The document discusses various techniques for hemodynamic monitoring, including both conventional and advanced methods. It provides an overview of the history of hemodynamic monitoring and outlines some of the goals of different monitoring devices. The document then reviews several specific monitoring techniques, such as arterial lines, central venous catheters, pulmonary artery catheters, echocardiography, pulse contour analysis, and electrical bioimpedance. Both advantages and disadvantages of each method are discussed.
Assessment of haemodynamics a critically ill patient and its management has always been a matter if debate. Over time a lot of studies and therapeutic interventions have been carried out. This presentation is a review of such interventions and their impact on the outcome.
comprehensive presentation on 2D echo use in ICu set up. helpful in finding causes of shock and also in monitoring of fluid status in critically ill patients.
Assessment of haemodynamics a critically ill patient and its management has always been a matter if debate. Over time a lot of studies and therapeutic interventions have been carried out. This presentation is a review of such interventions and their impact on the outcome.
comprehensive presentation on 2D echo use in ICu set up. helpful in finding causes of shock and also in monitoring of fluid status in critically ill patients.
The right ventricle (RV) is not important, until it is. Under normal conditions RV function merely keeps central venous pressure low and delivers all the venous return per beat into the pulmonary circulation under low pressure. If pulmonary artery pressures increase due to pulmonary vascular disease (embolism, ARDS, COPD), over-distention (COPD, asthma) or ischemia (embolism, pulmonary hypertension), the RV rapidly dilates decreasing left ventricular (LV) diastolic compliance via ventricular interdependence. Most clinicians presume that the RV is merely a weaker version of the LV, but follows that same rules. But this in not true. Normally, RV filling occurs without any measurable change in RV distending pressure owing to conformational changes in its shape rather than distention of its wall fibers. This effect allows central venous pressure to remain low despite major dynamic change sin venous return associated with breathing. RV ejection is exquisitely dependent of RV ejection pressure. Thus, if disease processes increase pulmonary artery impedance then RV dilation and failure will eventually occur. Furthermore, most of RV coronary blood flow occurs during systole, unlike LV coronary blood flow, which primarily occurs in diastole. Thus, systemic hypotension or relative hypotension where in pulmonary artery pressures equal or exceed aortic pressure must cause RV ischemia. Clinically these findings carry a common end result. For cardiac output to increase RV volumes must increase. If increasing RV volumes also result in increasing filling pressures then RV over distention may be occurring causing RV free wall ischemia. If relative systemic hypotension exists then selective increases in arterial pressure will improve RV systolic function. Accordingly, fluid resuscitation, if associated with rapid increases in central venous pressure should be stopped until evidence of acute cor pulmonale is excluded. Acute cor pulmonale can be treated by improving LV systolic function, coronary perfusion pressure or reducing pulmonary artery outflow impedance. The normal response of the RV to slowly increasing pulmonary artery pressures is to increase its intrinsic contractility (Anrep effect), but if the pressure load exceeds such adaptation, RV hypertrophy develops in an asymmetric fashion initially in the infundibulum before progressing to the RV free wall and septum. In chronic RV failure, dilation and RV wall thinning occurs as the heart reverts to preload to sustain stroke volume (Starling effect). Importantly, all these effects and their response to therapies can be assessed at the bedside using echocardiography and pulmonary arterial catheterization.
A neglected topic for way too long, the interest in fluid therapy seems to be quickly rising as the medical community is making a shift from looking at fluids as a mere method of stabilization towards the appreciation of its relevant side effects.
Many questions remain to be answered indeed:
Is the upgrade from saline 0.9% to balanced crystalloids worth the extra cost?
Does HES still have a place in the OR?
Do we have to fill the gap left by HES on ICU with crystalloids, other colloids or even albumin?
Is it really impossible to avoid fluid overload by using only crystalloids?
Is there still a definitive place for human albumin?
How do we treat and monitor specific patient populations, like patients with trauma, liver failure, brain edema and right heart failure among others?
How do we avoid a one-size-fits-all regimen in perioperative goal-directed therapy?
What with the fluids beyond resuscitation?
And what do the authors of the big fluid trials do in real life themselves?
The 9th International Fluid Academy Day will again be a 1 day concise meeting on all aspects of fluid managament and hemodynamic monitoring in the critically ill.
Date: October 26th 2019, 8:00 - 18:00
Point of critical care Ultrasound play a pivotal role in management of critically ill patients admitted in ICU . Its usage in this regard is ever growing . Here we discus about pearls and pitfalls of POCUS in Intensive care medicine.
Novel hemodynamic monitoring tool for major surgery and ICU patients. With minimally invasive doppler probe insertable through regular central line, Nilus is adding right side perspective back into hemodynamic monitoring.
