DOCSLIB.ORG

Comparison of Traditional and Plethysmographic Methods for Measuring Pulsus Paradoxus

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
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. Pulsus paradoxus was eter–pulse plethysmographic waveform offers a simple measured using the traditional auscultatory (PPausc) and noninvasive method for evaluating patients with air- method with a sphygmomanometer. Pulsus paradoxus way obstruction. was then measured using a blood pressure cuff observ- ing for the disappearance and reappearance of the Arch Pediatr Adolesc Med. 2004;158:48-51 ESPITE ADVANCES IN THE etry, blood gas sampling, and bedside spi- treatment and preven- rometry. However, a decrease in oxygen tion of asthma, it re- saturation may occur with only very mild mains one of the most airway obstruction or, conversely, may not common reasons for hos- occur at all even with severe airway ob- Dpitalization in the pediatric age group.1 Pe- struction. In addition, hypoxemia may be riodic assessment of the severity of air- masked by administration of small way obstruction is an integral part of the amounts of supplemental oxygen, such as management of status asthmaticus. How- with aerosol treatments. Spirometry, such ever, there are limitations to the various as peak expiratory flow rate, can be use- subjective and objective factors that are ful as an indicator of airway obstruction routinely used for assessment. There is a and as a measure of decreased pulmo- wide variation in how patients perceive and nary function from baseline in asthmatic describe their symptoms.2 The symp- individuals who use them regularly. De- toms of an attack such as cough, diffi- spite this, the utility of the peak expira- culty breathing, and wheezing frequently tory flow rate is limited in a child with se- do not correlate with severity. In addi- vere respiratory distress. Measurement of tion, there is a significant interobserver the partial pressure of arterial carbon di- From Critical Care Medicine, Department of Pediatrics, variability among physicians in evaluat- oxide (PaCO2) is a useful tool in evaluat- Children’s Hospital of ing physical signs such as the extent of ing alveolar ventilation. In mild and mod- Michigan, Wayne State wheezing and magnitude of respiratory dis- erate asthma the PaCO2 is usually low. University School of Medicine, tress.3,4 Some helpful tools in evaluating “Normalization” or significant elevations Detroit. the severity of asthma are pulse oxim- in PaCO2 are encountered only when air- (REPRINTED) ARCH PEDIATR ADOLESC MED/ VOL 158, JAN 2004 WWW.ARCHPEDIATRICS.COM 48 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 09/25/2021 way obstruction is severe enough to result in overall al- ting with the arm at the side, an appropriately sized arm cuff veolar hypoventilation. In addition, measurement of PaCO2 was inflated until all Korotkoff sounds disappeared. The cuff requires blood sampling. was deflated approximately 2 mm Hg per second until a few Pulsus paradoxus (PP) reflects an exaggeration of intermittent Korotkoff I sounds were heard. This pressure was the normal decrease in systolic blood pressure (SBP) dur- assumed to be the SBP during exhalation (Pex). The cuff pres- sure was similarly decreased until all Korotkoff I sounds were ing inspiration and is a quantifiable indicator of airway heard. This pressure was assumed to be the SBP during inspi- obstruction. It has been shown to correlate well with other ration (Pin). The difference between Pin and Pex was the PPausc. CO objective indicators of airway obstruction such as Pa 2 If Pex and Pin were not well defined during the initial deflation, and peak expiratory flow rate5,6; however, it is noninva- the cuff was reinflated once and an attempt at measurement sive and does not require cooperation with pulmonary was repeated. If Korotkoff I sounds were again not well heard, function tests. Pulsus paradoxus may be a useful ad- the cuff was deflated completely, and this process was re- junct in assessing the severity of airway obstruction at a peated after a short wait, a maximum of 3 times in total. The given time, as well as documenting response to therapy, first PP that was clearly heard was recorded as PPausc.IfPPwas especially in situations in which more invasive tests are not clearly discernible by auscultation, the patient was ex- not readily available, such as an office setting. Timing of cluded