Nursing Assessment of the Cardiovascular System Keith Rischer RN, MA, CEN #1 cause of death resulting in 42% of all deaths 1 million in US annually, more than the next 5 causes of death combined

Today’s Objectives… Review the anatomy and physiology of the cardiovascular system. Describe cardiovascular changes associated with aging. Identify factors that place patients at risk for cardiovascular problems. Explain and describe pre- and post-care associated with diagnostic cardiovascular testing. Explain the purpose of hemodynamic monitoring.

Aortic-Pulmonic Mitral-Tricuspid

Coronary Arteries Right Coronary Left Anterior Descending Circumflex

Cardiac Conduction SA node  Both Atria  AV Node Both Ventricles  Bundle of His Bundle Branches- Perkinje Fibers Heart muscle unique in that it can generate and rapidly conduct its own action potentials or electrical impulses Most myocardial cells capable of generating own action potentials do so at various rates-SA 60-100---AV 50-60 ventricles 20-40 Heart has 2 conduction systems one for atrial activity and ventricular activity…AV node connects the 2 SA node innervated w/ both parasympathetic/sympathetic nerve fibers…what is the influence of these??? SA node fastest and therefore usually dominant pacemaker AV node conduction slows slightly through the bundle of his.Delay allows the atria to completely empty w/atrial kick as they depolarize Bundle branches- divide off the AV node and depolarize at the same time Purkinje fibers- large fibers that allow for rapid conduction and depolarize ventricles in unison 5

Diastole Diastole Lower # in BP (120/80) Ventricles are relaxed Passively fill from atria Ventricular volume pressure becomes lower than atrial pressure resulting in passive flow from atria into ventricles 70% volume flows passively into ventricles Remaining 30% comes from atrial kick from synchronized atrial contraction as the SA node depolarizes the atria to AV node What rhythm causes a loss of this kick w/resultant loss of SV??? 6

Systole Higher # in BP (120/80) Ventricles are contracting and emptying SBP accurately reflects afterload Begins w/closure of AV valves and first heart sound Ventricles continue to contract until left ventricular pressure higher than aortic pressure & RV pressure higher than PA pressure 60% volume ejected in first quarter of systole and then remaining in next 2 quarters End of systole ventricles relax causing large drop in ventricular pressure…this causes semilunar valves to snap shut causing second heart sound and onset of diastole Avg content of LV is 120cc---on average healthy heart able to eject 65-70% this is the EJECTION FRACTION Decrease in EF classic sx of CHF Correlates w/AFTERLOAD Hi Nurse…. Could you tell me what Blood Pressure means ? ? ? I’ve always wanted to know that 7

CO = Stroke volume x heart rate SV (80cc) x HR (80)= 6400cc (6.4 lpm) Cardiac Output CO = Stroke volume x heart rate SV (80cc) x HR (80)= 6400cc (6.4 lpm) Daily pumps 1800 gallons 657,000 gallons every year Over 80 year lifetime: 52,560,000 gallons Every 10 days fills a 18000 gallon swimming pool Every year appx 36 pools Over lifetime appx 3000 pools Factors that influence CO are preload, afterload, myocardial contractility, and HR 8

Preload: Right side of heart Preload=primarily venous blood return to RA Right and left side of heart filling pressure (atria>ventricles) Pressure/Stretch in ventricles end diastole There are no valves where SVC-IVC empty into RA Preload is the filling pressure of the RV-LV and is influenced by venous return…higher venous return or blood volume in atria-the higher the SV will be…opposite is also true What cardiac meds will most strongly influence preload??? How will volume depletion such as by dehydration or blood loss affect preload??? 9

Starling’s Law of the Heart Maximum efficency of CO achieved when myocardium stretched appx 2 ½ times length Think rubber band CO decreased with lower preload/filling pressures or too high HF occurs when it takes higher filling pressures to accomplish normal contractile force Incr in preload cause a decrease in SV and higher LVEDP This causes back pressure into lungs causing leakage of fluid into alveoli causing PE 10

“AFTER” load: Left side of heart Force of resistance that the LV must generate to open aortic valve Correlates w/SBP Arterial vasodilation will decrease Important when in AMI we need to decr workload of heart by intentionally lowering afterload NTG indirectly affects afterload through decreasing preload What meds??? B-blockers….ACE inhibitors calcium channel blockers and arterial vasodilators such as hydralazine Epi will do what to afterload??? Go to page 11 of study guide 11

Contractility Ability of heart to change force of contraction without changing resting length Influenced by Ca++ Inotropic-Influencing contractility independent of Starling mechanism Positive inotropic Negative inotropic Inotropic Sympathetic drugs such as Dopamine-Dobutamine-Epi Negative-B-blockers Chronotropic-rate of HR…look at above for same examples 12

Assessment Techniques History Demographic data Age Gender Pre vs. post menopause Family history and genetic risk Personal medical history DM, HTN BCP use for women Diet

