BATES CHAP 9 and 12: The CV System; The Peripheral Vascular System

PAD Warning Signs:

-fatigue, aching, numbness, or pain that limits walking or exertion in the legs; if present, identify location, ask about erectile dysfunction -any poorly healing or nonhealing wounds of legs or feet -any pain present when at rest in the lower leg or foot and changes when standing or supine -abdominal pain after meals and associated "food fear" and weight loss -any first degree relative with abdominal aortic aneuryism (AAA) Risk factors: -50 years or more -smoking -diabetes -HTN -elevated cholesterol -African American -CAD

Abdomen PE: vascular:

Listen for aortic, renal, femoral bruits -Palpate and estimate width of abdominal aorta in epigastric area by measuring aortic width between two fingers, esp in older adults (higher risk of AAA) -Assess for a pulsatile mass

Point of maximal impulse (PMI):

Locates the left border of the heart and is found in the 5th intercostal space, or just medial to L midclavicular line (7-9 cm lateral to midsternal line) -Not always palpable Note: in pts with COPD, most prominent precordial impulse is the xiphoid or epigastric area due to R ventricular hypertrophy

DVT:

Location of edema suggests the location of hte occlusion: popliteal vein when lower leg or ankle is sweollen; iliofemoral veins when entire leg is swollen NOTE: Local swelling, redness, warmth and subcutaneous cord: superficial thrombophelbitis, which is a risk factor for DVT

Diminished/absent pulse:

Partial or complete proximal occlusion = 10x more likely -If the occlusion is at aortic or iliac level, all pulses distal are typically affected -Arterial occlusion (usually from atherosclerosis): causes intermittent claudication, posture color changes, trophic changes in skin

PAD:

Peripheral arterial disease: -Defined as: stenotic, occlusive, aneurysmal disease of the aorta, its visceral arterial branches, and the arteries of the lower extremities, exclusive of the coronary arteries -12% of the population, but is silent in half of those affected -INcreases with: age -PAD is a marker for CV morbidity and mortality, and functional decline -Note: thromboembolic disorders of the PVS is also a concern (pulmonary thromboembolism and deep venous thrombosis)

RV Area: Left sternal border in 3rd, 4th, and 5th interspaces PE:

Position: pt supine, head elevated to 30 degrees -Place tips of fingers in 3rd, 4th and 5th interspaces and feel systolic impulse of RV (have them breathe out and then hold breath to help) -If impulse is palpable, assess: location, amplitude, duration -Feel for potential S3 and S4 in 4th and 5th interspaces -In pts with increased anteroposterior diameter: palpate RV in epigastric or subxiphoid area

Measuring the JVP:

1) Make pt comfortable. Raise head slightly on a pillow to relax SCM muscles 2) Raise head of bed or examine table to 30 degrees; turn pt head slightly away from the side you are inspecting 3) Use tangential lighting and examine both sides of the neck. Identify external jugular on each side, then find internal pulsations 4) If necessary: raise or lower head until you can see the oscillation pt of internal jugular venous pulsations in lower half of neck 5) Focus on R internal jugular vein: look for pulsations in suprasternal notch (between SCM on sternum and clavicle) or just posterior to SCM. Distinguish pulses of internal jugular from those of carotid artery 6) Identify highest point of pulsation in R jugular vein. Extend rectangular object or card horizontally from this pt and ruler vertically from sternal angle, making right angle. Measure vertical distance in CM above sternal angle, and add to this distance 5 cm (distance from sternal angle to center of R atrium). the SUM=JVP

Location and timing of cardiac findings;

1) Note anatomical location of sounds -Midsternal line = more reliable zero point for msmt 2) Identify timing of impulses or sounds in relation to the cardiac cycle -S1 = first sound; S2= second; the long diastolic interval separates one pair from the next -Note: intensity of these sounds is helpful: S1 is louder than S2 at the apex; S2 is louder than S1 at the base

Palpating difficult pulses:

1) Position body and examining hand comfortably 2) place hand properly and linger there, varying pressure of fingers to pick up weak pulsation. Explore area if unsuccessful 3) Do not confuse their pulse with mine

Chest wall location correlated to origin of sound and murmurs:

1) Right 2nd interspace to the apex: AORTIC VALVE 2) Left 2nd and 3rd interspaces close to the sternum, but also at higher or lower levels: PULMONIC VALVE 3) At or near lower left sternal border: TRICUSPID VALVE 4) at our around the cardiac apex: MITRAL VALVE

What most commonly obstructs arterial circulation in thigh:

ATHEROSCLEROSIS -If it is in the thigh, the femoral pulse=normal but popliteal is decreased/absent

Myocardial contractility

Ability of the cardiac muscle to shorten, when given a load -Increases when: stimulated by action of SNS -Decreases when: blood flow or O2 delivery to myocardium decreases/impaired

Risk factor reduction:

Absence of CVD in the following optimal levels of 7 health metrics: 4 health behaviors: 1) BMI <25; 2) not smoking, 3) being physically active, 4) healthy diet 3 health factors: 1) untreated total cholesterol <200; 2) untreated BP <120/80; 3) fasting blood glucose <100 mg/dL 13% of US adults meet 5 or more of these criteria; 5% meet 6 or more, and virtually none meet 7 at ideal levels

Left lateral decubitus position:

Accentuates L sided S3 and S4 and mitral murmurs, esp mitral stenosis -This brings the LV close to the chest wall -Place bell of stethoscope lightly on apical impulse

S3 sound:

After Mitral valve opens, period of rapid ventricular filling as blood flows early in diastole from LA-->LV: may have a heart sound from rapid deceleration of column of blood against ventricular wall in children/young adults -In older adults, S3 gallop indicates pathologic change in ventricular compliance

Promoting Lifestyle Change and Risk factor modification:

HTN: optimal weight, <2.3 g sodium per day, regular aerobic exercise 3-4 times per week, moderate alcohol consumption per day <2 drinks for men and <1 for women, diet risk in fruits/veggies/whole grains/low fat dairy/reduced intake of saturated and total fats and sweets and red meat Tobacco use: Use the 5 As framework and Stages of Change model to develop strategies for quitting Obesity: healthy eating and weight loss: -Healthy fats (monosaturated fats, polyunsaturated fats, omega 3 fatty acids) -Unhealthy fats: high in saturated or trans fat Note: less than 1% of US pop meets most healthy dietary goals for fruits/veggies/fish/sodium/sugar/whole grains Physical activity: at least 150 min of moderate intensity cardio activity; muscle strengthening activties (2x weekly)

Assessment of the Carotid Pulse:

Amplitude and contour: -Pt lying down with head of bed elevated to 30 degrees -First inspect the neck for carotid pulsations medial to SCM msucles -Place index and middle fingers (or L thumb) on right carotid artery in lower third of neck, press posteriorly, feel for pulsations -Press just inside medial border of a relaxed SCM muscle, at level of cricoid cartilage (do not press on carotid sinus) -Slowly increase pressure until you feel max pulsation; then slowly decrease pressure until you best sense arterial pressure and contour. ASSESS THE FOLLOWING: 1) Amplitude of the pulse (correlates with pulse pressure) 2) Contour of the pulse wave (speed of upstroke, duration of summit, speed of downstroke --Normal: upstroke=brisk; summit=smooth; downstroke=less abrupt than upstroke) 3) Any variations in amplitude 4) Carotid upstroke timing in relation to S1 and S2 (note that normal carotid upstroke follows S1 and precedes S2) Note: carotid upstroke = delayed in aortic stenosis

