm Pressures
n Place deflated cuff 2.5 cm above antecubital space. Ensure that fit is snug and firm around the arm with the
bladder over the brachial artery.
n Palpate brachial pulse. Rapidly inflate cuff until brachial pulse is no longer felt.
n Place bell of stethoscope over brachial artery location and inflate to 30 mm above pulse loss and then deflate at
n Repeat blood pressure on the other arm. Arm readings should not differ by more than 5 mm Hg.
n The arm with the higher of the two readings should be recorded in the chart and used when taking future
a 24-hour ambulatory blood pressure evaluation prior to starting medications. (This can help rule out possible
white coat hypertension when readings are taken in the office.)
Leg Pressures (the patient starts prone)
n Popliteal Pressures: Place thigh cuff above the popliteal fossa. After determining location of popliteal artery
pulse, follow the same procedure as for arm pressures to determine the mmHg.
n Ankle pressures are determined by placing the appropriate size cuff on the lower leg and after palpating the
dorsalis pedis pulse or the posterior tibial artery pulse then following the same procedure as for arm pressures.
Ankle/Arm Index (Ankle Brachial Index)
n The ankle/arm index equals the ankle pressure divided by the brachial artery pressure. Normal values are 1.0
or greater. An ankle/arm index of <0.9 has a sensitivity of 88% and specificity of 82%3 for peripheral vascular
disease. An elevated ankle brachial index is associated with stiffening of the soft tissues of the lower extremity;
seen in some diabetics or those with marked peripheral vessel atherosclerosis.
in pulse of greater than 20 bpm), autonomic dysfunction (no increase in pulse from sitting to standing with
change in blood pressure and increased dizziness), baroreceptor dysfunction, or normo-pressure hydrocephalus.
Asymmetric measurement of blood pressures may suggest subclavian/brachial occlusion or steal syndrome. Marked
discrepancies between arm and leg pressures may suggest coarctation of the aorta. Greater than a 5 mmHg difference
in arm blood pressures is abnormal. Spinal cord injury, regional pain syndromes, or autonomic dysfunction can
impact the proximal/distal symmetry of blood pressures.
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Table 1: Blood Pressure (mmHg) Risk Assessment
No Other Risk Average Risk; Low Added Risk; Moderate Added Risk; High Added Risk;
Factors No BP intervention Lifestyle changes, Lifestyle changes for Lifestyle changes
needed exercise and diet several months then and consider
interventions drug treatment if drug treatment
BP uncontrolled
1–2 Risk Factors Low Added Risk; Moderate Added Risk; High Added Risk; Very High Added Risk;
Lifestyle changes, Lifestyle changes for Lifestyle changes Lifestyle changes
exercise and diet several months then and consider drug and immediate
interventions drug treatment if treatment drug treatment
BP uncontrolled
>3 Risk Factors, Moderate Added Risk; High Added Risk; High Added Risk; Very High Added Risk;
Metabolic Lifestyle changes for Lifestyle changes Lifestyle changes Lifestyle changes
Syndrome or several months then and consider and consider and immediate
Other Disease drug treatment if drug treatment drug treatment drug treatment
BP uncontrolled
Diabetes Moderate Added Risk; High Added Risk; High Added Risk; Very High Added Risk;
Lifestyle changes for Lifestyle changes Lifestyle changes Lifestyle changes
several months then and consider and consider and immediate
drug treatment if drug treatment drug treatment drug treatment
BP uncontrolled
Established CV Very High Added Risk; Very High Added Risk; Very High Added Risk; Very High Added Risk;
or Renal Disease Lifestyle changes Lifestyle changes Lifestyle changes Lifestyle changes
and immediate and immediate and immediate and immediate
drug treatment drug treatment drug treatment drug treatment
*Adapted from the JNC6 risk stratification, JNC7 grade guidelines. For drug treatment interventions refer to JNC8 guidelines below.
