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Advanced Assessment of the Cardiovascular System Mary Beerman, RN, MN, CCRN NUR 602 Interesting facts... The heart does not rest for more than a fraction of a second at a time During a lifetime it contracts more than 4 billion times Coronary arteries supply more than 10 million liters of blood to the myocardium in a lifetime Interesting facts…. Cardiac output (heart rate X stroke volume) can vary under physiologic conditions from 3 to 30 liters/minute Remember: Normal cardiac output for adults is 5-6 liters/minute Cardiac index corrects for body size (Cardiac output divided by body surface area) Common Diseases of the Heart Coronary artery disease Hypertension Rheumatic heart disease Bacterial endocarditis Congenital heart disease OTHER VERY COMMON DISEASES OF THE HEART CONGESTIVE HEART FAILURE CARDIOMYOPATHY ARRHYTHMIAS Review Structure and Physiology of the Heart in textbook Review of Symptoms Chest Pain This is the most important symptom of cardiac disease Pain could be from pulmonary, intestinal, gallbladder, or musculoskeletal sources but it may be from the heart itself Every complaint of chest pain must be taken very seriously! Differential Diagnoses of Chest Pain Angina Myocardial Infarction Other Ischemic C-V Origins Non-ischemic C-V Origins Pulmonary Gastrointestinal Psychogenic Neuromusculoskeletal Differential Diagnosis of Chest Pain - ANGINA Usually substernal Radiation – chest, shoulders, neck, jaw,arms Deep, visceral (pressure) – intense, not excruciating Duration- min., not sec. (5-15 min.) Differential Diagnosis of Chest Pain - ANGINA Associated with nausea, vomiting diaphoresis, pallor Precipitated by exercise & emotion Becomes Unstable when occurs during sleep, at rest, or increases in severity/frequency Relief with rest or NTG Differential Diagnosis of CP – Myocardial Infarction Same type of pain as angina Duration greater than 15 min. Occurs spontaneously, often sequela of unstable angina Relieved with Morphine, successful reperfusion of blocked coronary artery Differential Diagnosis of CP – Other C-V Ischemic Origins Aortic Stenosis/Regurgitation Idiopathic Hypertrophic Subaortic Stenosis (IHSS) Uncontrolled Hypertension Severe Anemia/Hypoxia Tachycardia/Arrhythmias Pulmonary Hypertension Differential Diagnosis of CP – Nonischemic C-V Origins Aortic Dissection – Sudden, excruciating pain (knife-like, tearing) – Migrating pain (depends on location of tear) – Frequently, hemodynamic instability – Appearance of shock with normal or elevated BP – Absent or unequal peripheral pulses Differential Diagnosis of CP – Nonischemic C-V Origins Pericarditis – Sharp or dull, retrosternal or precordial pain – Radiates to trapezius ridge – Aggravated by inspiration, coughing, recumbency, & rotation of trunk – Lessened by sitting upright & leaning forward – Relief - analgesics & anti-inflammatory meds Differential Diagnosis of CP – Nonischemic C-V Origins Mitral Valve Prolapse – Left anterior superficial, rarely visceral pain – Variable in character – Lasts minutes, not hours – Spontaneous onset with no pattern – Relieved with time Differential Diagnosis of CP Pulmonary Pulmonary Embolus /Infarct Pneumothorax Pneumonia with pleural involvement Pleurisy Differential Diagnosis of CP Pulmonary Pleuritic Pain – Visceral Pain arising from inferior portion of pleura – May be substernal and radiate to costal margins or upper abdomen – Lasts greater than 30 minutes – Often occurs spontaneously with associated dyspnea – Worsened with inspiration – Relief – time, rest, bronchodilators Differential Diagnosis of CP Gastrointestinal Esophageal Spasm – Substernal visceral (pressure) pain, radiates – Duration – 5 to 60 minutes – Spontaneous or provoked by cold liquids,exercise – Mimics angina – Relief with NTG Differential Diagnosis of CP Gastrointestinal GERD/Hiatal Hernia – Substernal & epigastric, rarely radiates – Duration is 10-60 min. – Provoked by recumbency, lack of food – Relieved by food, antacid Peptic Ulcer Disease – Substernal & epigastric pressure/burning – Duration – hours Differential Diagnosis of CP Gastrointestinal PUD (Cont.) – Precipitated by lack of food or “acidic” food – Relief with antacids & food Biliary Disease – Colicky or continuous, visceral epigastric & RUQ abdominal pain – Radiates to back & right shoulder – Occurs spontaneous & after heavy meal – Relief – analgesics & time Differential Diagnosis of CP Psychogenic Nonradiating, variable pain over chest Duration – 2-3 minutes May be associated with numbness/tingling of hands & mouth Precipitated by stress, emotional tachypnea Relief by removal of stimulus, relaxation Causes – depression, anxiety, self gain Differential Diagnosis of CP Neuromusculoskeletal Thoracic Outlet Syndrome Degenerative Joint Disease of cervical/thoracic spine – Superficial pain in arms & neck – Duration – variable, gradually subsides – Precipitated by head & neck movement, palpation – Relief – time, analgesia Differential Diagnosis of CP Neuromusculoskeletal Herpes Zoster (Shingle’s) – Pain follows dermatomal distribution of nerve Costochondritis (Tietze’s syndrome) – Superficial pain, reproducible with movement & palpation – May be localized or in multiple locations – Duration – variable – Relief – time, analgesia, anti-inflammatory meds Ask These Questions about Chest Pain Description of character Location Duration/Recurrence Precipitating factors Associated symptoms Relieving factors History of similar symptoms Angina Angina Pectoris is the true symptom of coronary artery disease. It is caused by hypoxia to the myocardium which leads to anaerobic metabolism and the production of lactic acid. The acid irritates the actual heart muscle and makes it hurt Angina, con’t Angina is due to an imbalance of oxygen delivery TO the heart and the oxygen needs OF the heart Levine’s Sign---Patients will describe angina by clenching their first and placing it over the sternum. PALPITATIONS Palpitations The uncomfortable sensations in the chest associated with a range of arrhythmias. Patients may describe palpitations as fluttering, skipped beats, pounding, jumping, stopping, or irregularity EXTRASYSTOLES Premature atrial contractions (PAC’s) Premature ventricular contractions (PVC’s) TACHYARRHYTHMIAS Sinus Tachycardia – Usually gradual onset and offset Paroxysmal Supraventricular Tachycardia (PSVT) – Sudden, abrupt onset and offset Atrial Fibrillation Ventricular Tachycardia CAUSES of ATRIAL FIBRILLATION Hypertension Hyperthyroidism Acute MI Pericarditis Coronary Artery Disease Congestive Heart Failure Valvular Heart Disease Acute or Chronic ETOH abuse Post-operative state ATRIAL FIBRILLATION Major complication – Peripheral embolization – CVA May present as CVA, Transient ischemic attack, Amaurosis fugax, ischemic limb, ischemic bowel or other viscera VENTRICULAR TACHYCARDIA Causes include: – Acute myocardial ischemia/infarct – Chronic Coronary artery disease – Cardiomyopathy – Prolonged QT interval (Congenital, druginduced, acquired) VENTRICULAR TACHYCARDIA May present as: – Sudden cardiac death VT degenerated into VF – Syncope – Wide complex tachycardia Often hemodynamically well tolerated BRADY - ARRHYTHMIAS Heart Block Sinus Arrest Common Causes of Palpitations DRUGS Bronchodilators – tachycardia Beta Blockers, Calcium Channel Blockers – bradycardia Digitalis – bradycardia, toxicity causes bradydysrhythmias Common Causes of Palpitations – More DRUGS Antidepressants – Prolong QT interval OTC medications – Antihistamines, Decongestants, Weight Loss preparations – Extrasystoles, Tachy-dysrhythmias Common Causes of Palpitations – OTHER Tobacco Caffeine Thyroid disorders Paroxysmal Nocturnal Dyspnea (PND) Occurs at night or when patient is supine. Patient awakens after being asleep about 2 hours and is “smothering”. Runs to window to get more air This is a specific sign of congestive heart failure Orthopnea Dyspnea when lying down Ask all patients: “How many pillows do you use in order to sleep?” To quantify the orthopnea, record “3pillow orthopnea for the past month” Dyspnea on Exertion (DOE) This is usually due to chronic CHF or severe pulmonary disease Quantify the severity by asking, “How many level blocks can you walk before you get short of breath? How many could you walk six months ago?” How to Chart about Dyspnea “The patient has had 1-block dyspnea on exertion for the past six months. Before 6 months ago, the patient was able to walk 4 blocks without shortness of breath. In addition, during the past month the patient has noted 4-pillow orthopnea. Previously he was able to sleep with just two pillows.” Common Causes of Congestive Heart Failure Uncontrolled Hypertension Myocardial ischemia/infarct Arrhythmias Lack of compliance – Diet – Drugs Fluid overload More Common Causes of Congestive Heart Failure Blood loss, Anemia Pulmonary embolism Systemic infection Valvular heart disease Nonischemic Dilated Cardiomyopathy Renal Artery Stenosis SYNCOPE Syncope Fainting or syncope is the transient loss of consciousness that is due to inadequate cerebral perfusion Syncope can be from cardiac or noncardiac causes Common Causes of Syncope Cardiac Neurocardiogenic Orthostatic Hypotension Metabolic Neurologic Psychogenic Common Causes of Syncope CARDIAC Obstruction to Blood Flow – Valvular stenosis – Hypertrophic cardiomyopathy – Prosthetic valve dysfunction – Atrial myxoma Common Causes of Syncope CARDIAC Obstruction to Blood Flow (cont) – Pericardial tamponade – Pulmonary hypertension – Pulmonary emboli – Congenital heart disease – Pump failure (MI or ischemia) Common Causes of Syncope CARDIAC Arrhythmias – Brady-arrhythmias Sinus bradycardia Sick sinus syndrome Atrioventricular block (AVB) Pacemaker malfunction Drug-induced bradycardia – Tachy-dysrhythmias VTach, SVT Common Causes of Syncope NEUROCARDIOGENIC Vasovagal Vasodepressor Carotid sinus hypersensitivity Situational – Cough, Micturition, Defecation, Deglutition Vasovagal Syncope This is the most common type of fainting and is one of the most difficult to manage. It has been estimated that 40% of all syncopal events are vasovagal in nature This occurs during periods of sudden, stressful, or painful experiences such as getting bad news, trauma, blood loss, sight of blood Vasovagal Syncope, con’t There is warning that the fainting is about to occur…pallor, nausea, weakness, blurred vision, lightheadedness, perspiration, yawning, diaphoresis, hyperventilation, or a “sinking feeling” Carotid Sinus Syncope This may occur in the elderly who may have a hypersensitive carotid sinus If they are wearing a tight shirt or collar or turn their neck in a certain way, there is increased stimulation of the carotid sinus, a sudden fall in systolic blood pressure, and a decrease in heart rate. Common Causes of Syncope – Orthostatic Hypotension Volume depletion Antihypertensive medications Antidepressant medications Common Causes of Syncope – METABOLIC Hypoglycemia Hyperventilation Hypoxia Common Causes of Syncope NEUROLOGIC – Epilepsy – Cerebrovascular disease PSYCHOGENIC Ask These Questions about Syncope “What were you doing just before you fainted?” “Have you had recurrent fainting spells? How often do they happen?” “Was there an abrupt onset to the fainting, or did you feel it coming?” “Did you totally lose consciousness?” Syncope Questions, con’t “In what position were you in when you fainted?” (possible orthostatic hypotension?) Was the fainting preceded by other symptoms like nausea, chest pain, palpitations, confusion, numbness, or hunger? …more syncope questions... “Was fainting episode witnessed by anyone? Who? “Did you have warning that you were going to faint?” “Did you have any black, tarry BMs before or after the fainting episode? “Did you experience any loss of urine or stool during the fainting episode?” And Just One More “On regaining consciousness, did you know where you were and who people were around you?” Fatigue This is a common symptom of decreased cardiac output. A common complaint from people with CHF and mitral valve disorder Fatigue may be the presenting symptom of a woman having an MI Not at all specific to heart disease, but you must consider it always Common Causes of Fatique Cardiac Anxiety/Depression Anemia Chronic Diseases Dependent Edema When peripheral venous pressure is high, fluid leaks out from the veins into tissues This is often the presenting symptom of right ventricular failure Edema will begin in legs and gets worse as the day progresses. Least evident in the a.m. after sleeping with the legs flat, worse as gravity pulls fluid to legs. More about Dependent Edema This indicates that there is excess fluid volume and 3rd spacing of fluids. People on bedrest will have edema of their sacral area In severe right or bi-ventricular heart failure, people often have abdominal distension, liver engorgement, constipation, and anorexia Anasarca may develop. Gross generalized edema Ask These Questions about Dependent Edema “When did you first notice the swelling?” “Do both legs swell equally?” “Did the swelling appear suddenly?” “What time of the day is it worse?” “Does it disappear after sleeping?” “Does propping your legs up make it go away?” More Questions about Edema... “What medicines do you take now?” “Do you have any kidney, heart, or liver disease?” “Do you have shortness of breath? Pain in your legs? Ulcers on your legs?” And, More Questions about Edema Have you noticed a difference in how your clothes fit, especially around the waist? Have you noticed recent problems with constipation? How is your appetite? More and More Do you add salt to food at mealtime and/or when cooking Do you eat out in restaurants or get take-out food frequently? Do you read labels on food before purchasing? Physical Exam for Edema Press fingers into the dependent areas for 2-3 seconds. If pitting is present, the fingers will sink into the tissue and when fingers are removed, the impression of the fingers will remain Edema is quantified from 1+ to 4+ depending on how deep