from the study. Pulsus paradoxus was then determined in the same pa- PP measurement to inspiration and expiration can be dif- tient using the PPpleth from a standard patient transport moni- ficult in asthmatic children who are tachypneic, tachy- tor (Marquette Electronics, Milwaukee, Wis). The pulse ox- cardic, and likely to be uncooperative. Therefore, in- imeter probe (Nellcor, Pleasanton, Calif) was placed on the stead of attempting to correlate SBP with phases of patient’s second or third finger of the same arm used for PPausc respiration, measurement of PP using variations in SBP and an adequate signal quality was ascertained by comparison 7 has been proposed in children. Nevertheless, such a mea- of the displayed PPpleths to the palpable pulse. The appropriate- surement is cumbersome and subject to considerable in- sized cuff was placed on the arm and inflated until the PPpleth terrater and intrarater variability as well as observer bias. disappeared from the monitor. The cuff pressure was then de- Improvements in the method of determining PP may al- creased at approximately 2 mm Hg per second in a similar fash- low it to be a more useful tool in evaluating airway ob- ion to PPausc determination, until intermittent PPpleths appeared and this pressure was assumed to be the SBP during Pex. The struction. cuff pressure was lowered further until all PP were dis- Newer pulse oximeters are equipped with a visual pleths played. This pressure was the SBP during Pin. The difference display of the pulse plethysmographic waveform (PPpleth). between Pex and Pin was the PPpleth. We proposed that the PPpleth of the pulse oximeter would Pulsus paradoxus by auscultation and PPpleth means (SDs) be an acceptable substitute for Korotkoff sounds for the were calculated, as well as the mean difference between the 2 measurement of PP. Our hypothesis was PP measured methods with 95% confidence intervals. Pearson product mo- by the pulse oximetry PPpleth would be greater in asth- ment correlation was used to compare values obtained by the matic children compared with nonasthmatic children. different methods. In addition, because of concerns regarding Furthermore, PP measured using the pulse oximeter ple- the use of the product moment correlation for the comparison thysmograph would have good agreement with the value of different methods of measurement, we also compared the readings using a Bland and Altman plot, giving an estimation obtained by the traditional method of auscultation of of agreement. Korotkoff sounds. RESULTS METHODS Thirty-six patients from the pediatric intensive care unit, emer- During a 4-month period, 36 patients were enrolled. Their gency department, and inpatient wards of the Children’s Hos- ages ranged from 27 months to 20 years, with a mean pital of Michigan, Detroit, were enrolled over a 4-month pe- (SD) age of 11.2 (4.7) years. Twenty patients were male, riod. Both asthmatic and nonasthmatic patients were evaluated. and 16 were female. Eleven were admitted having a di- All asthmatic patients were at the time of evaluation diag- agnosis of status asthmaticus; the remaining 25 patients nosed as having status asthmaticus, which was defined as the had various diagnoses none of which was expected to gen- acute onset of symptomatic expiratory airflow obstruction with- erate a significant PP (Table 1). Five patients were ex- out significant improvement after administration of aerosol- ized ␤-agonist treatments. Verbal consent was obtained by the cluded after consent owing to the inability to measure primary investigator (J.A.C.) from the guardian or patient and PPausc because of the patient’s inability to remain still dur- documented in the patient’s medical record. This study was ap- ing PP measurement. In all patients whose PPausc was dis- proved by the Wayne State University Human Investigations cernible, PPpleth was able to be measured as well. Committee. The patients were chosen by their ability to coop- The PP was significantly higher in the asthmatic erate with study requirements (ie, remain still) from the emer- group compared with the nonasthmatic group when mea- gency department and inpatient populations (generally aged sured by either auscultation or plethysmography from 0 to 18 years).
Load more

Recommended publications
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 3 Blood Pressure and Its Measurement
    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.
