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5/29/2012 BACK TO THE BASICS: ASSESSING YOUR PATIENT’S CARDIOVASCULAR STATUS WITHOUT ALL THE BELLS AND WHISTLES. NTI 2012 Session Number: 381 Presented By: Cynthia L. Webner, DNP, RN, CCNS, CCRN-CMC www.cardionursing.com 1 2 1 5/29/2012 CARDIAC DIASTOLE (ATRIAL & VENTRICULAR): EARLY PASSIVE VENTRICULAR FILLING 3 ATRIAL SYSTOLE & VENTRICULAR DIASTOLE: LATE ACTIVE VENTRICULAR FILLING Atrial Kick 4 2 5/29/2012 BEGINNING VENTRICULAR SYSTOLE: ISOVOLUMIC CONTRACTION 5 VENTRICULAR SYSTOLE: EJECTION 6 3 5/29/2012 HEART SOUNDS – THE BASIS FOR THE SOUNDS • Diastole • • Passive Ventricular Filling • S3 • Active Ventricular Filling • Atrial Kick – S4 • Valves Open • Mitral • Tricuspid • Don’t open well • Stenosis • Valves Closed • Aortic • Pulmonic • Don’t close well • Regurgitation Systole • Isovolumic contraction • Ejection of LV Contents • Valves Open: • Aortic • Pulmonic • Don’t open well • Stenosis • Valves Closed • Mitral • Tricuspid • Don’t close well • Regurgitation 7 BASIC HEART SOUNDS S1 • Closure of the M itral (M 1) valve and the Tricuspid (T1) valve • Beginning of Ventricular Systole and Atrial Diastole • Location: M itral area • Intensity: Directly related to force of contraction • Duration: Short • Quality: Dull • Pitch: High 8 4 5/29/2012 BASIC HEART SOUNDS S2 • Closure of Aortic (A2) and Pulmonic (P2) Valve • End of Ventricular Systole • Location: Pulmonic area • Intensity: Directly related to closing pressure in the aorta and pulmonary artery • Duration: Shorter than S1 • Quality: Booming • Pitch: High 9 DIASTOLIC FILLING SOUNDS S3 - VENTRICULAR GALLOP • Early diastolic filling sound • Caused by increased pressure and resistance to filling. • Most frequently associated w ith sy stolic dy sfunction • Associated w ith: • Fluid ov erload state • Right or left v entricular failure • Ischemia • Aortic regurgitation • Mitral regurgitation 10 5 5/29/2012 DIASTOLIC FILLING SOUNDS S3 - VENTRICULAR GALLOP • Patient position: left lateral decubitus position • Location: • Left-sided S3 – mitral area. • Right-sided S3 – tricuspid area. • Intensity • Left-sided heard best during expiration. • Right-sided heard best during inspiration. • • • • Duration: short. Quality : dull, thud like. Pitch: low . May be normal in children, y oung adults (up to 35-40) and in the 3rd trimester of pregnancy. 11 DIASTOLIC FILLING SOUNDS S4 - ATRIAL GALLOP • Late diastolic filling sound • Caused by atrial contraction and the propulsion of blood into a noncompliant (stiff) ventricle. • Most frequently associated with diastolic dysfunction • Associated with: • • • • • • Fluid overload state Systemic hypertension Restrictive cardiomyopathy Ischemia Aortic stenosis Hypertrophic cardiomyopathy • May be normal in athletes 12 6 5/29/2012 DIASTOLIC FILLING SOUNDS S4 - ATRIAL GALLOP • Patient position: left lateral decubitus position. • Location • Left-sided S4 – mitral area. • Right-sided S4 – tricuspid area. • Intensity • Left-sided louder on ex piration. • Right-sided louder on inspiration. • Duration: Short • Quality: Thud like • Pitch: Low 13 MURMURS • High blood flow through a normal or abnormal valve • Forward flow through a narrowed or irregular orifice into a dilated chamber or vessel • Backward or regurgitant flow through an incompetent valve 14 7 5/29/2012 HEART SOUNDS: THE BASIS FOR THE SOUNDS • Diastole • Passive Ventricular Filling • S3 • Active Ventricular Filling • Atrial Kick – S4 • Valves Open • Mitral • Tricuspid • Don’t open well • Stenosis • Valves Closed • Aortic • Pulmonic • Don’t close well • Regurgitation • Systole • Isovolumic contraction • Ejection of LV Contents • Valves Open: • Aortic • Pulmonic • Don’t open well • Stenosis • Valves Closed • Mitral • Tricuspid • Don’t close well • Regurgitation 15 PARADIGM SHIFT • Hemodynamics does not equal invasive monitoring • One must be comfortable with shades of grey!! 16 8 5/29/2012 The Heart as a Pump Goal: Forward propulsion of blood to perfuse the body. FLOW IS DETERMINED BY: √PRESSURE √ RESISTANCE √ VOLUME 17 18 9 5/29/2012 RIGHT SIDED VERSUS LEFT SIDED SYSTEM 19 BASIC HEMODYNAMIC FORMULA Cardiac Output Heart Rate X Stroke Volume Preload Afterload Contractility Same four components also determine myocardial oxygen demand20 10 5/29/2012 PRELOAD The ventricle is preloaded for ejection. It’s about stretch! 