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Advanced Hemodynamics: Hemodynamics in Every Area

Advanced Hemodynamics: Hemodynamics in Every Area. B.McLean CCNS-BC, CCRN, ANP-BC, FCCM Grady Memorial Hospital bamclean@mindspring.com. “The conventional view serves to protect us from the painful job of thinking.”. John Kenneth Galbraith (1908-2006).

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Advanced Hemodynamics: Hemodynamics in Every Area

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  1. Advanced Hemodynamics:Hemodynamics in Every Area B.McLean CCNS-BC, CCRN, ANP-BC, FCCM Grady Memorial Hospital bamclean@mindspring.com

  2. “The conventional view serves to protect us from the painful job of thinking.” John Kenneth Galbraith (1908-2006)

  3. Why are patients transferred to the ICU from the ward sicker than ED or OR admissions? • Why is their mortality higher, even corrected for how sick they are?

  4. Bedside monitoring • What is monitored? • TPR charts: temperature, pulse, respiratory rate, blood pressure & oxygen saturation most frequent measurements taken by health care professionals • These VITAL SIGNS are important indicators of the bodys response to stressors and form part of a routine physical assessment • measures of consciousness (AVPU), change in mental status • New hyperglycemia!!!!

  5. Bedside monitoring Who monitors? • Observations are usually taken by nursing staff – both registered and non registered. • Can often be delegated to more junior or less experienced members of the team Important that staff are aware of the significance of vital sign recording, and have the knowledge and skill to interpret them to ensure patient safety Safer Care for the Acutely Ill Patient: Learning from Serious Incidents. National Patient Safety Agency 2007

  6. Bedside monitoring Why is it important? • Important to provide baseline set of vital signs to identify subsequent changes in a patient’s condition • Critical events (cardiac arrests, deaths & unplanned ICU transfers) are often preceded by physiological deterioration (and often signs of physiological deterioration! Bedside monitoring can be perceived as basic and routine BUT plays a vital role to ensure safer patient care and early recognition of deterioration.

  7. All Shock Initial Assessment Traditional vs. New Acute vs. Ongoing Static vs. Dynamic Global vs. End Organ Resuscitation Endpoints • Mentation • Skin Perfusion • Pulse • Blood Pressure • Pulse Pressure • Shock Index • Urine Output pH Serum Lactate Base Deficit Echocardiography Arterial Wave analysis Stroke volume

  8. Two most important indicators • ΔRespiratory rate • ΔHeart rate

  9. Heart Rate • Compensating for inadequate circulatory blood flow • heart rate increase in response to stress and tissue demands for oxygen • maximum heart rate and VO2 • baroreflex control of BP • increase in ejection fraction • dependence on Frank-Starling mechanism to maintain stroke volume • vagal tone increases

  10. Sinus Tachycardia: • A “physiological response” • Our pulse can only go so fast under sympathetic stimulation: • UNLESS you are on Beta block therapy! Uh-Oh!!!!!

  11. The most common sign of illness . . . 220 minus age Tachycardia!!

  12. If you forget everything else that I say: • Remember that patients having near maximum sinus tachycardia at rest are at risk for dying!

  13. TACHYCARDIA is compensatory • Pain • Anxiety • Fever • Tissue oxygen deficit • Neurological

  14. Two most important indicators • ΔRespiratory rate • ΔHeart rate

  15. Rapid respiratory rate • Compensating for metabolic acidosis • Check the BMP: • Serum C02 20-28 • Anion Gap • Check ABG • Base deficit? + 2 to - 2 • Decreased Hc03- 22-26 • When any or all of these drop: ACID (H+ ↑ )

  16. Increasing respiratory rate • Always compensatory mechanism • Always evaluate for presence of metabolic acidosis

  17. Circulation • Peripheral pulses and blood pressure • Evidence of decreased perfusion • The most common cardiovascular disturbance in the seriously ill is hypotension caused by hypovolemia and/or sepsis

  18. Blood pressure Changes….. • A LATE sign of deterioration – patients will compensate (especially young) • Be aware of what is normal for patient • Organs are dependent on adequate pressures to ensure perfusion.

