Ventricular pump function is often compromised during critical illness and for a variety of reasons. The most common cause of a limited cardiac output in acutely ill patients is right ventricular (RV) dysfunction. Exacerbations of chronic obstructive lung disease or the use of high end-expiratory pressure sin acute lung injury to support arterial oxygenation can result in acute elevations of pulmonary arterial pressure impeding RV ejection, causing RV dilation, decreased left ventricular (LV) diastolic compliance. All these effects limit cardiac output and LV stroke volume. Importantly, the treatment is to sustain mean arterial pressure greater than pulmonary artery pressure to prevent RV ischemia and balance RV fluid status to avoid both over-distention (acute cor pulmonale) and under-filling. This delicate fluid balance is greatly facilitated by the immediate and repeated use of bedside echocardiography. Attempts to minimize lung over distention should be a primary focus of therapy. If one focuses only on the LV, these patients would be said to have a reversible form of diastolic dysfunction, in that LV ejection fraction would be normal but the LV not able to increase its end-diastolic volume without excess filling pressures promoting pulmonary edema. The second most common etiology of impaired heart functional reserve is chronic LV hypertrophy secondary to hypertension, wherein systemic afterload reduction is the primary treatment. Third, decreased systolic pump function is often seen in sepsis owing to reduced myocardial adrenergic responsiveness. However, this is often under-appreciated because of the usually co-existent peripheral vasodilation. In septic patients, measures aimed primarily to increase mean arterial pressure, such as the use of vasopressors often results in a decrease in cardiac output because the septic heart is not able to handle the increased load. Importantly, this form of systolic dysfunction is reversible once the sepsis state resolves, but may require inotropes during its height to sustain flow under pressure. Finally both chronic heart failure patients can also get sick and acute myocardial infarction will impair both diastolic and systolic function. Their treatments include reversing coronary ischemia, if present, afterload reduction and a balanced fluid response. A clear and logical approach to all critically ill patients is needed to quickly separate these diverse forms of heart failure from each other as they have markedly different therapies and clinical trajectories.
ICN Victoria presents Dr Aiden Burrell talking on the diagnosis, clinical features and treatment of right ventricular failure for the Intensive Care Specialist
Anaesthesia in Cardiac Patients for Non-cardiac SurgeryRashad Siddiqi
The reader should be able to:
(1) identify factors which will lead to increased cardiovascular risk for patients undergoing non-cardiac surgery
(2) decide which patients require further cardiovascular testing
(3) make optimization plan for such patients
(4) understand the principles of anaesthesia for patients with cardiac disease
ICN Victoria presents Dr Aiden Burrell talking on the diagnosis, clinical features and treatment of right ventricular failure for the Intensive Care Specialist
Anaesthesia in Cardiac Patients for Non-cardiac SurgeryRashad Siddiqi
The reader should be able to:
(1) identify factors which will lead to increased cardiovascular risk for patients undergoing non-cardiac surgery
(2) decide which patients require further cardiovascular testing
(3) make optimization plan for such patients
(4) understand the principles of anaesthesia for patients with cardiac disease
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.
Surgical procedures have been improved to reduce trauma to the pt, morbidity, mortality and hospital stay with consequent reduction in health care cost.
Many painful operations that once required prolonged hospitalizations are now being performed on an out Pt or short stay basis.
the implications for anesthesiologist are to use the technique that not only allows for optimal surgical conditions, but intraoperative Pt comfort and safety, and a rapid anesthetic recovery
The development of better equipment and facilities, along with increased knowledge and understanding of anatomy and pathology have allowed the development of endoscopy for diagnostic and operative procedure. Starting from 1970 used various pathologic gynecological conditions have been diagnosed and treated with laparoscope.
The two major causes of acute right ventricular (RV) failure in ICU patients are acute cor pulmonale (ACP) during acute respiratory distress syndrome (ARDS) and ACP during acute massive pulmonary embolism (PE).