BP = Blood pressure; DBP = diastolic blood pressure; SBP= systolic blood pressure; CV = cardiovascular; HTN = hypertension
Clinical Variables Influencing Prognosis (Risk Factors) Signs/Symptoms of Subclinical Organ Damage
1. Elevated Systolic or Diastolic Blood Pressures Influencing Prognosis
2. Age (>60) n Electrocardiogram showing left ventricular hypertrophy (LVH)
3. Race/Ethnicity
>38 mm
4. Smoking
n ECHO documented LVH (males >125 g/m2, females >110 g/m2)
5. Elevated Pulse Pressure in the elderly
n Carotid wall thickening (CIMT>0.9 mm) or plaque
6. Dyslipidemia
n Carotid-femoral pulse wave velocity >12 m/sec
n Total cholesterol >5.0 mmol/L (190 mg/dL)
n Ankle/Arm Index <0.9
n Low-density lipoprotein (LDL) >3.0 mmol/L
n Increase in plasma creatinine
(115 mg/dL)
n High-density lipoprotein (HDL): males <1.0 mmol/L Males: 115-133 mmol/L (1.3-1.5 mg/dL)
(40 mg/dL), females <1.2 mmol/L (46 mg/dL) Females: 107-124 mmol/L (1.2-1.4 mg/dL)
n Triglycerides >1.7 mmol/L (150 mg/dL) n Low glomerular filtration rate (<60 mL/min/1.73 m2) or creatinine
7. Fasting plasma glucose 5.6-6.9 mmol/L (102-125 mg/dL) clearance <60 mL/min
8. Abnormal 1 or 2 hour glucose tolerance test n Microalbuminuria 30-300 mg/24 hr or albumin/creatinine ratio
9. Abdominal obesity (waist circumference males >102 cm >22 (males) or >31 (females) mg/g creatinine
or >40 in, females >88 cm or >35 in) n Established cerebrovascular disease, stroke, or transient ischemic
10. Family history of premature cardiovascular disease
attack
(males <55, females <65) n Heart disease: myocardial infarction, angina, coronary
11. Diabetes mellitus
12. Autoimmune disease
revascularization, congestive heart failure, stent
n Renal disease: diabetic nephropathy, renal impairment, proteinuria
13. Heavy metal burden (lead, cadmium, arsenic, etc.)
n Peripheral artery disease or advanced retinopathy
14. Infections of the mouth, teeth, or gums
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Clinical Considerations for Modifiable Lifestyle Factors
Initiation of treatment outlined by JNC 8 is shown in Figure 1. The guidelines for treatment are influenced by age,
presence or absence of diabetes or chronic kidney disease, and race. The pharmacologic treatment interventions
vary depending on mechanisms (diuretic, calcium channel blockage, angiotension converting enzyme inhibition, or
angiotensin receptor blockage). Therapeutic lifestyle interventions should be addressed at all levels. These would include
sleep, nutrition, movement and exercise, mindfulness changes in thoughts and emotions, as well as relationships and habits.
Figure 1. JNC 8 Algorithm for Blood Pressure Goals and Intervention Management
Blood Pressure Goal and Therapy Intervention Based on Age, Race, Diabetes,
and Chronic Kidney Disease
Goal SBP<150 mmHg Goal SBP<140 mmHg Goal SBP<140 mmHg Goal SBP<140 mmHg
Goal DBP<90 mmHg Goal DBP<90 mmHg Goal DBP<90 mmHg Goal DBP<90 mmHg
Initiate thiazide-type diuretic or Initiate thiazide-type diuretic or ACEI, Initiate ACEI or ARB, alone or in
CCB, alone or in combination ARB, CCB, alone or in combo combination with other class
DM = diabetes mellitus; CKD = chronic kidney disease; SBP = systolic blood pressure; DBP = diastolic blood pressure; CCB = calcium channel blocker;
ACEI = angiotensin converting enzyme inhibitor; ARB = angiotensin receptor blocker
There are many diet and lifestyle habits that are associated with abnormal blood pressure. These have been well
documented in review articles that focus on nutrition-associated impacts on hypertension.4,5,8,9 Less-healthy diets are
often low in protein, potassium, and magnesium while being high in trans fats and sodium.
Nutritional interventions include eating healthy proteins, fats and oils, limiting simple carbohydrates, and adding
specific types of fiber. Attention to dietary minerals, soluble vitamins, and a wide variety of phytonutrients from
colorful vegetables and fruit is essential. Often adding a single food item can have a significant effect on systolic
blood pressure. Some of these effects are listed in Table 2.
Protein Reduces sympathetic activity, induces natriuresis, inhibits tyrosine kinase, reduces vascular
smooth muscle hypertrophy, lowers superoxide anion, decreases aldosterone. Whey protein
stimulates glutathione production.18-20 Carnitine limits end organ damage.22,23
n 1.5–1.8 g/kg body weight /day of non-animal protein
n Whey 30 g/day (ACEI)
n Carnitine 1g/bid
n Sardine muscle protein 3 g/d (ACEI)
n Bonito protein 1.5 g/d (natural ACEI)
n Soy protein 40 g/d (activates PPARs)
n Arginine up to 10 g/d from food or supplement; precursor vascular nitric oxide.23
n Taurine 6 g/day induces mild diuresis, vasodilation, increases atrial natriuretic factor,
improves insulin sensitivity, reduces homocysteine levels
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Table 2: Improving Nutrition Improves Blood Pressure4,5,8,9 (cont.)
