DOCSLIB.ORG

3 Blood Pressure and Its Measurement

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Chapter 3 / Blood Pressure and Its Measurement 49 3 Blood Pressure and Its Measurement CONTENTS PHYSIOLOGY OF BLOOD FLOW AND BLOOD PRESSURE PHYSIOLOGY OF BLOOD PRESSURE MEASUREMENT POINTS TO REMEMBER WHEN MEASURING BLOOD PRESSURE FACTORS THAT AFFECT BLOOD PRESSURE READINGS INTERPRETATION OF BLOOD PRESSURE MEASUREMENTS USE OF BLOOD PRESSURE MEASUREMENT IN SPECIAL CLINICAL SITUATIONS REFERENCES PHYSIOLOGY OF BLOOD FLOW AND BLOOD PRESSURE The purpose of the arterial system is to provide oxygenated blood to the tissues by converting the intermittent cardiac output into a continuous capillary flow and this is achieved by the structural organization of the arterial system. The blood flow in a vessel is basically determined by two factors: 1. The pressure difference between the two ends of the vessel, which provides the driving force for the flow 2. The impediment to flow, which is essentially the vascular resistance This can be expressed by the following formula: 6P Q = R where Q is the flow, 6P is the pressure difference, and R is the resistance. The pressure head in the aorta and the large arteries is provided by the pumping action of the left ventricle ejecting blood with each systole. The arterial pressure peaks in systole and tends to fall during diastole. Briefly, the peak systolic pressure achieved is determined by (see Chapter 2): 1. The momentum of ejection (the stroke volume, the velocity of ejection, which in turn are related to the contractility of the ventricle and the afterload) 2. The distensibility of the proximal arterial system 3. The timing and amplitude of the reflected pressure wave When the arterial system is stiff, as in the elderly, for the same amount of stroke output, the peak systolic pressure achieved will be higher. The poor distensibility causes a greater peak pressure. In addition, a stiff arterial system results in faster transmission and reflection of the pressure wave, thereby adding to the peak pressure. The narrow and peaked pressure seen in the more peripheral muscular arteries is the effect of such reflection. The level to which the arterial pressure will fall during diastole is primarily 49 50 Cardiac Physical Examination dependent on the state of the peripheral resistance, which controls the runoff. Conditions with low peripheral resistance and vasodilatation will cause the diastolic pressure to fall to low levels. The mean arterial pressure is the average of all the pressures obtained over an entire duration of a cardiac cycle. Since diastole is longer than systole, the mean pressure is estimated as the sum of 60% diastolic pressure and 40% systolic pressure. More accurate measurement will be derived by integrating the area under a recorded pressure curve. The pulse pressure, which is the difference between the systolic and the diastolic pres- sure, reflects not only the stroke volume but also the state of the peripheral resistance. Conditions associated with a large stroke volume and low peripheral resistance will be expected to give rise to a large pulse pressure, and this will be reflected in the amplitude of the arterial pulse by palpation. While the control of the cardiac output is usually determined by local tissue flow under physiological states, the control of the arterial pressure is independent of these and is regulated through a complex system, which involves nervous reflexes and neurohu- moral mechanisms for short-term needs (such as “flight,” “fright,” and “fight” type reactions or in situations like those following acute loss of blood volume) and neuroen- docrine, renin–angiotensin–aldosterone system, and renal mechanisms for long-term adaptation. These control systems in the normal as well as their alterations in hyperten- sion and in heart failure are well discussed in standard texts for physiology and medicine. In this chapter our focus will be mainly on measurement of blood pressure by the sphyg- momanometer and its use in special clinical situations. PHYSIOLOGY OF BLOOD PRESSURE MEASUREMENT The indirect measurement of blood pressure by the sphygmomanometer involves the application of a controlled lateral pressure by an inflatable cuff to occlude the artery by compression, thereby stopping the flow. The detection of the resumption of flow during slow deflation allows the determination of the pressure. The cuff is normally applied to the arm over the brachial artery. When the cuff pressure exceeds the systolic pressure, the brachial artery is fully occluded and the flow ceases. When the cuff is deflated to pressures just below the systolic peak, the flow begins to resume with each cardiac systole. The jet of blood coming through the partially occluded vessel is associated with tapping-type sounds, which can be recognized using a stethoscope placed over the bra- chial artery just distal to the cuff. These sounds, termed the Korotkoff sounds, help in identifying the systolic and the diastolic pressures in the artery. The detection of the first appearance