The Brachial Artery:

Assess this pulse in pts with carotid obstruction, kinking or thrills, applying previous techniques for amplitude and contour determination -Use index and middle fingers or thumb of opposite hand: cup hand under pt's elbow and feel for the pulse medial to the biceps tendon; pt's arm should rest with elbow extended, palm up -With free hand, may need to flew the elbow to a varying degree for optimal relaxation of muscles

Coarctation of aorta and dissecting aortic aneurism:

Asymmetric BP is seen

Arm lymph nodes:

Axillary lymph nodes: Drain most of the arm Epitrochlear nodes: drain ulnar surface of forearm/hand, little and ring fingers, adjacent surface of middle finger -These nodes are on medial surface of arm 3 cm above elbow

Amplitude abnormalities of RV:

Marked increase in amplitude with little or no change in duration=chronic volume overload (ex: atrial septal defect) Impulse with increased amplitude and duration occurs with pressure overload (pulm stenosis or pulm HTN) Obstructive pulm disease: hyperinflated lung prevents palpation of enlarged RV in L parasternal area -Impulse can be felt high in the epigastrium where heart sounds are also more audible

S4 heart sound

Marks atrial contraction--immediately precedes S1 of the next beat and can also reflect pathologic change in ventricular compliance -Not often heard in normal adults

Aortic regurg murmur full explanation:

Medium pitched, grade 2/6, blowing decrescendo diastolic murmur, heard best in 4th left interspace, with radiation to the apex

Lymph nodes of legs:

Have both deep and superficial systems, but only superficial are palpable. Superficial inguinal nodes: 1) Horizontal group: chain, high in anterior thigh below inguinal ligament -Drains superficial portions of the lower abdomen and buttock, external genitalia, anal canal, perianal area, lower vagina -Located just above femoral vein 2) Vertical group: upper saphenous vein (distal compared to horizontal group): drain corresponding region of leg -Located just distal to great saphenous vein Small saphenous vein: drains the heel and outer aspect of the foot -Join the deep system at the level fo the popliteal space

Cardiac physical exam:

BP and HR: -Pay attention to pt's color, resp rate, level of anxiety, BP, HR Jugular and venous pressure: -JVP parallels pressure in the RA or central venous pressure, related to volume in the venous system: best assessed from pulsations in the right internal jugular vein, which is directly in line with superior vena cava and RA -Pulsations in right external jugular vein can be used but examination can be impaired by obstruction at base of neck and by obesity -Note: inspection here is not useful in children under 12 because difficult to see the pulsations here Dominant movement of the JVP: inward, coinciding with the x descent -Dominant movement of carotid pulse: outward! --JVP: tells us a lot about volume status, R and L ventricular function, patency of tricuspid and pulm valves, pressures in pericardium, arrhythmias caused by junctional rhythms and AV blocks -Ex: JVP falls with loss of blood or dec venous vascular tone; increases with right or left HF, pulm HTN, tricuspid stenosis, AV dissociation, inc venous vascular tone, pericardial compression or tamponade

Afterload:

Degree of vascular resistance to ventricular contraction. Tone of walls of aorta, large arteries, and PV tree (arteries and arterioles), as well as the volume of blood in the aorta all provide resistance -Note: increases pathologically here=pressure overload

Pitting:

Depression caused by pressure from thumb (normally is none) -Severity of edema is graded on a four point scale (slight to very marked)

Dextrocardia and situs inversus

Dextrocardia: heart situated in right chest cavity with R sided apical impulse Situs inversus: heart, lung, stomach and spleen are on right side and liver/gall bladder are on left

Diaphragm vs bell:

Diaphragm: better for picking up high-pitched sounds of S1 and S2, murmurs of aortic and mitral regurg, and pericardial friction rubs **Listen throughout precordium, pressing firmly against chest The bell: more sensitive to low-pitched sounds of S3 and S4 and murmur of mitral stenosis -At the apex where you should start, then move medially along the lower sternal border

Diastolic vs systolic murmurs:

Diastolic: falls between S2 and S1 -Indicate valvular HD Systolic: falls between S1 and S2 (note murmurs are systolic if they coincide with carotid upstroke. Systolic murmurs=normally midsystolic or pansystolic) -Normal heart valves still with these murmurs

Varicose veins:

Dilated and tortuous -Walls may feel thickenend

Gradation of murmurs:

Grade 1: very faint, heard only after listener has "tuned in"; may not be heard in all positions Grade 2: Quiet, but heard immediately after placing stethoscope on chest Grade 3: Moderately loud Grade 4: Loud with palpable thrill Grade 5: Very loud with thrill. May be heard when stethoscope is partly off chest Grade 6: Very loud with thrill. May be heard with stethoscope entirely off chest

Paradoxical Pulse:

Greater than normal drop in Systolic pressure during inspiration -Use BP cuff to check: drop pressure slowly from first sounds that are heard, and drop it until sounds can be heard throughout the resp cycle. -Indication: a difference between the level of the highest systolic ressure (first Korotkoff sound) and the lowest systolic pressure is greater than 10 mmHg -Suggests: pericardial tamponade, constrcitve pericarditis, obstructive airway disease (most commonly)

Bilateral edema:

HF, Cirrhosis, nephrotic syndrome

Screening for AAA:

(Leading cause of death); Definition: infrarenal aortic diameter >3 cm, found in 50% of older male smokers Risk factors: -smoking -65 years or older -fam history -CAD -PAD -HTN -HLD (lipids) -Screening reduces mortality by 40%! -Recommended: one time screening in men between 65 and 76 years with hx of smoking -US is 95% sensitive, 100% specific for diagnosis of AAA -Palpation also useful when aortic diameter >4 cm

Pulse pressure:

the difference between systole and diastole pressures

Risk factors for lower extremity PAD:

-50 years, or younger if diabetes or atherosclerosis risk factor of smoking, dyslipidemia, HTN, hyperhornocysteinemia -50 to 69 years and history of smoking or diabetes -age 70 or older -leg syymptoms with exertion or ischemic rest pain -abnormal lower extremity pulses -known atherosclerotic coronary, carotid or renal artery disease

Screening for Renal Artery disease (RAD):

-7% of population 65 years and older; increases to 22%-55% with pts with PAD and 30% with those with CAD Recommend to screen with diagnostic studies starting with US of renal artery velocities, for the following pts: -HTN if age <30 years -Severe HTN if age >55 years -Accelerated, resistant, or malignant HTN -New worsening of renal function, or worsening after using angiotensin convering enzyme inhibitor or ARB -Unexplained small kidney -Sudden unexplained pulmonary edema, esp in worsening renal function pts

The health history: concerning or common symptoms vascular

-Abdominal, flank or back pain -Pain in arms or legs -Intermittent claudication -Cold, numbness, pallor in legs, hair loss -Swelling in calves, legs or feet -Color change in fingertips or toes in cold weather -Swelling with redness/tenderness Questions: -Abd, flank, back pain, esp in older smokers. Unusual constipation or distention? Check for urinary retention, difficulty voiding, renal colic -Ask about intermittent claudication -Ask about coldness, numbness, pallor in legs or feet, or loss of hair over anterior tibial surfaces