Carbohydrates n Fiber: Oatmeal fiber, psyllium, glucomannan, or betaglucan improves insulin sensitivity
Vitamins n Vitamin D to maintain adequate serum levels (36-50 ng/mL); many people need 5000 iu/d
to obtain and maintain optimum levels
n Vitamin E: 100 iu Vitamin E/1 g EFA
n Vitamin C: 250–500 mg twice a day if lack of adequate ascorbates from fruits/vegetables
n B2 (riboflavin): 25 mg/d
n Vitamin B6: 5 mg/kg/d reduces sympathetic nervous system activity, improves
insulin sensitivity
n Methyl folate or folinic acid if the patient is hyperhomocysteinemic
n B12 If the patient is hyperhomocysteinemic
ACEI = Angiotension converting enzyme inhibitor; EFA = essential fatty acid; EPA = eicosapentaenoic acid; K = potassium; N = nitrogen; NFkB = nuclear factor kappa B;
PPARs = peroxisomal proliferator-activated receptors
Diet, nutrition, and lifestyle interventions functionally change cellular systems and improve hypertensive
vascular disease.8,9
A more extensive listing of lifestyle and therapeutic dietary interventions that can reduce blood pressure is
provided in Table 3.
Evaluate and address Increasing heavy metal burden of lead, arsenic, cadmium, or mercury increases:
heavy metal burden n Endothelial dysfunction
n Oxidative stress
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Table 3: Lifestyle Interventions for Reducing Blood Pressure by Many Mechanisms4,5,8,9 (cont.)
Behavior Modifications All of the following can lower blood pressure by a number of many autonomic nervous
system, endocrine, and neurotransmitter blood pressure influencers:
n Stress management
n Biofeedback, relaxation
n Pilates, Yoga
n Psychotherapy
n Hypnosis
n Meditation
n Spiritual and religious practices
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Table 3: Lifestyle Interventions for Reducing Blood Pressure by Many Mechanisms4,5,8,9 (cont.)
Weight Reduction To ideal body weight (60% of hypertensive patients are 20% over ideal body weight)
Decrease in weight of 4–5 kg decreases systolic BP by 7 points, diastolic by 5 points.
Decreases waist circumference
Weight loss improves:
n Cardiac output
n Left ventricular filling pressure
n Insulin sensitivity
n Catecholamine levels
n Systemic vascular compliance
n Sodium retention
n Sympathetic tone
n Plasma renin activity
n Aldosterone levels
n hs CRP
n TNF, IL-6, inflammatory markers, and oxidative stress
ACE = angiotension converting enzyme; ARB = angiotension receptor blocker; MAO = monoamine oxidase; NSAID = nonsteroidal anti-inflammatory drug; TCA = tricyclic antidepressant;
hs CRP = high sensitivity C-reactive protein; TNFα = tumor necrosis factor; IL-6 = interleukin-6
Using nutrition as an antihypertensive is accomplished by understanding the therapeutic class of the food, much
as we understand the therapeutic classes of pharmaceutical interventions. The abilities of food to act as angiotensin
converting enzyme inhibitors, angiotensin receptor blockers, and beta and calcium channel blockers are real.
The diuretic, renin-inhibitory, vasodilatory, and central alpha agonist activities of foods and supplements are listed
in Table 4.9
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Table 4: Natural Antihypertensive Compounds Categorized by Class9 (cont.)
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Orthostatic Hypotension
The normal blood pressure response. When an adult assumes an upright position, there is a pooling of 500 to
1000 cc of blood in the splanchnic circulation and the lower extremities, which triggers a rapid decrease in venous
return to the heart. The reduced ventricular filling leads to a drop in cardiac output and a resultant drop in blood
pressure. The fall in blood pressure causes a reflex compensation of the central and peripheral sympathetic response,
with a decreased parasympathetic outflow involving baroreceptors. The increased sympathetic outflow increases
peripheral vascular resistance, venous return, and cardiac output, limiting the fall in blood pressure.32 This is the
normal baro-reflex response: an increase in heart rate and vascular resistance to maintain cardiac output and blood
pressure.33 Most of the time this reflex is intact; there is usually a small drop in systolic blood pressure (5 mmHg), an
increase in diastolic blood pressure (5 mmHg), and an increase in pulse rate of up to 10 beats per minute. Greater
changes in systolic and diastolic pressures or pulse rate, warrant further work-up.