of Korotkoff sounds (Phase I) as the cuff is being deflated corresponds to the systolic pressure, and the disappearance of Korotkoff sounds with further deflation of the cuff corresponds to the diastolic pressure. Korotkoff sounds generally become muffled first when the cuff is being deflated before they totally disappear. It is always advisable to take the diastolic pressure to the level at which the sounds disappear because it is less likely to introduce errors (1). The Mechanism of Origin of Korotkoff Sounds The exact mechanism of origin of Korotkoff sounds is not completely established. They have been thought to result from turbulence of flow coming through the partially occluded artery. This is thought to be supported by the following: they become muffled (Phase IV) and eventually disappear (Phase V) generally when the flow resumes in Chapter 3 / Blood Pressure and Its Measurement 51 diastole, i.e., when the cuff is deflated below the diastolic pressure, allowing the artery to be open throughout the cardiac cycle. In addition, before they become muffled and completely disappear, they may sound like a short bruit (initially as soft bruit in Phase II and louder bruit as in Phase III). However, they do not always sound like murmurs and often present as sharp sounds. The Waterhammer theory was suggested (not to be confused with the water-hammer pulse in aortic regurgitation) to explain the presence of distinct sounds (2). The sounds are thought to be produced by the deceleration of high-velocity flow coming through the vessel as it opens up from an occluded state against the stationary column of blood distal to the occlusion. The intensity of the sounds, however, may vary, being loud and persistent to low diastolic pressures or throughout diastole in certain situations such as in aortic regurgitation, in children, and in pregnancy. In aortic regurgitation, the stroke volume tends to be large with increased velocity of ejection. Children generally have hyperkinetic circulation, and pregnant women tend to have a high cardiac output with increased sym- pathetic tone. On the other hand, Korotkoff sounds tend to be poor in low-output states. When an oversized cuff is used it may lead to underestimation of the systolic blood pressure. It has been shown that the state of the distal vasculature in the limb where the blood pressure is being measured affects the intensity of the Korotkoff sounds. Vasodi- latation makes the sounds louder, and vasoconstriction softer (3,4). When the peripheral resistance in the arm distal to the cuff was changed by interventions such as heating, cooling, and induction of reactive hyperemia, the amplitude of the Korotkoff sounds appeared to change. Thus, these effects may lead to either over- or underestimation of both systolic and diastolic pressures (5). In fact, when the Korotkoff sounds are poorly heard, they are best augmented by raising the arm (decreasing venous distension) and having the patient open and close his or her fist on the side where the pressure is being measured a few times (6,7). This is thought to increase the forearm flow. Others have proposed that the pressure pulse wave itself may be the source of the Korotkoff sounds. The sounds may be attributed to “shock waves” where the flow velocity of blood in the narrowed segment may exceed the pulse wave propagation velocity and give rise to vibrations in the audible frequency range. This would be analo- gous to the sonic boom heard when the speed of a jet plane reaches and surpasses the speed of sound. It is also possible that the Korotkoff sounds are related to energy (vibrations) that results from sudden termination of the pressure pulse wave at the site of the inflated cuff, which leads to partial occlusion of the vessel, causing this to become a terminating site favoring reflection. Between the systolic peak and the diastolic pressures during which time the Korotkoff sounds are present there is a considerable degree of termination and reflection together with beginning onward transmission of the pressure pulse wave. Once the cuff pressure is lowered below the diastolic pressure, there is no more termi- nation or reflection at the site of the cuff application and the pressure pulse is further transmitted along the artery. Therefore, there is no sound to be heard. This may be supported by the fact that when an oversized cuff is used, it may lead to underestimation of the systolic blood pressure. In conditions where the Korotkoff sounds are loud and last longer to low levels of diastolic pressure such as aortic regurgitation, there is a more rapid and higher launching momentum to the pressure pulse wave because of the large stroke volume, which is ejected with a rapid velocity. Thus, there may be more energy for dissipation at the termination sites. In significant aortic regurgitation, one often feels 52 Cardiac Physical Examination “pistol shots” over the femoral arteries, which are also often sites of reflection because of bifurcation.
Recommended publications
  • General Physical Examination Skills for Ahps