    [Show full text]
  • Pulsus Paradoxus in a Neonate with Interrupted Aortic Arch
    CORRESPONDENCE Pulsus Paradoxus in a Neonate with Interrupted Aortic Arch Pulsus paradoxus is an exaggerated inspiratory fall (>10 mmHg) of systolic blood pressure (BP). It has been reported with cardiac tamponade, asthma, pericarditis, croup, hemorrhagic shock and cardiomyopathy [1-3]. We report a novel association with interrupted aortic arch [left ventricular outflow tract (LVOT) obstruction]. A full-term, 2.8 kg, 8-day-old male neonate presented with congestive cardiac failure and shock (heart rate- 152/ min, respiratory rate 80/min, cold/pale extremities, right upper limb BP 31/12 mmHg, chest retractions, and hepatomegaly). His femoral pulses were feeble and were disappearing during inspiration. His right brachial pulse was constant throughout respiratory cycle. His lower limb BP was unrecordable. The respiratory variation in pulses FIG. 1 (a) Pulse oximetry tracing showing normal amplitude was also appreciated on pulseoximetry (Fig. 1a). His pulse waveform during expiration (thin arrows), and low cardiac examination was unremarkable except increased amplitude pulse wave form during inspiration (thick arrows); precordial activity. Echocardiography and computed (b) Computed tomography angiography image showing tomography angiography (Fig. 1b) confirmed interrupted interrupted aortic arch (arrow). aortic arch. With Prostaglandin E1 (PGE1) infusion and supportive care, his lower limb pulses and BP improved circulation can detect impending ductal closure, in LVOT [45/28 mmHg (mean 34)]. The respiratory variation in obstruction. Whereas, differential pulses suggest LVOT pulseoximetry gradually disappeared. Disappearance of obstruction, pulsus paradoxus in such setting might pulses during inspiration and respiratory variation in pulse indicate impending ductal closure and is thus an ominous waveforms was consistent with pulsus paradoxus [4,5].
    [Show full text]
  • Pulsus Paradoxus from Anterior Mediastinal Mass
    Annals of Case Reports & Reviews doi: 10.39127/2574-5747/ACRR:1000239 Case Report Tanking C, et al. Annal Cas Rep Rev: ACRR-239 Pulsus Paradoxus from Anterior Mediastinal Mass Chonthicha Tanking*1, Chanwit Wuttichaipradit1, Chatree Wongsinkongman1, Chayanee Samdaengpan2 1Cardiology unit, Chulabhorn Hospital, 906 Kamphaeng Phet 6 Rd, Lak Si, Bangkok 10210, Thailand 2Oncology unit, Chulabhorn Hospital, 906 Kamphaeng Phet 6 Rd, Lak Si, Bangkok 10210, Thailand *Corresponding author: Chonthicha Tanking, MD, Chulabhorn Hospital, Bangkok, Thailand. Tel: (+66)81-985-5882; E-mail: [email protected] Citation: Tanking C, Wuttichaipradit C, Wongsinkongman C, Samdaengpan C (2021) Pulsus Paradoxus from Anterior Mediastinal Mass. Annal Cas Rep Rev: ACRR-239. Received Date: 09 May 2021; Accepted Date: 13 May, 2021; Published Date: 20 May 2021 Abstract Spontaneous breathing comprises a variation of intrathoracic pressure transmitting to heart and great vessels. Under normal circumstance, arterial blood pressure falls with inspiration and rises with expiration, fluctuates within 10 mmHg range. Exaggeration of normal systolic blood pressure decrease during inspiration is defined as pulsus paradoxus [1]. Classical prototype scenarios are cardiac tamponade and acute asthma. Other causes of pulsus paradoxus include pulmonary embolism, constrictive pericarditis and pulmonary disease with large variations in intrathoracic pressure [2]. Few other conditions have been reported such as superior vena cava obstruction, thoracic outlet syndrome, etc. [3]. This report demonstrates a case of a young female patient who was sent for echocardiography due to dyspnea. There is minimal pericardial effusion seen; however, we found an exaggerated inflow variation without evidence of pericardial disease on echocardiography. On examination, pulsus paradoxus was positive by sphygmomanometer as well as with palpation.