The right ventricle (RV) is not important, until it is. Under normal conditions RV function merely keeps central venous pressure low and delivers all the venous return per beat into the pulmonary circulation under low pressure. If pulmonary artery pressures increase due to pulmonary vascular disease (embolism, ARDS, COPD), over-distention (COPD, asthma) or ischemia (embolism, pulmonary hypertension), the RV rapidly dilates decreasing left ventricular (LV) diastolic compliance via ventricular interdependence. Most clinicians presume that the RV is merely a weaker version of the LV, but follows that same rules. But this in not true. Normally, RV filling occurs without any measurable change in RV distending pressure owing to conformational changes in its shape rather than distention of its wall fibers. This effect allows central venous pressure to remain low despite major dynamic change sin venous return associated with breathing. RV ejection is exquisitely dependent of RV ejection pressure. Thus, if disease processes increase pulmonary artery impedance then RV dilation and failure will eventually occur. Furthermore, most of RV coronary blood flow occurs during systole, unlike LV coronary blood flow, which primarily occurs in diastole. Thus, systemic hypotension or relative hypotension where in pulmonary artery pressures equal or exceed aortic pressure must cause RV ischemia. Clinically these findings carry a common end result. For cardiac output to increase RV volumes must increase. If increasing RV volumes also result in increasing filling pressures then RV over distention may be occurring causing RV free wall ischemia. If relative systemic hypotension exists then selective increases in arterial pressure will improve RV systolic function. Accordingly, fluid resuscitation, if associated with rapid increases in central venous pressure should be stopped until evidence of acute cor pulmonale is excluded. Acute cor pulmonale can be treated by improving LV systolic function, coronary perfusion pressure or reducing pulmonary artery outflow impedance. The normal response of the RV to slowly increasing pulmonary artery pressures is to increase its intrinsic contractility (Anrep effect), but if the pressure load exceeds such adaptation, RV hypertrophy develops in an asymmetric fashion initially in the infundibulum before progressing to the RV free wall and septum. In chronic RV failure, dilation and RV wall thinning occurs as the heart reverts to preload to sustain stroke volume (Starling effect). Importantly, all these effects and their response to therapies can be assessed at the bedside using echocardiography and pulmonary arterial catheterization.
A neglected topic for way too long, the interest in fluid therapy seems to be quickly rising as the medical community is making a shift from looking at fluids as a mere method of stabilization towards the appreciation of its relevant side effects.
Many questions remain to be answered indeed:
Is the upgrade from saline 0.9% to balanced crystalloids worth the extra cost?
Does HES still have a place in the OR?
Do we have to fill the gap left by HES on ICU with crystalloids, other colloids or even albumin?
Is it really impossible to avoid fluid overload by using only crystalloids?
Is there still a definitive place for human albumin?
How do we treat and monitor specific patient populations, like patients with trauma, liver failure, brain edema and right heart failure among others?
How do we avoid a one-size-fits-all regimen in perioperative goal-directed therapy?
What with the fluids beyond resuscitation?
And what do the authors of the big fluid trials do in real life themselves?
The 9th International Fluid Academy Day will again be a 1 day concise meeting on all aspects of fluid managament and hemodynamic monitoring in the critically ill.
Date: October 26th 2019, 8:00 - 18:00
Point of critical care Ultrasound play a pivotal role in management of critically ill patients admitted in ICU . Its usage in this regard is ever growing . Here we discus about pearls and pitfalls of POCUS in Intensive care medicine.
Novel hemodynamic monitoring tool for major surgery and ICU patients. With minimally invasive doppler probe insertable through regular central line, Nilus is adding right side perspective back into hemodynamic monitoring.
Hemodynamic monitoring of critically ill patientsV4Veeru25
Hemodynamic monitoring measures the blood pressure inside the veins, heart, and arteries. It also measures blood flow and oxygen proportion in the blood. Monitoring hemodynamic events provides information about the adequacy of a patient's circulation , perfusion, and oxygenation of the tissues and organ systems. The effectiveness of hemodynamic monitoring depends both on available technology and on physician ability to diagnose and effectively treat the disease
central venous pressure and intra-arterial blood pressure monitoring. invasiv...prateek gupta
central venous pressure and intra-arterial blood pressure monitoring. various sites for cvp and Ibp insertion. working principle for cvp and ibp. indication and complication. various waveform of cvp and ibp
fluid optimization concept based on dynamic parameters of hemodynamic monitoringSurendra Patel
Recent advances in hemodynamic monitoring to assess fluid responsiveness of patients in acute circulatory failure is based on dynamic parameters like SPV, PPV, SVV and PVI. These parameters are more accurate than static but needs advanced and sensitive monitoring tools.
Post cardiac arrest brain injury Jan 2023.pptxmansoor masjedi
Post cardiac arrest period is a critical period after return of spontaneous circulation . Optimal care and management is associated with best outcome with least neurological devastating sequella.