    General Physical Examination Skills for Ahps

    General Physical Examination Techniques for the Rheumatology Clinic This manual has been developed as an overview of the general examination of the rheumatology patient. Certain details have been specifically omitted because they have no relevance when examining a stable out patient in the rheumatology clinic. Vital Signs 1. Heart rate 2. Blood pressure 3. Weight 1. Heart Rate There are two things you want to document when assessing heart rate: The actual rate and the rhythm. Rate: count pulse for at least 15 – 30 seconds (e.g., if you count the rate for 15 seconds, multiply this result by 4 to determine heart rate). The radial pulse is most commonly used to assess the heart rate. With the pads of your index and middle fingers, compress the radial artery until a pulsation is detected. Normal 60-100 bpm Bradycardia <60 bpm Tachycardia >100 bpm 2. Heart Rhythm The rhythm should be regular. A regularly irregular rhythm is one where the pulse is irregular but there is a pattern to the irregularity. For example every third beat is dropped. An irregularly irregular rhythm is one where the pulse is irregular and there is no pattern to the irregularity. The classic example of this is atrial fibrillation. 3. Blood Pressure Blood pressure should be measured in both arms, and should include an assessment of orthostatic change How to measure the Brachial Artery Blood Pressure: • Patient should be relaxed, in a supine or sitting position, with the arms positioned correctly(at, not above, the level of the heart) • Remember that measurements should be taken bilaterally • Choice of appropriate cuff size for the patient is important to accuracy of measured blood pressure.
  • Hypertension – Adult – Clinical Practice Guideline

    Hypertension – Adult – Clinical Practice Guideline

    Hypertension – Adult – Clinical Practice Guideline Table of Contents EXECUTIVE SUMMARY ........................................................................................................... 3 SCOPE ...................................................................................................................................... 4 METHODOLOGY ...................................................................................................................... 5 INTRODUCTION ....................................................................................................................... 5 RECOMMENDATIONS .............................................................................................................. 5 Establish the Diagnosis ........................................................................................... 5 Patient Evaluation ................................................................................................... 7 Treatment Goals ..................................................................................................... 7 Lifestyle Modifications ............................................................................................. 8 Table 4 – Lifestyle Modifications ........................................................................ 9 Medication Treatment............................................................................................ 11 Figure 1 - Initiation and Titration of Antihypertensive Medication ..................... 13 Table 7 - Antihypertensive
  • Essentials of Bedside Cardiology CONTEMPORARY CARDIOLOGY

    Essentials of Bedside Cardiology CONTEMPORARY CARDIOLOGY

    Essentials of Bedside Cardiology CONTEMPORARY CARDIOLOGY CHRISTOPHER P. CANNON, MD SERIES EDITOR Aging, Heart Disease and Its Management: Facts and Controversies, edited by Niloo M. Edwards, MD, Mathew S. Maurer, MD, and Rachel B. Wellner, MD, 2003 Peripheral Arterial Disease: Diagnosis and Treatment, edited by Jay D. Coffman, MD, and Robert T. Eberhardt, MD, 2003 Essentials ofBedside Cardiology: With a Complete Course in Heart Sounds and Munnurs on CD, Second Edition, by Jules Constant, MD, 2003 Primary Angioplasty in Acute Myocardial Infarction, edited by James E. Tcheng, MD,2002 Cardiogenic Shock: Diagnosis and Treatment, edited by David Hasdai, MD, Peter B. Berger, MD, Alexander Battler, MD, and David R. Holmes, Jr., MD, 2002 Management of Cardiac Arrhythmias, edited by Leonard I. Ganz, MD, 2002 Diabetes and Cardiovascular Disease, edited by Michael T. Johnstone and Aristidis Veves, MD, DSC, 2001 Blood Pressure Monitoring in Cardiovascular Medicine and Therapeutics, edited by William B. White, MD, 2001 Vascular Disease and Injury: Preclinical Research, edited by Daniell. Simon, MD, and Campbell Rogers, MD 2001 Preventive Cardiology: Strategies for the Prevention and Treatment of Coronary Artery Disease, edited by JoAnne Micale Foody, MD, 2001 Nitric Oxide and the Cardiovascular System, edited by Joseph Loscalzo, MD, phD and Joseph A. Vita, MD, 2000 Annotated Atlas of Electrocardiography: A Guide to Confident Interpretation, by Thomas M. Blake, MD, 1999 Platelet Glycoprotein lIb/IlIa Inhibitors in Cardiovascular Disease, edited by A. Michael Lincoff, MD, and Eric J. Topol, MD, 1999 Minimally Invasive Cardiac Surgery, edited by Mehmet C. Oz, MD and Daniel J. Goldstein, MD, 1999 Management ofAcute Coronary Syndromes, edited by Christopher P.
  • Comparison of Traditional and Plethysmographic Methods for Measuring Pulsus Paradoxus