Abnormalities with Waves of the JVP:

-Abnormally prominent a waves: increased resistance to RA contraction (tricupsid stenosis, severe 1st 2nd and 3rd degree AV block, supraventricular tachy, junctional tachy, pulm HTN, pulm stenosis) -Absent a waves: signal a fib -Increased v wave: tricuspid regurg, atrial septal defects, constrictive pericarditis

CVD:

HTN, CHD, HF, stroke -CVD=leading cause of death in US -Rates are declining due to reduction in CV risk factors (primary prevention) and improvements in treatments following clinical CVD events like stroke/MI (secondary prevention) -Still accounts for 1 in 3 deaths in the US

Screening early:

-Assess lifetime risk in asymptomatic patients early on -Early risk asessment can lead to more timely interventions to lower the burden of CVD

Risk factors for diabetes:

-BMI >25! -Physical inactivity -First degree relative with diabetes -Members of a high risk ethnic pop: African American, Hispanic/Latino, Asian American, Pacific Islander -Mothers of infants > 9 lbs at birth or diagnosed with gestational diabetes -HTN >140/90 or on therapy for HTN -HDL cholesterol <35 and or triglycerides >250 mg/dL -Women with polycystic ovary syndrome (PCOS) -HbA1C>57%, impaired glucose tolerance, or impaired fasting glucose -Other conditions associated with insulin resistance (severe obesity, etc) -History of CVD

Arms PE (vascular):

1) Inspect both arms from fingertips to shoulders, noting: size, symmetry, swelling -Venous pattern -Color of the skin and nail beds and texture of skin (note: prominent veins in edematous arm suggest venous obstruction) 2) Palpate radial pulse: with pads of fingers on flexor surface of wrist laterally. Partially flexing the patient's wrist may help you feel this pulse. Compare in both arms. If you suspect arterial insufficiency: -feel for brachial pulse -flex patient's elbow slightly, palpate artery medial to biceps tendon in antecubital crease 3) Feel for one or more epitrochlear nodes: -Pt elbow flexed to 90 degrees and forearm supported by my hand, reach around behind arm and feel in the groove between biceps and triceps, 3 cm above medial epicondyle -If node is present, note its size, consistency, tenderness (enlarged node here: local or distal infection, or generalized lymphadenopathy)

Hypovolemic vs hypervolemic:

Hypovolemic: the JVP will be low, so you will need to lower the head of the bed sometimes to 0 degrees to see the oscillation point best Hypervolemic: if the pt is volume overloaded, and then the JVP will be high and you will raise the head of the bed

Common or concerning cardiac symptoms:

-CP, palpitations, S OB (dyspnea, orthopnea, or paroxysmal nocturnal dyspnea), swelling/edema, fainting/syncope

Media:

-Composed of smooth muscle cells that dilate and constrict to accomodate BP and flow -Boundaries: internal and external elastic laminae (membranes made of elastin) -Vasa asorum arterioles perfuse the media

Intermittent claudication:

-Defined as any pain or cramping in the legs during exertion that is relieved by rest within 10 min

Technique of exam: CARDIAC OBJECTIVES

-Describe chest wall anatomy and identify key listening areas -Evaluate jugular venous pulse, carotid upstroke, presence or absence of carotid bruits -Palpate and describe PMI -Auscultate S1 and S2 in six positions from the base to the apex -Recognize effect of PR interval on intensity of S1 -Identify physiologic and paradoxical splitting of S2 -Auscultate and recognize abnormal sounds in early diastole, including an S3 and O2 of mitral stenosis -Auscultate and recognize an S4 later in diastole -Distinguish systolic and diastolic murmurs -Evaluate and interpret paradoxical pulse

Interventions that reduce onset and progression of PAD:

-EXERCISE (walk) -Tobacco cessation -treatment of hyperlipidemia -control of diabetes and HTN -use of antiplatelet agents -foot care and well fitted shoes -surgical revascularization if necessary

Jugular Venous Pulsations:

-First elevation: presystolic a wave: reflects the slight rise in atrial pressure that accompanies atrial contraction. Occurs just prior to S1 and before carotid upstroke -Following this is the x descent (first trough): starts with atrial relaxation; continues as the RV pulls floor of atrium downwar during systole, and ends just before S2. Note that during systole, blood is still flowing into RA from venae cavae -Tricuspid valve is closed, chamber fills, RA pressure increases, creating second elevation (v wave!): Blood flows passively into RV, RA pressures fall, creating y descent (the second trough) NOTE: -A is for atrial contraction -C is for carotid transmission (closure of tricuspid valve) -V for venous filling --To the naked eye: the 2 descents (x and Y0 are most visible events of the cycle of atrial contraction, relaxation, filling, and emptying again (followed by contraction)--x is most prominent of the two -a wave precedes S1 and carotid pulse -x descent is systolic collapse -v wave coincides almost with S2 -y descent follows early in diastole

Elevated JVP:

-Highly correlated with both acute and chronic HF -Also seen in: tricuspid stenosis, Chronic pulm HTN, suerior vena cava obstruction, cardiac tamponade, constrictive pericarditis -Note: those with lung disease it can appear elevated on expiration, but veins collapse on inspiration--not indicative of HF -Elevated JVP is >95% specific for an increased LV end diastolic pressure and low LV EF

When ausculation alone does not suffice:

-Intensities of S1 or S2 may be abnormal; HR may be rapid; duration of diastole may be short' etc=all reasons why auscultation alone is difficult How to deal with it: PALPATE carotid artery during auscultation to aid in timing the sound or murmur -Since carotid upstroke (When the arteries are filling) always occurs in systole immediately after S1, sounds or murmurs at this time are systolic; sounds or murmurs occurring after completion of the upstroke=diastolic EXAMPLE: S1 is diminished in 1st degree heart block; S2 is diminished in aortic stenosis

Factors affecting BP:

-LV stroke volume -Distensibility of aorta and large arteries -Peripheral vascular (PV) resistance, particularly at arteriolar level -Volume of blood in arterial system --Changes in any of these alter systolic pressure, diastolic pressure, or both -BP changes throughout the day varying with: physical activity, emotions, pain, noise, environmental temp, time of day, coffee/tobacco/drug use

Key components of Peripheral Arterial Exam:

-Measure BP in both arms -Palpate carotid upstroke, auscultate for bruits -Auscultate for aortic, renal, femoral bruits; palpate aorta and determine max diameter -Palpate brachial, radial, ulnar, femoral, popliteal, dorsalis edis, posterior arteries -Inspect ankles and feet for color, temp, skin integrity, note any ulcerations; check for hair loss, trophic skin changes, hypertrophic nails

If you detect unilateral edema (leg PE vascular cont...):