Optimal chest compression point , Does one size fit all 0- Dr Masjedi.pptxmansoor masjedi
Cardiopulmonary resuscitation is a life saving process . over years it has undergone changes most prominently in the field of chest compression because high quality chest compression deeply affects outcomes . Chest compression point plays a important role in this regard . Guidelines has changed little in this fundamental part of high quality CPR although ever increasing data denotes its utmost importance .
Challenges in optimal thromboprophylaxis dose in COVID 19 ICU patients.PPTXmansoor masjedi
COVID 19 global epidemy was associated with a lot of unresolved entities amongst them , thromboprophylaxis . This presentation encompasses a brief review of this important aspect of COVID 19 .
Complications & troubleshooting in continuous renal replacement therapymansoor masjedi
Acute kidney injury is a common and important issue in critical care patients . Among different extra corporeal supporting modalities , continuous renal replacement therapy is a common selection especially in unstable conditions . As any other intervention , there are some related complications that should be diagnosed and treated as early as possible .
Diagnostic imaging in COVID 19 pts in intensive care unitsmansoor masjedi
In the era of COVID19 , early diagnosis , ruling out other differential diagnosis , determination of its severity , monitoring the course of the disease , prediction of outcome and response to treatment are so important . CT scan and ultrasound could help physicians in this way . This presentation is part of an international webinar discussing this entity .
A case based approach to the treatment of sepsis in critical caremansoor masjedi
sepsis is the leading cause of death in intensive care units Emergence of multi drug resistance micro organisms should be suspiciously considered early in critically ill patients .
ECMO and its emerging role in trauma ICU 15th ECCC Dubai April 2019mansoor masjedi
Although there are some special considerations & important obstacles , extra-corporeal life support is increasingly used in multiple trauma patients admitted in ICU , with acceptable results.
As a newly emphasized modality to treat infectious complications and also to folloew non-antibiotic regimens against infection, Probiotics has recieved more and more attention now a days.
Vascular sonography 4th international congress on critical care Tehran Iranmansoor masjedi
a review on application of sonography for vascular evaluation and intervention in critical care , sonography is an invaluable tool in both central and peripheral vascular access with proved efficacy to reduce comlications and increase the success rate and ease of catheter insertion
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
263778731218 Abortion Clinic /Pills In Harare ,ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group ABORTION WOMEN’S CLINIC +27730423979 IN women clinic we believe that every woman should be able to make choices in her pregnancy. Our job is to provide compassionate care, safety,affordable and confidential services. That’s why we have won the trust from all generations of women all over the world. we use non surgical method(Abortion pills) to terminate…Dr.LISA +27730423979women Clinic is committed to providing the highest quality of obstetrical and gynecological care to women of all ages. Our dedicated staff aim to treat each patient and her health concerns with compassion and respect.Our dedicated group of receptionists, nurses, and physicians have worked together as a teamof receptionists, nurses, and physicians have worked together as a team wwww.lisywomensclinic.co.za/
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
5. • 1960s: golden age of vasopressors
• 1970s: golden age of inotropes
• 1980s:
• 1990s till now:
History of Monitoring
Pressure, arterial line & CVP
Cardiac output, PA catheter
SvO2 , relative balance between oxygen supply and
demand
Better understanding of tissue oxygenation,
Right & left ventricular function ,
Functional monitoring,PiCCO, continuous CO
Less invasive, TEE
6. Hemodynamic monitoring
trutH
•No monitoring device, no matter how simple
or complex, invasive or non-invasive, inaccurate
or precise will improve outcome
•Unless coupled to a treatment , which itself
improves outcome
Pinsky & Payen. Functional Hemodynamic Monitoring, Springer, 2004
7. Goals of Monitors
To assure the adequacy of perfusion
Early detection of inadequacy of perfusion
To titrate therapy to specific hemodynamic end point
To differentiate among various organ system
dysfunctions
Hemodynamic monitoring for individual patient should be
physiologically based and goal oriented
8. Different Environments Demand
Different Rules
Emergency Department
Trauma ICU
Operation Room
ICU & RR
Rapid, invasive, high specificity
Somewhere in between ER and OR
Accurate, invasive, high specificity
Close titration, zero tolerance for complications
Rapid, minimally invasive, high sensitivity
10. Old equipments
• Arterial line
– Real time SBP, DBP, MAP
– Pulse pressure variation (∆PP)
• ΔPP (%) = 100 × (PPmax - PPmin)/([PPmax + PPmin]/2)
• >= 13% (in septic pts,) discriminate between fluid responder and
non respondaer (sensitivity 94%, specificity 96%)
Am J Respir Crit Care Med 2000, 162:134-138
11. Arterial line
• Advantages
– Easy setup
– Real time BP monitoring
– Beat to beat waveform display
– Allow regular sampling of blood for lab tests
• Disadvantages
– Invasive
– Risk of haematoma, distal ischemia, pseudoaneurysm
formation and infection
12. Old equipments
• Central venous catheter
– Measurement of CVP, medications infusion
and modified form allow for dialysis
13. Limitation of CVP
Systemic venoconstriction
Decrease right
ventricular
compliance
Obstruction of the
great veins
Tricuspid regurgitation
Mechanical
ventilation
14. Central venous catheter
• Advantages
– Easy setup
– Good for medications infusion
• Disadvantages
– Cannot reflect actual RAP in most situations
– Multiple complications
• Infections, thrombosis, complications on insertion,
vascular erosion and electrical shock
16. Indications for PAP monitoring
• Shock of all types
• Assessment of cardiovascular function
and response to therapy
• Assessment of pulmonary status
• Assessment of fluid requirement
• Perioperative monitoring
17. PAC
• Advantages
– Provide lot of important haemodynamic
parameters
– Sampling site for SvO2
• Disadvantages
– Costly
– Invasive
– Multiple complications (eg arrhythmia, catheter
looping, balloon rupture, PA injury, pulmonary
infarction etc)
– Mortality not reduced and can be even higher
Crit Care Med 2003;31: 2734-2741
JAMA 1996;276 889-897
18.