the indentation is The Physical Examination Inspection General Appearance Is the patient in acute distress? Is breathing labored or easy? Is there use of accessory muscles? Is there cyanosis? Pallor? Are xanthomata present (stony hard, yellowish masses on extensor tendons of the fingers. Due to hypercholesterolemia Inspection... Inspect nails. Splinter hemorrhages are associated with infective endocarditis Inspect the face. People with supravalvular aortic stenosis have wideset eyes, stabismus, low-set ears, upturned nose, hypoplasia of the mandible Moon face suggests pulmonic stenosis More inspection... Expressionless face with puffy eyelids and loss of the outer 1/3 of the eyebrow is seen in hypothyroidism Inspect eyes. Yellow plaques on eyelids (xanthelasma) may be due to hyperlipoproteinemia Opacities of the cornea may be sarcoidosis …and more inspection... Conjunctival hemorrhage is commonly seen with infective endocarditis Petechiae on the palate may be seen with infectious endocarditis High arched palate may be seen with Marfan’s Syndrome Arm Breadth greater that body height is also seen in Marfan’s Inspection of the Chest Wall The heart and chest develop at the same time in embryo, so anything that interferes with development of the chest may interfere with the heart Pectus Excavatum (caved-in chest) is seen in Marfan’s syndrome and sometimes MVP Pectus Carinatum (pigeon breast) also seen in Marfan’s syndrome Inspection of the chest, con’t Are there any visible cardiac motions? Inspection of the extremities Look for edema (pitting and nonpitting) Observe color Babies with atrial septal defects may have an extra finger or toe. Long, slender fingers suggest Marfan’s with possible aortic valve deformity Inspection of Extremities Continued Loss of hair may indicate hypothyroidism or PVD Assessment of Blood Pressure Always measure in both arms sitting Then take BP standing Orthostatic Hypotension Have the patient lie down for 5 minutes and measure BP and pulse Have patient stand and repeat reading immediately. Allow 90 seconds for maximum orthostatic changes A drop in systolic BP of 20 mmHg or more when standing is orthostatic There is usually an increase in HR Rule out Supravalvular Aortic Stenosis If there is hypertension in the right arm, take BP in the left arm as well In supravalvular aortic stenosis, there will be hypertension in the right arm and hypotension in the left arm Rule out Coarctation of the Aorta If the patient is hypertensive in both arms, have patient lie on abdomen, put cuff around lower thigh, listen to BP at the popliteal artery A leg blood pressure lower than the arm BP suggests coarctation Normally BP higher in leg arteries than arm Rule out Cardiac Tamponade An exageration of the normal inspiratory fall in systolic BP (it should normally fall about 5 mmHg during inspiration You should check for a paradoxical pulse any time there is low arterial BP and a rapid, feeble pulse Checking for Paradoxical Pulse Have the patient breathe normally, inflate BP cuff until no sounds are heard. Gradually deflate cuff until sounds are heard on expiration only and note this number Continue to deflate the cuff until sounds are heard during inspiration as well. Note this number A Positive Paradoxical Pulse If the difference in BP exceeds 10 mmHg, this is abnormal and indicates possible cardiac tamponade Assessment of the Arterial Pulse Grasp both radial arteries, count for 30 seconds, and multiply by 2 Determine rhythm. The slower the rate, the longer you should palpate. If the rhythm is irregular, is there a pattern to the irregularity? Arterial Pulse, con’t Premature beats are isolated extra beats in a regular rhythm A grossly irregular rhythm is most likely atrial fibrillation Palpate the carotid artery by standing at the patients’ right side with him resting on his back. Listen first for possible bruit and do not palpate if you hear one Arterial Pulse, con’t Never palpate both carotids at the same time Jugular Venous Pulse Remember that the internal jugular vein provides information about right atrial pressure The pulsation of the internal jugular vein are beneath the sternocleidomastoid muscle and are visible as they are transmitted through surrounding tissue The vein itself cannot be seen Jugular Venous Pressure, con’t Because the right internal jugular vein is straighter than the left, only the right IJV is evaluated To determine jugular waveform, have patient lie without pillow at about 25 degree angle. Turn head slight to the right and slightly down to relax the right sternocleidomastoid muscle Jugular Venous Pulse, con’t Standing on the right side of the patient, place your right hand