21 PRELOAD • End-diastolic stretch on myocardial muscles fibers • Determined by: • Volume of blood filling the ventricle at end of diastole • Greater the volume the greater the stretch (muscle fiber length) Ð • Greater the stretch the greater the contraction Ð • Greater the contraction the greater cardiac output TO A POINT 22 11 5/29/2012 NON INVASIVE ASSESSMENT OF PRELOAD Right Ventricular Preload Left Ventricular Preload • JVD • Orthopnea / PND/ Dyspnea • Hepatojugular reflux • CXR report of vascular / interstitial edema • Peripheral edema * • Rales/crackles • Weight* • Consider role of lymph drainage • S3 Gallop • Frothy sputum • Hypoxemia from decreased diffusion of oxygen • Pre-renal AKI (BUN/creatinine ratio 20:1) • Weight* 23 MEASURING JVD • Raise HOB 30 – 45 degrees • Normal JVP level is < 3 cm above the sternal angle • Internal preferred • Sternal angle is 5cm above right atrium • M ay use external • Use tangential light • Use centimeter ruler • JVP of 3 cm + 5cm = estimated CVP of 8cm H2O • Difficult to assess if HR>100 24 12 5/29/2012 Estimated CVP> 8 cmH2O Increased blood volume Usually RV failure Tricuspid valve regurgitation Pulmonary hypertension JVD (JUGULAR VENOUS DISTENSION) Additional assessment tip: Sitting or standing patient up to see top of column. 26 13 5/29/2012 JVD (Jugular Venous Distension) Jugular Vein No pulsations palpable. Carotid Artery Palpable pulsations. Pulsations obliterated by pressure above the clavicle. Pulsations not obliterated by pressure above the clavicle. Level of pulse wave decreased on inspiration; increased on ex piration. No effects of respiration on pulse. Usually two pulsations per systole (x and y descents). One pulsation per systole. Prominent descents. Descents not prominent. Pulsations sometimes more prominent with abdominal pressure. No effect of abdominal pressure on pulsations. 27 FACTORS INFLUENCING PRELOAD • Body Position • Circulating blood volume • Venous Tone • Hypervolemia • Intrathoracic pressure • Third spacing • Intrapericardial pressure • Dysrhythmias • Atrial Kick • LV Function • Hypovolemia • Distribution of blood volume • Sepsis • Anaphylaxis • Venous vasodilators 28 14 5/29/2012 AFTERLOAD After the ventricle is loaded, it must work to eject the contents! It’s about pressure! 29 AFTERLOAD • Pressure ventricle needs to overcome to eject blood volume • Left ventricle: • Systemic vascular resistance (SVR) • Other components • Valve compliance • Viscosity of blood • Arterial wall compliance • Aortic compliance • Right ventricle: • Pulmonary vascular resistance 30 15 5/29/2012 BP AND AFTERLOAD • Blood pressure does not equal afterload Blood Pressure (MAP) = Cardiac Output x Systemic Vascular Resistance (Afterload) 31 BP = CO X SVR • Low BP could be due to: • Low CO • HR too slow or too fast • Preload too low or too high • Contractility low • Low SVR • Vasodilation due to sepsis, anaphylaxis, altered neurological function, drugs 32 16 5/29/2012 MORE ON VASCULAR TONE • Increased vascular tone is usually associated with compensation for low Stroke Volume • Acute Cardiogenic shock • Hypovolemic shock • Decreased vascular tone is usually due to abnormally pathology • Sepsis • Anaphylaxis • Altered neurological control 33 NON INVASIVE ASSESSMENT OF AFTERLOAD Right Ventricular Afterload Left Ventricular Afterload • NOTE: Any hypoxemia, positive pressure ventilation, and PEEP increase the workload of the right ventricle. • Diastolic BP is closest noninvasive measurement • Evaluate the pulse pressure 34 17 5/29/2012 USE OF PULSE PRESSURE & HEART RATE • PP < 35 with tachycardia • PP > 35 with tachycardia (in absence of beta blocker) • Early sign of oxygenation failure • Early sign of inadequate blood volume • Delivery cannot meet demand 35 CAUSES OF INCREASED LV AFTERLOAD CAUSES OF DECREASED LV AFTERLOAD • Arterial vasoconstrictors • Arterial vasodilators • Hypertension • Hyperthermia • Aortic valve stenosis • Vasogenic shock states (sepsis and anaphylactic) where the body cannot compensate with vasoconstriction • Increased blood viscosity • Hypothermia • Compensatory vasoconstriction from hypotension in shock • Chronic Aortic Regurgitation – hyperdynamic cardiac output therefore lowering systemic vascular resistance 36 18 5/29/2012 INCREASED RIGHT SIDED AFTERLOAD • Pulmonary hypertension • mPAP > 25 mmHg or > 30 mmHg w ith ex ercise • PVR > 250 dy nes/sec/cm -5 • Causes • • • • • • Hy pox emia Acidosis Inflammation Hy pothermia Ex cess sy mpathetic stimulation Pulmonary endothelial dy sfunction • Impaired nitric oxide and prostacyclin (PGI2) release • Primary pulmonary hy pertension 37 CONTRACTILITY • Ability of myocardium to contract independent of preload or afterload • Velocity and extent of myocardial fiber shortening • Inotropic state 38 19 5/29/2012 CONTRACTILITY • Related to degree of myocardial fiber stretch (preload) and wall tension (afterload). • Influences myocardial oxygen consumption • Ï contractility Ö Ï myocardial workload Ö Ï myocardial oxygen consumption 39 IMPORTANT POINTS ABOUT CONTRACTILITY • No accurate w ay to measure contractility Noninvasive Assessment: Ejection Fraction • Low cardiac output does not necessarily mean diminished contractility (i.e. hy pov olemia) • Correct preload and afterload problems first in a patient w ith a low ejection fraction. • Increasing contractility w ith medications w ill also increase my ocardial ox y gen demand. 40 20 5/29/2012 FACTORS ALTERING CONTRACTILITY • Decreased contractility • • Excessive preload or afterload • Drugs – negative inotropes Increased contractility • Drugs • Positive inotropes • Myocardial damage • Hyperthyroidism • Ischemia • Adrenal Medulla Tumor • Cardiomyopathy • Hypothyroidism • Changes in ionic environment: hypoxia, acidosis or electrolyte imbalance 41 HEART RATE • M athematically heart rate increases cardiac output • Physiological limit where increased heart rate will decrease cardiac output due to decreased filling time (decreased preload) • Consider as first line strategy to increase cardiac output when temporary pacemaker in place 42 21 5/29/2012 ADJUSTING TO MAINTAIN CARDIAC OUTPUT THE BODY KNOWS THE ALGORHYTHM • When perfusion to the tissues decrease for whatever reason the body launches a response • The body begins to adjust to improve cardiac output • Two primary responses • Sympathetic nervous system • Renin angiotensin aldosterone system ACTIVATION OF SNS • First Responder • Decreased CO → ↓ BP → activates baroreceptors and vasomotor regulatory centers in medulla • Increase circulating catecholamines • Stimulates alpha and beta receptors • Increase HR • Peripheral vasoconstriction • Contractility Positive effect: ↑ CO and BP Negative effect: ↑ O2 demand → ischemia, arrhythmias, sudden death 44 22 5/29/2012 ACTIVATION OF RAAS • Kidney’s response to decreased perfusion due to decreasing CO • Concentrations of angiotensin II, and aldosterone rise as end result • Potent vasoconstriction • Venous – enhanced preload • Arterial – enhanced afterload • Enhanced Aldactone • Sodium/water absorption increases • Enhanced preload 45 DELIVERY OF OXYGEN TO THE TISSUES Oxygen Hemoglobin Cardiac Output 46 23 5/29/2012 OXYGEN DELIVERY TO TISSUES • Oxygen delivery measured as DO2 • Volume of oxygen delivered to tissues each minute • DO2 = cardiac output x arterial oxygen content • Arterial oxygen content = hemoglobin x arterial oxygen saturation • DO2 formula = CO x HGB x SaO2 x 13.4 (constant) • Normal DO2 = 900- 1100 ml/min (1000 ml/min) 47 OXYGEN CONSUMPTION / RESERVE • Oxygen consumption is measured as VO2 • Volume of oxygen consumed by the tissues each minute • Normal VO2: 200–300 ml / min (250 ml / min) • Measured by mixed venous oxygen saturation (SVO2) • Normal 60-80% (75%) • May also be measured by SCV02 • Normal 80-85% • Trends the same as SV02 48 24 5/29/2012 KEY POINTS • Tissues were delivered 1000 ml / min (DO2) • Tissues uses 250 ml / min (VO2) • This leaves a 75% reserve in venous blood • Oxygen delivery and oxygen consumption are independent until a critical point of oxygen delivery is reached • Tissues will extract the amount of oxygen needed independent of delivery because delivery exceeds need 49 CAUSES OF INCREASED VO2 • Fev er per 1 degree C • 10% • Shiv ering • 50-100% • Suctioning • 7-70% • Sepsis • 5-10% • Non Family Visitor • 22% • Position Change • 31% • Sling Scale Weight • 36% • Bath • 23% • CXR • 25% • Multi Organ Failure • 20-80% CNEA / KEY CHOICE 50 25 5/29/2012 RELATIONSHIP OF DELIVERY TO CONSUMPTION DO2 VO2 (extraction is SVO2 (SV0 2 will independent of delivery) improve when you increase delivery) 1000 cc 250 cc (25%) 75% 750 cc 250 cc (33%) 67% 500 cc 250 cc (50%) 50% 51 WHEN YOU HAVE ALTERATIONS IN OXYGEN SATURATION, HEMOGLOBIN OR CARDIAC OUTPUT YOU MAY HAVE ALTERATIONS IN OXYGENATION. 