19. Advance in haemodynamic assessment
• Modification of old equipment
• Echocardiogram and esophageal doppler
• Pulse contour analysis and transpulmonary thermodilution
• Partial carbon dioxide rebreathing with application of Fick
principle
• Electrical bioimpedance
20. Objective To compare measurements of cardiac output using a new pulmonary artery catheter with
those obtained using two " gold standard " methods: the periaortic transit time ultrasonic flow probe
and the conventional pulmonary artery thermodilution.Design Prospective clinical
trial.Setting Cardiac surgery operating room and surgical ICU in a university hospital.Material and
methods In the operating room, a new pulmonary artery catheter (truCCOMS system) was inserted in
eight patients. A periaortic flow probe was inserted in four of them. Measurements of cardiac output
obtained with the truCCOMS catheter and with the flow probe were compared at different phases of
the surgical procedure. In the intensive care unit, the cardiac output displayed by the truCCOMS
monitor was compared with the value obtained after bolus injection performed
subsequently.Results In the operating room (70 measurements), the coefficient of correlation between
cardiac output measured by the flow probe and the truCCOMS system was r2
= 0.79, the bias was
+0.11 l/min with a precision of 0.47 l/min, and limits of agreement –0.83 to +1.05 l/min. In the intensive
care unit (108 measurements), the coefficient of correlation between cardiac output measured by
thermodilution and the truCCOMS system was r2
= 0.56, the bias was –0.07 l/min, the precision was
0.66 l/min, and the limits of agreement were –1.39 to +1.25 l/min.Conclusion The truCCOMS system is
a reliable method of continuous cardiac output measurement in cardiac surgery patients.
21. TruCCOMS system
• Advantage
– Continuous CO monitoring
– Provision of important haemodynamic parameter
as PAC
• Disadvantage
– Invasive
– Costly
– Complications associated with PAC use
22.
23.
24. Transthoracic echo
• Assessment of
– cardiac structure
– ejection fraction
– cardiac output
• Based on 2D and doppler flow
technique
25. Static (much like central venous pressure
[CVP]/pulmonary artery occlusion
pressure [PAOP] )
Eyeballing
Left ventricular end-diastolic area (LVEDA)
Mitral early to late filling velocities (E/A)
Early mitral filling velocity to early
diastolic mitral annular velocity (E/E’)
CO
Dynamic
Aortic blood flow
Respiratory variation
Vena cava collapsibility
Passive leg raising
STATIC VERSUS DYNAMIC PARAMETERS
26. LVEDA
Left parasternal short-axis view, mid-papillary level
Normal LVEDA is 9.5–22 cm2
; very low (<5.5 cm2
/m2
body
surface area) suggests
hypovolemia
Beware suboptimal image
quality (especially border
definition and midpapillary
positioning (
Mostly useful as a reality
check for eyeballing
27. EYEBALLING
Echocardiography has been validated for left
ventricular (LV) volume measurements.
Such measurements are often adequate to
guide fluid volume therapy, but only at extremes
of cardiac filling and function.
30. PASSIVE MECHANICAL VENTILATION
Exaggerates hemodynamic effects noted with passive,
PPventilation in hypovolemic subjects
Right ventricular (RV) preload effects
LV stroke volume effects
Passive = paralyzed or heavily sedated, not initiating breaths
Requires at least 8 mL/kg tidal volume, by convention
Requires sinus rhythm
31. ECHOCARDIOGRAPHY FOR STROKE VOLUME VARIABILITY
Various techniques exploit the net effects of positive-
pressure ventilation on stroke volume/LV filling in
hypovolemic patients
Echocardiography provides a useful, informative
alternative to Swan-Ganz, indicator-dilution, thoracic
bio-impedance/reactance, etc.