    Comparison of Traditional and Plethysmographic Methods for Measuring Pulsus Paradoxus

    ARTICLE Comparison of Traditional and Plethysmographic Methods for Measuring Pulsus Paradoxus Jeff A. Clark, MD, FAAP; Mary Lieh-Lai, MD, FAAP; Ron Thomas, PhD; Kalyani Raghavan, MD; Ashok P. Sarnaik, MD, FAAP, FCCM Background: In the evaluation of patients with acute (PPpleth) on the pulse oximeter. Mean difference and asthma, pulsus paradoxus (PP) is an objective and non- 95% confidence intervals were calculated for each invasive indicator of the severity of airway obstruction. method. The 2 methods were also analyzed for correla- However, in children PP may be difficult or impossible tion and agreement using the Pearson product moment to measure. Indwelling arterial catheters facilitate the mea- correlation and a Bland and Altman plot. surement of PP, but they are invasive and generally re- served for critically ill patients. Results: Patients with status asthmaticus had higher PPausc and PPpleth readings compared with nonasthmatic pa- Objective: To determine the utility of the plethysmo- tients. Pulsus paradoxus measured by plethysmography graphic waveform (PPpleth) of the pulse oximeter in mea- in patients with and without asthma was similar to PPausc suring PP. readings (mean difference, 0.6 mm Hg; 95% confidence interval, −0.6 to 2.1 mm Hg). Individual PPpleth readings Methods: Patients from the pediatric intensive care showed significant correlation and agreement with PPausc unit, emergency department, and inpatient wards of a readings in patients both with and without asthma. tertiary care pediatric hospital were eligible for the study. A total of 36 patients (mean age [SD], 11.2 [4.7] Conclusion: Measurement of PP using the pulse oxim- years) were enrolled in the study.
  • Blood Pressure (BP) Measurements in Adults

    Blood Pressure (BP) Measurements in Adults

    Page 5 Blood Pressure (BP) Measurements in Adults Ramesh Khanna, MD Karl D. Nolph, MD Chair in Nephrology Professor of Medicine Director, Division of Nephrology University of Missouri-Columbia Uncontrolled high blood pressure is present in every 3rd person in the American community and is attributed to be a major risk factor for progression of chronic kidney disease, coronary artery disease, and stroke. Therefore, blood pressure recording is the most common measurements at home and by healthcare professionals in all of clinical medicine. It might come as a surprise that majority of recordings are done in a less than ideal circumstances and consequently performed inaccurately. BP measurements using mercury sphygmomanometer by a trained health care professional is the gold standard for clinical assessment of blood pressures. The appearance of the 1st Korotkoff sound signals the systolic blood pressure and the disappearance of the 5th sound denotes the diastolic blood pressure. The hypertension experts believe and have increasing evidence to suggest that this method frequently either over diagnose hypertension or fail to recognize masked hypertension (blood pressure that is normal in the physician’s office setting but high at other times including at home). The four commonly recognized reasons for this are: Avoidable inaccuracies in the methods, The inherent variability of blood pressure; and The tendency for blood pressure to increase in the presence of a health care professional (the so-called white coat effect). Failure to standardize blood pressure measurement dos and don’ts. It is believed and also to some extent evidence based that the health care providers including physicians often do not follow established guidelines for blood pressure measurement.
  • Blood Pressure Year 1 Year 2 Core Clinical/Year 3+