  19. Arterial Pressure Monitoring • Systolic pressure • Response of artery to LV ejection • Diastolic pressure • Run-off of volume related most to vascular tone Davidson CJ, et al. Cardiac Catheterization. In: Heart Disease: A Textbook of Cardiovascular Medicine, Edited by E. Braunwald, 5th ed. Philadelphia: WB Saunders Company, 1997

  20. Interventions to improve patient outcomes • “Track and trigger” systems • Used on paper-based and electronic observation charts • Periodic observation of selected vital signs (the “tracking”) with pre-determined • criteria (the “trigger”) for requesting the attendance of more experienced staff

  21. Albert, BL, et al, DIMENS CRIT CARE NURS. 2011;30(5):283/292] http://www.ihi.org/knowledge/Pages/ImprovementStories/EarlyWarningSystemsScorecardsThatSaveLives.aspx

  22. Benefits of the MEWS • Increased frequency of monitoring and assessments in high-risk patients • Can trend data on form to better identify subtle changes • Increases communication among healthcare providers • Shift-to-shift report • Report between disciplines • Increased Critical Thinking knowledge

  23. Principles of hemodynamics evaluation FULL cardiovascular monitoring Measurement and evaluation of filling pressures, cardiac output and tissue oxygenation should provide information regarding both the systemic and pulmonic circulations PressureReflection of compliance when a chamber is filled with volume Cardiac outputThe amount of volume ejected by the heart per minute (represents blood flow) Tissue Oxygenation The amount of volume ejected by the heart per minute (represents blood flow) • Blood pressure is necessary to maintain proper blood flow between arterial and venous circulations • From systemic arteries to capillaries to systemic veins • From pulmonary arteries to alveolar capillaries to pulmonary veins • Blood flow is necessary to provide adequate oxygen uptake and carbon dioxide removal • At the system capillary level to cells • At the pulmonary capillary level to the alveolus • Blood flow is necessary to provide adequate oxygen uptake and carbon dioxide removal At the system capillary level to cells • At the system capillary level to cells • At the pulmonary capillary level to the alveolus

  24. Hemodynamic Profiles M Pinsky. Functional hemodynamic Monitoring. Current Opinion Critical Care 2007;13:318 LOW total volume, LOW flow High venous volume, LOW flow High venous volume, LOW flow High arterial volume, High flow Occlusion to perfusion

  25. Shock states

  26. Circulatory shock • Decreased ability of blood flow to meet metabolic demands of the system • Tissue hypoperfusion is the common denominator in all forms of shock • Assuring blood flow and endpoints representing tissue perfusion are the cornerstones of hemodynamics

  27. Hemodynamic monitoring in the PICU • Early recognition and treatment of inadequate tissue perfusion and oxygenation • Prevention development of SHOCK • Anticipatory management • Physical examination + basic monitoring • Advanced hemodynamic monitoring • cardiac output • prediction fluid responsiveness • DO2 / VO2 relationship • quantification (pulmonary) edema

  28. Inadequate Volume • Hypovolemia (abnormally low circulating blood volume) • low total volume • low arterial volume • Venous pooling • ↑Interstitial “third-spacing” • ↑insensible losses (fever, RR) • Hemorrhagic shock • ONLYarterial volume is meaningful

  29. Inadequate Heart (Cardiac Output) • Inadequate volume in veins • Inadequate cardiac contractile strength • Inadequate heart rate • Excessive work and failure to fill • Valvular disturbances that promote backward flow • ONLYarterial volume is meaningful

  30. Inadequate Vascular Tone • Dilated small arterioles and capillaries • Vessel leak • OR • Vasoconstriction and failure to mobilize blood volumes • OR • loss of ability to constrict or dilate depending on the tissue needs • ONLYarterial volume is meaningful

  31. The problem: How do I decide if my hypotensive patient needs fluids, pressors, or an inotrope? • Septic patients require volume • Giving pressors to an under-resuscitated patient can cause tissue hypoxemia and ischemia • Giving too much fluid may lead to prolonged ventilatory support • Giving fluid is deleterious when the patient will not respond to the fluids with an increase in Cardiac output

  32. What endpoints do we resuscitate to?

  33. Delivering and Measuring Tissue perfusion MACRO: Blood Flow MICRO: Tissue perfusion Base deficit lactate Anion gap V-A CO2 • Cardiac Output (HR{SV}) • Stroke volume • Systolic blood pressure • Pulse pressure • Urine output in mls/Kg/hr Guiding fluid resuscitation in critically ill patients: how to evaluate the available tools? Polderman KH, Bein B, Kluge S, Saugel B.Intensive Care Med. 2015 May;41(5):962-4. doi: 10.1007/s00134-015-3741-1. Epub 2015 Mar 27.