32. Pulsed Wave Doppler
VTI = Area Under Curve
AORTIC VELOCITY TIME INTERVAL (VTI(
RESPIRATORY VARIATION
33. PEAK VELOCITY: SURROGATE FOR VTI
2001 study by Feissel et al studied 19
patients
Feissel M, Michard F, Mangin I, et al. Respiratory changes in aortic blood velocity as
an indicator of fluid responsiveness in ventilated patients with septic shock. Chest.
2001;119:867-873.
40. AORTIC VELOCITY VARIABILITY PITFALLS
Beware RV failure:
Cor pulmonale
Severe ARDS
Severe pul. hypertension
Resp. distress with huge pressure swings,
e.g., status asthmaticus
Usual aortic velocity variability (AoV) pegged to typical
intrathoracic pressure shifts
Cardiac translation can exaggerate AoV variability
High positive end-expiratory pressure
41. VENA CAVA COLLAPSIBILITY:
A SURROGATE FOR RV PRELOAD
Superior Vena Cava
Only accessible via
transesophageal
echocardiography (TEE(
Intrathoracic
Beware superior vena cava
(SVC) syndrome
Inferior Vena Cava
Generally accessible via
transthoracic
echocardiography (TTE)
Extrathoracic
Beware abdominal
compartment syndrome
43. na cava collapsibility = (Dmax - Dmin)/Dmax x 10
SVC Collapsibility
Patients who had an SVC collapsibility index o
>36% were volume responsive.
Patients with an SVC collapsibility index of
<36% were not volume responsive.
46. IVC DISTENSIBILITY INDEX
Feissel M, et al. Intensive Care Med. 2004;30:1834-
1837.
Barbier C, et al. Intensive Care Med. 2004;30:1740-
1746.
• Patients intubated
• No respiratory
efforts
• VT >8 mL/kg
PBW
49. IVC PITFALLS
Beware of movement in and out of plane, which will
exaggerate IVC collapsibility. Many authors
recommend short-axis view of IVC to confirm.
Beware the hepatic vein confluence.
Do not mistakenly interrogate aorta.
50. 2012 SEPSIS GUIDELINES
20-40 mL/kg
CVP to 8-12 mm Hg
Norepinephrine for a MAP
<65 mm Hg
Dobutamine for ScVO2 <70%
or organ hypoperfusion
Lactate or oliguria
Limited Echocardiography
Guide
Parasternal
Apical 4-chamber
Subcostal
Biventricular function
Pericardial evaluation
IVC diameter
1. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis
Campaign: international guidelines for management of severe
sepsis and septic shock: 2012. Crit Care Med. 2013;41:580-
637.
2. Kanji HD, McCallum J, Sirounis D, et al. Limited
echocardiography-guided therapy in subacute shock is
associated with change in management and improved
outcomes. J Crit Care. 2014:29:700-705.
51. ACTIVE VENTILATION
Active spontaneous, negative-pressure ventilation
Includes many pts on the ventilator
)though poorly studied(
Highly variable stress on cardiac filling/function
Thwarts most efforts at stroke volume variability
Postural change: bring the blood
to the heart
52. PASSIVE LEG RAISE (PLR(
Wait 90 seconds to 3 minutes between measurements
Observe privacy
Use straight arms
53. PASSIVE LEG RAISING
12%
Lamia B, et al. Intensive Care Med.
2007;33:1125-1132.
Maizel J, et al. Intensive Care Med.
2007;33:1133-1138.
PLR-induced changes in VTIAo
54. Determining Probability
Rarely is a single measure definitive
Integrate multiple inputs to make a prediction,
e.g., AoV variability + IVC + CVP + clinical instinct
Then assess results: echocardiography
provides a useful and rapid method
English statistician,
philosopher and
Presbyterian minister
55. SUMMARY
Static measures rarely predict fluid
responsiveness.
Dynamic measures often predict fluid
responsiveness.
Passively ventilated
LV stroke volume effects: aortic VTI/Vpeak variability
RV preload: IVC/SVC variability
Actively ventilated
Passive leg raise
Synthesize multiple inputs to make assessment
56.
57. QUESTION
This image is from a 51-year-old
man with septic shock. Is this
patient fluid responsive?
A.Yes
B.No
C.Uncertain
LVEDA 18 cm2
GET MORE DATA
58. QUESTION
This image is from a 40-year-old
woman with septic shock. Is this
patient fluid responsive?
A.Yes
B.No
C.Uncertain
59. QUESTION
This image is from a 40-year-old
woman with septic shock. Is this
patient fluid responsive?
