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PHYS DX TEST #2 – BOOK NOTES

CH 14 – HEART

General Considerations

Major forms of heart disease are coronary heart disease, hypertension, rheumatic heart disease, bacterial endocarditis, and congenital heart disease. Heart disease is by far the nation’s #1 killer claiming 39% of all deaths. Cardiovascular disease (CVD) calms more lives than the next seven causes combined. In women coronary heart disease kills one in 3 women over the age of 65. Women have a higher mortality rate from infarct than men. People with higher systolic and diastolic pressures have greater incidence of heart disease and death attributed to heart disease.

Structure and Physiology

L side of heart and arteries = high pressure delivery system

R side of heart and veins = low pressure delivery system

Pericardial Sac = envelops the heart and is adhered to the diaphragm and the sternum.

Visceral Pericardium = Epicardial/outermost layer of cells of the heart

Parietal pericardium = outer sac

Pericardial Fluid = sits between the parietal and visceral pericardium and lubricates the heart allowing for motion

Outside to Inside

Pericardial Sac -------- Parietal Pericardium ------- Pericardial Fluid -------- Visceral Pericardium

Innervations & Pain

Parietal pericardium is innervated by the phrenic nerve. The parietal pericardium carries pain fibers. The visceral pericardium does not contain pain fibers (pain insensitive).

Impulse Conduction

1. SA Node = Generates impulses…Located at the junction of superior vena cava and right atrium

2. AV Node = Located in the interatrial septum near the coronary sinus and slows the signals

3. Bundle of His = Receives the signals after the AV node

4. R and L Bundle branches = Specialized tissue that conducts the impulse

5. Perkinje’s Fibers = Conduct the message to the ventricles

Autonomics

Both parasympathetic and sympathetic fibers are present in the SA and AV nodes as well as the atrial. The ventricles primarily have sympathetics (lack parasympathetics). Parasympathetics travel with the vagus nerve VS. Sympathetics that travel with thoracic nerves T1-T5 to the ventral roots and synapse and the sympathetic ganglia to postganglionics traveling in the cardiac nerves. Cardiac nerves (sympathetics) join up with parasympathetics at the cardiac plexus (located near the aortic arch and tracheal bifurcation).

Sympathetics = Norepinephrine….Increased HR and contractility

Parasympathetics = Acetylcholine…Decreases HR and contractility

Medullary CV Center: The center has excitatory and inhibitory areas that regulate output to autonomic fibers. The system relies on stretch receptors and pressure receptors located in the aortic arch and carotid sinus.

Decreased pressure and activity triggers sympathetic efferent activity with decreased parasympathetics to restore BP, HR and contractility

VS

Increased pressure and activity triggers parasympathetic efferent activity with decreased sympathetics to drop BP, HR, and contractility.

Heart Anatomy and Location

RV = makes most of the anterior cardiac surface

RA = 3rd-5th rib to R of sternum

LV = Left and behind the RV

Apex = 5th intercostal space at MC line (5ICS-MCL) – THIS LOCATION IS CALLED THE APICAL IMPULSE OR THE POINT OF MAXIMUM IMPULSE (PMI)

Aortic = 2nd intercostal space, Right sternal border (2ICS-RSB)

Pulmonic = 2nd intercostal space, Left Sternal border – (2ICS-LSB)

Tricuspid = Left Lower Sternal Border (LLSB)

Mitral = Cardiac Apex (5ICS-MCL)

Erb’s Point = 3rd left intercostal space…the areas where the pulmonic and aortic sounds are best heard

Base of Heart = 2nd ICS to R and L of sternum

*** Know the locations for the exam ***

Cardiac Cycle

S1 = Closure of the AV valves (mitral and tricuspid) produces the first heart sound of S1

S2 = Closure of the SL valves (aortic and pulmonic) produces the second heart sound of S2.

Opening of the valves is ONLY HEARD WHEN THEY ARE DAMAGED!

Snaps and Clicks

Opening Snap = AN AV VALVE THAT OPENS WHEN STENOTIC PRODUCES A SNAPPING SOUND DURING DIASTOLE!

A). Mitral Opening Snap = Occurs with a stenotic mitral valve. The mitral valve opens when pressure in the LA exceeds LV pressure causing blood to flow from the LA into the LV past the mitral valve. Stenosis causes valve “hardening.” Pushing blood from the LA into the LV against a “hardened valve” creates a snapping sound during mitral opening and is termed mitral valve opening snap.

B). Tricuspid Opening Snap = Occurs with a stenotic tricuspid valve. The tricuspid valve opens when pressure in the RA exceeds RV pressure causing blood to flow from the RA into the RV past the tricuspid valve. Stenosis causes valve “hardening.” Pushing blood from the RA into the RV against a “hardened valve” creates a snapping sound during tricuspid opening and it termed tricuspid valve opening snap.

Vs

Ejection Click = AN SL VALVE THAT OPENS WHEN STENOTIC MAKES A CLICKING SOUND DURING SYSTOLE!

A). Aortic Ejection Click = Heard with a stenotic aortic valve when the pressure in the left ventricle exceeds diastolic pressure in the aorta forcing blood in the aorta. This process opens the Aortic valve. Stenosis can cause valve problems pushing blood passed a “hardened” valve producing the click.

B). Pulmonic Ejection Click = heart with a stenotic pulmonary valve when the pressure in the right ventricle exceeds the diastolic pressure in the pulmonary artery. This process opens the pulmonary valve. Stenosis can cause valve problems pushing blood passed a “hardened” valve producing an audible click.

Opening & Closing Sequence

Mitral Valve Closes ---- Tricuspid Closes ---- Pulmonary Opens ---- Aortic Valve Opens --- Aortic Valve Closes ---- Pulmonary Closes --- Tricuspid Opens ---- Mitral Valve Opens

S1 Sound Broken Down

S1 Mitral Portion = occurs when mitral valve closes, when the left ventricular pressure rises above the left atrial pressure…It is called M1

S1 Tricuspid Portion = occurs when tricuspid valve closes, when the RV pressure rises above the RA pressure…It is called T1

M1 + T1 = S1 ----- Mitral + Tricuspid = Heart Sound 1

Isovolumetric Contraction

Time between closure of the AV valves and opening of the SL valves

Ejection = time between opening and closing of the SL valves.