The increase in pulmonary vascular resistance (PVR) in ARDS can be secondary either to « structural » mechanisms related to lung injury per se and to « functional » mechanisms related to the effects of mechanical ventilation with positive end expiratory pressure (PEEP). The latter mechanism is enhanced when PEEP overdistends more than it recruits lung volume and when tidal volume (VT) is high. The recommended protective ventilation with low VT and PEEP adjusted to driving pressure can also reduce the RV afterload. A reduced central blood volume can also play a role in the increase in PVR (extension of the West’s zone 2). In this case, volume administration can reduce the PVR and improve the RV function. Finally, prone positioning also exerts a beneficial effect on RV afterload through a decrease in PVR (lung recruitment, decrease in hypoxic vasoconstriction, increase in central blood volume with decrease in the extent of zone 2).
In acute PE, RV dysfunction is associated with poor outcome. Thrombolytic treatment, which is indicated in cases of severe PE with shock, prevents hemodynamic decompensation in patients with intermediate risk PE, but also results in increased risk of severe hemorrhage and stroke. In the case of PE with low cardiac output and no RV dilatation, fluid administration can be indicated to improve cardiac output. In cases of systemic arterial hypotension, vasopressors such as norepinephrine can be indicated to restore adequate RV perfusion pressure. Indication of inotropic agents such as dobutamine, which improves the RV-pressure artery coupling should be evaluated individually. Surgical pulmonary embolectomy can be indicated when the thrombolytic therapy is contra-indicated in acute PE with shock.
An excellent tool to treat refractory hypoxia. Target audience are ICU junior physicians and Respiratory Therapists. It will take away the fear of "What is APRV?" from your hearts and you will feel ready to give it a try.
Jehowah's witnesses and blood conservation strategies by Dr.Minnu M. PanditraoMinnu Panditrao
dr. Mrs. Minnu M. Panditrao explains the problems faced by anesthesiologists in anesthetising the Jehowah's Witness patients because of their beliefs. Ina ddition she also discribes various strategies of Blood conservation.
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.
Surgical procedures have been improved to reduce trauma to the pt, morbidity, mortality and hospital stay with consequent reduction in health care cost.
Many painful operations that once required prolonged hospitalizations are now being performed on an out Pt or short stay basis.
the implications for anesthesiologist are to use the technique that not only allows for optimal surgical conditions, but intraoperative Pt comfort and safety, and a rapid anesthetic recovery
The development of better equipment and facilities, along with increased knowledge and understanding of anatomy and pathology have allowed the development of endoscopy for diagnostic and operative procedure. Starting from 1970 used various pathologic gynecological conditions have been diagnosed and treated with laparoscope.
The two major causes of acute right ventricular (RV) failure in ICU patients are acute cor pulmonale (ACP) during acute respiratory distress syndrome (ARDS) and ACP during acute massive pulmonary embolism (PE).
The increase in pulmonary vascular resistance (PVR) in ARDS can be secondary either to « structural » mechanisms related to lung injury per se and to « functional » mechanisms related to the effects of mechanical ventilation with positive end expiratory pressure (PEEP). The latter mechanism is enhanced when PEEP overdistends more than it recruits lung volume and when tidal volume (VT) is high. The recommended protective ventilation with low VT and PEEP adjusted to driving pressure can also reduce the RV afterload. A reduced central blood volume can also play a role in the increase in PVR (extension of the West’s zone 2). In this case, volume administration can reduce the PVR and improve the RV function. Finally, prone positioning also exerts a beneficial effect on RV afterload through a decrease in PVR (lung recruitment, decrease in hypoxic vasoconstriction, increase in central blood volume with decrease in the extent of zone 2).
In acute PE, RV dysfunction is associated with poor outcome. Thrombolytic treatment, which is indicated in cases of severe PE with shock, prevents hemodynamic decompensation in patients with intermediate risk PE, but also results in increased risk of severe hemorrhage and stroke. In the case of PE with low cardiac output and no RV dilatation, fluid administration can be indicated to improve cardiac output. In cases of systemic arterial hypotension, vasopressors such as norepinephrine can be indicated to restore adequate RV perfusion pressure. Indication of inotropic agents such as dobutamine, which improves the RV-pressure artery coupling should be evaluated individually. Surgical pulmonary embolectomy can be indicated when the thrombolytic therapy is contra-indicated in acute PE with shock.
