Relax and Learn At the Farm 2012

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1 Relax and Learn At the Farm 2012 Session 7: Noninvasive Hemodynamic Assessment Without the Bells and Whistles Carol Jacobson RN, MN Cardiovascular Nursing Education Associates Tom Ahrens HEMODYNAMIC MONITORING Function of the Cardiovascular System Supply every cell in the body with enough O2 and nutrients to do its job Blood Flow Oxygenation Heart Arteries Veins Volume DEFINITIONS Cardiac Output: Volume of blood ejected by the ventricle each minute Normal: 4-8 liters/minute Cardiac Index: Adjustment made for body size Normal cardiac index: liters/minute/m 2 Stroke Volume: Volume of blood ejected with each beat. Normal ml / beat Systolic BP as non invasive indicator Ejection Fraction: Percent of blood ejected from the ventricle Normal: 55% to 70% RIGHT SIDE VERSUS LEFT SIDE SYSTEMS Anatomically the heart sits between the two lungs, but physiologically the lungs sit between the right heart and the left heart. 1

2 DETERMINANTS OF CARDIAC OUTPUT CO = HR x SV Preload Afterload Contractility HEART RATE Mathematically heart rate increases cardiac output (CO = HR X SV) At normal HR ranges HR is not the cause of decreased CO Both bradycardia and tachycardia can decrease CO Tachycardia decreases cardiac output by decreasing diastolic filling time ( preload) Drugs that affect HR Increase: atropine, dopamine, dobutamine, epinephrine, norepinephrine Decrease: beta blockers, Ca ++ blockers, digoxin, antiarrhythmics, adenosine COMPENSATORY MECHANISMS Venous tone Body Position Intrathoracic Intrapericardial pressure pressure Sympathetic Nervous System Tachycardia is the first change and occurs for a reason! Patients on beta blockers may not be able to mount a compensatory tachycardia Peripheral vasoconstriction to maintain MAP Will result in increased diastolic BP and decreased pulse pressure If you monitor HR and diastolic BP over time you can see your patient compensating before they crash! Blood Volume Distribution of Atrial Kick LV Function blood volume PRELOAD Preload is end diastolic ventricular fiber length Volume determines fiber length the longer the fibers the better the contraction up to a point (Starlings Law) CVP is the invasive clinical indicator of RV preload JVD is physical assessment parameter that reflects RV preload PWP is the invasive clinical indicator of LV preload Lung sounds are physical assessment parameter that reflect LV preload CONDITIONS THAT ALTER PRELOAD Hypovolemia (low preload) Hemorrhage Dehydration Burns Overdiuresis Third Spacing (low albumin, capillary leak secondary to CPB, ARDs) High Preload Hypervolemia (overhydration CHF Renal disease Pulmonary HTN Tamponade Tension pneumo Pressure higher but not volume Altered Size of Vascular Space Sepsis Neurogenic shock Spinal or epidural anesthesia Anaphylaxis Rewarming after cardiac surgery Venous dilating drugs NTG ACEI Ca ++ blockers NON INVASIVE ASSESSMENT OF PRELOAD RIGHT VENTRICULAR JVD Hepatojugularreflux Symptoms of high RV preload Peripheral edema Weight gain LEFT VENTRICULAR Rales/crackles S3 Gallop Symptoms of high LV preload Frothy sputum Hypoxemia Orthopnea / PND/ Dyspnea 2