    [Show full text]
  • Cardiac Tamponade: Emergency Management
    Cardiac Tamponade: Emergency Management Subject: Emergency management of cardiac tamponade Policy Number N/A Ratified By: Clinical Guidelines Committee Date Ratified: December 2015 Version: 1.0 Policy Executive Owner: Clinical Director, Medicine, Frailty and Networked Service ICSU Designation of Author: Consultant Cardiologist Name of Assurance Committee: As above Date Issued: December 2015 Review Date: 3 years hence Target Audience: Emergency Department, Medicine, Surgery Key Words: Cardiac Tamponade, Pericardiocentesis 1 Version Control Sheet Version Date Author Status Comment 1.0 Dec Dr David Brull Live New guideline. 2015 (Consultant) Rationale: This guideline has been written Dr Akish Luintel as part of the coordinated response to a (Cardiology recent serious incident. Registrar) This guideline is based on current best practice utilising our links to the Barts Heart Centre where all our Tertiary Cardiology is sent 2 Clinical signs of Tamponade – Management algorithm Clinical Signs of Tamponade 1. Tachycardia, tachypnoea 2. Raised JVP, Hypotension & quiet heart sounds (Beck’s Triad) 3. Pulsus Paradoxus 4. Kussmaul’s Sign 5. Hepatomegaly 6. Pericardial rub Medical Emergency: Organise URGENT Echo Bleep Cardiology on 3038/3096 in hours Out of hours Call Bart’s Heart Centre: Barts Heart Electrophysiology SpR 07810 878 450 Cardiology SpR Interventional 07833 237 316 Bart’s Heart Switchboard 0207 377 7000 Management of Tamponade (Monitor in Intensive Care or Coronary Care) Transfer to Barts for Emergency Pericardiocentesis Treat on-site if patient peri-arrest Supportive Management (as required) Do not delay pericardiocentesis Volume expansion Oxygen Inotropes Positive pressure ventilation should be avoided 3 Criteria for use This is a guideline for the emergency management of patients presenting with cardiac tamponade.
    [Show full text]
  • Cath Lab Essentials: “Pericardial Effusion & Tamponade”
    Cath Lab Essentials: “Pericardial effusion & tamponade” Pranav M. Patel, MD, FACC, FSCAI Chief, Division of Cardiology Director, Cardiac Cath Lab & CCU University of California, Irvine Division of Cardiology Acknowledgments No financial disclosures Case A 52-year-old man with a 3-day history of progressively worsening dyspnea on exertion to the point that he is unable to walk more than one block without resting. He has had sharp intermittent pleuritic chest pain and a nonproductive cough. He is taking no medications. Case Temp is 37.7 °C (99.9 °F), blood pressure is 88/44 mm Hg, pulse is 125/min, and respiration rate is 29/min; BMI is 27. Oxygen saturation is 95%. Pulsus paradoxus is 15 mm Hg. JVP is 12 cm H2O. Cardiac examination discloses muffled heart sounds with no rubs. Lung auscultation reveals normal breath sounds and no crackles. There is 2+ pedal edema. ECG-electrical alternans Chest X-ray Question What is the most appropriate treatment? A. Dobutamine to increase BP B. Broad spectrum antibiotics C. Pericardiocentesis D. Surgical pericardiectomy Echocardiogram: RV collapse in diastole Most commonly involves the RV outflow tract (more compressible area of RV) Occurs in early diastole, immediately after closure of the pulmonary valve, at the time of opening of the tricuspid valve When collapse extends form outflow tract to the body of the right ventricle, this is evidence that intrapericardial pressure is elevated more substantially https://www.youtube.com/channel/UCPgiLlKxXci7WX8VrZ9g0wQ FN Delling 2007 Subcostal view FN
    [Show full text]
  • Pulsus Paradoxus