S2 Sound Broken Down

Incisura/Dicrotic Notch/A2 = Occurs during aortic component of S2, when the aortic valve closes…it is called A2

P2 = Pulmonic component of S2 that occurs when the pulmonic valve closes. The pulmonic valve closes at the point when the RV pressure falls below the pulmonary diastolic pressure.

Isovolumetric Relaxation

The time between the closure of the SL valves and the opening of the AV valves.

S3

S3 can occur at the end of rapid filling period. S3 occurs after S2. S3 is normal in children and young adults. In adults over 30, it signifies a volume overload to the ventricle. The cause may be regurgitation of the valves or CHF.

S4

May be heard at the end of diastole (atrial contraction). S4 is normal in children and young adults. In people over 30, it indicates a stiff or noncompliant ventricle. The ventricle hypertrophies due to pressure overload typically from CHD.

S3 and S4 are often called “Gallop Sounds.”

Locations of Where the Heart Sounds are Heard Best

S1 = Apex

S1 Splitting = Tricuspid Area

S2 = Base

S2 is split into A2 and P2 components ----- Aortic Closure + Pulmonic Closure = Heart Sound #2. A2 precedes P2 as the aortic valve closes before the pulmonic valve. The pulmonic valve remains open longer than the aortic valve because it takes longer to fill the right ventricle to eject blood into the pulmonary artery. A2 and P2 normally split during inspiration (called physiologic splitting of S2).

Arterial Pulse

Arterial Pulse = Produced by the ejection of blood into the aorta.

Anacrotic Notch = A slight notch in the arterial pulsation toward the end of the rapid ejection period.

Dicrotic Notch = Closure of the aortic valve that corresponds with decreased intensity when graphed

Dicrotic wave = Follows the dicrotic notch and is a small upstroke/positive wave

Percussion wave = an early wave, preceding the dicrotic notch that is associated with peak rate and velocity of flow into the artery.

Tidal wave = Occurs after the percussion wave and is related to peak systolic pressure. The tidal wave is typically smaller than the percussion wave and can be increased in hypertensive or elderly patients.

Order of Events: Anacrotic Notch (depression after rapid ejection) --- Upstroke in the graph ----- Percussion wave ---- Tidal wave ---- Dicrotic notch ---- Dicrotic Wave --- Return to baseline

The content and volume of the arterial pulse are determined by left ventricular stroke volume, ejection velocity, compliance of the arteries, capacities of the arteries, and pressure waves from Anterograde flow of blood.

Blood Pressure

Blood Pressure = Lateral Pressure exerted by a column of blood against the arterial wall. BP is the result of cardiac output and the peripheral vascular resistance. BP depends on the volume of blood ejected, its velocity, and the distensibility of the arterial wall, the viscosity of the blood and the pressure within the vessel after the last ejection.

Systolic = Peak pressure in the arteries, regulated by SV (stroke volume) and compliance of the blood vessels.

Vs.

Diastolic = Lowest pressure in the arteries and depends on peripheral resistance.

Pulse Pressure = Difference between systolic and diastolic. Typically the reading is 15-20 greater in the UE.

There is normally a decline in systolic BP with inspiration (called Inspiratory decline) of up to 10 mm Hg during quit respiration. The decline during quiet inspiration is NORMAL.

Jugular Venous Pulse

The reading provides direct information about the pressures in the right side of the heart because the jugular system is in direct proximity with the RA (right atrium).

The RV (right ventricle) monitors the pressures in the LA and LV in a normal, non-stenotic heart.

The MOST COMMON cause of R sided heart failure = L sided heart failure.

A). A Wave of the Jugular Venous Pulse = Caused by R atrial contraction occurring after the P wave. The time delay is present because of the normal delay from the impulse to be interpreted and cause contraction of the atria with subsequent appearance in the neck.

B). X descent of the Jugular Venous Pulse = Caused by atrial relaxation and just before ventricular contraction that shows up as a descent in the wave when graphed...

C). C wave of the Jugular Venous Pulse = Occurs following the X descent. There is a slight increased in RA Pressure due to the tricuspid valve closure and secondary to R ventricular contraction.

D). X prime descent = Descent of the base of the heart following contraction is the cause for the X prime descent. Mild decreases in RA pressure are also present as the size of the atrium slightly increases (increase in size results in decreased pressure).

E). V wave = The RA begins to fill with blood returning by the vena cava following completion of ventricular systole. The increase in RA pressure is viewed as a spike (V wave) when graphed.

F). Y Descent = Occurs at the end of ventricular systole, when RV pressure decreases rapidly. When RA pressure exceeds RV pressure the tricuspid valve opens and blood rushes into the RV. The blood rushing from RA to RV causes a descent when graphed (Y descent).

Sequence of Events: A wave ----- X descent ---- C wave ----- X prime descent ---- V wave ---- Y descent

Typically only the A and V waves are visible on examination. The C wave is typically not observed, so the X and X prime are often summated on exam. If a C wave is present, it could indicate an enlarged carotid artery pulsation artifact.

Review of Specific Symptoms

The most important symptoms are chest pain, palpitations, dyspnea, syncope, fatigue, dependent edema, hemoptysis, and cyanosis.

Chest Pain

The most important symptom of cardiac disease but it can occur with other non-cardiac pathology, such as: pulmonary, intestinal, gallbladder, musculoskeletal disorder.

Angina Pectoris = the true symptom of CHD. A consequence of hypoxia of the myocardium from an imbalance between coronary supply and myocardial demand.

Levine’s Sign = The patient clenches the fist and places it over the sternum. THIS IS A CLASSIC SIGN FOR ANGINA AND CVD PROBLEMS!