An abnormal blood pressure response. In patients with symptomatic orthostatic hypotension, one or more steps
in this reflex process result in a greater decline in blood pressure without a normal compensation in heart rate.34
There are many conditions and diseases associated with symptomatic orthostatic hypotension. Nutrition adequacy
plays a role in improving many of these conditions.
The prevalence of postural change in blood pressure increases with older age and with higher blood pressure levels
regardless of age.35 Aging individuals who develop cardiac, endocrine, or neurodegenerative conditions and are
treated with medications are more likely to have symptomatic orthostatic hypotension.32-34,36,37 For example, up to
25 percent of diabetic patients have altered autonomic response to position change and symptomatic orthostatic
hypotension.37 Examples of the medications and the associated conditions that exacerbate orthostatic hypotension
are summarized in Table 5. Heat intolerance, adrenal insufficiency, or situational or induced malnutrition (starvation,
anorexia nervosa, complications of bariatric surgery) also are associated with orthostatic hypotension. Specific
genetic single nucleotide polymorphisms affecting nutrient availability are being identified and may play a weak role
in maintaining the reflexes of normal blood pressure.38
Table 5: Medications and Associated Medical Conditions that Cause or Exacerbate Orthostatic Hypotension36
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A severe form of orthostatic hypotension includes reflex syncope.Vasovagal syncope, situational syncope, cardiac
sinus syncope, and atypical forms lead to an altered, neurally-mediated, transient loss of consciousness due to
vasodilation, bradycardia, systemic hypotension, and cerebral hypoperfusion.39 Nutrition intervention would be
considered as a secondary, not primary intervention in these conditions.40
Therapeutic uses of nutrition in symptomatic hypotension are entertained by addressing the root causes of the
conditions. Increasing protein in the sarcopenic orthostatic patient might be the intervention of choice when
the reasons for the sarcopenia are fully considered. Many underlying disease dysfunctions have nutrition levers.
Interventions can be quite specific: e.g., improving insulin response in the person with metabolic syndrome,
lessening the peak insulin levels and the resultant physiologic effects of insulin leading to increased orthostasis, or
addressing vitamin D deficiency in the elder with orthostatic hypotension.41,42 Reflexes that maintain blood pressure
are also influenced by nutrition.
The extensive range of interventions for the hypertensive patient reflects the many roles of nutrition in maintaining
a healthy blood pressure. The literature offers nutritional considerations for orthostatic hypotension in specific
conditions.42–45 For example, in postural orthostatic tachycardia (POTS), vitamin B1245 and vitamin D43,44 have
been identified as therapeutic treatments. In the case of orthostatic hypotension in the elderly, addressing alpha
hydroxylation insufficiency by using calcitriol in the vitamin D-deficient patient is therapeutic.42 Whether the
patient is a diabetic with neuropathy or a severely depleted anorexic, a Functional Medicine workup addressing the
adequacy of the diet as far as macronutrients, protein, healthy fats and oils, carbohydrates, and the many minerals
and vitamins that are needed to maintain the physiologic reflexes associated with a healthy blood pressure must
be completed.37,46–48
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Functional Medicine Matrix Model
When addressing the underlying causes of elevated blood pressure, consideration must be given to each of the areas
of possible system imbalance shown in the Functional Medicine Matrix in Figure 2. This figure highlights some of
the antecedents, triggers, and mediators of hypertension, as well as diet and lifestyle influences.
Retelling the Physiology and Function: Organizing the Patient’s Clinical Imbalances
Patient’s Story
Antecedents
Assimilation Defense & Repair
(e.g., Digestion, (e.g., Immune,
(Predisposing Factors— Absorption, Microbiota/GI, Inflammation,
Genetic/Environmental) Respiration) Infection/Microbiota)
Mental Emotional
e.g., cognitive e.g., emotional
Structural function, regulation, grief, Energy
Integrity perceptual sadness, anger, (e.g., Energy
Regulation,
Triggering Events (e.g., from Subcellular patterns etc.
Membranes to Mitochondrial
(Activators) Function)
Musculoskeletal
Structure)
Spiritual
e.g., meaning &
purpose,
Communication relationship with Biotransformation
Mediators/Perpetuators (e.g., Endocrine,
something greater
& Elimination
(Contributors) Neurotransmitters, Immune (e.g., Toxicity,
messengers) Detoxification)
Transport
(e.g., Cardiovascular, Lymphatic System)
Conclusion
The correct measurement of blood pressure is part of the ABCDs of Functional Nutrition Evaluation. Improving
blood pressure to low-risk or normal levels requires an evaluation of underlying nutritional causes of chronic
disease. The practitioner must understand systemic imbalance and how to intervene to correct the root causes of
blood pressure abnormalities. This means addressing and correcting the drivers of oxidative stress and immune
or inflammatory imbalance causing endothelial dysfunction. Elevated blood pressure is a symptom of imbalance;
improving blood pressure to normal levels promotes health instead of disease.