52 26 5/29/2012 HOW CARDIAC CONDITIONS ALTER MYOCARDIAL PERFORMANCE 53 SYSTOLIC VS DIASTOLIC DYSFUNCTION 54 27 5/29/2012 SYSTOLIC DYSFUNCTION • Impaired wall motion and ejection • Dilated chamber • 2/3 of Heart Failure Population • Hallmark: Decreased LV Ejection Fraction < 40% • Ischemia is cause in 2/3 of patients • Multiple other causes including • Mitral Regurgitation • Dilated Cardiomyopathy • Untreated diastolic dysfunction 55 DIASTOLIC DYSFUNCTION • • • • • Filling impairment Normal chamber size 20 to 40% of patients with HF have preserved LV function Normal EF or elevated Caused by • • • • • • Hypertension Restrictive myopathy Ischemic heart disease Ventricular hypertrophy Valve disease Idiopathic 56 28 5/29/2012 DIASTOLIC DYSFUNCTION • Diagnosis is made when rate of ventricular filling is slow • Elevated left ventricular filling pressures when volume and contractility are normal 57 HEART FAILURE 58 29 5/29/2012 HEART FAILURE DEFINED • Heart Failure is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricle to either fill or eject 59 HEART FAILURE PATHOPHYSIOLOGY • Complex process involving continually emerging symptoms and deterioration • M yocardial dysfunction initially results from any number of triggers • Compensatory mechanisms designed to improve cardiac output eventually cause harm 60 30 5/29/2012 PATHOPHYSIOLOGY THE REAL CULPRIT: NEUROHORMONAL RESPONSE Two significant events occur • Sy mpathetic Nerv ous Sy stem (SNS) stimulation • Increase Heart Rate • Increase Contractility • Activ ation of the Renin-Angiotensin-Aldosterone Sy stem (RAAS) • Vasoconstriction • Venous – Increased Preload • Arterial – Increased Afterload • Enhanced Aldactone: Sodium and Water Retentions • Increased preload 61 STAGES OF HEART FAILURE AMERICAN COLLEGE OF CARDIOLOGY / AMERICAN HEART ASSOCIATION GUIDELINES Stage A Stage B Stage C Stage D At high risk f or HF but without structural heart disease or sy mptoms of HF. Structural heart disease but without signs or sy mptoms of Heart Failure Structural heart disease with prior or current sy mptoms of HF. Ref ractory HF requiring specialized interv entions. HPTN CAD DM Obesity Metabolic syndrome Family HX CM Prev ious MI LV Remodeling including LVH and low EF Asy mptomatic v alv ular disease Know structural disease and SOB, f atigue, reduced exercise tolerance. Marked sy mptoms of HF at rest despite maximal medical therapy. 62 31 5/29/2012 STAGES TO GUIDE THERAPY Stage A Stage B Class IA-C) •Treat HTN •Treat DM • Smoking Cessation • Treat Lipids • Regular Exercise • DC Alcohol / Drug Use •Treat thy roid disorders • ACE-I in select patients • All measures as stage A Stage C •All measures under stage A • Dietary salt restriction • Daily Weight • Medications for routine use: •ACE-I in Diuretics select patients ACE – I • Beta Blockers Beta-Blockers in select Digitalis patients Aldosterone Antagonists Hydralizine/Isordil African Americans • Implantable def ibrillators • Exercise training • Devices in select patients Resynchronization Therapy Implantable defibrillators Stage D • All measures under A, B and C • Mechanical assist • Transplantation • Palliativ e Care • Hospice 63 CARDIAC RESYNCHRONIZATION THERAPY 64 32 5/29/2012 NORMAL VENTRICULAR DEPOLARIZATION 65 VENTRICULAR DEPOLARIZATION WITH LBBB 66 33 5/29/2012 VALVULAR HEART DISEASE Aortic Stenosis Mitral Regurgitation 67 VALVE DYSFUNCTION Decreased Cardiac Output Compensatory Changes 68 34 5/29/2012 PATHOPHYSIOLOGY Remember: Stenosis = Pressure Regurgitation = Volume 69 AORTIC STENOSIS PATHOPHYSIOLOGY 70 35 5/29/2012 COMPENSATORY MECHANISMS Aortic Valve Orifice Narrows Î ____Afterload Î ____LV Workload Î ____LV Wall M ass Î ____LV Hypertrophy Î ___________ Dysfunction Works well for years – even decades. Compensatory system ultimately fails Î Symptoms http://www.marvistavet.com/assets/images/aortic_stenosis.gif 