-Measure legs: 1) forefoot, 2) smallest circumference above ankle, 3) largest circumference at calf, 4) midthigh. COMPARE SIDES (1 cm diff above ankle or 2 cm at calf=suggests edema) **Calf asymmetry=likely DVT If edema is present: -How far up the leg does it go? -Look for possible causes in PVS. Is swelling unilateral or bilateral? -Are veins unusually prominent? -Identify any venous tenderness (accompany DVT sometimes, but only 50% of pts have this) -Palpate groin medial to femoral pulse for tenderness of femoral vein -Palpate calf (pt leg flexed at knee and relaxxed) -Note color of skin -Is there local redness? Note temp if so (Feel for thrombosis of vein) -Are there brownish areas near ankles? -Note ulcers in skin, where are they? (Brown discoloring or ulcers above malleolus=chronic venous insufficiency) -Ask pt to stand, inspect saphenous system for varicosities: feel for any varicosities NOTE: venous distention suggests venous cause of edema

Auscultation:

-Most widely used method of screening for valvular heart disease Inching your stethoscope: -Start at apex and inch to the base: move from PMI medially to L sternal border, superiorly to 2nd interspace, then across sternum to 2nd interspace at R sternal border (or do the opposite) Timing S1 and S2: -By carefully noting the intensities of S1 and S2, can confirm each of these sounds and correctly identify systole (interval between S1 and S2) and diastole (interval between S2 and S1)

How to get blood in LE veins back to heart:

-One way valves of the deep, superficial and perforating veins propel blood forward, prevent pooling, venous stasis, and backward flow -Contraction of calf muscles during walking also squeezes blood against gravity-->up

Changes over life span:

-PMI is less easily palpated in adults with age as the chest in anteroposterior diameter deepens and the impulse is harder to find -Splitting of S2 is also harder to hear in older people (same as above reason) -Heart murmurs with absence of CV illness often develop with age and are benign

Abnormal displacement of LV:

-Pregnancy or high L diaphragm may displace apical impulse upward and to the L -Lateral displacement from cardiac enlargement: HF, cardiomyopathy, ischemic heart disease (lat displacement makes cardiac enlargement and low left ventricular EF 3-4 and 10 times more likely, respectively) PMI: in left lateral decubitus position, a diffuse PMI with diameter 3 cm indicates LV enlargement; if PMI is > 4 or 5 cm when pt is supine, LV overload is 5x more likely) Increased amplitude: hyperthyroidism, severe anemia, aortic stenosis (pressure overload of LV); mitral regurg (volume overload of LV) Sustained, high amplitude impulse: LVH from pressure overload (HTN); if displaced laterally, volume overload Dilated cardiomyopathy: sustained low amplitude (hypokinetic) impulse Brief middiastolic impulse: S3 Impulse just before the systolic apical beat=S4

Sit up, lean forward, exhale completely, stop breathing in expiration:

-Press diaphragm of stethoscope on chest, listen along left sternal border and at apex, pausing some so pt may breathe -Accentuates aortic murmurs (diastolic murmur of aortic regurg)

Diastole and systole:

-Pressure in L atrium exceeds that in the relaxed left ventricle, so it flows from LA to LV across open mitral valve -Just before onset of systole, atrial contraction produces slight pressure rise in both chambers -Systole: L ventricle starts to contract, ventricular pressure rapidly exceeds LA pressure, closing mitral valve -CLOSURE OF MITRAL VALVE IS FIRST HEART SOUND (S1) -LV pressure continues to rise, exceeding aortic pressure and the aortic valve is forced open; and normally maximal LV pressure = systolic BP -As LV ejects blood, pressure falls again, when the pressure drops below aortic pressure, the aortic valve close -CLOSURE OF AORTIC VALVE=SECOND HEART SOUND (S2)

Topics for health prom and counseling:

-Screening for PAD, ankle brachial index (ABI) -Screening for renal artery disease -Screening for AAA (abd aortic aneurism)

ABI:

-Sensitivity of 95%; specificity of 99% -Measure SBP in arms and pedal pulses using US Note: -Those with ABIs in lowest categories have a 20-25% annual mortality risk -Those with higher daily physical activity (spec treadmill walking) lower both risk of mortality and CV events

Cardiac output and SV:

-The volume of blood ejected from each ventricle during 1 minute (product of HR x SV) SV: the volume of blood ejected with each heartbeat -Depends on 1) preload 2) myocardial contractility 3) and afterload

Tips to identify murmurs:

-Timing -Shape -Location of maximal intensity: determined by the site where it originates -Radiation or transmission from pt of maximal intensity: reflects site of origin and intensity of murmur, direction of BF, bone conduction in thorax -Pitch: high, medium or low -Quality: blowing, harsh, rumbling, musical Other characteristics: variation with resp, variation with position of pt, and other special maneuvers

Bruits and their significance:

-Usually caused by atherosclerotic narrowing of internal carotid artery; can also be from external carotid arterial disease, aortic stenosis, hypervascularity of hyperthyroidism, external compression from thoracic outlet syndrome -NOTE: asymptomatic carotid bruits increase with age, reaching 8% in adults 75 years and older

Special techniques to identify murmurs and HF:

1) Standing and squatting: venous return to heart dec, as does peripheral vascular resistance -Arterial BP, SV, and volume of blood in LV all decline -When squatting, changes occur in the opposite position! These can help to 1) identify prolapsed mitral valve and 2) distinguish hypertrophic cardiomyopathy from aortic stenosis --Listen to the heart in tthe squatting and standing position 2) Valsalva maneuver: BP reponse is 4 phases: -Transient increase during onset of the strain phase when pt bears down -Normalization during the strain phase -Drop of both BP and LV volume during the release phase -Overshoot several seconds later USES: 1) distinguish hypertrophic cardiomyopathy: ask pt to bear down, and listen to the area of the lower left sternal border (the hypertrophic cardiomyopathy murmur=the only one that increases during strain phase of Valsalva maneuver due to INC outflow tract obstruction) 2) identify HF and pulm HTN:take BP, keeping it locked at 15 mmHg above systolic pressure baseline while they perform the valsalva maneuver, listen for sounds of BP over the brachial artery. IN healthy patients, phase 2 (the strain phase) is silent and Korotkoff sounds are heard after straining is released, or during phase 4 --In HF patients: Korotkoff sounds are heard during phase 2 strain phase but not phase 4 release (the square wave response); correlated with volume overload and elevated LV end diastolic pressure and pulmonary capillary pressure) 3) Isometric handgrip: increases systolic murmurs of mitral regurg, aortic regur, and ventricular septal defect, as well as diastolic murmurs of pulm stenosis and mitral stenosis 4) Transient arterial occlusion: transient compression of both arms by bilateral blood pressure cuff inflation to 20 mmHg greater than peak systolic BP augments the murmurs of mitral regurg, aortic regur, and ventricular septal defects

Special populations:

1) Women: -CVD is the leading cause of death in women -CVD and CHD risk factors highest in black women compared to white women -Women >65 have high HTN than men, and higher prevalence of uncontrolled HTN (black women have highest prevalence of both) -2/3 of women in US are overweight or obese, contributing to type 2 diabetes and risks for MI and stroke -Women account for 60% of stroke deaths in US; higher risk than men -Stroke risk factors: pregnancy, hormone therapy, early menopause, preeclampsia; atrial fibrillation is also higher in women and a risk factor for stroke 2) African Americans: -Higher risk factors than white population

Artery anatomy:

