Hemodynamics presentation


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Hemodynamics presentation

  1. 1. Objectives  The participant will be able to discuss hemodynamic definitions (cvp, pa, pcwp, co, ci, svr and pvr) and how they relate to the respiratory patient.  •The participant will use critical thinking skills in assessing changes in respiratory status/ventilation with changes in hemodynamic status.
  2. 2. INDICATIONS FOR HEMODYNAMIC MONITORING Shock  Pulmonary edema of uncertain etiology  Postcardiac surgery  Cardiac tamponade  Acute respiratory failure  Need to evaluate for fluid status/guideline for fluid resuscitation  Need to evaluate hemodynamic response to potent pharmacologic agents MI  especially with an acute right or left ventricular failure  Refractory pain  Significant hypotension or hypertension
  3. 3. Blood pressure  Blood pressure=CO X SVR  Changes in blood pressure are caused by either a change in cardiac output or by systemic vascular resistance  MAP Mean arterial pressure=  SBP + (DBP x 2)= 70-105 mm Hg 3  The average blood pressure occurring in the aorta and its major branches during the cardiac cycle
  4. 4. Stroke volume: CO ÷HR The amount of blood ejected by the left ventricle during systole. N= 60-120 ml/beat Stroke Index: SV ÷BSA The SV indexed for differences in body size by dividing by BSA. N= 30-65 ml/m2/beat Ejection Fraction: % of blood in the ventricle that is ejected during systole. Normally, greater than 50%.
  5. 5. SBP + (DBP x 2)= 70-105 mm Hg 3 CHECK YOURSELF Calculation of Mean Arterial Pressure (MAP) Blood Pressure = 100/60 MAP = _________________ Blood Pressure = 180/98 MAP=_________________ Blood Pressure = 150/70 MAP = _________________
  6. 6. Stroke volume is the volume of blood pumped out of the heart with each heartbeat. If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output. This is known as compensatory tachycardia. Tachycardia is an effective compensatory mechanism up to a point. At heart rates greater than 150 bpm, diastolic filling time becomes so short that the tachycardia itself produces a drop in stroke volume, and cardiac output can no longer be maintained. Stroke volume is affected by three factors, preload, afterload, and contractility.
  7. 7. Preload  Preload is defined as the amount of stretch on the cardiac myofibril at the end of diastole (when the ventricle is at its fullest). The amount of stretch is directly affected by the amount of fluid volume in the ventricle thus preload is most directly related to fluid volume.
  8. 8. Preload  As preload (fluid volume) increases, cardiac output will also increase until the cardiac output levels off.  If additional fluid is added after this point, cardiac output begins to fall. This reaction of the heart muscle to stretch can be likened to a slingshot.  The same is true of the heart.  Too little preload and the cardiac output cannot propel enough blood forward, too much and the heart will become overwhelmed leading to failure. Just the right amount of preload produces the best possible cardiac output; finding this level of preload is called “preload optimization.”
  9. 9. Preload  How is preload measured? There is not a practical way to measure myofibril stretch in living beings, nor is there a widely available method to measure ventricular end-diastolic volume.  Physical assessment of preload includes assessment parameters one would use to evaluate fluid volume status.
  10. 10. Preload Signs of inadequate preload include :  poor skin turgor  dry mucous membranes  low urine output  Tachycardia  Thirst  weak pulses  flat neck veins.  Signs of excess preload in a patient with adequate cardiac function include:  distended neck veins  crackles in the lungs  Bounding pulses  Increased preload in a patient with poor cardiac function presents with:  crackles in the lungs  an S3 heart sound  low urine output  Tachycardia  cold clammy skin with weak pulses,  edema. Insufficient preload is commonly called hypovolemia or dehydration.
  11. 11. Afterload  Afterload is defined as the resistance that the ventricle must overcome to eject its volume of blood. The focus in this packet is afterload of the left ventricle.  The most important determinant of afterload is vascular resistance.  Other factors affecting afterload include blood:  viscosity  aortic compliance  valvular disease As arterial vessels constrict, the afterload increases; as they dilate, afterload decreases.
  12. 12. Afterload  High afterload increases myocardial  The pulse pressure is calculated by subtracting the diastolic blood pressure (DBP) from the systolic blood pressure (SBP). The normal work and decreases stroke volume. Patients with high afterload present with signs and symptoms of arterial vasoconstriction including: pulse pressure at the brachial artery is 40 mm Hg.  cool clammy skin  capillary refill greater than 5 seconds  narrow pulse pressure. Pulse Pressure = SBP - DBP Patients with low afterload present with symptoms of arterial dilation such as: • warm flushed skin • Bounding pulses • wide pulse pressure. If the afterload is too low, hypotension may result.