71 72 36 5/29/2012 ALTERATION IN MYOCARDIAL PERFORMANCE AORTIC STENOSIS • Diastolic Dysfunction • Poor Ventricular Filling • To improve filling • Preload • Volume management may be precarious • Longer diastole (slower heart rates) • Gently adjust volume either way • Relaxed left ventricle • Cautious use of venous vasodilators • Elevated heart rate impacts filling time 73 ALTERATION IN MYOCARDIAL PERFORMANCE AORTIC STENOSIS • Afterload • Elevated due to stenotic aortic valve • SVR remains normal if cardiac output maintains perfusion • Arterial vasodilatation with exercise needs an effective increase in cardiac output to prevent hypotension • Contractility • Increased left ventricular ejection fraction • Strong pump • Heart Rate • Increased heart rate will decrease filling time • Severity of AS may prevent effective increase in CO • May develop dizziness 74 37 5/29/2012 SYSTOLIC EJECTION MURMUR • May be present before any significant hemodynamic changes occur • More severe AS Î longer murmur • Timing: Midsystolic • Location: Best heard over aortic area • Radiation: Toward neck and shoulders • May radiate to apex • Configuration: Crescendo-decrescendo • Pitch: Medium to high • Quality: Harsh 75 S4 - ATRIAL GALLOP • Late diastolic filling sound • Caused by atrial contraction and the propulsion of blood into a noncompliant (stiff) ventricle. • Most frequently associated with diastolic dysfunction • Associated with: • • • • • • Fluid overload state Systemic hypertension Restrictive cardiomyopathy Ischemia Aortic stenosis Hypertrophic cardiomyopathy • May be normal in athletes 76 38 5/29/2012 LEFT OR RIGHT SIDED S4 • Patient position: left lateral decubitus position. • Location • • • Left-sided S4 – mitral area. Right-sided S4 – tricuspid area. Intensity • Left-sided louder on expiration. • Right-sided louder on inspiration. • Duration: Short • Quality : Thud like • Pitch: Low • D:\Track07.cda 77 MITRAL REGURGITATION PATHOPHYSIOLOGY 78 39 5/29/2012 MITRAL REGURGITATION PATHOPHYSIOLOGY During systole as the LV contracts blood is ejected from left ventricle through the open aortic valve AND some is diverted retrograde through dysfunctional mitral valve Ä ______left atrial volume and pressure AND Ä left atrium responds by _________ Ä atrium sends _________volum e to ventricle Ä LV adjusts by ________________ AND Ä LV increases _____________to assure forward flow Works well for years – even decades. Compensatory system ultimately fails Î __________ Dysfunction Î Symptoms 79 ALTERATION IN MYOCARDIAL PERFORMANCE MITRAL REGURGITATION • Systolic Dysfunction • Reduced ejection • Afterload • SVR increased • Preload • Elevated • Reduced ejection activates normal compensatory mechanisms • Sympathetic nervous system • Renin angiotensin system • Contractility • Reduced • Heart Rate • Elevated with compensatory changes • Too much or too little volume problematic 80 40 5/29/2012 MITRAL REGURGITATION SYSTOLIC MURMUR • Timing: Holosystolic • Location: Mitral area • May be louder in aortic area depending on leaflet involved • Radiation: To the left axilla or posteriorly over lung bases • Quality: Blowing, harsh or musical • Configuration: Plateau • Pitch: High 81 CARDIOMYOPATHY Dilated Restrictive Hypertrophic 82 41 5/29/2012 CARDIOMYOPATHY • Heterogeneous group of diseases of the myocardium • Associated with mechanical and / or electrical dysfunction • Usually (but not invariable) exhibit inappropriate ventricular hypertrophy or dilation • Due to a variety of causes • Maron, B.J. et al Contemporary Definitions and Classification of the Cardiomyopathies: An American Heart Association Scientific Statement From the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention Circulation, Apr 2006; 113: 1807 - 1816. 