*** KNOW LEVINE’S SIGN FOR THE EXAM, FINAL, AND NATIONAL BOARDS ***

Table 14-1 Characteristics of Chest pain

Angina = Location = Retrosternal, Diffuse…Radiation = Left arm, Jaw, Back…Description = Aching, Dull, Pressing, Squeezing, Viselike…Intensity = Mild to severe…Duration = Minutes…Precipitated by = Effort, emotion, eating, cold…Relieved by = Rest, nitroglycerin

Not Angina = Location = Left inframmary, localized…Radiation = Right arm…Description = Sharp, shooting, cutting…Intensity = Excruciating…Duration = Seconds, hours, days…Precipitated by = Respiration, posture, motion…Relieved by = Nonspecific

*** Know how to distinguish between Angina and Not Angina for the exam ***

Table 14-2 Common Causes of Cardiac Pain

Cardiac: Coronary artery disease, aortic valvular daises, pulmonary hypertension, mitral valve prolapse, pericarditis, idiopathic hypertrophic subaortic stenosis

Vascular: Dissection of the aorta

Pulmonary: pulmonary embolism, pneumonia, pleuritis, Pneumothorax

Musculoskeletal: Costochondritis (Called Tietze’s syndrome – an inflammation of the costal cartilage), arthritis, muscular spasm, bone tumor

Neural: Herpes Zoster

GI: Ulcer disease, Bowel disease, hiatal hernia, pancreatitis, cholecystitis

Emotional: Anxiety, Depression

*** Just know that there are many different causes of chest pain ***

Palpitations

Uncomfortable sensations in the chest associated with arrhythmias. These sensations are described as “fluttering”, “skipped beats”, “pounding”, “jumping,” “stopping,” or “irregularity.” Palpitations are common and may not indicated serious problems. Palpitations are associated with cardiovascular causes, thyrotoxicosis, hypoglycemia, fever, anemia, pheochromocytoma, anxiety, hyperthyroidism, caffeine, tobacco, drugs, sympathetic amines used to treat bronchoconstrictions, and panic disorders.

Table 14-3 Common Causes of Palpitations

Extrasystoles: Premature Atrial Contraction, Nodal premature beats, Ventricular Premature beats

Tachyarrhythmias: Paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, multifocal atrial tachycardia, ventricular tachycardia

Bradyarrhythmias = Heart block, Sinus Arrest

Drugs = Bronchodilators, digitalis, Antidepressants

Smoking

Caffeine

Thyrotoxicosis

*** Know this chart for the exam, particularly the first 4 (extrasystoles, tachyarrhythmias, bradyarrhythmias, and drugs ***

Dyspnea as a Cardiac Symptom

1. PND (paroxysmal nocturnal dyspnea) = Occurs at night or when the patient is supine. Increased introthoracic blood volume occurs. The increased volume cannot be handled by a weakened heart. Linked with CHF! The patient awakens during sleep and presents with dyspnea, coughing and seeks relief by getting up to get more air.

2. Orthopnea = Patient requires more pillows to sleep due to positionally associated dyspnea.

3. DOE (dyspnea on exertion) = Due to chronic congestive heart failure or severe pulmonary disease. Clarify the severity of the condition by asking how many blocks can you walk now vs. 6 months ago.

4. Trepopnea = A rare positional dyspnea that occurs when the patient assumes a sidelying posture. The cure is to flip over to the other side. (Ex. Patient experiences dyspnea while laying on the Right side --- The cure would be to flip on the Left side).

Table 14-4 Common Causes of Dyspnea

Cardiac = Left ventricular failure, mitral stenosis

Pulmonary = obstructive lung disease, asthma, restrictive lung disease, pulmonary embolism, pulmonary hypertension

Emotional = Anxiety

High Altitude = Decreased oxygen pressure

Anemia = Decreased oxygen carrying capacity

*** This chart is a review of dyspnea covered in the 1st test, but it may be covered on the 2nd exam, particulary cardiac causes of dyspnea ***

Syncope

Fainting or a transient loss of consciousness due to inadequate cerebral perfusion. It is important to note if exercise/activity preceded the syncope. Valvular stenosis, idiopathic hypertrophic subaortic stenosis and primary pulmonary hypertension are all linked to syncope due to activity.

A patient may have palpitation before the syncope, indicating arrhythmia. The condition may affect cardiac output.

Types:

A). Orthostatic Hypotension/Syncope = A postural syncope resulting from a peripheral autonomic limitation. There is s a sudden fall in systemic blood pressure resulting from failure of reflexes to compensate to the standing position. Symptoms include: dizziness, blurred vision, weakness, and syncope. Classic is an older person, on medication, that awakens at night from bed.

B). Micturition Syncope = Occurs when straining with nocturnal urination. Classic is older men that strain during urination that have consumed significant amounts of alcohol.

C). Vasovagal Syncope = The most common type of syncope and the most difficult to manage. This form occurs during periods of sudden, stressful or painful experiences, surgery, trauma, and loss of blood or the sight of blood. Symptoms include pallor, nausea, weakness, blurred vision, lightheadedness, perspiration, yawning, diaphoresis, hyperventilation, epigastric discomfort, and a “sinking feeling.” There is a sudden fall in systemic vascular resistance without compensations (increased cardiac output). The situation can be avoided if the person sits or lies down promptly.

D). Carotid Sinus syncope = Associated with a hypersensitive carotid sinus. This condition commonly affects the elderly. Increased stimulation of the carotid sinus causes a fall in systemic pressure and results in syncope. There are 2 types of carotid sinus Syncope:

1). Cardioinhibitory: Bradycardia results

2). Vasodepressor: Hypotension without bradycardia

E). PostTussive Syncope = Occurs in a patient with COPD. Coughing causes increased intrathoracic pressure that decreases venous return and decreases cardiac output. There can also be a rise in CSF pressure and decreased brain perfusion.