An excellent tool to treat refractory hypoxia. Target audience are ICU junior physicians and Respiratory Therapists. It will take away the fear of "What is APRV?" from your hearts and you will feel ready to give it a try.
Jehowah's witnesses and blood conservation strategies by Dr.Minnu M. PanditraoMinnu Panditrao
dr. Mrs. Minnu M. Panditrao explains the problems faced by anesthesiologists in anesthetising the Jehowah's Witness patients because of their beliefs. Ina ddition she also discribes various strategies of Blood conservation.
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.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
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.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
3. Determinants of Cardiac Pump Function as
Viewed from the Left Ventricle
Preload (Frank-Starling)
Contractility (Anrep)
Afterload
Heart Rate
Synchrony
4. Heart Failure in the ICU is
Condition Specific
• Post-op hearts
• Stunned myocardium
decreased contractility, decreased lusotropy
• RV dysfunction
• Dyssynchrony
• Sepsis
• VA Decoupling, decreased adrenergic response
• COPD/ARDS
• RV dysfunction
• Anterior chest trauma
• RV contusion
7. Rosenblueth et al. Arch Int Physiol 67: 358, 1959
Starling versus Anrep
Heterometric v. Homeometric autoregulation of the heart
Sudden increase and decrease in venous return
EDV
ESV
Starling
Anrep
Increased Preload
Increased Contractility
Preload
Contractility
8. Cardiac Contractility
Contractility proportional to the rate
and amount of Ca+2 flux into the
sarcolema of the contracting
myocytes
All known positive inotropes increase Ca+2 flux
All known negative inotropes decrease Ca+2 flux
9. Cardiac Contractility
• Autonomic Tone
Exercise, Stress; Diabetes
• Coronary Blood Flow
• Kojima et al. Am J Physiol 264:H183-9, 1993
• Serum ionic Ca+2
• Marquez et al. Anesthesiology 65:457-61, 1986
• Local Catecholamine Stores
Chronic stress
• Catecholamine Receptors
Sepsis
• Extrinsic Catecholamine Supplements
14. Isometric LV Ejection
LV Volume (mL)
LV
Pressure
(mm Hg)
End-
Systolic
Developed
Pressure
CBA
Suga et al. Circ Res 32:314-322, 1973
15. Isometric LV Ejection
LV Volume (mL)
LV
Pressure
(mm Hg)
CBA
End-Systolic Pressure-
Volume Relationship
Suga et al. Circ Res 32:314-322, 1973
16. LV Ejection from a Common EDV
LV Volume (mL)
LV
Pressure
(mm Hg)
A
B
CEnd-Systolic Pressure-
Volume Relationship
Suga et al. Circ Res 32:314-322, 1973
18. LV Pressure-Volume loops at variable venous return
before and after epinephrine
Suga et al. Circ Res 32:314-322, 1973
19. Effect of Changes in Contractility on the
End-Systolic Pressure-Volume Relationship
LV Volume (mL)
LV
Pressure
(mm Hg)
Decreased Contractility
Increased Contractility
Normal
Failure
Augmented
Suga et al. Circ Res 32:314-322, 1973
20. End-Systolic Pressure Volume Relationship
(generated by IVC occlusion)
Ees
Diastolic compliance
IVC
Occlusion
Ejection
21. Determinants of Afterload
LV Wall Stress
r
P
LaPlace’s Law
Tension = Px r
Maximal tension
at maximal P x r
which usually occurs at the opening
of the aortic value: EDV, diastolic pressure
22. Chronotropy
Increases in heart rate increase Ca+2 influx
into the sarcolema of the myocytes
increasing force of contraction
Bers. Nature 415:198-205, 1998
Optimal heart rate? > 60 but < 120
23. Effect of Changes in Heart Rate on Contractility
Force-Frequency Relationship
Liu et al. Circulation 88:1893-906, 1993
70 min-1 70 min-1100 min-1 100 min-1
120 min-1 160 min-1 120 min-1 150 min-1
Chronotropy Diastolic Dysfunction
24. Clinical Applications of
LV Pressure-Volume Relations
Acute Myocardial Ischemia
• Useful in understanding the pathophysiolgy of
acute myocardial ischemia
• Explains rationale for pharmacological
approaches to optimize ventricular pump function
25. LV
Pressure
(mm Hg)
LV volume (mL)
Ees
Effect of Acute Myocardial Ischemia on
Left Ventricular Pressure-Volume Relationship
Ischemia
Ees
Ischemia
Acute LV
Failure
26. Effect of Inotropic Support
following Acute Myocardial Ischemia
LV
Pressure
(mm Hg)
LV volume (mL)
Ees
Dobutamine
Ees
27. Effect of Vasodilator Therapy & Inotropic Support
following Acute Myocardial Ischemia
LV
Pressure
(mm Hg)
LV volume (mL)
Ees
Ees
Decreased
LV ejection
Pressure
Nitroprusside
28. Is Myocardial Contractility Depressed
in Human Septic Shock?