83 DILATED CARDIOMYOPATHY • Most common form of cardiomyopathy • Dilated LV with LVEF < 40% • Systolic Dysfunction • Causes • • • • • • • • • • Idiopathic Ischemic Genetic disorders Hypertension Viral / Bacterial Infection Hyperthyroidism Valvular Heart Disease Chemotherapy Peripartum Syndrome Related to Toxicity Cardiotoxic Effects of Drugs or alcohol 84 42 5/29/2012 STAGES TO GUIDE THERAPY Stage A Stage B Class IA-C) •Treat HTN •Treat DM • Smoking Cessation • Treat Lipids • Regular Exercise • DC Alcohol / Drug Use •Treat thy roid disorders • ACE-I in select patients • All measures as stage A Stage C Stage D •All measures under stage A • Dietary salt restriction • Daily Weight • Medications for routine use: •ACE-I in Diuretics select patients ACE – I • Beta Blockers Beta-Blockers in select Digitalis patients Aldosterone Antagonists Hydralizine/Isordil African Americans • Implantable def ibrillators • Exercise training • Devices in select patients Resynchronization Therapy Implantable defibrillators • All measures under A, B and C • Mechanical assist • Transplantation • Palliativ e Care • Hospice 85 RESTRICTIVE CARDIOMYOPATHY • Rigidity of myocardial wall • Results in decreased ability of chamber walls to expand during ventricular diastole • Diastolic Dysfunction • Least common form of Cardiomyopathy • 5% of all primary heart muscle diseases (Goswami & Reddy, 2003) 86 43 5/29/2012 RESTRICTIVE CARDIOMYOPATHY Primary Causes • Endomyocardial Diseases Secondary Causes • • Eosinophilic Endomyocardial Fibrosis Infiltrative disorders • Amyloidosis • Endocardial Fibrosis • 90% of RCM in North America • Cardiac Transplant • Sarcoidosis • Anthracycline Toxicity • Radiation carditis • Idiopathic • Loffler’s Endocarditis • Storage Diseases • Hemochromatosis • Glycogen storage disease • Fabry’s Disease 87 ALTERATION IN MYOCARDIAL PERFORMANCE RESTRICTIVE CARDIOMYOPATHY • Diastolic Dysfunction • Poor Ventricular Filling • Work to improve filling • Preload • Volume management may be precarious • Longer diastole (slower heart rates) • Gently adjust volume either way • Relaxed left ventricle • Use caution with venous vasodilators • Elevated heart rate impacts filling time 88 44 5/29/2012 ALTERATION IN MYOCARDIAL PERFORMANCE RESTRICTIVE CARDIOMYOPATHY • Afterload • No change in afterload • Contractility • Not initially impacted. • Heart Rate • Increased heart rate will decrease filling time • Can develop arrhythmias due to infiltrates 89 HYPERTROPHIC CARDIOMYOPATHY 1 of every 500 (Maron et al, 2003) Primary genetic cardiomyopathy Effects men and women equally Hypertrophy of myocardial muscle mass in the absence of increased ventricular afterload • Associated with decreased ventricular filling and decreased cardiac output • Diastolic dysfunction • M ost common cause of sudden death in young adults • Cause unknown • • • • • 50% transmitted genetically 90 45 5/29/2012 HYPERTROPHIC CARDIOMYOPATHY • Disarray of cardiac myofibrils with hypertrophy of myocytes • Cells take on a variety of shapes • Myocardial scarring and fibrosis occurs 91 HYPERTROPHIC CARDIOMYOPATHY • Usually only effects Left Ventricle • Changes may be symmetrical • Asymmetrical septal hypertrophy is more common 92 46 5/29/2012 ALTERATION IN MYOCARDIAL PERFORMANCE RESTRICTIVE CARDIOMYOPATHY • Diastolic Dysfunction • Poor Ventricular Filling • Work to improve filling • Preload • Volume management may be precarious • Longer diastole (slower heart rates) • Gently adjust volume either way • Relaxed left ventricle • Use caution with venous vasodilators • Elevated heart rate impacts filling time 93 ALTERATION IN MYOCARDIAL PERFORMANCE RESTRICTIVE CARDIOMYOPATHY • Afterload • No change in afterload • Contractility • Usually increased. • Increased with obstruction • Heart Rate • Increased heart rate will decrease filling time 94 47 5/29/2012 ASSESSMENT IN ACUTE DECOMPENSATION 95 ASSESSING FOR ADEQUATE CARDIAC OUTPUT Forwards Flow: CI, Skin temp (warm or cold) 5 4 3 Normal Hemodynamics (I) No pulmonary congestion: • PWP < 18; Dry lungs No hypoperfusion: • CI > 2.2; Warm skin 2 Forwards Failure (III) 1 No pulmonary congestion • PWP < 18; Dry lungs Hypoperfusion • CI < 2.2; Cold skin Backwards Failure (II) Pulmonary congestion • PWP > 18; Wet lungs No hypoperfusion • CI > 2.2; Warm skin The Shock Box (IV) Pulmonary congestion • PWP > 18; Wet lungs Hypoperfusion • CI < 2.2; Cold skin 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 Preload: PWP, lung sounds (dry or wet) 96 48 5/29/2012 FLUID OVERLOAD VS. HYPOPERFUSION • Fluid Overload • Hypoperfusion • Weight gain • Narrow pulse pressure • Peripheral edema • Resting tachycardia • Jugular venous distention • Cool Skin • SOB • Altered mentation • Crackles in lungs • Decreased