Table 14-5 Common Causes of Syncope

Cardiac = Decreased CSF (secondary to cardiac rhythm disturbance), Left Ventricular output obstruction

Metabolic = Hypoglycemia, Hyperventilation, Hypoxia

Psychiatric = Hysteria

Neurologic = Epilepsy, Cerebrovascular Dissease (Stroke)

Orthostatic Hypertension = Volume Depletion, Antidepressants, Antihypertensives

Vasovagal = Vasodepression

Micturition = Vasodepression

Cough = Chronic Lung Disease

Carotid Sinus = Vasodepressor Response to carotid sinus sensitivity

*** Know this chart for the exam, final and national Boards ***

Fatigue

Not specific for cardiac conditions. When linked to cardiac conditions, the cause can be attributed to decreased cardiac output conditions like CHF and Mittal valve disease. Overall the most common cause of fatigue is not cardiac related and is related to anxiety and depression (psychogenic fatigue).

A). Psychogenic Fatigue = “Tired all the time”…more tired at home than at work. They often feel worst in the morning and feel best at the end of the day.

B). Organic/Cardiac Fatigue = Fatigue with exertion…These people feel best in the mornings and fatigue later in the day/evening. Position (standing all day) and exertion (having performed a day’s work) increase the fatigue as the day progresses.

Dependent Edema

Swelling of the legs…CHF presents with symmetrical edema of the lower extremities that worsens as the day progresses and dyspnea….Severe bedridden patients may have sacral area edema.

Hemoptysis

Mitral stenosis and rupture of the bronchial veins can produce hemoptysis.

Cyanosis

Differential Cyanosis = Cyanosis noted only in the LE due to an R to L shunt through a PDA (patent ductus arteriosus). The shunt results from pulmonary hypertension. Blood crosses the PDA below the level of the carotid and L subclavian arteries. Deoxygenated blood is pumped to the Lower extremity as a result causing cyanosis only in the lower body.

Impact of Cardiac Disease

Fear, depression, and anxiety are often present in patients with cardiovascular disease.

Physical Examination

Inspection of the patient, Blood pressure assessment, Assessment of the arterial pulse, assessment of the jugular venous pulse, percussion of the heart, palpation of the heart, auscultation of the heart, examination for dependent edema

Inspection – Evaluate General Appearance

Checking for acute distress, labored breathing, use of accessory muscles of respiration

Inspection – Inspect the Skin

Inspect for cyanosis (central, peripheral, and differential), Pallor, temperature (increased warmth with anemia, beriberi, thyrotoxicosis & decreased warmth with intermittent claudication), xanthomata, erythema marginatum, and Osler’s Nodes.

A). Tendon Xanthomata = Stony hard, yellowish masses often found in the extensor tendons of the fingers, Achilles tendon, and plantar tendons that are a result of hypercholesterolemia. This condition often occurs when serum cholesterol exceeds 450 mg/dL.

B). Primary Biliary Cirrhosis = Can present with multiple xanthomata due to extremely elevated cholesterol levels (1000-1500 mg/dL). Primary biliary cirrhosis is rare, progresive, and often fatal liver disease seen mostly in women. Xanthomata often presents on the palms, soles, knees, elbow, and hands.

C). Eruptive Xanthomata = Typically occurs with familial pathology of fat metabolism. It is often present on chest, buttocks, abdomen, back, face and arms. This condition can be seen with diabetes mellitus and hypertriglyceridemia. Serum levels are often in excess of 15000 mg/dL. The lesions develop often after excessive alcohol consumption.

D). Erythema Marginatum = Reddened, disc shaped areas with raised edges…If linked with fever, it can indicate rheumatic fever

E). Osler’s Nodes = Painful lesions on the fingers and toes that occurs with infective endocarditis.

Inspection -- Inspect the Nails

Splinter Hemorrhages = Small, reddish-brown lines in the nail bed. Classically associated with infective endocarditis. This is a non-specific finding since trauma as well as other pathology can lead to splinter hemorrhages.

Inspection – Inspect the Facies

A). Supraclavicular Aortic Stenosis = A congenital problem, that presents with widely set eyes, strabismus, low set ear, upturned nose, and hypoplasia of the mandible.

B). Pulmonic Stenosis = Moon facies, widely set eyes

C). Hypothyroidism = Expressionless face, puffy eyelids, loss of the outer third of eyebrow

D). Earlobe Crease/Lichtenstein’s Sign = Oblique ear crease, often found bilaterally in people over 50 INDICTING CHD. This sign is classic for CHD, but has high levels of false + and false -.

Inspection – Inspect the Eyes

A). Xanthelasma = Yellow plaques on the eyelids that indicates a hyperlipoproteinemia.

B). Arcus Senilis = A white ring at the edge of the cornea that is linked with hypercholesterolemia. In patients younger than 40 the suspicion of hypercholesterolemia is present.

C). Sarcoidosis = Opacity of the cornea linked with cor pulmonale.

D). Displacement of the Lens = Linked with Marfan’s syndrome and aortic regurgitation

E). Conjunctival Hemorrhages = Seen with infective endocarditis.

F). Hypertelorism = Widely set eyes…Associated with congenital heart disease (pulmonic stenosis, supravalvular aortic stenosis).

G). Roth Spots = Present with infective endocarditis

Retinal Inspection is indicated due to the impact of diabetes, hypertension ad atherosclerosis.

Inspection – Inspect the Mouth

A). Highly arched palate = Indicates congenital heart problems like mitral valve prolapse

B). Petechiae on the Palate = Indicates Infective endocarditis

Inspection Inspect the Neck

Webbing = Linked with Turner’s Syndrome and Noonan’s Syndrome. Both syndromes are sexually linked diseases of development that show retarded sexual development, webbed neck, pulmonic stenosis and abnormal sex chromosomes (Turners – Female 45 X0…..Noonan’s – Male 46 XY).

Inspection – Inspect the Chest Configuration

A). Pectus Excavatum = Caved in chest linked with Marfan’s and mitral valve prolapse.