    Blood Pressure Year 1 Year 2 Core Clinical/Year 3+

    Blood Pressure Year 1 Year 2 Core Clinical/Year 3+ Do Do • Patient at rest for 5 minutes • Measure postural BP and pulse in patients with a • Arm at heart level history suggestive of volume depletion or • Correct size cuff- bladder encircles 80% of arm syncope • Center of cuff aligns with brachial artery -Measure BP and pulse in supine position • Cuff wrapped snugly on bare arm with lower -Slowly have patient rise and stand (lie them down edge 2-3 cm above antecubital fossa promptly if symptoms of lightheadedness occur) • Palpate radial artery, inflate cuff to 70 mmHg, -Measure BP and pulse after 1 minute of standing then increase in 10 mmHg increments to 30 mmHg above point where radial pulse disappears. Know Deflate slowly until pulse returns; this is the • Normally when a person stands fluid shifts to approximate systolic pressure. lower extremities causing a compensatory rise in • Auscultate the Korotkoff sounds pulse by up to 10 bpm with BP dropping slightly -place bell lightly in antecubital fossa • Positive postural vital signs are defined as -inflate BP to 20-30mmHg above SBP as determined symptoms of lightheadedness and/or a drop in by palpation SBP of 20 mmHg with standing -deflate cuff at rate 2mmHg/second while auscultating • Know variations in BP cuff sizes -first faint tapping (Phase I Korotkoff) = SBP; • A lack of rise in pulse in a patient with an Disappearance of sound (Phase V Korotkoff)=DBP orthostatic drop in pressure is a clue that the Know cause is neurologic or related or related to -Korotkoff sounds are lower pitch, better heard by bell medications (eg.
  • Does This Patient Have Aortic Regurgitation?

    Does This Patient Have Aortic Regurgitation?

    THE RATIONAL CLINICAL EXAMINATION Does This Patient Have Aortic Regurgitation? Niteesh K. Choudhry, MD Objective To review evidence as to the precision and accuracy of clinical examina- Edward E. Etchells, MD, MSc tion for aortic regurgitation (AR). Methods We conducted a structured MEDLINE search of English-language articles CLINICAL SCENARIO (January 1966-July 1997), manually reviewed all reference lists of potentially relevant You are asked to see a 59-year-old articles, and contacted authors of relevant studies for additional information. Each study woman with liver cirrhosis who will be (n = 16) was independently reviewed by both authors and graded for methodological undergoing sclerotherapy for esopha- quality. geal varices. When she was examined by Results Most studies assessed cardiologists as examiners. Cardiologists’ precision for her primary care physician, she had a detecting diastolic murmurs was moderate using audiotapes (k = 0.51) and was good pulse pressure of 70 mm Hg. The pri- in the clinical setting (simple agreement, 94%). The most useful finding for ruling in mary care physician is concerned about AR is the presence of an early diastolic murmur (positive likelihood ratio [LR], 8.8- the possibility of aortic regurgitation 32.0 [95% confidence interval {CI}, 2.8-32 to 16-63] for detecting mild or greater AR (AR) and asks you whether endocardi- and 4.0-8.3 [95% CI, 2.5-6.9 to 6.2-11] for detecting moderate or greater AR) (2 tis prophylaxis is necessary for sclero- grade A studies). The most useful finding for ruling out AR is the absence of early di- astolic murmur (negative LR, 0.2-0.3 [95% CI, 0.1-0.3 to 0.2-0.4) for mild or greater therapy.
  • Pulsus Paradoxus

    Pulsus Paradoxus

    ERJ Express. Published on December 6, 2012 as doi: 10.1183/09031936.00138912 Pulsus paradoxus Olfa Hamzaoui1, Xavier Monnet2,3, Jean‐Louis Teboul2,3 1. Hôpitaux Universitaires Paris‐Sud, Hôpital Antoine Béclère, Service de Réanimation Médicale, 157, rue de la Porte de Trivaux, 92141 Clamart, France. 2. Hôpitaux Universitaires Paris‐Sud, Hôpital de Bicêtre, service de réanimation médicale, 78, rue du Général Leclerc, Le Kremlin‐Bicêtre, F‐94270 France. 3. Université Paris‐Sud, Faculté de médecine Paris‐Sud, EA4533, Le Kremlin‐Bicêtre, 63, rue Gabriel Péri, F‐94270 France. Address for correspondence: Prof. Jean‐Louis Teboul Service de réanimation médicale Centre Hospitalier Universitaire de Bicêtre 78, rue du Général Leclerc 94 270 Le Kremlin‐Bicêtre France e‐mail: jean‐[email protected] Phone: + 33 1 45 21 35 47 Fax: + 33 1 45 21 35 51 1 Copyright 2012 by the European Respiratory Society. Abstract Systolic blood pressure normally falls during quiet inspiration in normal individuals. Pulsus paradoxus is defined as a fall of systolic blood pressure of more than 10 mmHg during the inspiratory phase. Pulsus paradoxus can be observed in cardiac tamponade and in conditions where intrathoracic pressure swings are exaggerated or the right ventricle is distended, such as severe acute asthma or exacerbations of chronic obstructive pulmonary disease. Both the inspiratory decrease in left ventricular stroke volume and the passive transmission to the arterial tree of the inspiratory decrease in intrathoracic pressure contribute to the occurrence of pulsus paradoxus. During cardiac tamponade and acute asthma, biventricular interdependence (series and parallel) plays an important role in the inspiratory decrease in left ventricular stroke volume.
  • A Review of Pericardial Diseases: Clinical, ECG and Hemodynamic Features and Management