urine output • Increased BUN/Creatinine • Cheyne Stokes Respirations 97 STAGES OF SHOCK: SIGNS AND SYMPTOMS • Sub clinical Hypoperfusion • CI 2.2-2.5 • No clinical indications of hypoperfusion yet something seems different or not right • Compensatory with SNS Stimulation • CI 2.0 – 2.2 • Restlessness / confusion • Tachycardia • Narrowed pulse pressure • Tachypnea • Cool Skin • Oliguria • Decreased Bowel sounds 98 49 5/29/2012 STAGES OF SHOCK: SIGNS AND SYMPTOMS • Shock: Progressive with hypoperfusion (CI < 2.0) • Dysrhythmias • Hypotension • Tachypnea • Cold, clammy skin • Anuria • Absent bowel sounds • Lethargy to coma • Shock: Refractory with profound hypoperfusion (CI < 1.8) • • • • • • • • • Life threatening dysrhythmias Hypotension despite vasopressors ARDS DIC Hepatic failure ATN Mesenteric ischemia Myocardial ischemia Cerebral ischemia 99 WHEN TO ALTER PRELOAD • Pulmonary Congestion • Subset II patients (Backwards Failure) • Goal: Decrease preload • Therapy: Diuretics, venous dilators • Hypotension Secondary to Hypovolemia • Subset III patients (Forward Failure) • Goal: Increase preload • Therapy: Fluids 100 50 5/29/2012 WHEN TO ALTER AFTERLOAD • Combined forward and backward failure • Subset IV patients: Shock Box • Goal: Decrease pulmonary congestion and increase forward flow • Therapy • Arterial dilator drugs • ACEI, ARBs, Nitroprusside, Ca++ blockers, Milrinone, Nesiritide • IABP 101 WHEN TO ALTER CONTRACTILITY • Subset III patients with adequate preload • Subset IV patients: Shock box • Assume a contractility problem • Patients with low CO but optimal preload, afterload, and HR CO = HR, preload, afterload, contractility • Therapy: • Inotropes (dobutamine, dopamine, milrinone, epinephrine, digoxin) • Increase MVO2, use with caution in acute MI 102 51 5/29/2012 TREATMENT FOR ACUTE DECOMPENSATED HEART FAILURE 103 ACUTE DECOMPENSATED HEART FAILURE • Reduce Preload • Diuretics • Venous vasodilators • Low dose Nitroglycerin • Neseritide • Increase Contractility • Positive Inotropes • Dobutamine • Milronone • Ultrafiltration • Reduce Afterload • Arterial vasodilators • High dose Nitroglycerin • Nitroprusside • Neseritide • Intra aortic balloon pump 104 52 5/29/2012 Antman et al, 2004. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to 105 Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). 106 53 5/29/2012 REMEMBER • Low BP could be due to: • Low CO • HR too slow or too fast • Preload too low or too high • Contractility low • Low SVR • Vasodilation due to sepsis, drugs, anaphylaxis 107 COMPARISON OF 2 HYPOTENSIVE PATIENTS 88/70 Vasodilators 82/30 Cardiogenic Shock Septic Shock Cause: Decreased C.O. Cause: Decreased SVR Treatment may involve afterload reduction to increase cardiac output Treatment is focused on filling tank and restoring vascular tone. Vasopressors 54 5/29/2012 CASE STUDY If you listen to the patient and they will tell you what is wrong with them! 109 PATIENT PRESENTATION • 85 year old female living independently at home with help of family is admitted to the hospital with shortness of breath. • She has become increasingly short of breath the past 2 days. Her weight is up 6 pounds from 3 days ago. • She has not taken her medications for 4 days because her prescriptions ran out and she was waiting on her oldest son to get back in town to get them filled. 55 5/29/2012 HOME MEDS AND HISTORY • Furosemide (only 20 mg daily) • Lisinopril • Metoprolol • Aldactone • Baby ASA • Warfarin • Synthroid • OTC NSAIDs for pain HISTORY • • • • • • • History of ischemic cardiomyopathy CABG @ age 70 History of atrial fibrillation History TIA Last known ejection fraction 30% Osteoarthritis Hypothyroidism 56 5/29/2012 STAGES OF HEART FAILURE ACC / AHA Stage A Stage B Stage C Stage D At high risk f or HF but without structural heart disease or sy mptoms of HF. Structural heart disease but without signs or sy mptoms of Heart Failure Structural heart disease with prior or current sy mptoms of HF. Ref ractory HF requiring specialized interv entions. Know structural disease and SOB, f atigue, reduced exercise tolerance. Marked sy mptoms of HF at rest despite maximal medical therapy. HPTN CAD DM Obesity Metabolic syndrome Family HX CM Prev ious MI LV Remodeling including LVH