3 NECK VEINS Blood in jugular veins assumes level corresponding with right atrial pressure so estimates CVP Right jugular vein reflects pressure best Normal CVP = < 9 cm H 2 0 Position patient so internal jugular is visible (30-45 degrees) Angle of Louis is 5 cm above right atrium Place ruler vertically at Angle of Louis Measure in cm how far above Angle of Louis the neck vein is visible Add this measurement to 5 = estimated CVP JVD (JUGULAR VENOUS DISTENSION) Normal JVD level is 3 cm above the sternal angle Sternal angle is 5cm above right atrium JVD of 3 cm + 5cm = estimated CVP of 8cm Estimated CVP > 8 cm H 2 O is abnormal Increased blood volume Usually RV failure Tricuspid valve regurgitation Pulmonary hypertension Most common cause of RV failure is LV failure 7 cm Level of neck vein Angle of Louis 5 cm Right atrium CVP = 12 cm H 2 O MORE ABOUT NECK VEINS Abdominojugular reflux seen in RV failure Press on upper right quadrant for seconds while watching neck veins Rise in neck veins of 1 cm or more = positive abdominojugular reflux Kussmaul s sign (paradoxical elevation of jugular venous pressure during inspiration) Normally the neck veins empty during inspiration as intrathoracic pressure drops and venous return to the heart increases In restrictive disease (cardiac tamponade, constrictive pericarditis, cardiomyopathy, diastolic HF) the heart cannot handle the increased venous return so neck veins elevate when venous return increases during inspiration DYNAMIC PRELOAD INDICATORS Passive Leg Raise Test Systolic Pressure Variation (SPV) Stroke Volume Variation (SVV) Pulse Pressure Variation (PPV) All 3 measure the difference between the maximum and minimum values over a full respiratory cycle. Are dependent on intrathoracic pressure changes and tidal volume in ventilated patients PASSIVE LEG RAISE (PLR) Form of reversible volume challenge that can be used to evaluate which patients will benefit from intravenous fluid and increased preload. Elevating legs transfers fluid from lower extremities to central circulation Estimated between 150 to 300 ml up to 750 ml in some studies. If the heart is preload-responsive, PLR should result in increased stroke volume & cardiac output. Requires that both the right and left ventricles be preloaddependent. If the right ventricle cannot increase cardiac output with increased preload, the left ventricle will not see the increased preload, and cardiac output will not improve. 3

4 Respiratory Indices of Fluid Responsiveness: SVV, PPV, SPV Positive pressure inspiration causes: intrathoracic pressure during inspiration RV filling volume RV stroke volume LV stroke volume SBP during expiration (due to pulmonary transit time) Comparison of the pulse pressure, stroke volume, or SBP during inspiration and during expiration demonstrates the degree to which the heart is preload dependent. Increased PPV, SVV, or SPV is a predictor of fluid responsiveness Inspiration Expiration Pulse oximetry waveform may also show these changes in some patients INTERPRETATION OF PPV, SPV, SVV Respiratory variation cannot be used in: Spontaneously breathing patients Cardiac arrhythmias Tidal volumes less than 8 ml/kg (all parameters are very dependent on VT) High positive end-expiratory pressures Use of vasoactive drugs With open chest Elevated intra-abdominal pressure Right ventricular failure Sympathetic NS & Arteriolar Tone SVR Circulating vasodilator or vasoconstrictor mediators Aortic Pressure & Compliance AFTERLOAD Afterload is the work done by a ventricle to eject its volume PVR is clinical indicator of RV afterload SVR is clinical indicator of LV afterload Diastolic BP is a reflection of LV afterload Aortic Stenosis HOCM CONDITIONS THAT ALTER AFTERLOAD Vasodilation Sepsis Spinal or epidural anesthesia Anaphylaxis Rewarming after cardiac surgery Arterial dilating drugs Nipride ACEI ARBs Milrinone Ca ++ channel blockers Antihypertensives Vasoconstriction Hypertension SNS stimulation Compensatory vasoconstriction (hypothermia, pump failure) Drugs Phenylephrine (Neosynephrine) Norepinephrine (Levophed) High-dose dopamine Epinephrine Vasopressin MORE ON VASCULAR TONE Increased vascular tone is usually associated with compensation for low SV Cardiogenic shock Decompensated heart failure Hypovolemic shock Decreased vascular tone is usually due to abnormally pathology Sepsis Anaphylaxis Altered neurological control 4

5 AFTERLOAD INDICATORS EVALUATING BLOOD PRESSURE Right ventricular afterload Known pulmonary HTN Causes of increased RV work Hypoxemia Pulmonary embolus Positive pressure ventilation PEEP Left ventricular afterload Diastolic BP is closest noninvasive measurement Narrow pulse pressure BP does NOT equal afterload Diastolic BP is a noninvasive indicator of LV afterload Systolic BP is affected by LV stroke volume Peak rate of LV ejection Distensibility of blood vessel walls Diastolic BP is mostly affected by peripheral vascular resistance BP does not equal perfusion BP value does not tell you WHY the BP is low must evaluate determinants of BP and treat the cause Low BP could be due to: Low CO HR too slow or too fast Preload too low or too high Contractility low Low SVR BP = CO X SVR Vasodilation due to sepsis, drugs, anaphylaxis Paradoxical BP (pulsus paradoxus) Exaggerated decrease in systolic BP during inspiration (normal is < 10 mm Hg drop during inspiration) Normally there is some pooling of blood in the lungs during inspiration, so less blood enters LV and LV stroke volume is slightly reduced With tamponade, the RV can t distend into the pericardial space to accommodate increased venous return during inspiration so it pushes the septum toward the LV, further reducing LV filling and causing a > 10 mm Hg drop in systolic BP during inspiration To measure: have patient breathe normally. Gradually deflate cuff until first sound is heard during expiration, then note when sounds heard during both inspiration and expiration. Example: 140/120/70 Pulsus Paradoxus on Arterial Line > 10 mmhg drop in systolic BP during inspiration SBP = 116 mm Hg SBP = 136 mm Hg Inspiration Expiration Inspiration BP = 136/116/84 Pu lsus paradoxus can be seen in: Cardiac tamponade/constrictive pericarditis Asthma/COPD Restrictive cardiomyopathy Pulmonary embolism Hypovolemic shock Orthostatic BP changes Normally, systolic falls less than 10 mm Hg, diastolic increases about 5 mm Hg, HR increased 5-20 bpm Orthostasis = drop in systolic BP of 20 mm Hg or more or a drop in diastolic of at least 10 mm Hg within 3 minutes of standing To measure Patient supine for 10 minutes, then measure BP and HR Have patient stand (may need to sit first) and measure BP & HR immediately and after 2 minutes May continue to monitor every 2 minutes for 10 minutes 5