Modifiable Risk Factors Cigarette smoking Physical inactivity Obesity Psychological factors Chronic disease Cigarette smoking Most significant risk factor for CV disease Nicotine and CO most significant Physical inactivity Goal is 30” light to moderate exercise daily Obesity 64% are obese in US w/BMI 25-30 Psychological factors Highly competive…overly concerned w/meeting deadlines….angry/hostile or type A Chronic disease

Changes with Aging Calcification in valves Pacemaker cells decrease in number Conduction time increases Left ventricle increases Aorta and large vessels thicken and become stiffer Baroreceptors less sensitive

Women & CAD Vague-atypical chief c/o Only 53% have CP as chief c/o Fatigue chief c/o Typically develop CAD 10+ years later then men Mortality twice as high Less likely to have definitive 12 lead EKG Smaller coronary arteries Higher prevalence of silent ischemia CABG higher mortality rate/complications After first MI-more likely to suffer fatal event Women > 50 pay must address HTN, high cholesterol, family history, diabetes #1 cause of death of women Vague- weakness-SOB-nausea-anorexia-pain in back/epigastric 16

Men Women Develop 10-15 years earlier Initial event AMI Classic CP sx Develop greater collateral circulation compared to women Influence of menopause…4x risk Causes more deaths in women than men Initial event angina Atypical CP sx…fatigue Menopause before women have higher HDL cholesterol and lower LDL levels-after menopause LDLlevels increase Deaths for women CAD causes 10x more deaths than breast CA…only 15% consider CAD their greatest health risk 17

Elderly & CAD More likely to have vague, atypical c/o SOB, fatigue, syncope or falls Any fall must be investigated for mitigating circumstances Less likely to have radiation

Clinical Manifestations:Dyspnea Can occur as a result of both cardiac and pulmonary disease Difficult or labored breathing experienced as uncomfortable breathing or shortness of breath Dyspnea on exertion (DOE) Orthopnea dyspnea when lying flat Paroxysmal nocturnal dyspnea (PND) after lying down for several hours

Other Clinical Manifestations Fatigue Palpitations Weight gain Syncope Extremity pain Ischemia Venous insufficiency Fatigue Determine timing Palpitations From change in heart rate or rhythm Weight gain Weight gain is the best indicator of fluid retention 1 liter =2.2 lbs Syncope Brief LOC can be near syncopal as well… Any condition that suddenly reduces CO resulting in decr cerebral blood flow Extremity pain

CV Physical Assessment General appearance Integumentary system Skin color Skin temperature Extremities Blood pressure Orthostatic Arterial pulses Jugular venous distention General appearance Skin color…LOC, confusion SOB Integumentary system Color and temp of skin…use nail beds and mucous membranes Skin color Assess for cool, pale or moist skin Bluish color to skin is cyanosis….central is oxygenation problem…bluisk tinge mucous membranes and tongue Peripheral cyanosis-decr blood flow to peripheral extremities due to vasoconstriction Skin temperature Touch with back of hands Extremities Assess for edema in LE-pitting vs. non-pitting Blood pressure HTN 135/85 Why a problem with cardiac pt??? Arterial pulses Jugular venous distention

Precordium Auscultation Normal heart sounds…S1S2 Paradoxical splitting Gallops S3 S4 Murmurs Systolic most common Pericardial friction rub Assessment of the precordium (area over the heart) involves:

Serum Markers of Myocardial Damage Troponin B-Natruetic Peptide Serum lipids C-reactive protein Lytes K+ Mg++ Blood coagulation PT & INR Troponin Myocardial muscle protein released with injury

Brain Natriuetic Peptide:BNP 95 % of BNP resides in ventricles As pressure inc in ventricles in HF-BNP is released Bodies own ACE/B-blocker Only lab test that measures HF Normal is less than 100 Elevated 100-500 + for CHF >500 Uses: dx- assess response to tx Bnp is a peptide released when excessive stretch present in ventricles due to excessive end diastolic filling pressures Works is bodies own ACE inhibitor-causes rapid diuresis and inhibits aldosterone and renin secretion and works as antagonist to angiotensin II and inhibits release of nor-epinephrine 24

Cardiac Catheterization Client preparation Possible complications: myocardial infarction, stroke, thromboembolism, arterial bleeding, lethal dysrhythmias, and death Pre-procedure: Review procedure (video) Consent NPO or light breakfast Cath site shaved Premeds - sedative

Cardiac Catheterization Procedure Pt awake – report any chest pain or symptoms May proceed to Stent Placement Follow-up care: Restricted bedrest, insertion site extremity kept straight Assess groin site and distal pulses closely Monitor vital signs Force fluids Assess for complications

Cardiac Catheterization Report

Other Diagnostic Tests 12 lead EKG Holter monitor (ambulatory) Electrophysiologic (EP) study Exercise Stress test Echocardiography Pharmacologic stress echocardiogram Transesophageal echocardiogram Thallium imaging

Hemodynamic Monitoring: Arterial Line Invasive system used in critical care areas to provide quantitative information about vascular capacity, blood volume, pump effectiveness, and tissue perfusion

Hemodynamic Monitoring: Pulmonary Artery catheter

Hemodynamic Monitoring Strips