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Acknowledgements
IFM would like to acknowledge and thank the development team for their research, organization, and creation of the ABCDs of Functional
Nutrition Physical Exam series. P. Michael Stone MD, MS and topic specific contributors developed the materials. The Functional Nutrition
Evaluation; Blood Pressure materials were co-developed with Mark Houston, MD. The development team also included Kristi Hughes, ND,
Nicole Dotson, ND, Deanna Minich, PhD, and Nicholas Morgan, ND, who all did excellent work in support of the materials.
To cite: Stone PM, Houston M: Functional Nutrition Evaluation; Anthropometrics: Blood Pressure Companion Guide. Federal Way (WA):
Institute for Functional Medicine: 2016.
IFM n Blood Pressure n N Sight Videos and Resources: nsight.org © 2018 The Institute for Functional Medicine 14
44. Chaudhari SA, Sacerdote A, Bahtiyar G. 1- hydroxylation defect in postural orthostatic tachycardia syndrome: remission with calcitriol supplementation. BMJ Case Rep. 2012 Aug 13;2012. pii:
bcr0220125730. doi: 10.1136/bcr.02.2012.5730.
45. Öner T, Guven B, Tavli V, et al. Postural orthostatic tachycardia syndrome (POTS) and vitamin B12 deficiency in adolescents. Pediatrics. 2014 Jan;133(1):e138-42. doi: 10.1542/peds.2012-3427. Epub 2013
Dec 23
46. Marzola E, Nasser JA, Hashim SA, et al. Nutritional rehabilitation in anorexia nervosa: review of the literature and implications for treatment. BMC Psych. 2013; 13: 290.
47. Miller KK. Endocrine dysregulation in anorexia nervosa update. J Clin Endo Metab. 2011;96(10):2939-2949. doi:10.1210/jc.2011-1222.
48. Abed J, Judeh H, Abed E, et al. “Fixing a heart”: the game of electrolytes in anorexia nervosa. Nutr J. 2014 Sep 5;13:90. doi: 10.1186/1475-2891-13-90.
Additional Resources:
JNC8
James PA, Oparil S, Carter BL, et al. 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee
(JNC 8). JAMA. 2013 Dec. doi: 10.1001/jama.2013.284427.
Weber MA, Schiffrin EL, White WB, Mann S, Lindholm LH, Kenerson JG, et al. Clinical practice guidelines for the management of hypertension in the community: a statement by the American Society of
Hypertension and the International Society of Hypertension. J Clin Hypertens. 2014 Jan;16(1):14-26. doi: 10.1111/jch.12237.
JNC7 http://www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.htm
JNC6 http://www.nhlbi.nih.gov/health-pro/guidelines/archive/hypertension-jnc6
DASH Diet http://www.nih.gov/news/pr/apr97/Dash.htm
National High Blood Pressure Education Program http://www.nhlbi.nih.gov/about/nhbpep/indes.htm,
http://www.nhlbi.nih.gov/hbp/index.html.
Video Resources:
Campbell NR, Chockalingam A, Fodor JG, McKay DW. Accurate, reproducible measurement of blood pressure. CMAJ: Canadian Medical Association Journal. 1990;143(1):19-24.
Handler J. The Importance of Accurate Blood Pressure Measurement. The Permanente Journal. 2009;13(3):51-54.
Kurtz KJ. Bruits and Hums of the Head and Neck. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990
Chapter 18. Available from: https://www.ncbi.nlm.nih.gov/books/NBK289/
Ogedegbe G, Pickering T. Principles and techniques of blood pressure measurement. Cardiology clinics. 2010;28(4):571-586. doi:10.1016/j.ccl.2010.07.006.
Pessi, T. et al. Bacterial signatures in thrombus aspirates of patients with myocardialinfarction. 2013, Circulation 12(11):1219-1228. doi: 10.1161/CIRCULATIONAHA.112.001254.
Pickering TG, et al. Recommendations for blood pressure measurement in humans and experimental animals. Circulation. 2005 Feb 8;111(5):697-716.
Tolonen H, et al. Challenges in standardization of blood pressure measurement at the population level. BMC Medical Research Methodology. 2015;15:33. doi:10.1186/s12874-015-0020-3.
Wong DH et al. Acute cardiovascular response to passive leg raising. Crit Care Med. 1988 Feb;16(2):123-5.
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