holding a pinlight on the patients sternum and shine the light tangentially across the right side of the patient’s neck. Shadows of the pulsation will be cast on the sheet. Chart: “JV pulsation seen at 25 degrees” Jugular Venous Distension Hepatojugular Reflex A useful test for assessing high jugular venous pressure (also called abdominal compression) By applying pressure over the liver, you can grossly assess RV function. People with RV failure have dilated sinusoids in the liver. Pressure over right upper quadrant pushes blood out and increases JV pressure How to Check for Hepatojugular Reflex Have patient lie in bed, mouth open, breathe normally to prevent valsalva maneuver. Place right hand over RUQ and apply firm pressure for 10 seconds Normally there will be a short increase in venous dilation followed by fall to baseline How to Check for Hepatojugular Reflex – Cont. If there is RV failure, neck veins will stay elevated during entire time of compression Percussion Not helpful in CV assessment CXR shows heart size and borders very accurately Palpation Point of Maximal Impulse (PMI) Stand on the right side of the patient with him sitting. Place fingertips at 5th ICS, MCL and you should feel PMI PMI is usually within 10 cm of the midsternal line and no larger than 2-3 cm diameter PMI that is lateral or displaced suggests cardiomegaly PMI, con’t About 70% of the time you will be able to feel PMI with patient sitting. If you can’t, turn patient to his left side, lying down. A PMI that is over 3 cm diameter indicates left ventricular hypertrophy and is 86% predictive of increased left ventricular end diastolic pressure General Motion After palpating with the fingertips for PMI, use palm of your hand to palpate any large areas of sustained outward motion (“heave” or “lift”) Palpate all 4 cardiac areas Any condition that increases the rate of ventricular filling can produce a palpable impulse “Have you ever felt a thrill?” Thrills are superficial vibratory sensations felt on the skin overlying an area of turbulence The presence of a thrill indicates that you will hear a loud murmur (grade 46) Simply an indication of what you will hear when you listen. Auscultation General Principles of Auscultation Close your eyes when listening Never listen through any kind of clothing Listen at all 4 cardiac areas: Aortic --2nd ICS, RSB Pulmonic---2nd ICS, LSB Mitral--cardiac apex, 5th ICS, MCL Tricuspid---left lower sternal border Principles of Auscultation, con’t Normally only the closing of valves can be heard. Closure of the tricuspid and mitral valves (AV valves) produce the 1st heart sound. Closure of the aortic and pulmonic valves produce the 2nd heart sound. Opening of valves can only be heard if they are very damaged (opening “snap” Third Heart Sound When AV valves open, the period of rapid filling of ventricles occurs. 80% of ventricular filling occurs now. At the END of rapid filling, a 3rd heart sound may be heard S-3 is normal in children and young adults, but not in people over age 30. It means there is volume overload of ventricle What an S3 Sounds Like... SLOSH-ing-in, Slosh-ing-in, Slosh- ing-in Or Ken-tuck-y Fourth Heart Sound At the end of diastole, atrial contraction contributes to the additional 20% filling of the ventricle If the left ventricle is stiff and noncompliant, you will hear an S4. It sounds like this: a-STIFF-wall, aSTIFF-wall, a-STIFF-wall Or sounds like TEN-ne-see Gallop Rhythms The presence of an S3 and an S4 creates a cadence resembling the gallop of a horse. Hence the term “gallop rhythm” Auscultation Procedure Stand at the patient’s right side while he is flat on his back. Listen to all 4 valve areas, inching the stethoscope along from area to area While listening at the apex and left lower sternal border with the bell, you’ll be able to determine if an S3 or S4 are present Procedures, con’t Next have the patient turn to his left side and listen to the apex for lowpitched diastolic murmurs with bell Have patient sit upright and listen everywhere with diaphragm. Have patient sit and lean forward, exhale, and hold breath while you listen with diaphragm to hear high diastolic murmur Procedure, con’t To interpret heart sounds correctly, you must clearly identify what sound is S1. To do this, palpate the carotid artery while you listen. The sound that you hear when you feel the carotid pulse is S1. S2 will follow the pulse Procedure, con’t Please see pictures on pages 255-256 of your textbook for approach to auscultation Murmurs They are produced when there is turbulent blood flow within the heart Turbulence may be due to a narrowed opening of a valve (stenosis) or a valve that does not