3 layers: -Intima: -Media -Adventitia -Internal elastic membrane: borders the intima and media -External elastic membrane: separates the media from the adventitia Note: injury to these vascular endothelial cells provokes thrombus formation, atheromas, and vascular lesions of hypertension Aorta and immediate branches: large/highly elastic arteries (common carotid and iliac) -->medium sized muscular arteries (coronary and renal arteries); these have lots of smooth muscle and elastic recoil -->small arteries -->arterioles (resistance to BF occurs PRIMARILY HERE) -->capillaries (endothelial lining, no media, allowing for rapid diffusion of O2 and CO2)

Grading pulses:

3+ Bounding 2+ Brisk, expected (normal) 1+ Diminished, weaker than expected 0 Absent, unable to palpate

Aneurysmal vs aortic insufficiency, arterial occlusion

Aneurysmal: if an artery is widely dilated Aortic insufficiency: bounding carotid, radial and femoral pulses Arterial occlusion: asymmetric diminished pulses occur here from atherosclerosis or embolism

Inspection and Palpation: L Ventricular area

Apical impulse: normally the PMI -If cannot identify it in supine, ask pt to roll partly on the L side (left lateral decubitus position; can ask them to hold their breath for a few seconds to help too) Note: pathologic conditions can make it so the PMI is not at at apex (enlarged RV, dilated pulm artery, anuerysm of aorta, etc) Note: apex beat=palpable only in 25-40% of healthy adults in supine position and 50% of healthy adults in the lateral position (esp those thin pts) ASSESS THE FOLLOWING: location, diameter, amplitude, duration, S 3 and S4 Location: Locate two points: the interspaces (5th or maybe 4th) for the vertical location and distance in cm from midclavicular line for horizontal location Diameter: palpate the size (supine usually is <2.5 cm) Amplitude: usually small and feels brisk and tapping Duration: most useful characterstic of the apical impulse for identifying hypertrophy of LV--listen to heart sounds as you feel apical impulse (or watch stethoscope movement as you listen)--estimate the portion of systole occupation by apical impulse (normlaly, lasts through first 2/3 of systole or less) S3 and S4: pt should lie partly on L side, breathe out, briefly stop breathing. Inking an X on the apex, may be able to see these movements

Atheroma:

Begins in the intima as lipid filled foam cells, then becomes fatty streaks Complex atheromas: thickened asymmetric plaques that narrow the lumen, reducing BF and weaken underlying media

The health history: CARDIAC

Chest pain: begin with open ended questions, then have the pt point to the source of the chest pain, clarify with 7 features of a symptom -Note that most present with exertional angina, but women may also have the following: upper back pain, neck or jaw pain, SOB, paroxysmal noctural dyspenea, nausea/vomiting, fatigue Palpitations: skipping,fluttering, pounding, stopping of the heart -For this group of symptoms, an EKG is indicated SOB: -Dyspnea (often seen in pts with cardiac or pulmonary problems)--uncomfortable awareness of breathing that is inappropriate to a given level of exertion -Orthopnea: when pt is supine -PND: awaken the pt from sleep; episodes of sudden dypnea and orthopnea Swelling (edema): focus on location, timing, setting, and associated symptoms -Are rings tight on your fingers? Eyelids puffy or swollen in morning? Letting out your belt? Clothes gotten tight around the middle? -Causes: often cardiac (R or L ventricular dysfunction; Pulm HTN) or pulmonary (obstruction); nutritional (hypoalbuminemia), positional too -Dependent edema: appears in lowest parts of body Fainting/syncope: most commonly caused by neurocardiogenic (neutrally mediated vasodepressor syncope or vasovagal syncope) and cardiac origin from arrhythmias (20%)

Adventitia

Connective tissue containing nerve fibers and the vasa vasorum arterioles

SPECIAL TESTS: vascular

Evaluating arterial supply to hand: 1) Try to feel for ulnar pulse if suspect arterial insufficiency in arm or hand 2) Allen test: helps us if we suspect arterial insufficiency in arm or hand; also ensures patency of ulnar artery -Have pt make tight fist with one hand; compress both radial and ulnar arteries -Ask pt to open the hand into a relaxed, slightly flexed position. THe palm is pale -Release the pressure over the ulnar artery. If the ulnar artery is patent, the palm flushes within 3-5 seconds; patency of the radial artery is tested by doing the opposite (releasing RA and compressing UA still) (NOTE: persistence of pallor indicates occlusion of UA or its distal branches Postural color changes or chronic arterial insufficiency: 1) Raise both legs to 60 degrees until max pallor of feet (note: MARKED PALLOR UPON ELEVATION OF THIS TEST: arterial insufficiency) -Ask pt to sit up with legs dangling down: compare feet, noting time required for: 1) Return of pinkness to skin (10 sec or less), filling of veins of feet and ankles (15 sec) (IF STILL PALE: arterial insufficiency) -Look for any rubor (dusky redness) to replace pallor of dependent foot (persisting rubor on dependent foot suggests arterial insufficiency -Note: normal responses accompanied by diminished arterial pulses=good collateral circulation developed around an arterial occlusion MAPPING VARICOSE VEINS: -Transmit pressure waves along blood filled veins -With pt standing, place palpating fingers gently gently on a vein and, with other hand below it, compress vein sharply -Feel for a pressure wave transmitted to the fingers of your upper hand -A palpable pressure wave indicates the two parts of the vein ar connected EVALUATING COMPETENCY OF VENOUS VALVES: -Retrograde filling (Trendelenburg) test: assess valvular competency in both communicating veins and saphenous system -Start with pt supine: elevate one leg to 90 degrees to empty venous blood -Occlude great saphenous vein in upper thigh by manual compression (do not occlude deeper vessels too, however) -Ask pt to stand. Normally, the vein fills from below, taking 35 sec as blood flows through capillary bed into venous system NOTE: rapid filling of superficial veins while saphenous vein is occluded indicates incompetent valves in communicating veins (blood flows quickly in a retrograde direction from deep to saphenous veins) -After pt stands for 20 sec, release compression and look for sudden additional venous filling -Normally there is none: competent valves in saphenous vein block retrograde flow. Slow venous filling ocntinues (NOTE: sudden additional filling of superficial veins after releasing compression indicates incompentent valves in saphenous vein) -When both steps are normal, response =negative negative (vs positive positive, or neg pos, or pos neg)

Chest pain abnormal causes/issues:

ExertionalCP, pressure, shoulder/neck/back or arm: angina pectoris--seen in 18% of pts with an acute MI Acute coronary syndrome: clinical syndromes caused by an acute MI (unstable angina, NONSTEMI, and STEMI) Causes of CP in absence of CAD: microvascular coronary dysfunction, abnormal cardiac nocioception) Acute aortic dissection: anterior CP, tearing or ripping/radiating into back or neck

Abnormalities with auscultatory sounds:

Expiratory splitting: abnormal Persistent splitting: from delayed closure of pulm valve or early closure of aortic valve Loud P2: pulm HTN

AHA CV Risk categories for women:

High risk: -> 1 of the high risk states, including existing CVD or CHD or PAD, abdominal aortic aneurism, DM, renal disease -10 year predicted risk of >10% At risk: -->1 major risk factors of smoking, high BP or treated HTN, total cholesterol >200, treate dyslipidemia, obesity, poor diet, phys inactivity, fam history of premature CVD --Evidence of atherosclerosis, metabolic syndrome, poor exercise capacity on stress test treadmill -Systemic autoimmune collagen vascular disease (lupus, rheumatoid arthritis) -History or preeclampsia, gestational diabetes, pregnancy induced HTN Ideal CV Health (ALL OF THESE): -Total cholesterol <200 mg/dL -BP < 120/80 -Fasting glucose <100 -BMI <25 kg/m2 -Abstinence from smoking -Phys activity at goal: >150 min/week moderate; >75 min vigorous; combo -Healthy diet

Oscillation point of JPV:

Highest point of oscillation in internal jugular vein (or point where external jug vein appears collapsed) -Measured in vertical distance above sternal angle -Allows us to estimate level of the JVP -Note: measuring the top of the internal jugular vein from the sternal angle -JVP measured at >3 cm above sternal angle; or >8 cm above right atrium=abnormal VOLUME STATUS: may need to alter the elevation of the head or bed depending on volume status to accurately measure between the two points -Usual starting position is 30 degrees when assessing the JVP; pt head turned slightly to L and then R, to identify hte external jugular vein on each side -Then focus on Internal jugular vein pulsations on the right--JVP is HIGHEST OSCILLATION PT of these pulsations

S3 and s4 sounds

In adults over 40, these diastolic sounds are generally pathologic, correlated with heart failure and acute myocardial ischemia

Inspection and Palpation: Cardiac

Inspect anterior chest to look for: apical impulse or PMI, or less commonly S3 and S4 (if identified, palpate the PMI) -General palpation: reveals thrills, timing of S1 and S2, and ventricular movements of S3 and S4 -Palpate for: heaves, lifts, thrills: using palm and/or fingerpads held flat against chest. -For lifts and heaves=sustained impulses from enlarged ventricle or atrium; will feel the rhythm lifting fingers if present) -For thrills: press bell of hand pad on chest to check for a buzzing or vibratory sensation from underlying turbulence from heart murmurs. Auscultate if present. More easily palpated when pt leans forward (whatever position makes murmur more accentuated) -Palpating for S1 and S2: R hand on chest wall; left index and middle fingers palpate carotid artery in lower 3rd of neck. Identify S1 just before carotid upstroke and S2 just after upstroke; palpate for S3 and S4 using lighter pressure at cardiac apex for any extra movement detection -Assess RV by palpating that area at lower L sternal border and in subxiphoid area; pulm artery in left 2nd interspace; aortic area in righ 2nd interspace

Distinguishing JVP from Carotid pulsations:

Internal jugular pulsations: -Rarely palpable -Soft biphasic undulating quality (2 elevations) characteristic inward deflection (x descent) -Pulsations eliminated by light pressure on vein just above sternal end of clavicle -Height of pulsations change with position, normally dropping as the pt sits more upright -Height of pulsations usually falls with inspiration Carotid pulsations: -Palpable -More vigorous thrust with a single outward component -Pulsations not eliminated by pressure on veins at sternal end of clavicle -Height of pulsations unchanged by position -Height of pulsations not affected by inspiration

Murmur types:

Midsystolic murmur: after S1 and before S2; has a gap between murmur and heart sounds. Typically from blood flow across semilunar (aortic and pulmonic) valves Pansystolic murmur: starts with S1 and stops at S2, without a gap between murmur and heart sounds -Regurgitant (backward) flow across AV valves Late systolic murmur: usually starts in mid-or late systole and persists up to S2 -Murmur of the mitral valve prolapse and is often, not always, preceded by systolic click Early diastolic murmur: starts immediately after S2, without discernible gap, then fades into silence way before S1 -Accompany regurgitant flow across incompetent semilunar valves Middiastolic murmur: starts a short time after S2. May fade, or merge into a late diastolic murmur -Turbulent flow across AV valves Late diastolic/presystolic murmur: starts late in diastole and continues up to S1 -Turbulent flow across AV valves A continuous murmur: begins in systole and extends into all or part of diastole -Congenital causes sometimes

Valves and circulation:

Mitral and tricuspid valves: AV valves Aortic and pulmonic valves: Semilunar valves Systole: contraction in ventricles; L ventricle pressure rises from 5 mmHg to 120 mmHg Early diastole: ventricular relaxation; ventricular pressure falls below 5 mmHg and blood flows from atrium to ventricle Late diastole: ventricular pressure rises slightly during inflow of blood from atrial contraction During systole: Aortic (or pulmonic too) valves are open; mitral valve (or tricuspid too) valves are closed to prevent backflow During diastole: aortic (or pulmonic too) valves are closed to prevent back flow from aorta (in the L ventricle) and mitral (or tricuspid too) valves are open

BLOOD PRESSURE categories:

Normal: <120/80 Pre HTN: 120-139 systolic; 80-89 diastolic Stage 1 HTN: -Age >18 to <60 years: 140-159; 90-99 -Age >60 years: 150-159; 90-99 Stage 2 HTN: ->160; >100 If diabetes or renal disease: <140; <90 INDICATIONS for pharm therapy to lower BP: 1) Age >60 years: SBP >150 or DBP >90 (strong recommendation) 2) Age >60 years: SBP >140 (expert opinion) 3) Age >18 years with chronic kidney disease or diabetes: SBP >140; DBP >90 mm (Expert opinion) Note: lowering bp below 130/80 may be appropriate for some pts with CAD, previous MIs, history of stroke, carotid artery disease, PAD, abdominal aortic aneuryism

PMI irregularities:

PMI >2.5 cm =LVH from HTN or aortic stenosis Displacement of the PMI atleral to midclavicular line: LVH and also ventricular dilatation from an MI or HF

Atherosclerotic PAD:

Pain with walking or prolonged standing, radiating from spinal area into buttocks, thighs, lower legs, feet. Present in neurogenic claudication with a likelihood ratio of 7.4 for spinal stenosis if pain is releived by sitting and a lR over 6 if pain is relieved by bending forward or if bilateral buttock or leg pain present

HEART Physical exam:

Positioning: supine with head of bed 30 degrees -Turn to the left side to assess PMI (left lateral decubitus position) -To listen for aortic sufficiency, have pt sit up, lean forward, and exhale Sequence of the cardiac exam: 1) Supine with head elevated 30 degrees: -Inspect and palpate precordium: 2nd R and L interspaces; RV; LV; apical impulse (diameter, location, amplitude, duration) 2) Left lateral decupitus: -Palpate apical impulse (listen at apex with bell) (Low pitched extra sounds/diastolic rumble=mitral stenosis) 3) Supine with head elevated 30 degrees: -Listen at 2nd R and L interspaces, along L sternal border, across apex with the diaphragm 4) Sitting, leaning forward, after exhalation: -Listen at R sternal borer for tricuspid murmurs and sounds with the bell (Diastolic murmur=aortic insufficiency)

Preload:

Preload: the load that stretches the cardiac muscle before contraction (ex: volume of blood in the RV at the end of diastole constitutes its preload for the next beat) -Increases preload: RV preload is increased by increasing venous return to the R heart -Physiologically: inspiration and increased volume of blood flow from exercising muscles also increase preload -Pathologically: increased blood volume from a dilated RV in heart failure increases preload -Decreases of RV preload: exhalation, decreased LV output, pooling of blood in venous system -Pathologic increases here is called volume overload