    A Review of Pericardial Diseases: Clinical, ECG and Hemodynamic Features and Management

    REVIEW SHAM IK AIKAT, MD SASAN GHAFFARI, MD Department of Cardiology, Cleveland Clinic Department of Cardiology, Cleveland Clinic A review of pericardial diseases: Clinical, ECG and hemodynamic features and management ABSTRACT ECAUSE PERICARDIAL DISEASES are com- mon and often misdiagnosed, physi- Pericardial diseases are common, have multiple causes, and cians need to he familiar with their presenta- are often misdiagnosed. Physicians need to recognize the tions and distinguishing features. characteristic and distinguishing features of the three most This article reviews the clinical features, important pericardial conditions: acute pericarditis, cardiac diagnosis, and management of acute pericardi- tamponade, and constrictive pericarditis. In these tis, cardiac tamponade, and constrictive peri- conditions, proper diagnosis and appropriate management carditis. can significantly reduce morbidity and mortality. • THE PERICARDIUM KEY POINTS The pericardium envelopes the heart, extend- ing on to the adventitia of the great vessels. It Acute pericarditis is an important part of the differential is 1 to 2 mm thick and consists of an outer and diagnosis of chest pain syndromes and needs to be an inner layer. The tough, fibrous outer layer is distinguished from acute myocardial infarction both called the parietal pericardium, and the serous clinically and electrocardiographically. inner layer is called the visceral pericardium. The parietal and visceral pericardium are sep- Suspect pericardial tamponade in any patient with acute arated by fluid: 15 to 50 mL of an ultrafiltrate dyspnea, especially in the presence of a pericardial rub, of plasma that acts as a lubricant.1-2 elevated jugular venous pressure, and hypotension. The pericardium limits excessive cardiac movement and acute cardiac distension.
  • Unit 10 Shock,Resuscitation Part A

    Unit 10 Shock,Resuscitation Part A

    Vanderbilt University Medical Center Emergency General Surgery Service Surgical Residency Rotation and Curriculum UNIT 10SHOCK, RESUSCITATION, AND SURGICAL CRITICAL CARE PART A: SHOCK AND RESUSCITATION UNIT OBJECTIVES: 1. Demonstrate an understanding of the pathophysiology of shock and its categories. 2. Demonstrate an understanding of the mechanisms and pathophysiology of cardiopulmonary arrest. 3. Demonstrate the ability to manage the treatment of shock and cardiopulmonary arrest. COMPETENCY-BASED KNOWLEDGE OBJECTIVES: 1. Define the categories of shock based upon type, and explain the etiology and pathophysiology of each type of shock: a. Cardiogenic b. Hypovolemic c. Distributive (septic, anaphylactic, neurogenic, and adrenal insufficiency mediated) d. Obstructive (cardiac tamponade, tension pneumothorax, pulmonary embolus) 2. Summarize the clinical presentation and hemodynamic parameters associated with each type of shock. 3. Propose an algorithm for diagnosing and initiating treatment for each shock type. 4. Discuss the pathophysiology, including the mechanism of arrest, for each of the following situations: a. Acute myocardial infarction f. Substance abuse b. Acute dysrhythmia g. Hypothermia c. Congestive heart failure h. Acute stroke d. Pulmonary embolus i. Hemorrhagic shock e. Tension pneumothorax 5. Explain the indications for and the pharmacokinetics of each of the following drugs: a. Lidocaine g. Quinidine b. Bretylium h. Isoproterenol c. Digoxin i. Amiodarone d. Propanolol j. Dopamine e. Verapamil k. Dobutamine f. Pronestyl l. Adenosine (Adenocard®) 6. Summarize the indications and the appropriate techniques for cardioversion and defibrillation. Vanderbilt University Medical Center Emergency General Surgery Service Surgical Residency Rotation and Curriculum 7. Outline the signs and symptoms of acute airway obstruction and define the appropriate intervention in adult and pediatric patients.
  • An Examination of Vascular Responses to Acute Isometric Handgrip Exercise and a Complementary Ischemic-Reperfusion Cuff Protocol