A.Yes
B.No
C.Uncertain
LVEDA 5 cm2
60. QUESTION
This is an image of a 75-year-old man with a urinary
tract infection and shock. Is this
patient fluid responsive?
A.Yes
B.No
C.Uncertain
61. QUESTION
This is an image of a 75-year-old man with a
urinary
tract infection and shock. Is this patient fluid
responsive?
A.Yes
B.No
C.Uncertain
∆Vpeak = (0.63 - 0.46)/[(0.63 + 0.46)/2] x
100
∆Vpeak = 31.2%
62. Transthoracic echo
• Advantages
– Fast to perform
– Non invasive
– Can assess valvular structure and myocardial function
– No added equipment needed
• Disadvantages
– Difficult to get good view (esp whose on ventilator / obese)
– Cannot provide continuous monitoring
63. Transesophageal echo
• CO assessment by Simpson or doppler flow technique as
mentioned before
• Better view and more accurate than TTE
• Time consuming and require a high level of operator skills
and knowledge
64. Esophageal aortic doppler US
• Doppler assessment of
descending aortic flow
• CO determinate by
measuring aortic blood flow
and aortic CSA
• Correlate well with CO
measured by thermodilution
Crit Care Med 1998 Dec;26(12):2066-72
Decending
aorta
65. Esophageal aortic doppler US
• Advantages
– Easy placement, minimal training needed (~ 12 cases)
– provide continuous,real-time monitoring
– Low complications
– Minimal infective risk
• Disadvantages
– High cost
– Poor tolerance at awake pt, so for those intubated
– Probedisplacement can occur during prolonged
monitoring and patient’s turning
– High interobserver variability when measuring changes
in SV in response to fluid challenges
66.
67. What is the PiCCO-Technology?
2 - Pulse Contour Analysis
CV
Bolus
injectio
n
PULSIOCAT
H
CALIBRATIO
N
1 - Transpulmonary Thermodilution injection
t
T
P
t
A unique combination of 2 techniques
for advanced hemodynamic and volumetric management
69. SVSVmaxmax
SVSVminmin
SVSVmeanmean
SVSVmaxmax – SV– SVminmin
SVV =SVV =
SVSVmeanmean
Stroke Volume Variation: Calculation
Stroke Volume Variation (SVV) represents the variation of stroke volume (SV)
over the ventilatory cycle.
SVV is...
... measured over last 30s window
… only applicable in controlled mechanically ventilated patients with regular heart
rhythm
70. Pulse Pressure Variation: Calculation
PPPPmaxmax – PP– PPminmin
PPV =PPV =
PPPPmeanmean
PPPPmaxmax
PPPPmeanmean
PPPPminmin
Pulse pressure variation (PPV) represents the variation of the pulse pressure
over the ventilatory cycle.
PPV is...
…measured over last 30s window
…only applicable in controlled mechanically ventilated patients with regular beat
rhythm
71. Decision tree for hemodynamic / volumetric monitoring
CI (l/min/m2
)
GEDI (ml/m2
)
or ITBI
(ml/m2
)
ELWI* (ml/kg)
(slowly responding)
>3.0<3.0
>700
>850
<700
<850
>700
>850
<700
<850
ELWI* (ml/kg)
GEDI (ml/m2
)
or ITBI
(ml/m2
)
CFI (1/min)
or GEF (%)
<10 >10 <10 <10 <10>10 >10 >10
V+ V+! V+!V+Cat Cat
OK!
V-
>700
>850
700-800
850-1000
>4.5
>25
>5.5
>30
>4.5
>25
700-800
850-1000
Cat
>5.5
>30
>700
>850
700-800
850-1000
700-800
850-1000
≤10 ≤10 ≤10 ≤10
V-
V+ = volume loading (! = cautiously) V- = volume contraction Cat = catecholamine / cardiovascular agents
** SVV only applicable in ventilated patients without cardiac arrhythmia
>700
>850
<10Optimise to SVV** (%)<10 <10 <10
R
E
S
U
L
T
S
T
A
R
G
E
T
T
H
E
R
A
P
Y
1.