    Pulsus paradoxus. R Shabetai, … , J C Fenton, M Masangkay J Clin Invest. 1965;44(11):1882-1898. https://doi.org/10.1172/JCI105295. Research Article Find the latest version: https://jci.me/105295/pdf Journal of Clinical Investigation Vol. 44, No. 11, 1965 Pulsus Paradoxus * RALPH SHABETAI, NOBLE 0. FOWLER,t JOHN C. FENTON, AND MANUEL MASANGKAY (From the Cardiac Research Laboratory and Division of Cardiology, Department of Medicine, University of Cincinnati, Cincinnati, Ohio) Previous studies from this laboratory (1-3) left ventricular stroke output was demonstrated in have shown that the paradoxical pulse of experi- cardiac tamponade, but the mechanism that inter- mental cardiac tamponade is produced by an ex- fered with left ventricular filling during inspiration aggerated inspiratory decline of left ventricular was not identified. The studies to be described in stroke volume. Most investigators have concen- this paper were designed to evaluate the signifi- trated on one of three principal mechanisms of this cance of the following factors, which may reduce inspiratory decrease of left ventricular stroke out- inspiratory left heart filling during cardiac tam- put. An early postulate (4) was that because of ponade and thus cause a paradoxical pulse: 1) in- high intrapericardial pressure throughout the re- spiratory rise of transpericardial pressure, 2) in- spiratory cycle, extrapericardial venous pressure spiratory pooling of blood in the pulmonary veins, falls more than atrial pressure during inspiration, and 3) inspiratory increase of venous return to the thus reducing cardiac filling and stroke volume right heart. (5-7). With this mechanism, inspiratory pul- The respiratory variation in transpericardial monary venous pooling would be expected to oc- pressure was measured in dogs with cardiac tam- cur.
    [Show full text]
  • Student's Corner–2
    Published online: 2020-12-31 THIEME 364 Student’s Student's CornerCorner–2 Jyotsna et al. Student’s Corner–2 Dayasagar Rao2 P. Sampath Kumar3 1Cardiology Department, KIMS, Hyderabad, Telangana, India Address for correspondence Maddury Jyotsna, MD DM FACC 2Cardiology Department, Osmania, Hyderabad, Telangana, India FESC FICC, NIMS (Nizam institute of medical sciences), Punjagutta, Hyderabad, Telangana, 500082, India (e-mail: [email protected]). Ind J Car Dis Wom:2020;5:364–367 Q1. Why DBP Does not Vary with AV In the above question, for the patient with AV dissociation Dissociation and Atrial Fibrillation and atrial fibrillation (preferably isolated), there is no change in peripheral resistance, which is the key determinant of DBP. Answer by Prof. Dayasagar Rao Hence, no change in DBP. Systolic blood pressure (SBP) is mainly determined by stroke volume, while diastolic blood pressure (DBP) is determined For Students, a Few Important Formulae Relevant to the by systemic vascular resistance (SVR), compliance of the Question is Mentioned Below arterial wall and duration of diastole. Normally, diastole is longer than systole; hence, mean arte- When we say atrioventricular (AV) dissociation, we mean rial pressure is not arithmetic mean of systolic and diastolic that the atria and the ventricles have independent rates and blood pressure. rhythms with a loss of synchrony, whereas in atrial fibrillation, Mean BP: DBP + 1/3rd of pulse pressure the extremely high-heart rates make atrial contractions inef- Pulse pressure: SBP − DBP fective while reducing the diastolic filling time between two Systolic pressure = diastolic pressure + pulse pressure beats, leading to reduced ventricular filling. The variation in Pulse pressure = stroke volume/arterial capacitance SBP in AV dissociation is due to variation in preload to ventricle Mean arterial pressure = cardiac output × total peripheral proportional to atrial contribution to ventricle filling.