close completely, allowing blood to slosh backwards (regurgitation or insufficiency) Describing Murmurs When in the cardiac cycle do you hear the murmur? Systole? Diastole? Pansystolic? Location (in which of the 4 cardiac areas do you hear it the loudest?) Radiation (does the sound travel throughout the chest?) Duration of the murmur The Intensity of Murmurs Grade I = lowest intensity, not heard by inexperienced listener Grade II = low intensity, usually audible to everyone Grade III = medium intensity but no palpable thrill Grade IV = medium intensity with a thrill Intensity of murmurs, con’t Grade V = loudest murmur audible when stethoscope is on the chest. Has a thrill Grade VI = loudest intensity, audible when stethoscope is removed from the chest. Has a thrill Other Ways to Describe Murmurs Pitch (high? Low?) Quality (rumbling? blowing? harsh? musical? scratchy?) Is there any relationship to the respiratory cycle? Systolic Murmurs These are ejection murmurs May be caused by turbulence across the aortic or pulmonic valves if they are stenosed May be caused by turbulence across the mitral or tricuspid valves if they are incompetent (regurgitant) Systolic Murmurs, con’t The murmur falls between S1 and S2 Sounds like, LUB-shhh-dub Diastolic Murmurs Mitral and tricuspid stenosis can cause a diastolic murmur Aortic or pulmonic regurgitation can cause a diastolic murmur Sounds like this: Lub-dub-shhh Pericardial Friction Rub These are extra-cardiac sounds of short duration that have a sound like scratching on sandpaper May result from irritation of the pericardium from infection, inflammation, or after open heart surgery Best heard when patient sits and holds breath Friction Rub, con’t A rub that disappears when the patient holds his breath does NOT come from the heart. This is probably a pleural friction rub There are three components to a friction rub…one systolic (during ejection) and two diastolic (during rapid filling of the heart and again during atrial contraction) Refer to excellent charts regarding Extra Cardiac Sounds and Murmurs on pages 258-259 in textbook. Assessment of the Peripheral Vascular System Introduction Peripheral vascular disease - very common, may involve arteries or veins. Arterial diseases include cerebrovascular, aortoiliac, femoropopliteal, renal, and aortic occlusive or aneurysmal disease Narrowing of vessels causes a decreased blood supply, resulting in ischemia. Abdominal Aortic Aneurysms The abdominal aorta is the artery most frequently involved in the development of an aneurysm Usually occur below the renal arteries Few symptoms until it ruptures. You may discover a pulsatile mass in the abdomen Usually first sign is catastrophic rupture Microvascular Disease Diabetes is the most common cause of microvascular disease New recommendations - blood sugar should be covered with insulin in hospitalized patients for BG over 150 Peripheral venous disease often progresses to venous stasis and thrombotic disorders (we fear pulmonary emboli the most) Review of Symptoms Pain This is the principal symptom of atherosclerosis. Pain is often in calf, arch of foot, thighs, hips, or buttocks while walking (“intermittent claudication”) Leriche’s Syndrome…chronic aorto-iliac obstruction. Pain in buttocks and thigh, as well as erectile dysfunction Skin Changes Color changes are common with vascular disease Chronic arterial insufficiency produces a cool, pale extremity Chronic VENOUS insufficiency produces a warmer-than-normal extremity (leg becomes red, erosions develop, increased pigmentation, swelling, aching, heaviness Deep Vein Thrombosis People with DVT have secondary inflammation of the tissue around the vein. This produces warmth, redness, and fever Swelling of one leg more than 2 cm at the ankle or mid-calf should be considered significant Edema Lymphedema results from obstruction to flow in which there is stasis of lymph fluid in the tissues This produces firm, non-pitting edema Seen in women post-mastectomy with lymph node removal Ulceration Persistent ischemia of a limb is associated with ischemic ulceration and gangrene Ulceration is almost inevitable once the skin has thickened and circulation is compromised Ulceration can occur with just the slightest trauma Ulceration, con’t Rapidly developing ulcers are commonly caused by arterial insufficiency, whereas slowly developing ulcerations are usually the result of venous insufficiency Emboli Thrombi form from stasis or hypercoagulability Bedrest, CHF, obesity, pregnancy, recent extended travel on planes, and oral contraceptives have been associated with thrombus formation and emboli Symptoms depend on where clot lodges The Physical