6 PULSE PRESSURE Difference between systolic BP and diastolic BP Normal = 40 mmhg (120/80 = 40 mmhg PP) Influenced by stroke volume and arterial compliance (beat-to-beat change reflects SV) PP can be increased due to high stroke volume ( preload, contractility) or high compliance (vasodilation) PP can be decreased due to low stroke volume ( preload, contractility) or low compliance (vasoconstriction) PULSE PRESSURE Decreased pulse pressure (narrow PP) is an early sign of decreased cardiac output First BP change is a rise in diastolic BP due to compensatory vasoconstriction Causes: hypovolemia, LV dysfunction (heart failure, cardiogenic shock), aortic stenosis, HOCM, cardiac tamponade Increased pulse pressure (wide PP) can occur with increased SBP or decreased DBP Aortic regurgitation (increased stroke volume) Hypertension & aortic atherosclerosis (increased SBP) Increased ICP Vasodilated states (sepsis, anaphylaxis,neurogenic) SNS Adrenals H + CO 2 O 2 Ventricular Catecholamines Metabolic Drugs Muscle Mass State CONTRACTILITY Contractility is how efficiently the fibers shorten regardless of how long they are No good direct measure of contractility Hypoxemia Ischemia CONDITIONS THAT ALTER CONTRACTILITY Increase SNS stimulation Pheocromocytoma Hyperthyroidism Positive inotropic drugs Dobutamine Dopamine Levophed Milrinone Digoxin Decrease Myocardial infarction Cardiomyopathy Ischemia Hypoxia Acidosis Negative inotropic drugs Beta blockers Ca ++ blockers Antiarrhythmics Some chemo agents Some anesthetics, sedatives IMPORTANT POINTS ABOUT CONTRACTILITY No accurate way to measure contractility Noninvasive assessment: ejection fraction Normal EF = 50%-70% Low cardiac output does not necessarily mean decreased contractility (CO = HR X SV) Bradycardia, tachycardia, hypovolemia, vasoconstriction Correct preload and afterload problems first in a patient with a low ejection fraction. Increasing contractility with medications will also increase myocardial oxygen demand. OXYGENATION VS VENTILATION Oxygenation involves loading hemoglobin with oxygen for delivery to the tissues Measured by ABG: PaO 2 = > 80 mmhg Measured by O 2 saturation: SaO 2 = % Ventilation involves removal of CO 2 from the blood via the lungs Measured by PaCO 2 : mmhg Measured by PETCO 2 : normal mmhg ETCO2 is 2-5 mmhg lower than PaCO 2 Reflects metabolism, circulation, and ventilation 6