B). Pectus Carinatum = Pigeon breast…also linked with Marfan’s

Inspection – Inspect the Extremities

A). Atrial Septal Defects = May have an extra phalanx, extra finger, or toe

B). Marfan’s = Long, slender fingers and aortic regurgitation

C). Turner’s Syndrome = Short stature, cubitus valgus, medial deviation of forearm

Blood Pressure -- Blood Pressure Assessment

*** This section goes over how to take blood pressure and was covered in PHYS DX. #1 ***

Auscultory Gap = Silence by disappearance of the Korotkoff sounds after the initial appearance and their reappearance at a lower pressure. The gap is present where there is a decreased blood flow to the extremities as is found in hypertension and in aortic stenosis. The importance lies in the fact that the systolic blood pressure may be mistake for lower blood pressure, the point of reappearance.

Blood Pressure -- Determine Blood Pressure by Palpation

*** Covered in Phys Dx #1 ***

Blood Pressure -- Determine Blood Pressure by Auscultation

*** Covered in Phys Dx #1 ***

Blood Pressure -- Rule Out Orthostatic Hypotension

Orthostatic Hypotension (definition) = A drop in systolic BP of 20 mm Hg or more upon standing with the development of dizziness, syncope, and increased HR. The procedure involves having the patient resting in a supine/recumbent position for 5 minutes and takes their BP. Have the patient stand and immediately take their BP standing. Subtract the systolic measurements (Supine – Standing) and note any signs/symptoms present.

Blood Pressure -- Rule Out Supravalvular Aortic Stenosis

Supravalvular Aortic Stenosis = A difference in BP in the arms with hypertension in one arm and hypotension in the other arm.

Blood Pressure -- Rule Out Coarctation of the Aorta

Coarctation of the Aorta = Occurs when systolic blood pressure is lower in the leg (LE) than the arm (UE)…The assessment occurs when BP is taken in both the UE and LE and compared.

Blood Pressure – Rule Out Cardiac Tamponade

A) Cardiac tamponade = Should be ruled out when there is a low arterial blood pressure with a rapid, feeble pulse. Cardiac tamponade is an increase in intrapericardial pressure that interferes with normal diastolic filling.

1). Paradoxical pulse = linked with cardiac tamponade, pericardial effusions, constrictive pericarditis, asthma and emphysema. Paradoxical pulse is characterized by the exaggeration of the normal Inspiratory fall of systolic pressure (a fall of greater than 10 mm Hg during inspiration).

Paradoxical pulse is tested for:

1). Inflate the cuff into no sounds are heard with the patient respirating normally

2). Gradually deflate the cuff until sounds are heard in expiration only

3). Note the pressure at which sounds are heard

4). Continue to deflate the cuff until sounds are heard during inspiration

5). Note this pressure

6). If f the difference is greater than 10 mm Hg, paradoxical pulse is present.

Arterial Pulse

Rate, rhythm, contour, amplitude

Arterial Pulse – Determine the Cardiac Rate

Cardiac rate is assessed by the radial pulse. Pulse should be taken for at least 30 seconds from the radial artery in regular/healthy individuals. In irregular conditions (like atrial fibrillation), auscultation of the heart should be done because there is varying length of diastolic filling leading to weak pulse waves during ventricular contraction. Some of the pulse waves may not be felt, making the pulse measurement at the radial artery inaccurate.

Arterial Pulse – Determine the Cardiac Rhythm

A). Regular = Normal, typical, not pathological

B). Regularly Irregular = An irregular beat that occurs in a definite pattern

1). Premature Beats – Presence of isolated extra beats during regular rhythm

2). Bigeminy = Coupled rhythm of beats in pairs (first beat is sinus….second beat is usually a premature ventricular beat)

C). Irregularly Irregular = Does not have a definite pattern (Ex. Arial fibrillation – grossly irregular without a definite pattern and pulse)

Arterial Pulse – Palpate the Carotid Artery

Procedure:

1). Dr. on the R side of patient…Patient is supine

2). Auscultate the Carotid arteries for bruits

a). If bruit present, do not palpate the carotid artery

b). If a cholesterol plaque is present, do not palpate the carotid

3). Palpate the carotid (if indicated) with index and third fingers by going to the thyroid cartilage and sliding laterally between the trachea and SCM (just medial to the SCM is the location).

4). Palpate low in the neck to avoid pressure on the carotid sinus

5). Evaluate the other artery (each artery separately)

Arterial Pulse – Evaluate the Characteritics of the Pulse

Contour and Amplitude is assessed:

1). Contour = Shape of the wave described as the speed of the upslope, speed of the down slope, and duration of the wave.

2). Amplitude = Graded 0-4

Other descriptors

1). Normal: Smooth with the upstroke steeper and more rapid than the down stroke.

2).Diminished: Small and weak

3). Increased: Large, Strong, hyperkinetic with increased rise of ascending limb and a brisk tap at the peak.

4). Double Peaked: Prominent percussion and tidal wave with or without a dicrotic wave.

Jugular Venous Pulse

The R internal jugular vein gives information about wave forms and R atrial pressure.

Jugular Venous Pulse – Determine the Jugular Wave Forms

Process of Finding the Pulse:

1). Patient lying flat and with trunk flexed 25 degrees (slightly elevated)

2). The head is turned to the right and down to relax the SCM

3). The doctor is on the R side

4). The doctor shines a light on the patient’s R neck

5). The doctor views the pulsation waves

Table 14-6 – Differentiation of Jugular and Carotid Wave Forms

Internal Jugular Pulse: Palpation: Not palpable…Wave forms: Multiform (2 or 3 components)…Quality: Soft, undulating…Pressure: Wave forms obliterated (light pressure on the vessel above the sternal end of the clavicle)…Inspiration: Decreased Height of wave forms…Sitting up: Decreased height of wave forms…Valsalva: Increased height of wave forms

Carotid Pulse = Palpation: Palpable…Wave forms: Single…Quality: Vigorous…Pressure: No effect…Inspiration: No effect…Sitting up: No effect…Valsalva: No effect

*** Know this chart for the exam and final ***

Chart of Pulse Types

Anacrotic = Description: Small, slow rising, delayed pulse with a notch or shoulder on the ascending limb…Cause: Aortic Stenosis