Examination Points to Consider in Exam Inspect for symmetry of extremities Examine arterial pulses Auscultate carotid artery with diaphragm (slightly elevate head on pillow and turn slightly away from the side being auscultated) If a bruit is noted, do NOT palpate! Should not be able to palpate abdominal pulse unless very thin. Err on side of caution. Get abdominal ultrasound to R/O aneurysm. Often too late when bulging mass felt. Exam, con’t Palpate abdomen deeply but gently for a mass with laterally expansive pulsation (surgical mortality for a nonruptured abdominal aneurysm is only 5%, but rupture increases mortality to over 90%) Listen for bruits over major arteries with patient lying flat. Listen 2 inches above umbilicus for presence of aortic bruit Exam, con’t Renal artery bruits may be heard about 2 inches above umbilicus and 1-2 inches laterally from mid-line Palpate femoral pulse. The lateral corners of the pubic hair triangle is where you will find the pulse. Feel both femorals so you can judge equality …more of the exam... Palpate popliteal pulse…often hard to feel. Place thumbs on patella and press remaining fingers of both hands in popliteal fossa. Have legs in mid-flexed position Palpate dorsalis pedis (top of foot) and posterior-tibial pulse (inside ankle bone) Grading Pulses 0 = absent pulse (check with doppler!) 1+ = diminished 2+ = normal 3+ = increased 4+ = bounding Capillary Refill Evaluate capillary refill by compressing the toe or fingernail tufts until they blanche. Color should return in 3-5 seconds Prolonged time for color to return is a sign of arterial vascular insufficiency Allen’s Test: Evaluating arterial supply in arms Occlude the radial artery by firm pressure. Ask patient to clinch his fist, then open the fist and observe the color of the palm Then compress ulnar artery, clinch fist, and observe color of palm Pallor of the palm during compression of one artery indicates occlusion of the OTHER artery! Acute Arterial Occlusion: The Five P’s Pain Pallor Paresthesia Paralysis Pulselessness Raynaud’s Disease Poor peripheral circulation to distal fingers and toes You may see three distinct color changes: white (pallor) due to decreased blood supply, blue (cyanosis) due to increased peripheral extraction of oxygen, and then red (rubor) due to the return of blood flow Diagnostic Tests Venous doppler flow studies Arterial doppler flow studies CARDIAC LABORATORY TESTS COMPLETE BLOOD COUNT (CBC) WBC – Increases with inflammation & phagocytosis MI Large hematoma Pericarditis – Increases with use of steroids Treatment of Pericarditis Treatment of allergic reactions to IV contrast RBC, HG, HCT, INDICES Evaluate for anemia as cause of chest pain, dyspnea Evaluate safety for initiation and continued use of anticoagulant and antiplatelet therapy PLATELETS Evaluate safety for initiation of & continued use of anticoagulant and antiplatelet therapy Decreases may be due to adverse drug effect – Heparin-induced Thrombocytopenia (HIT) – H-2 blockers (Pepcid, Tagamet, Zantac) – Aspirin, Plavix COMPLETE METABOLIC PROFILE (CMP) SODIUM (Na) Increases – Dehydration – Increases Na intake Decreases – Volume overload – Decreased Na intake – Diuretics POTASSIUM (K) MUST keep in tight range Decreases due to: – – – – – – – Diuresis Decreased potassium intake Diarrhea Nausea & Vomiting Gastric Suctioning Hypoglycemia Alkalosis POTASSIUM (K) Increases due to: – Renal failure – Dehydration – Acidosis – Hyperglycemia – Increased potassium intake – ACE inhibitors – Hemolysis HYPOKALEMIA Often presents as: – PVC’s – Atrial tachycardia – Ventricular tachycardia – Ventricular fibrillation – Leg Cramps HYPERKALEMIA Often presents as: – Bradycardia – Heart block – Idioventricular rhythms – VTach – VFib – Ventricular arrest – Muscle weakness – Tetany POTASSIUM Potassium level should be maintained 4.0 to 5.0 in cardiac patients, especially with acute MI, Cardiomyopathy, history of Ventricular arrhythmias, and diuretic therapy (as long as normal renal function). CARBON DIOXIDE Measures bicarbonate level of blood Measures metabolic state BLOOD UREA NITROGEN (BUN) Increased level (azotemia) with impaired renal function caused by: – CHF, Dehydration, Shock, Stress, Acute MI Increased levels also with renal disease and GI bleed CREATININE (CR) Increased level indicates worsening renal function GLUCOSE (BG) May elevate with stress such as with MI LIVER FUNCTION TESTS AST, ALT, Alkaline Phosphatase May elevate in CHF due to hepatic congestion Will elevate in low perfusion states causing “shock liver” due to ischemia. Common with cardiac arrest S/P resuscitation, prolonged hypotension, shock states, embolic event. Liver Function