Legs: PE (vascular):

Pt position: lying down, draped with legs fully exposed, no socks Inspection: -Examine both legs from groin and buttocks to feet, noting: -Size, symmetry, any swelling -Venous pattern and any venous enlargement -Any pigmentation, rashes, scars, ulcers -Color and texture of skin, color of nail beds, distribution of hair on lower legs, feet, toes (Warmth and redness over calf=cellulitis) -Inguinal lymph nodes: palpate superficial inguinal nodes (horizontal and vertical groups). Note: size, consistency, discreteness, tenderness (normal: nontender, discrete inguinal nodes) -Peripheral arteries: palpate pulses for arterial circulation assessment. 1) Femoral pulse 2) Popliteal pulse: knees flexed with leg relaxed (if cannot feel, try with pt prone and have them flex knee 90 degrees with lower leg reaxed against my shoulder) 3) Dorsalis pedis pulse 4) Posterior tibial pulse (absence in pedal pulses with normal femoral/popliteal pulses=atherosclerosis way more likely, seen in DM) - Note temperature of feet and legs, with backs of my fingers. Compare both sides (bilateral coldness=most often caused by a cold environment/anxiety; unilateral coldness=inadequate arterial perfusion) Peripheral veins: -Look for edema: compare foot and leg with other side, noting size/prominence of veins, tendons, bones -Check for pitting edema: press firmly but gently with thumb for atleast 2 sec: 1) over dorsum of each foot, 2) behind each medial malleolus; 3) over shins.

Pulmonic Area and Aortic Area

Pulm Area--L 2nd Interspace: -over the pulmonary artery -As pt holds expiration: look and feel for impulse and transmitted heart sounds (Note: Prominent pulsation here=dilatation or increased flow into pulm artery. A palpable S2 suggests increased pressure in PA (pulm HTN) Aortic Area--Right 2nd Interspace: overlies aortic outflow tract. Search for pulsations and palpable heart sounds (Note: Palpable S2 suggests systemic HTN. Pulsation suggests dilated or aneurysmal aorta)

Murmurs originating in R vs L side:

R side of heart: vary with respiration MORE Than those starting from L side heart

Jugular venous pressure (JVP) and Pulsations:

Reflects R atrial pressure, which equals central venous pressure and right ventricular end-diastolic pressure -Best estimated from R internal jugular vein (most direct channel into R atrium) A wave: produced by atrial contraction in jugular veins just before S1 and systole X descent: atrial relaxation V wave: occurs as R atrial pressure begins to rise with inflow from the vena cava during right ventricular systole Y descent: blood passively empties into RV during early and middiastole

Pulsus Alternans:

Rhythm of the pulse remains regular, but the force of the arterial pulse alternates because of alternating strong and weak ventricular contractions -Indicates severe L-sided HF -Apply light pressure on the radial or femoral arteries to feel it: use a BP cuff to confirm finding--lower the pressure in the cuff slowly to systolic level, and you will hear the softer sounds of the alternating weak beats within the Korotkoff sounds -Indicated by: alternately loud and soft Korotkoff sounds or a sudden doubling of apparent HR as the cuff pressure declines

Right sided heart sounds:

Right sided cardiac events occur slightly later than left--instead of hearing a single heart sound for S2, likely will hear first from L sided A2 and the second from right sided closure of P2 Inspiration: leads to the P2 lagging slightly behind the A2 due to the increased SV in the RV, delaying closure of the pulmonary valve Expiration: the two A2 and P2 sounds are one unison S2 sound

Heart anatomy: R and L ventricles

Right ventricle: most of the anterior cardiac surface; inferior border is below sternum/xiphoid process junction -RV narrows at top, joining pulm artery at sternal angle (base of the heart)--the superior aspect of the heart at the right and left 2nd interspaces adjacent to sternum Left ventricle: behind RV and to left, forms lateral left margin of heart--tapers inferiorly at cardiac apex. Produces the apical pulse! (point of maximal impulse--PMI)

Auscultatory Sounds:

S1: note intensity and any apparent splitting. Normal splitting=detectable along lower left sternal border S2: Note intensity Split S2: listen for splitting of this sound in 2nd and 3rd L interspaces. Ask pt to beathe quietly, then more deeply than normal. Does S2 split into 2 components, as it normally does? If not, ask pt to 1) berathe more deeply or 2) sit up. Listen again. Thick chest wall may make the pulm component of S1 inaudible -Width of split: how wide? it is normally narrow -Timing of split: when in the resp cycle does it happen? normally heard in late inspiration (should disappear during exhalation) Intensity of A2 and P2: compare intensity of the two components (A2 is usually louder) Extra sounds in systole:: such as ejection sounds or systolic clicks; note location/timing/intensity/pitch/effects of resp on the sounds (Systolic click of mitral valve prolapse=most common extra sound in systole) Extra sounds in diastole: S3, S4. Note location/timing/intensity/pitch/effects of resp on sounds (S3 or S4 in athletes=normal) Systolic and diastolic murmurs: differentiated from S1 and S2 and extra sounds by their longer duration

Where to listen for S1 and S2:

S2: Loudest at the Base of the heart (Note: 2nd and 3rd left interspaces close to the sternum=best place to hear P2 specifically) S1: throughout precordium but loudest at the apex of the heart (tricuspid, because softer, is best heard at lower left sternal border) **Note: splitting does not vary with respiration for the S1 sound

Screening steps for CVD: STEP TWO

STEP 2: Calculate 10 year and lifetime CVD risk using online calculator: -Risk estimates incorporate age, gender, smoking history, total cholesterol level, HDL cholesterol level, systolic BP, antihypertensive therapy, diabetes -Provide gender and race specific risk estimates for a first MI, CHD death, or fatal/nonfatal stroke

Screening steps for CVD: STEP THREE

STEP 3: track individual risk factors 1) HTN: 1/3 of US adults >20 years have HTN--BP >140/90 -Primary htn (essential): most common cause. Risk factors: age, genetics, black race, obesity, weight gain, excessive sodium intake, physical inactivity, excessive alcohol use -Secondary htn: <5%--causes; sleep apnea, chronic kidney disease, renal artery stenosis, meds, thyroid disease, parathyroid disease, Cushing syndrome, etc -Substantially higher in blacks than whites (generally similar between men and women) 2) Diabetes: -only 26.1% are treated and controlled; 39.5% are treated and uncontrolled; 26.5% are not treated and undiagnosed; 8% are not treated but aware -Diagnosing: fasting glucose >126 mg/dL and HbA1C >6.5% -Screening: adults with no risk factors begin at 45 years; repeat at 3 year intervals; adults with BMI >25 and additional risk factors Diagnostic Criteria: -HbA1C: >6.5% is diabetes; 5.7-6.4% is prediabetes -Fasting plasma glucose: >126 is diabetes; 100-125 is prediabetes -2 hour plasma glucose/tolerance test: >200 is diabetes; 140-199 is prediabetes -Random glucose if classic symptoms: >200 for diabetes 3) Dyslipidemias: recommendations lipid screening for all men >55, women >45 who are at increased risk for CHD; also for those at 20 years with diabetes, HTN, obesity, tobacco use, noncoronary atherosclerosis, fam history of early CVD -For pts with clinical CVD (secondary prevention) or LDL cholesterol levels >190 (primary prevention): prescirbe high intensity statin therapy -For pts with diabetes and or LDL cholesterol levels from 70 to 189, determine 10 year risk of atherosclerotic CVD. Strong evidence of starting statin therapy for those with a 10 year risk >7.5%; still considere for risks between 5-7.5% 4) Metabolic syndrome: criteria is to meet 3 of the 5 -Waist circumference: men >102 cm; women >88 cm -Fasting plasma glucose: >100, or being treated -HDL cholesterol: men <40, women <50; or being treated -Triglycerides: >150 or being treated with drugs -BP: >130/85 or being treated with drugs 5) Other risk factors: Smoking, Fam Hx, Obesity -Smoking: increases risk of CHD and stroke by 2-4 fold (14% of cardiac deaths are attributed to smoking) -13% report fam history of MI or angina before 50 years; this risk factor is associated with 50% increased lifetime risk for CVD and CHD -Obesity: BMI >30--associated with a 13% of CVD deaths compared to normal weights