Waterhammer = Description: Rapid, sudden systolic expansion…Causes: Aortic Regurgitation

Bisferiens = Description: Double peaked pulse with a midsystolic dip…Causes: Aortic Regurgitation, Combined aortic stenosis and aortic regurgitation, Idiopathic hypertrophic subaortic stenosis

Alternans = Description: Alternating amplitude of pulse pressure…Cause = CHF

Paradoxical = Description: Detected by blood pressure assessment. An exaggerated drop in systolic blood pressure during inspiration…Cause = Tamponade, Constrictive Pericarditis, COPD

*** Know this chart for the exam, final and National Boards, particularly anacrotic, alternans and paradoxical as they have been mentioned several times in the textbook and in class ***

Jugular Venous Pulse – Estimate the Jugular Venous Pulse

*** This procedure was covered in Phys Dx. #2 Lab ***

When the height is equal to or lower than the sternal angle in the supine position the venous pressure is normal.

Jugular Venous Pulse – Evaluate the Hepatojugular Reflex

*** This procedure was covered in Phys Dx. #2 Lab ***

The tests assesses right ventricular function. Patients with RV failure have dilated liver sinusoids, so pressure over the liver forces blood into the vena cava and into the R side of the heart. The presentation manifests as dilated neck veins.

A). Normal Response = Slight distention of the neck veins during the 10 seconds of pressure, with a quick return to baseline in the last seconds of pressure

B). Abnormal Response = Increased distention of neck veins during and after the 10 seconds of pressure, with distention falling rapidly on sudden release of the compressing hand. A + test indicates right ventricular failure or elevated pulmonary artery wedge pressure.

Percussion – Percuss the Heart’s Borders

The heart is percussed at the 3rd, 4th, and 5th ICS from axillary line to axillary line.

A). Normal = A change in sound from resonance to dullness 6 cm lateral to the left of the sternum

B). Abnormal

1). Greater than 10.5 CM = Dullness greater than 10.5 cm from the L 5th ICS is sensitive for increased left ventricular end-diastolic volume, left ventricular mass or cardiomegaly

Palpation

Apical Impulse, RV, Pulmonary Artery, Left Ventricular Motion, Presence of Thrills, PMI (Point maximum impulse)

A). Thrills = Low frequency cutaneous vibrations associated with loud heart murmurs

B). PMI = Outward motion of the cardiac apex as it rotates counterclockwise as view from below, stroking the anterior chest wall during isovolumetric contraction.

Palpation – Palpate the PMI

Process:

1). Examiner on the R side of patient with the patient seated

2). Fingertips are used in the 5th ICS – MC line to assess local motion.

3). PMI is noted; if not present, move fingertips to cardiac apex.

4). If still not noted with the patient supine, have the patient assume the left lateral decubitus position

PMI is usually within 10 cm or midsternal line and no larger than 2-3 cm in diameter. Laterally displaced PMI’s indicates cardiomegaly. Pulses greater than 3 cm indicate increased left ventricular end diastolic volume and left ventricular enlargement.

In RV enlargement: The heart rotates clockwise and the PMI can be create by the RV instead of the LV. The RV impulse is more diffuse than the LV.

IN COPD: PMI moves down and to the right. The PMI is felt over the epigastric area at the lower end of the sternum.

IN COPD with normal PMI Location: Indicates cardiomegaly

Palpate for Localized Motion

The presence of a systolic impulse in the second ICS to the L of the sternum is suspect for pulmonary hypertension. This is attributed to the closure of the pulmonic valve under increased pressure.

Palpate for Generalized Motion

The doctor uses the proximal hand to palpate for:

A). Heave/lift = A large area of sustained outward motion.

B). R Ventricular Rock = Sustained left parasternal impulse associated with lateral retraction and Large R Ventricle

C). Second Impulse = Any condition that increased rate of ventricular filling during early diastole can produce a second palpable impulse after the main ventricular impulse. The impulse is felt over the PMI and felt with S3.

Palpate for Thrills

Thrills = Superficial vibratory sensations felt on the skin overlying an area of turbulence. The presence of a thrill indicates a loud murmur.

Auscultation

1). Bell = Lightly applied to the skin used for low pitched sounds such as gallop rhythms or murmur of AV stenosis,

2). Diaphragm = Pressed tightly on the skin and used to hear high pitched sounds like valve closure, systolic events, regurgitation murmurs.

Always inspect before auscultating.

Auscultation – Auscultate the Cardiac Areas

4 Areas to auscultate: 1). Aortic 2). Pulmonic 3). Tricuspid 4). Mitral

Dr. should determine presence of S3 or S4 at the apex and left lower sternal border.

Auscultation – The Standard Auscultation Positions

4 positions: 1). Supine 2). Left Lateral Decubitus 3). Upright 4). Upright, leaning forward

Process:

1. Pt. starts supine and all 4 areas (listed above) are auscultated.

2. The patient then flips into the left lateral decubitus position. The examiner listens to the ape for a low pitched diastolic murmur of mitral stenosis, best heard with the bell.

3. Patient then sits upright and all areas examined with the diaphragm

4. The patient is then asked to lean forward from the seated position. The patient exhales and holds breath. Doctor uses the diaphragm and listens for high-pitched diastolic murmur or aortic regurgitation at R and L second ICS.

Auscultation – The Influence of Breathing

Most murmurs originating in the R side of the heart ARE ACCENTUATED WITH RESPIRATION! This is due to the return of blood occurring with inspiration and increased RV output. S3 and S4 ARE ACCENTUATED DURING INSPIRATION!