and low EF Asy mptomatic v alv ular disease 113 CLASSIFICATION OF HEART FAILURE NEW YORK HEART ASSOCIATION Class I Class II Class III Cardiac disease Cardiac disease no Cardiac disease resulting limitation with slight limitation with marked in phy sical activity. of phy sical activity. limitation on phy sical activity. Ordinary activ ity f ree of f atigue, palpitation, dy spnea or anginal pain. Comf ortable at rest but ordinary activity results in f atigue, palpitations, dy spnea, or anginal pain. Class IV Cardiac disease resulting in inability to carry out any phy sical activity without discomf ort. May hav e sy mptoms of Comf ortable at rest cardiac but less than insuf ficiency at rest. ordinary activ ity results in f atigue, palpitations, dy spnea, or anginal pain. 114 57 5/29/2012 PHYSICAL ASSESSMENT BP: 88/70 HR: 110’s to 130’s Rhythm: Atrial Fib Frequent ventricular ectopy RR 28-32 SaO2 88% on 4L nasal cannula Pale and cool to touch Somewhat lethargic M ild right sided weakness Faint pedal pulses Heart Sounds S3 Systolic murmur 3/6 Lungs with crackles ½ up bilaterally JVD Right Upper quadrant tenderness 2+ peripheral edema to mid calf Urine output is 10cc in first hour DIAGNOSTICS First troponin .04 BNP 1200 K+ 5.1 H & H 9.2 / 30.1 BUN 42 / Creatinine 2.0 PaCO2 43 mmHg, PaO2 59 mmHg Chest x-ray consistent with congestion and bilateral pleural effusions • ECG/ Rhythm • • • • • • • 58 5/29/2012 EVALUATION • Are tissues receiving adequate oxygenation? • What are the 3 parameters that determine delivery of oxygen to the tissues? • What is probable cause of myocardial decompensation? 59 5/29/2012 EVALUATION BP: 88/70 HR: 110’s to 130’s RR 28-32 Pale and cool to touch Somew hat lethargic S3 Systolic murmur 3/6 5 th ICS LMCL Lungs: Crackles ½ up JVD RUQ quadrant tenderness 2+ edema Urine output is 10cc/hr SaO2 88% on 4L / NC PaCO2 43 mmHg PaO2 59 mmHg) Mild right sided w eakness K+ 5.1 H & H 9.2 / 30.1 BUN 42 / Creatinine 2.0 EVALUATION OF DELIVERY OF OXYGEN • Is SaO2 adequate? • • • • What should PaO2 be? What type of pulmonary problem is present? How does it need to be treated? Are there any concerns about ventilatory status? • Is hemoglobin adequate? • Is transfusion indicated? • What needs considered? • Is cardiac output adequate? • What assessment indicators give you indication? What is the value of the BUN/creatinine ratio? 60 5/29/2012 EVALUATION OF CARDIAC OUTPUT Cardiac Output • What is the formula for Cardiac Output? • What non invasive parameter correlates with SV? What would invasive hemodynamic monitoring add? Diagnosis? Guiding therapy? SVO2 value? • Preload? • JVD • Lung sounds • S3 • Afterload? • Pulse pressure • Contractility? • EF • HR? • Compensation • Beta blockade HEMODYNAMIC PROFILE FOR CARDIOGENIC SHOCK • CO • SV • Preload • Afterload • Contractility • HR What is the profile for our patient? 61 5/29/2012 CAUSE OF DECOMPENSATION • Stopping medications? • MI? • Valve dysfunction? • Anemia? • Atrial fibrillation? • Impact of BBB? Profiles of Advanced Heart Failure Congestion at Rest No Low Perfusion at Rest No Yes Warm and Wet Warm and Dry Congestion No congestion No hypoperfusion No hypoperfusion CI 2.2 Yes Cold and Dry No congestion Hypoperfusion Cold and Wet Congestion Hypoperfusion PWP 18 62 5/29/2012 CORRECTING DECOMPENSATED HEART FAILURE • What parameters are a priority for correcting? • What are the results of therapy on myocardial oxygen demand? What is a non pharmacological method of decreasing afterload? Therapies of Advanced Heart Failure Congestion at Rest No No Low Perfusion at Rest CI 2.2 Yes Yes Preload Reduction Diuretics Nitrates Inotropes Dobutamine Milrinone Afterload Reduction Hydralazine Nitroprusside Milrinone Inotropes PWP 18 63 5/29/2012 ADDITIONAL QUESTIONS • Co-existing pneumonia? • Potassium • Why so high? What about non steroidals? • Right sided weakness • New or old? • Atrial fib • New or old? • Other reasons for warfarin? CLINICAL ASSESSMENT WITHOUT BELLS AND WHISTLES IS MORE CHALLENGING. PROVIDERS AT THE BEDSIDE MAKE THE DIFFERENCE IN THE LIFE AND DEATH OF THE PATIENT. Make sure your skills are the best they should be. 128 64 5/29/2012 www.cardionursing.com BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE COUNTING ON IT! 129 65