Screening steps for CVD: STEP ONE

STEP ONE: Screen for Global Risk Factors: -begin at 20 years for individual risk factors or "global" risk of CVD, family history of premature heard disease (age was >55 years in men or <65 in females) Family history of premature CVD: update regularly Cigarette smoking: screen at each visit; goal is cessation Poor diet: screen at each visit; goal is improved eating Phys inactivity: screen at each visit; goal is 30 min daily Obesity: screen at each visit; goal BMI 20-25; circumference <40 in for men; GOAL <35 in for women HTN: screen at each visit; goal <140/90 for adults <60 or adults >60 with diabetes/chronic kidneys disease; <150/90 for all other adults >60 Dyslipidemias: screen every 5 years if low risk; every 2 years if strong risk; GOAL initiate statin therapy if meeting ACC/AHA guidelines Diabetes: every 3 years (if normal) screening beginning at 45 years; more frequently at any age if risk factors exist--goal is to prevent or delay diabetes for those with HbA1c of 5.7-6.4% Pulse: screen at each visit; GOAL to identify and treat a fib

Superior vena cava and Inferior vena cava:

SVA: Veins from upper trunk, arms, and head and neck drain here -This empties into the RA IVA: -Veins from legs and lower trunk drain upward here -Weaker wall structure in lower extremity veins, so they are susceptible to irregular dilatation/compression/ulceration/etc

Functional murmur:

Short, early, midsystolic murmur that decreases with intensity with maneuvers that reduce LV volume, like standing up/sitting up/straining during Valsalva maneuver -Often heard in healthy pts and not pathologic

Intima:

Surrounds lumen of all blood vessels, made up of endothelial cells -Functions: -metabolizes regulators of thrombosis -produces prothrombotic moecules -modulates BF and vascular reactivity by synthesizing both vasoconstrictors and dilators -Regulates immune and inflammatory reactions

Lympathic system and lymph nodes:

System: extensive vascular network draining lymph from body tissues and returning it to venous circulation -Starts peripherally as lymph capillaries--->moves centrally as thin vascular channels-->collecting ducts-->empties into major veins at neck -Filtered through lymph nodes along the way! Lymph nodes: -Round, oval, bean shaped that vary in size depending on location -Palpable ones on PE: the superficial ones: cervical, axillary, and nodes in arms/legs

Techniques of Exam Vascular:

The Arms: -size, symmetry, skin color -Radial pulse, brachial pulse -Epitrochlear lymph nodes Abdomen: -Aortic width -Pulsatile mass Legs: -Size, symmetry, skin color -Femoral pulse and inguinal lymph nodes -Popliteal, dorsalis pedis, posterior tibial pulses -Peripheral edema

VEINS:

Thin walled and highly distensible Venous intima: nonthrombogenic endothelium Media: elastic tissue and smooth muscle that change vein caliber in response to minor changes in venous pressure DEEP veins of legs: -Deep veins carry approx 90% of venous return from the LE -Well supported from tissues SUPERFICIAL veins of legs: -subcutaneous, with relatively poor tissue support 1) Great saphenous vein: originate on dorsum of foot, pass anterior to medial malleolus, continues up medial leg, joins femoral vein of DVS below inguinal lig -Anastomosis connects the two of these 2) Small saphenous vein: begins on lateral side of foot, passes along posterior calf, joins DVS in popliteal fossa NOTE: -Perforating veins connect superficial with deep system

Thrills and Bruits:

Thrills: humming vibrations Bruit: murmurlike sound arising from turbulent arterial blood flow -Ask pt to stop breathing for a few seconds, auscultate with diaphragm (better at detecting bruits than the bell) -Place diaphragm near upper end of thyroid cartilage below jaw angle, where common carotid artery bifurcates into internal carotid. Bruit here: less likely to be confused with transmitted murmur from heart or subclavian or vertebral artery bruits

Fluid exchange; capillary bed

Toward arterial end: Hydrostatic pressure: within capillary bed, near arteriolar end, forcing fluid out into tissue spaces -Additionally, interstitial colloid oncotic pressure of the proteins within the tissues pull for the nutrients/aid the hydrostatic pressure within the capillary bed -These forces are opposed by hydrostatic pressure of the tissues -At this point, the net flow of fluid is outward from the arterioles Toward venous end: Colloid oncotic pressure of pasma proteins: gains dominance towrad the venous end of the capillary bed (the hydrostatic pressure falls here too) and this pullls fluid back into the vascular tree -Now the net flow is inward on the venous side -Lymph capillaries (also play a role in this equilibrium) remove excessive fluid, including proteins, from interstitial space

Arterial pulses:

Upper body Arterial pulses: brachial, radial, ulnar Leg arterial pulses: -Femoral artery (just below inguinal lig) -Popliteal artery (extension of femoral artery, passes medially behind femur, palpable behind the knee--divides into 2 arteries listed below:) -Dorsalis pedis: dorsum of foot lateral to extensor tendon of big toe Posterior tibial artery: behind medial malleolus of ankle

Percussion:

Use this only when you cannot feel the apical impulse (as palpation has replaced percussion for estimation of cardiac size) -Percuss from resonance (starting to the L on the chest) toward cardiac dullness in 3rd, 4th, 5th and possibly 6th interspaces

Shape of a murmur:

determined by itss intensity over time Crescendo murmur: grows louder -Presystolic murmur of mitral stenosis in normal sinus rhythm Decrescendo murmur: grows softer -Early diastolic murmur of aortic regurg Crescendo-decrescendo murmur: first rises in intensity, then falls -Aortic stenosis and innocent flow murmurs (midsystolic murmurs) Plateau murmur: same intensity throughout -Pansystolic murmur of mitral regurg

Lymphadenopathy:

enlargement of the nodes, with or without tenderness. Localized: causative lesion in drainage area Generalized: enlarged nodes in at least 2 other noncontiguous lymph node regions

Exaggerated, widened femoral or popliteal pulse:

femoral aneuyrism or popliteal aneurysm (respectively) which is--(dilatation pathologic of artery) --Usually caused by atherosclerosis

Gangrene:

hair loss over anterior tibiae occurs with decreased arterial perfusion -Dry or brown black ulcers from gangrene may ensue after