Auscultation – Time the Cardiac Events

1). S1 = The sound that precedes the carotid pulse

2). S2 = Follows the carotid pulse

Table 14-7 Approach to Cardiac Auscultation

Supine: Evaluate: S1 (all areas), S2 (all areas), Systolic murmurs or sounds in all areas

Left Lateral Decubitus: Diastolic events at apex with bell of stethoscope

Upright: S1 (all areas), S2 (all areas), Systolic murmurs or sounds in all areas, Diastolic murmurs or sounds in all areas

Upright, leaning forward: Diastolic events at the base with the diaphragm of stethoscope

*** Know for the exam ***

Auscultation -- Describe Any Murmurs Present

Descriptions: 1). Timing 2). Location 3). Radiation 4). Duration 5). Intensity 6). Pitch 7). Quality 8). Relationship to respiration 9). Relationship to body position

1). Timing:

A). Holosystolic/Pancystolic Murmur = Murmurs occurring throughout systole, beginning with S1 and ending with S2.

B). Systolic Ejection Murmur = Murmur that begins after S1 and ends before S2.

C). Holodiastolic Murmur = Persists throughout the entire diastolic period

2). Location = Where is the murmur best heard

3). Radiation = Common locations are the axilla, neck, or back

4). Intensity = Graded 1-6, based on loudness

1 = Lowest intensity, often not heard by inexperienced listeners

2 = Low intensity, usually audible by inexperience listeners

3 = Medium intensity without a thrill

4 = Medium intensity with a thrill

5 = Loudest murmur that is audible when the stethoscope is placed on the chest…Associated with a thrill

6 = Loudest intensity: audible when stethoscope is removed from the chest. Associated with a thrill.

5). Quality = rumbling, blowing, harsh, musical, machinery, or scratchy.

The intensity of a murmur tells nothing about the severity of the clinical state.

Auscultation -- Describe Any Pericardial Rubs

Friction Rubs = Extracardiac sounds of short duration that have unique quality described as sandpaper scratching, resulting from irritation of the pleura (pleural rub) or pericardium (pericardial rub).

A). Pericardial Rubs: Have 3 components (1 systolic and 2 diastolic)

1). Systolic = Occurs during ejection

2). Diastolic = During Rapid filling and atrial contraction

Pericardial rubs are head best with patient sitting while holding breath in expiration. Pericardial rubs are made better when the patient sits forward. A rub that disappears while patient holds the breath is pleural.

Auscultation -- The Goals of Auscultation

1). Intensity of S1 in all areas 2). Intensity of S2 in all areas 3). Systolic Sounds 4). Diastolic Sounds

Normal = 1). S1 is loudest normally at the apex 2). S2 is loudest normally at the base 3). S2 split into A2 and P2 is best heard at the pulmonic area while patient is supine (supine position increases venous return and widens the split)

Examination for Edema

Pitting edema may be present from CHF

Examination for Edema – Test for Edema

Procedure:

1). Depress fingers into an area for 2-3 seconds

2). When fingers removed, the impression will remain (+ for pitting edema)

Edema is graded from 1+ to 4+ depending on how long pitting remains. Bedridden patients have edema in the sacrum

Clinicopathologic Correlations

Types of Pathology: 1). Abnormalities of S1 2). Abnormalities of S2 3). Systolic Clicks 4). Diastolic Opening Snaps 5). Murmurs

Abnormalities of the First Heart Sound – Abnormalities of the First Heart Sound

The intensity of S1 is based on: 1). Rate of rise of ventricular pressure 2). Condition of the Valve 3). Position of the valve 4). Distance of the heart from the chest wall

Scenarios:

1. Faster the rate of rise of LV pressure = Louder the Mitral sound of S1

2. Increased Contractility = Increases the sound of S2

3. Decreased Contractility = Softens S1

4. Mitral Stenosis = Louder S1 (initially)…As time progresses the valve becomes more calcified and the sound will later be more softly.

5. Shorter PR interval = Louder S1 Sound

6. Longer PR interval = Softer S1 Sound (Wienkebach)

7. Heart further from chest wall = Soft S1 sound

8. Obesity, COPD, Pericardial Effusion = Soft S1

Impact of Valve Position = Valve position at ventricular contraction impacts S1 intensity.

Arc of Coaptation = Angle through which the valve closes. Wider arc means louder S1. Wider arc corresponds to short PR interval on ECG. The short interval occurs because the ventricular contraction occurs quickly after atrial contraction. The mitral valve stays open longer and closes later than normal, accentuating S1.

Abnormalities of the Second Heart Sound – Abnormalities of the Intensity of the Second Heart Sound

S2 is changed by: 1). Changes in Systolic pressure 2). Condition of the valve

Scenarios:

1). Increased S2 = Increased systolic pressure (ex. Hypertension – raises aortic systolic pressure and causes a loud A2 and therefore increases S2 intensity)

2). Decreased S2 = Lowered Systolic Pressure (calcification of SL valves, fibrosis of the SL valves, or decreased BP)…Fibrosis of the SL valves due to anatomical makeup of the valves causes decreased sound vs. Fibrosis of the AV valves which causes increased sounds

Abnormalities of the Second Heart Sound – Splitting of the Second Heart Sound

Normally an S2 split should be present.

Abnormal Splits include widening, paradoxical and fixed splitting.

A). Scenarios for Widened Split: PULMONIC STENOSIS, RBBB, MITRAL REGURGITATION, VENTRICULAR SEPTAL DEFECT (VSD), PATENT DUCTUS ARTERIOSUS (PDA)

1). Delayed ventricular Systole/Delayed P2 = Widens S2 Split

2). R Bundle Branch Block/R Ventricular Emptying Delay = Widened Split of S2

3). Pulmonic delay of S2 during inspiration and expiration = Widened Split of S2

4). Shortened Left Ventricular Systole (Early A2) = Widened Split of S2

a). Examples of Shortened LV Systole = Mitral regurgitation, Ventricular septal defect, PDA (shortening S1 to A2)

1). In Ventricular septal Defect with L to R shunt = LV systole is shorter and RV systole is prolonged causing a VERY WIDE S2 SPLIT (via a “double whammy”)\

B). Scenarios for Paradoxical Split: AORTIC STENOSIS, LBBB

1). Delays in LV emptying = Paradoxical Split of S2

a). Examples = Left Bundle Branch Block, Aortic Stenosis, LV failure, Severe HTN, …both conditions delay closure of the aortic valve after RV systole and P2 wave causing a reversal of A2 – P2 sequence. Widened P2-A2 split during expiration (that normally shouldn’t occur) and is termed paradoxical.