7 PULSE OXIMETRY VS CAPNOGRAPHY Pulse Oximetry Assesses oxygenation Measures saturation of Hb with O 2 Waveform correlates with arterial line and peripheral perfusion Capnography Assesses ventilation Measures exhaled CO 2 Waveform correlates with tissue metabolism, cardiac output, and pulmonary function EVALUATING OXYGENATION Arterial blood gas Provides a PO 2 which measures only the small amount (2%) of oxygen that is dissolved in plasma Painful, does not provide immediate or continuous data Pulse oximetry has become the standard for continuous noninvasive assessment of arterial oxygen saturation : the "fifth vital sign" Measures saturation of hemoglobin with O 2 (SaO 2 ) Reflects the 98% of arterial O2 content that is carried by hemoglobin OTHER USES FOR PULSE OXIMETRY? Monitor perfusion to extremity after cardiac cath procedure Place probe on toe for femoral access and on index finger for radial access Waveform might be usable to assess for fluid responsiveness similar to arterial waveform Limitations of Pulse Oximetry Does not assess ventilation Administration of O2 can maintain SaO2(normal pulse ox reading) even with severe hypoventilation Reliance on pulse ox alone can delay detection of clinically significant hypoxemia SaO 2 won t fall until PO 2 decreases to about mmhg Pulse ox results are signal-averaged over several seconds, so the pulse oximeter may not detect a hypoxemic event until well after it has occurred Carboxyhemoglobin (carbon monoxide poisoning, smoke inhalation) absorbs light the same as oxyhemoglobin, so pulse ox reading may be normal even with severe desaturation (same true with methemoglobinemia) OTHER FACTORS IMPACTING TISSUE OXYGENATION Affinity of hemoglobin for O 2 for proper uptake in lungs and unloading to tissues Shift to Left: easy to Load O 2 in lungs but harder to release it to tissues Hypothermia, alkalosis, 2,3 DPG (banked blood) Shift to Right: hard to pick up O 2 in lungs but easy to Release it to tissues Acidosis, hyperthermia, 2,3 DPG Utilization of O 2 by the cells Sepsis (cells unable to use O 2 ) SHIFT TO THE RIGHT 2,3-DP R I G H T ise n + (acidosis) emperature More about 2,3-DPG 2,3-DPG is a substance in RBCs that controls how much O 2 is released to tissues. Decreased levels seen in hemolytic anemia and after large blood transfusions (banked blood rapidly loses 2,3-DPG and ability to deliver O 2 ). Increased levels in conditions in which the body needs more oxygen: anemia, COPD, cystic fibrosis, congenital heart disease, hyperthyroidism, high altitudes. 7

8 CLINICAL USES FOR ETCO 2 MONITORING THE NORMAL WAVE FORM Intubated Patients Verify ET tube placement during intubation Monitor ET tube placement during transport Monitor CPR quality Detect ROSC Control ventilation in closed head injury & increased ICP Non Intubated Patients Detect bronchospasm Asthma, anaphylaxis, COPD Detect hypoventilation Sedation, HF, stroke Low cardiac output HF, cardiogenic shock, hypovolemia Hyperventilation Phase I = inspiration of CO 2 -free air (ETCO 2 level is 0 mmhg) Phase II = beginning of expiration (CO 2 starts being detected as dead space air mixes with exhaled CO 2 ) Phase III = expiration (CO 2 -rich gas from the alveoli) Phase 0 = inspiration (CO 2 level rapidly falls as O 2 enters airways) Normal waveform: PETCO 2 about 40 mmhg CPR: PETCO 2 should be at least 10 mmhg If below 10 mmhg, need to improve CPR quality ROSC: sudden sustained rise in PETCO 2 Apnea or dislodged ET tube Hypoventilation CO 2 levels rising, > 45 mmhg Esophageal intubation Hyperventilation CO 2 levels falling, < 35 mmhg 8

9 Bronchospasm: shark fin appearance indicates delay in exhalation due to obstruction Asthma, COPD, anaphylaxis Shark fin shape may become more pronounced as attack progresses ETCO2 values may be normal at first and then rise as attack progresses in severity Curare cleft Occurs when paralytics begin to wear off and patient tries to breathe on own Indicator to give more paralytic if still needed FACTORS AFFECTING PETCO 2 INCREASED PETCO 2 DECREASED PETCO 2 Metabolic Factors Pain Hyperthermia Shivering Respiratory System Hypoventilation Respiratory depression COPD Analgesia/sedation Circulatory System Increased cardiac output Metabolic Factors Hypothermia Metabolic acidosis Respiratory System Hyperventilation Bronchospasm Mucus plug Circulatory System Hypotension Hypovolemia Cardiac arrest Pulmonary embolism Acute Cardiac Decompensation MI Acute decompensated heart failure Cardiac tamponade Acute Pulmonary Embolism Tension Pneumothroax Acute Aortic Dissection Shock States Hypovolemic Cardiogenic Distributive Obstructive 3 CLINICAL PROFILES OF DECOMPENSATED HEART FAILURE Patients with volume overload Pulmonary &/or systemic congestion Patients with profound depression of cardiac output Hypotension, renal insufficiency, other signs of hypoperfusion Patients with signs and symptoms of both fluid overload and shock PROFILES OF ADVANCED HF Low Perfusion at Rest Is skin warm or cold? Warm Cold Congestion at Rest Dry Warm and Dry No congestion No hypoperfusion Cold and Dry No congestion Hypoperfusion (forwards failure) Are lungs wet or dry? Wet Warm and Wet Congestion No hypoperfusion (backwards failure) Cold and Wet Congestion Hypoperfusion 9