• Used transesophageal echocardiographic measures
of LV volume over time linked to arterial pressure
during brief episodes of nitroprusside-induced
hypotension to generate LV ESPVR
Gorcsan et al. Anesthesiology 1994, 81:553-562
• Repeated measures following dobutamine infusion
(5 mg/kg/min)
• Repeated measures at 5 days and at recovery (10d)
Cariou et al. Hopital Cochin, Paris V, 1999-2001
30. Gorcsan et al. Circulation 1994;89:180-90
Transesophageal Echocardiography-ABD
and LV Pressure
31. LV Contractile Reserve in Sepsis
0
10
20
30
Day 1 Day 5 Day 9
Baseline
Dobutamine
E’es
*
P < 0.05
n = 10
Depressed
contractility?
Decreased Adrenergic
Responsiveness?
Cariou et al. Intensive Care Med 34: 917-22, 2008
32. Contractility is Depressed in
Human Sepsis
• E’es is depressed relative to paired recovery
values
• Ees increases less in response to dobutamine
during sepsis relative to paired recovery
values
• Myocardial depression persists following
initial recovery from severe sepsis
Cariou et al. Intensive Care Med 34: 917-22, 2008
33. Determinants of Cardiac Pump Function as
Viewed from the Left Ventricle
Preload
Contractility
Afterload
Heart Rate
Synchrony
34. Phase angles in Regional Dyskinesis
a
b
sum
Baseline
Normal Decreased Force Asynchrony
Series Loss Phase loss
36. Phase Angles & Regional End-systole
during Esmolol-induced Dyskinesis
R R
ECG
Sum
Basal
Chordal
Papillary
Apical
R R
360
0
Global End-systole
A B C
0
0
-10
0
0
0
45
0
60
0250
0
238
0
200
0
190
0
200
0
0
o
Phase angles (R) Phase angles (Global)Stroke volumes
Asynchronous regions
SVt
Strum & Pinsky. A&A 90:252-61, 2000
37. Two-Point Assessment of
Regional Asynchrony
LV
RV
LBBB Patient
2
-2
cm/s
1.1 sec
Septum
Posterior Wall
Septum
Posterior Wall
Normal Control
2
-2
cm/s
1.5 sec
Dohi et al. Am J Cardiol 96:112-6, 2005
38. Contractile Dyssynchrony
• Most common cardiac dysfunction:
Regional wall motion abnormality
• Degree of dysfunction twice a large as seen
• Increased inotropy can help
– If delayed segments increased contraction rate
• Increase inotropy can hurt
– If only normal segments increased contraction
40. Acute Heart Failure in the ICU
• Very Common
• Multi-factorial even if resulting in one effect
• Filling pressures can be misleading
• Context specific: MI, ARDS, sepsis, GOK?
• Requires assessment to treat effectively
– Fluids are not always good
– Increased inotropy is not always good