  13. 13. CLINICAL APPLICATION Afterload A key component of treatment for heart failure is afterload reduction using beta-blockers and ACE inhibitors. By decreasing the resistance to ventricular ejection the cardiac output is increased and myocardial workload is decreased. The increase in cardiac output frequently improves the functional status of these patients.
  14. 14. Contractility & Compliance  Contractility is enhanced by:  Exercise  Catecholamines  positive inotropic drugs It is decreased by:  Hypothermia  Hypoxemia  Acidosis  negative inotropic drugs.  Myocardial compliance refers to the ventricle’s ability to stretch to receive a given volume of blood.  If compliance is low, small changes in volume will result in large changes in pressure within the ventricle.  If the ventricle cannot stretch, it will be unable to increase cardiac output with increased preload as described by the curve.
  15. 15. Right Atrial Pressure-RAP               Normal Value 2-8 mm Hg Clinical Significance: Equivalent to central venous pressure. Abnormalities: Increased –Right ventricular failure, tricuspid valve abnormalities (stenosis or regurgitation), cardiac tamponade, right ventricular infarct, VSD with a left to right shunt. –Pulmonary stenosis, Positive Pressure ventilation –Pulmonary Hypertension Active: hypoxemic pulmonary vasoconstriction Pa02 < 60 mm Hg. –Pulmonary Embolus –COPD –ARDS Passive: –Mitral valve dysfunction either stenosis or regurgitation
  16. 16. Right Atrial Pressure-RAP Decreased:  Hypovolemia  Anything that vasodilates the body  Systemic vasodilation  Septic Shock  Neurogenic Shock,  Anaphylactic Shock  Venous vasodilation  Nitroglycerin or Morphine
  17. 17. Pulmonary Artery Pressure PAP  Systolic: 15-30 mm Hg  Diastolic: 5-12 mm Hg  Mean: 10-20 mm Hg  Clinical Significance: PAP is equal to right ventricular pressure during systole while the pulmonary valve is open.
  18. 18. Pulmonary Artery Pressure PAP  Abnormalities: Increased:  Hypervolemia, VSD with left to right shunt, Pulmonary HTN, Positive pressure ventilation, Mitral valve dysfunction (both), Tamponade,  Left ventricular failure Decreased:  Hypovolemia  Excessive vasodilation
  19. 19. Pulmonary capillary wedge pressure PCWP  Normal value 5-12 mm Hg  Clinical Significance: pcwp is normally equal to left atrial presure; sensitive indicator of pulmonary congestion or left sided CHF. Abnormalities:  Increased  Left ventricular failure with resultant pulmonary congestions, acute mitral insufficiency, tamponade, decreased left ventricular compliance (hypertropy, infarction).
  20. 20. Pulmonary capillary wedge pressure PCWP  Decreased  –Hypovolemia  –Vasodilation
  21. 21. PCWP
  22. 22. Cardiac Output CO  Normal Value 4-8 L/min.  Clinical Significance: CO=SV x heart rate/1000 Abnormalities:  Increased  Sympathetic nervous system innervation(stress/exercise)  Exogenous catecholamines(ie. epinephrine, dobutrex, dopamine, isuprel)  Other positive inotrope: digitalis  Infection, early sepsis  Hyperthyroidism  Anemia
  23. 23. Cardiac Output CO  Decreased  –Cardiac dysrhythmias, decreased contracting muscle mass (myocardial infarction, ischemia) mitralinsufficiency, VSD.  –Increased SVR (afterload)-systemic or Pulmonary HTN, Aortic or Pulmonicstenosisor polycythemia  –Significantly increased or decreased heart rate.  Either hyper or hypovolemia
  24. 24. Cardiac Index CI  Value: 2.5-4 L/min.  Clinical Significance: CI= CO/BSA Abnormalities:  Increased:  high output failure secondary to fluid overload, hepato cellular failure, renal disease, septic shock  Decreased:  hypovolemia, cardiogenicshock, pulmonary embolism, hypothyroidism, CHF with failing ventricle.
  25. 25. Systemic Vascular resistance SVR  Normal Value 900-1300 dyne/sec/cm.  SVR= (MAP-RAP) x 80 /CO•Clinical Significance: Resistance against which the left ventricle must work to eject its stroke volume. Abnormalities:  Increased:  Hypervolemic vaso constrictive states (hypertension, cardiogenic shock, traumatic shock).  Decreased:  septic shock, acute renal failure, pregnancy.
  26. 26. Remember!  There is a inverse relationship with CI and SVR.  •If the CI is UP, the SVR will be DOWN.  •If the CI is DOWN, the SVR will be UP.
  27. 27. Pulmonary Vascular Resistance PVR  Normal Value: 150-250 dyne/sec/cm-5.  •Clinical Significance: PVR=(mPAP-PCWP) x 80/CO. Abnormalities:  Increased:  corpulmonale, pulmonary embolism, valvular heart disease, CHF.  Decreased:  Hypervolemic states, pregnancy
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