2. <10 <10 <10 <10
72. Pulse contour analysis
• Advantages
– Almost continuous data of CO / SV / SV variation
– Provide information of preload and EVLW
• Disadvantages
– Minimal invasive
– Optimal arterial pulse signal required
• Arrhythmia
• Damping
• Use of IABP
73. Partial carbon dioxide rebreathing
with application of Fick principle
• Fick principle is used for CO measurement
• CO = VO2 / (CaO2 – CvO2) = VCO2 / (CvCO2 – CaCO2)
• Based on the assumption that blood flow through the
pulmonary circulation kept constant and absence of shunt
• Proportional to change of CO2 elimination divided by change
of ETCO2 resulting from a brief rebreathing period
• The change was measured by NICO sensor
74. Partial carbon dioxide rebreathing
with application of Fick principle
• Advantages
– Non invasive
• Disadvantages
– Only for those mechanically ventilated pt
– Variation of ventilation modality and presence of
significantly diseased lung affect the CO reading
– Not continuous monitoring
75. • Electrodes are placed in specific areas on the neck & thorax
• A low-grade electrical current, from 2 - 4 mA is emitted &
received by the adjacent electrodes
• Impedance to the current flow produces a waveform
• Through electronic evaluation of these waveforms, the timing
of aortic opening and closing can be used to calculate the left
ventricular ejection time and stroke volume
77. Haemodynamic monitoring enable early
detection of change in pt’s conditions
New techniques provide reasonably good
results & less invasive
Always correlate the readings / findings with
clinical pictures in order to provide the best
treatment options
Many factors in the literature attempt to determine whether patients will respond to volume expansion. These factors are grouped as static and dynamic parameters. Static factors don’t change over time: for example, central venous (CVP) or pulmonary artery occlusion pressure (PAOP) and end-diastolic area. These dynamic parameters change with time over different ventricular loading conditions.
In a parasternal short axis view, an area can be calculated from a tracing. The problem with that is the normal end-diastolic area is wide, somewhere between 10 and 20 cm2. It&apos;s not useful to determine where a patient falls on the Frank-Starling curve. A low end-diastolic area (less than 5 cm2) suggests hypovolemia. Eyeballing or tracing the border isn&apos;t helpful most of the time, because most people fall into the normal range.
First echo is sepsis with hyperdynamic hypovolemia and low LVEDA (~8cm2), while second echo is normal. Third echo is sepsis but LVH and normal LVEDA (~12cm2). The LV volumes look smaller because the RV is dilated.
The literature touts certain surrogates for wedge pressure. These can be calculated with Doppler through the mitral valve or the pulmonary vein. But the wedge pressure doesn&apos;t indicate whether the patient is going to respond to fluid, so these procedures aren&apos;t that useful.
In patients who are receiving passive mechanical ventilation—meaning heavily sedated and the ventilator is doing all the work—check the aortic blood flow variation and whether or not the vena cava is collapsible. In those who are spontaneously breathing, these measures are not as accurate, so raise the legs to see if cardiac output increases.
Huang et al, Crit Care Med. 2008, used PiCCOplus monitor to establish that high positive end-expiratory pressure (PEEP) and low tidal volume in ARDS patients also causes wide RV preload effects.
Echocardiology reveals stroke volume variation in a noninvasive manner.
To look at respiratory variation of the aortic velocity time interval, obtain an apical five-chamber view. Use pulsed wave Doppler instead of continuous wave, and place the cursor at the left ventricle outflow tract. Each resulting waveform is essentially the stroke volume going through the outflow tract or the aortic annulus. Next, trace the biggest and smallest curves to determine the area under the curve for each. These areas provide the difference between the maximum and the minimum velocity time intervals (VTI), which are analogous to the largest and smallest stroke volume and how volume changes with respiration.
A study by Feissel, et al (Chest. 2001;119:867-73) looked at 19 sedated patients in septic shock.
The larger the variation of VTI, the more dramatic the increase in cardiac output following a fluid bolus.
It is a little cumbersome to have to trace the VTI and so, as a surrogate of the VTI, use the maximum velocity of each of those curves. Again, use the five-chamber view. With the pulsed wave Doppler, use the peak velocity. Peak velocity varies with respiration, providing variation of the maximum and minimum, not just one value.
Add the maximum and minimum peak velocity to this equation. Basically, it&apos;s the difference between the maximum and minimum divided by the average of the two, then multiplied by 100 to get a percentage.
The bigger the difference between minimum and maximum peak velocity, the more dramatic the increase in cardiac output with volume expansion. In this study, the authors split their patients between who responded to fluid and who didn&apos;t. The magic number seemed to be 12% or 12.5%. If the variation is more than 12.5% in sinus rhythm at 8 mL/kg, the patient is more likely to respond to fluid. If it is less than 12.5%, do not give fluid.
The end-diastolic area didn&apos;t seem to separate responders from non-responders. It&apos;s just not that helpful.
Let’s run through some examples. We see maximum of 0.63 in this patient and an minimum of 0.46. If you put that into the equation, the variation is 31%. So, that&apos;s somebody that you are going to give fluid to.
Here’s another patient. Without even doing the math, you can appreciate the sinusoidal wave; how big the difference is between the maximum peak velocity and the minimum peak velocity. Doing the math, again, this patient has a variation of 24% and would respond to fluid.
Lastly, these waves are very consistent, with changes that are not very dramatic. If you do the math on this patient, that&apos;s somebody that doesn&apos;t respond to fluid. So, it&apos;s a fairly straight-forward concept.