    [Show full text]
  • Cardiac Tamponade Non Invasive Assessment by Echo
    Cardiac Tamponade Non Invasive Assessment by Echo Fahmi Othman, MD Cardiology Consultant Non-invasive lab, Heart hospital, Hamad Medical Corporation Declaration of interest • I have nothing to declare Objectives •Introduction •Why Echo is important in cardiac tamponade. • Take home messages Introduction: • Cardiac tamponade is a life-threatening, slow or rapid compression of the heart due to the pericardial accumulation of fluid, pus, blood, clots or gas as a result of inflammation, trauma, rupture of the heart or aortic dissection. • Can be classified based on the: • Onset to (acute, subacute) or (chronic if more than three months). • The size mild (<10 mm), moderate (10–20 mm) or large (>20 mm) • Distribution (circumferential or loculated) • 10-50 ml of pericardial fluid is normally present. • 100 ml of pericardial fluid is enough to cause circumferential effusion. • 300-600 ml of non hemorrhagic pericardial fluid can cause tamponade. Pressure/volume curve of the pericardium with fast accumulating pericardial fluid leading to cardiac tamponade with a smaller volume (A) compared with the slowly accumulating pericardial fluid reaching cardiac tamponade only after larger volumes (B Feb 2018 August 2018 Why Echo is Important in Cardiac Tamponade? •To make the diagnosis •For triage •To guide and monitor the pericardiocentesis Diagnosis Symptoms Of Cardiac Tamponade Sensitivity of the physical examination in the diagnosis of cardiac tamponade Signs of cardiac tamponade Pulsus paradoxus Pulsus paradoxus Sensitivity Of The ECG In The Diagnosis Of Cardiac Tamponade Sensitivity Of The Chest Radiograph In The Diagnosis Of Cardiac Tamponade Echocardiographic Signs Of Cardiac Tamponade Echocardiography in Cardiac Tamponade • Chamber collapse • Doppler Signs of Increased Ventricular Interdependence • Inferior Vena Cava Plethora Chamber collapse • The lower pressure cardiac chambers (atria) are affected before the higher pressure cardiac chambers (ventricles).
    [Show full text]
  • Pericardial Disease: Tamponade and Constriction
    STATE-OF-THE-ART ECHOCARDIOGRAPHY Pericardial Disease: Tamponade and Constriction FEBRUARY 16, 2016 Sanjiv J. Shah, MD, FASE Associate Professor of Medicine Director, Heart Failure with Preserved EF Program Division of Cardiology, Department of Medicine Northwestern University Feinberg School of Medicine [email protected] N O R T H W E S T E R N U N I V E R S I T Y F E I N B E R G S C H O O L O F M E D I C I N E Questions • In a patient with pericardial effusion, how can I diagnose tamponade (i.e., who needs an urgent pericardiocentesis?) • Why is there no Kussmaul sign in tamponade? Why is there loss of Y-descent? • What are the echo clues to constriction? • Why is septal > lateral e’ in constriction? • In constriction, why does hepatic vein flow reversal increase with expiration but JVP goes up with inspiration (+Kussmaul)? Cardiac tamponade Case presentation • 52-year-old woman with malaise, CP » Low-grade fever, malaise, fatigue x 2 weeks » CP x 1 week, pleuritic, worse when supine, better when sitting forward, positional » No lightheadedness, dizziness, orthopnea, PND, syncope, or palpitations • No prior medical history, no medications Case presentation (continued) • Laboratory work-up: » ANA, rheumatoid factor: normal » Chem panel, CBC: normal » PPD: nonreactive; HIV: negative • Echocardiogram: normal • Prescribed NSAIDs • Symptoms resolved within 2-3 days Case presentation (continued) • 2 weeks later: recurrence of malaise, fatigue, low grade fevers, pleuritic CP; +SOB/dizziness • Physical exam: » 99.8, 98/80, 110, 22,
    [Show full text]
  • Heart Sounds That Matter
    Slide 1 ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________ Slide 2 ___________________________________ HEART SOUNDS ___________________________________ THAT MATTER Willard Baker, Jr. MMS PA-C ___________________________________ DFAAPA ___________________________________ ___________________________________ ___________________________________ ___________________________________ Slide 3 ___________________________________ Objectives • After attending this workshop the attendees will be able to distinguish between normal and abnormal heart sounds ___________________________________ • Attendees will utilize case study histories, and physical findings to determine the etiology of the heart sounds. • Attendees will utilizes the Student Auscultation Manikin II (SAM II) system. This will allow the attendees to audibly distinguish between ___________________________________ various cardiac sounds using an infrared stethoscope. • Utilize the mnemonic TPLRP to help identify specific murmurs. ___________________________________ ___________________________________ ___________________________________ ___________________________________ Slide 4 ___________________________________ First Things First! History ___________________________________ ___________________________________ ___________________________________ ___________________________________ ___________________________________
    [Show full text]