10 SHOCK CLASSIFICATIONS HEMODYNAMIC PARAMETERS IN SHOCK Hypovolemic Cardiogenic Distributive Anaphylactic Septic Neurogenic Nonspecific vasodilatory Obstructive Pulmonary embolism Cardiac tamponade Tension pneumothorax Aortic dissection Hypovolemic (volume problem) Cardiogenic (pump problem) Distributive (vessel problem) Preload Afterload Pump Function (compensatory) (compensatory) (early) Tissue Perfusion (SvO 2 ) (vasodilation) (late) (O 2 delivered but unused) CLINICAL SIGNS OF HYPOVOLEMIA Tachycardia Low urine output Flat neck veins Pulsus paradoxus sometimes seen CVP decreases before BP decreases Hypotension eventually occurs BP is maintained by HR and vasoconstriction until decompensation occurs STAGES OF SHOCK Sub clinical Hypoperfusion CI No clinical indications of hypoperfusion yet something seems different or not right Clinical Hypoperfusion (Compensatory SNS Stimulation) CI Tachycardia Narrowed pulse pressure Tachypnea Cool Skin Oliguria Restlessness,confusion STAGES OF SHOCK TREATMENT FOCUS IN SHOCK Shock (Progressive hypoperfusion) CI < 2.0 Arrhythmias Hypotension Tachypnea Cold, clammy skin Anuria Absent bowel sounds Lethargy to coma Refractory Shock (Profound hypoperfusion) CI < 1.8 Life threatening arrhythmias Hypotension despite vasopressors ARDS DIC Hepatic failure ATN Mesenteric ischemia Myocardial ischemia Cerebral ischemia Hypovolemic Replace volume Stop volume loss Cardiogenic Increase stroke volume Decrease preload (diuretics, venous dilation) Decrease afterload (vasodilators, IABP or Impella) Increase contractility (inotropes) Septic (Distributive) Fill up container (volume first!) Restore vascular tone (vasopressors) Treat underlying cause 10

11 SIGNS OF CARDIAC TAMPONADE Beck s Triad JVD - may increase with inspiration (Kussmaul s sign) Hypotension Muffled heart sounds Tachycardia, decreased ECG voltage Narrowing of pulse pressure Pulsus paradoxus Inspiration Inspiration Inspiration ACUTE PULMONARY EMBOLUS Risk factors (Virchow s triad) Stasis of blood flow (i.e. prolonged bedrest) Vascular endothelial injury Inherited or acquired hypercoagulable state Tachypnea (most common sign) Respiratory Alkalosis (due to rapid respiratory rate) Dyspnea (at rest or with exertion), cough, orthopnea Pleuritic chest pain Tachycardia Hypotension with JVD or elevated CVP ECG signs of right heart strain (not always present) Right axis deviation, RBBB Tall P waves SI, QIII, TIII Pulmonary embolus can be asymptomatic TENSION PNEUMOTHORAX Risk factors (conversion to positive pressure ventilation, existing chest tube, chest trauma) Tachypnea, dyspnea Pleuritic chest pain Lung sounds diminished or absent on one side Tachycardia, hypotension JVD Hypoxemia Mediastinalshift (very late sign) ACUTE AORTIC DISSECTION Risk factors (HTN most common, chest trauma) Chest or back pain sharp, severe, tearing, ripping Diastolic murmur of aortic regurgitation BP difference between arms (> 20mmHg) 4 extremity pulse variation Symptoms of shock diaphoresis, tachycardia, cool clammy skin Oliguria if renal artery involved Signs of cardiac tamponade if pericardial sac involved Type A (ascending arch) dissection is surgical emergency CO = HR X SV BP: 88/64 BP = CO X SVR HR 116 sinus tachycardia Pulse pressure = 24 (normal is 40) Is the problem cardiac output or SVR? Is it HR or SV that is the problem? How to treat? Evaluate preload: neck veins, lung sounds If hypovolemia fluids, try PLR to test fluid responsiveness If tamponade - pericardiocentesis If contractility - inotropes Stroke Volume Preload Afterload Contractility CO = HR X SV BP: 82/30 BP = CO X SVR HR 120 sinus tachycardia Pulse pressure = 52 (normal is 40) Is problem cardiac output or SVR? How to treat? Low SVR probably due to sepsis Volume to fill tank Vasopressors to increase SVR and BP 11