There are some things to be cautious about when you are using this. This does not work as well in patients with RV failure, whether it&apos;s from ARDS or standing pulmonary hypertension; it&apos;s not as predictive of who will benefit. High PEEP also can cause problems and, again, you need sinus rhythm for that. If you are in an arrhythmia, every stroke volume is different. So, you can&apos;t really say that this is going to work for somebody in atrial fibrillation, for example.
Another dynamic parameter is vena cava collapsibility. You can use either the superior vena cava if you&apos;re able to do transesophageal echocardiography, or you can use the inferior vena cava.
This is the TTE scan of the ascending aorta, the right pulmonary artery, the main pulmonary artery, and the SVC. In a subcostal view with the transducer pointed cephalad and caudad, the IVC is visualized emptying in the right atrium next to the liver.
This is the equation for vena cava collapsibility. It&apos;s the difference between the maximum diameter of the IVC or SVC minus the smallest diameter, and it ultimately is divided by the maximum diameter. This is not divided by the average, like the aortic variation. Notice that this has nothing do with how big the IVC or SVC is; the maximum diameter of the IVC could be massive, but variation would indicate fluid responsiveness. The absolute number is unimportant; collapsibility is the meaningful factor.
Putting the SVC variation into this equation, patients in this study who had greater than 36% collapsibility were likely to respond to fluid expansion. Patients with less than 36% collapsibility were unlikely to respond.
The best way to look at collapsibility is to use M-mode because the maximum diameter or minimum diameter of the IVC or SVC will not be missed. M-mode captures about 200 pictures per second, whereas two-dimensional echocardiography scans at maybe 30 pictures per second. Here&apos;s an example of M-mode scanning through the SVC and plotting 200 times per second. We can measure the minimum and maximum diameter of the IVC, then put it into the appropriate equation. Here the variation is over 36% so this patient would respond to fluid.
Conversely, here&apos;s an SVC without much variation. The equation result is less than 36%, so no fluid for this patient.
Looking now at the IVC, the more variation there is in the IVC collapsibility, the more dramatic the increase in cardiac output or stroke volume with volume expansion.
Feissel, et al used the formula: Divc max - Divc min / mean x 100%.
They called this the “IVC variation” and set a threshold of &gt;12%. The maximum diameter of the IVC did not predict fluid responsiveness. So, don&apos;t look at the IVC size; what is important is collapsibility.
Here are some more examples. This is an M-mode scan. Applying the equation isn’t necessary. This is completely collapsed. This patient will respond to fluid.
Here, don&apos;t focus on how wide the IVC is; just focus on the fact that that&apos;s not collapsing at all. So no fluid is needed.
There are a couple of matters to keep in mind.
Sometimes that IVC will move in and out of the ultrasound plane, so maintain a good picture throughout the whole respiratory cycle.
If the mid-portion of the IVC is visualized half the time and only the corner of it the remainder of the time, collapsibility will be exaggerated.
The hepatic vein empties into the IVC near where it all empties into the right atrium. If M-mode is performed there, the IVC diameter will appear falsely large.
Remember that the aorta is very close to the IVC.
Historical control, and not an RCT.
Until now, the discussion has focused on patients on passive ventilation, who are not generating a lot of intrathoracic negative pressure. Patients who are breathing on their own are going to get off the ventilator sooner. So might these individuals respond to an autotransfusion?
Slow transition to emphasize the patience required.
Pitfalls:
- Abdominal compartment syndrome
- Open abdomen
- Unstable pelvic/low lumbar fracture
These results illustrate how this maneuver works. The responders to the leg raise had an increase in VTI, whereas the non-responders didn&apos;t. Both groups returned to baseline with the legs lowered. Following volume administration, passive leg raise responders also responded to volume. So, this leg maneuver predicts the patients that are going to respond.
No single parameter is the perfect measure. You may wish to combine IVC and aortic variation, CVP and urine output. Look at a couple of findings to improve an educated guess.
What are the take-home messages?
Try to use the dynamic parameters to predict patient responsiveness.
If the patient is receiving passive ventilation, it&apos;s helpful to use IVC collapsibility or stroke volume variation based on aortic VTI.
If the patient is actively breathing, autotransfusion via passive leg raise can predict who will respond to volume.
Use all available input to make a decision.
The parasternal long-axis view is foreshortened, so one must exercise caution in interpreting it (first answer is C).
But the parasternal short axis, with confirmed low LVEDA, suggests fluid responsiveness (second answer is A).
C. Aortic velocity variability is unreliable in the presence of RV failure. The systolic excursion velocity (RV S’) could be used. In this case it’s likely to be slow, making aortic velocity variation (AoVV) unreliable. 2 clips, 1 question.
C. Aortic velocity variability is unreliable in the presence of RV failure. The systolic excursion velocity (RV S’) could be used. In this case it’s likely to be slow, making aortic velocity variation (AoVV) unreliable. 2 clips, 1 question.