    An Examination of Vascular Responses to Acute Isometric Handgrip Exercise and a Complementary Ischemic-Reperfusion Cuff Protocol

    University of Windsor Scholarship at UWindsor Electronic Theses and Dissertations Winter 2014 An examination of vascular responses to acute isometric handgrip exercise and a complementary ischemic-reperfusion cuff protocol Joshua Seifarth University of Windsor, [email protected] Follow this and additional works at: http://scholar.uwindsor.ca/etd Recommended Citation Seifarth, Joshua, "An examination of vascular responses to acute isometric handgrip exercise and a complementary ischemic- reperfusion cuff protocol" (2014). Electronic Theses and Dissertations. Paper 5031. This online database contains the full-text of PhD dissertations and Masters’ theses of University of Windsor students from 1954 forward. These documents are made available for personal study and research purposes only, in accordance with the Canadian Copyright Act and the Creative Commons license—CC BY-NC-ND (Attribution, Non-Commercial, No Derivative Works). Under this license, works must always be attributed to the copyright holder (original author), cannot be used for any commercial purposes, and may not be altered. Any other use would require the permission of the copyright holder. Students may inquire about withdrawing their dissertation and/or thesis from this database. For additional inquiries, please contact the repository administrator via email ([email protected]) or by telephone at 519-253-3000ext. 3208. An examination of vascular responses to acute isometric handgrip exercise and a complementary ischemic-reperfusion cuff protocol By: Joshua Seifarth A Thesis Submitted to the Faculty of Graduate Studies through the Faculty of Human Kinetics in Partial Fulfillment of the Requirements for the Degree of Master of Human Kinetics at the University of Windsor Windsor, Ontario, Canada 2013 © 2013 Joshua Seifarth An examination of vascular responses to acute isometric handgrip exercise and a complementary ischemic-reperfusion cuff protocol By: Joshua Seifarth APPROVED BY: _____________________________ Dr.
  • Cardiac Tamponade Management Clinical Guideline

    Cardiac Tamponade Management Clinical Guideline

    Cardiac Tamponade Management Clinical Guideline V1.0 August 2020 Summary Cardiac Tamponade Management Clinical Guideline V1.0 Page 2 of 20 1. Introduction 1.1 Cardiac tamponade is a clinical syndrome caused by the accumulation of fluid, blood, pus, clots or gas in the pericardial space, resulting in reduced ventricular filling and subsequent haemodynamic compromise. This includes a haemodynamic spectrum ranging from incipient or preclinical tamponade (when pericardial pressure equals right atrial pressure but it is lower than left atrial pressure) to haemodynamic shock with significant reduction of stroke volume and blood pressure, the latter representing a life-threatening medical emergency. 1.2 The diagnosis of cardiac tamponade is essentially a clinical diagnosis requiring echocardiographic confirmation of the initial diagnostic suspicion. In most patients, cardiac tamponade should be diagnosed by clinical examination that typically shows elevated systemic venous pressure, tachycardia, muffled heart sounds and paradoxical arterial pulse. Systemic blood pressure may be normal, decreased, or even elevated. Clinical signs may also include decreased electrocardiographic voltage with electrical alternans and an enlarged cardiac silhouette on chest X-ray with slow-accumulating effusions. 1.3 Once a clinical diagnosis of tamponade is suspected, an echocardiogram should be performed without delay. The diagnosis is then confirmed by echocardiographic demonstration of several 2D and Doppler-based findings (i.e. evidence of pericardial effusion with variable cardiac chambers’ compression, abnormal respiratory variation in tricuspid and mitral valve flow velocities, inferior vena cava plethora). 1.4 This should immediately trigger On-call Consultant Cardiologist review in order to stratify the patient risk, identify specific supportive and monitoring requirements and guide the optimal timing and modality of pericardial drainage.