  34. Can We Use BP Alone? Bland, ShoemakerJ Surg Obst 1978: • 74 % of survivors achieved normal values • 76% of NON-SURVIVORS achieved normal vital signs

  35. Crit Care Med – Jan 2013 Crit Care Med 2013; 41:34–40

  36. Crit Care Med – Jan 2013 • 27,022 simultaneous NIBP & A-line BPs • 4,957 patients • University teaching hospital ICU • NIBP overestimatedSBP in hypotension • Mean from NIBP and A-line consistent • MAP < 60 associated with AKI & death Crit Care Med 2013; 41:34–40

  37. AKI: aline versus cuff

  38. Acute Kidney Injury: MAP

  39. Static CVP PAOP Blood Pressure Volume Assessment Parameters • Dynamic • SVV • PPV • SPV • IVC collapse • PLR

  40. Hemodynamic Monitoring Pulmonary Artery Catheter • Not advocated for hypovolemic shock • Dynamic response of the systems too slow to guide therapy • Use: • May benefit geriatric trauma • Sepsis goal directed therapy Central Venous Pressure • Not advocated for hypovolemic shock • Poor relationship between CVP and blood volume • Unreliable for assessing response to fluid • Use: • Acute air embolus • Acute PE • Rt Ventricular infarction • Acute lung injury

  41. While only 47% of intensivists believed that CVP should guide resuscitation, 86% used it because of the Surviving Sepsis Campaign Guidelines.

  42. What’s wrong with this picture?

  43. The four major factors which affect Stroke Volume and Cardiac Output • Heart rate increased is what we see • Sttoke volume is what we TREAT! • Preload : treat with volume • Degree of stretch of myocardial fibers before (pre) ejection • Determined by the volume of blood and compliance (stretch) of ventricle at end of diastole • Measured as preload pressure • Afterload: treat with vasoactive therapy • Degree of tension developed by the ventricle in order to overcome resistance to or after ejection • Measured as calculated resistance • Contractility: treat with inotropes • the intrinsic strength of cardiac muscles: making preload move against afterload • Inferred by Stroke Volume and Frank Starling curve

  44. Stroke Volume (SV) and Stroke Volume Index: • Stroke Volume • Volume of blood that is ejected during systole • SV = end diastolic volume (EDV) – end systolic volume (ESV) • Normal: 60 to 100 ml/beat • Max SV: 120 to 200 ml/beat, depending on size, heredity, and conditioning • Stroke Volume Index • Stroke index is defined as the amount of blood ejected per beat indexed to BSA • Normal: 25 to 35 ml/m2 Most important function Delivery of oxygen to tissues ( left heart dynamics) Delivery of carbon dioxide to alveoli (right heart dynamics) Achieved by maximizing function of both ventricles

  45. We can measure SV…..

  46. Stroke Volume (SV) • MOST important: SV • We can assume by Systolic pressure (SP) • We can assume by Pulse Pressure (PP) • We can assume by Pleth perfusion (PI)

  47. Continuous stroke volume monitoring is the gold standard to monitor the response to a fluid challenge.

  48. preload-independence preload-dependence Volume expansion will increase stroke volume only if ventricles are preload-dependent Stroke Volume Ventricular preload

  49. Passive LegRaising Pathophysiology: Transfers the blood trapped in the lower limbs centrally and increass preload of the heart similar to a fluid bolus ~300mL Baseline: 1.Placept in semirecumbent position (HOB at 45°) for 3 consecutively recorded minutes Challenge: Lower HOB to supine position .Elevate patient’s legs to 45° for 3 minutes consecutively recorded minutes Fluid Responsiveness Increase in SV >10% from prechallenge baseline Duus et al, 2015. Journal of Crit Care

  50. Five rules of PLR • Bed to 45 0, assess CO and SV • Use the bed adjustment and lay patient flat: DO NOT TOUCH patient • Use the bed adjustment and lift the legs to 45 0 (try not to touch) • After 2 minutes, assess CO, SV, SVV • Return to normal position • Assess again!

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