Tests May elevate due to anti-lipidemic drugs. Usually not a problem unless 2X normal range. MISCELLANEOUS LABS Amylase & Lipase – Increases with pancreatitis or GB disease – May order if suspect GI source of chest pain Magnesium – Decreased levels cause arrhythmias – Always check in atrial & ventricular arrhythmias and QT prolongation MISCELLANEOUS Thyroid Function Tests – Thyroid abnormalities can cause: Arrhythmias Fatique Anemia – Usually start by checking TSH. If abnormal, check full thyroid panel CARDIAC ISOENZYMES Total CK (Creatine Kinase) – Enzyme found in heart, skeletal, and brain muscle cells. Enzyme is released with injury to cells – Increases with acute MI, myocarditis, postCABG, cardioversion(defibrillation) – Can also elevate with rhabdomyolysis. May see with cocaine intoxication & adverse effect from statin drugs for hypercholestolemia CARDIAC ISOENZYMES CK-MB – Specific to myocardium – Increases with acute MI, myocarditis , post-CABG, cardioversion – May also elevate with chronic renal failure – With acute MI, MB occurs in serum in 6-12 hrs. & remains for 18-32 hrs. – Presence is diagnostic of MI CARDIAC ISOENZYMES MB Index – Percentage of MB in comparison with total CK *** Three sets of cardiac isoenzymes should be ordered 8 hrs. apart to diagnose/confirm acute MI. TROPONIN I and T Troponin I more specific Unique to heart muscle Released with very small amounts of damage as early as 1-3 hrs. after injury Peaks in 12-48 hrs. Levels return to normal in 7-10 days. Useful in delayed diagnosis of MI also TROPONIN T May also elevate in unstable angina, myocarditis, chronic renal failure, acute muscle trauma, rhabdomyolysis, polymyositis, and dermatomyosis. MYOGLOBIN Oxygen-binding protein of striated muscle. Released with injury to muscle. Used as early marker of muscle damage in MI Elevates in 2-4 hrs. Peaks in 8-10 hrs. Returns to normal in 24 hrs. B-type NATRIURETIC PEPTIDE (BNP) Hormone produced by ventricles of the heart that increases in response to ventricular volume expansion and pressure overload. Marker of ventricular systolic and diastolic dysfunction Useful in diagnosing CHF Normal is less than 100 ng/L CARDIAC DIAGNOSTIC TESTS ELECTROCARDIOGRAM (EKG or ECG) Cardiac rhythm Chamber enlargement Conduction abnormalities Electrolyte and toxic disorders – Peaked T-waves = Hyperkalemia – U waves = Hypokalemia – QT prolongation = toxic drug effects EKG cont. Acute MI – T wave inversion = ischemia – ST elevation = acute injury – Q waves = Transmural MI – CAN HAVE AN MI WITH NORMAL EKG!! – Cannot read with Left Bundle Branch Block CHEST X-RAY (CXR) Heart size Calcification on valves and arteries Evidence of CHF – Pulmonary vascular congestion – Pleural effusions Masses ECHOCARDIOGRAM (ECHO) Structural Abnormalities – Anatomical – Presence of thrombi, vegetations, – Presence of pericardial effusion/tamponade Chamber sizes Valvular function Left ventricular function – Wall motion, Ejection Fraction (EF) TYPES OF ECHOCARDIOGRAM TRANSTHORACIC (TTE) – Most common Transesophageal (TEE) – Usually ordered to evaluate for vegetations, valvular disorders, and thrombi. STRESS TESTING Exercise Treadmill testing Myocardial Perfusion Imaging (MPI) – Often called misnomer, Thallium scan – Types – Exercise, Persantine, Adenosine, Dobutamine Stress Echocardiogram – Types – Exercise, Dobutamine All done to evaluate for myocardial ischemia RADIONUCLIDE ANGIOGRAPHY Often called MUGA scan – stands for multiple gated angiography Determines ejection fraction Almost always automatically done with MPI now COMPUTED TOMOGRAPHY (CT) Helical CT – Uses IV Contrast – Used to diagnose Aortic dissection, Pulmonary emboli Plain CT – Abnormal masses (with or without contrast) – Hematoma or retroperitoneal bleed – better with IV contrast CT cont. Ultrafast CT – No contrast used – Detection of coronary artery calcification as indicator of atherosclerosis – The higher the score, the more calcium detected CARDIAC CATHETERIZATION Uses IV contrast Reveals: – Pressures in chambers/Aorta – LV wall motion and ejection fraction – Visualization of coronary anatomy – Valvular function ARRHYTHMIA MONITORING Telemetry Holter monitor – continuous recording of heart rhythm, usually for 24 hrs. Event recorder – records specific events to correlate symptoms with possible arrhythmia, worn for several weeks Loop recorder – implanted in chest wall, continuous recording, then explanted. ELECTROPHYSIOLOGY STUDY (EPS) Evaluation of conduction system Inducibility of arrhythmias Effectiveness of Antiarrythmic therapies Ventilation-Perfusion Scan (VQ Scan) Used to diagnose Pulmonary embolism Will read as high, moderate, or low probability for PE