C). Scenarios for Fixed Splitting of S2: ATRIAL SEPTAL DEFECT (ASD)

1). ATRIAL SEPTAL DEFECT (CLASSIC) = Fixed S2 split

A). The Fixed S2 split is wide and does not change with respiration. The mechanism for this is a shunt present from L to R that keeps the volume in the RA constant during respiration and therefore normal splitting does not occur

Systolic Clicks

Ejection Clicks = High pitched sounds that occur, early in systole at the onset of ejection and are produced by the opening of the pathologically deformed SL valves. Pulmonic or aortic stenosis produce ejection clicks. The clicks are best heard at their associated valves. Over time as the condition progresses, the clicks disappear as mobility of the valve decreases.

Midsystolic Clicks = Occurs in the middle of systole and can be single or multiple can change in position during the cardiac cycle. THE MOST COMMON CAUSE OF A MIDSYSTOLIC CLICK IS MITRAL OR TRICUSPID VALVE PROLAPSE!

Diastolic Opening Snaps

Opening Snap = Diastolic event that is the sound of a pathologically deformed AV valve. The sound is sharp and high pitched.

A). Mitral Opening Snap = Mitral stenosis occurring after A2

B). Tricuspid Opening Snap = Tricuspid Stenosis after P2

Severe Mitral Stenosis is characterized by a very short S2-OS interval. (The mitral valve opens earlier than normal due to pressure changes and as LV pressure drops below La pressure shortening the interval).

Murmurs

Types of Murmurs:

1). Blowing Murmurs: Produced by large gradients with variable flow volumes

2). Rumbling Murmurs: Result for areas of small gradients that are dependent on flow

3). Harsh Murmurs: Result from large gradients and high flow.

4). Ejection Murmur: Produced by turbulence across a semilunar valve during systole (ex. Aortic stenosis or pulmonic stenosis)…described as diamond shaped and “crescendo-decrescendo” beginning after S1 and ending before S2. The ejection murmur is medium pitched and best heard with the diaphragm of the stethoscope. Intensity does not indicate extend of pathology.

5). Regurgitant Systolic Murmurs: Produced by retrograde flow from a high pressure area back to a low pressure area during systole (ex. Mitral or tricuspid regurgitation). The murmur can be holosystolic/pansystolic beginning with S1 and ending after S2.

6). S3 murmur: Indicative of volume overload to the ventricle that is high pitched and best heard with the diaphragm. The S3 murmur is often called regurgitation, incompetence, and insufficiency. (Ex. Holosystolic AV valve regurgitation murmur)

7). Diastolic AV murmur: Begins after S2 with the opening of the AV valve. Ex. – Mitral Stenosis and tricuspid stenosis. There is a pause between S2 and the beginning of the murmur. The murmur is decrescendo in shape and begins with an opening snap. The murmur is low pitched and best heard with the bell with the patient in the L Lateral position. The murmur intensity is increased at the end of diastole/pre-systole in conditions of normal sinus rhythm.

8). Diastolic Semilunar Murmurs: Begin immediately after S2 and heard with aortic or pulmonic regurgitation. NO delay after S2 to the beginning of the murmur. The murmur is high pitched and decrescendo. The murmur is best heard with the diaphragm of the stethoscope with the patient sitting up and leaning forward.

Table 14-8 Cardiac Sounds

Early Systolic: Ejection Click, Aortic Prosthetic Valve

Mid-Late Systolic: Midsystolic Click, Rub

Early Diastolic: Opening Snap, S3, Mitral prosthetic valve opening sound, Tumor plop

Mid-diastolic: S3, Summation Gallop (with fast heart rates the diastolic period shortens and S3 and S4 are summated into a single sound called a summation gallop)

Late diastolic/Presystolic: S4, Pacemaker sound

Systolic Murmurs

Aortic Stenosis = Location: Aortic area…Radiation: Neck…Shape: Diamond…Pitch: Medium…Quality: Harsh…Associated signs: Decreased A2, Ejection Click, and S4, Narrow pulse pressure, Slow rising and delayed pulse

Mitral Regurgitation = Location: Apex…Radiation: Axilla…Shape: Holosystolic…Pitch: High…Quality: Blowing…Associated Signs: Decreased S1, S3, Laterally displaced diffused PMI

Diastolic Murmurs

Mitral Stenosis = Location: Apex…Radiation: No…Shape: Decrescendo…Pitch: Low…Quality: Rumbling…Associated Signs: Increased S1, Opening snap, RV rock, Presystolic Accentuation

Aortic Regurgitation = Location: Aortic Area…Radiation: No…Shape: Decrescendo…Pitch: High…Quality: Blowing…Associated Signs: S3, Laterally displaced PMI, Wide pulse pressure (cause for aortic regurgitation), Bounding pulses, Austin Flint murmur (apical diastolic murmur heard with aortic regurgitation that mimics mitral stenosis), Systolic ejection murmur (flow murmur across a valve that is narrow for the increased blood volume due to aortic regurgitation)

Table 14-9 Differentiation of Other Systolic Murmurs

Pulmonic Stenosis = Location: Pulmonic Area…Radiation: Neck…Shape: Diamond…Pitch: Medium…Quality: Harsh

Tricuspid Regurgitation = Location: Tricuspid area…Radiation: Right of sternum…Shape: Holosystolic…Pitch: High…Quality: Blowing

Ventricular Septal Defect = Location: Tricuspid area…Radiation: Right of Sternum…Shape: Holosystolic…Pitch: High…Quality: Harsh

Venous Hum = Location: Above clavicle…Radiation: Right neck…Shape: Continuous…Pitch: High…Quality: Roaring, humming

Innocent Murmur = Location: Widespread…Radiation: Minimal…Shape: Diamond…Pitch: Medium…Quality: Twanging, vibratory

CHAPTER 15 PERIPHERAL VASCULAR SYSTEM

General Considerations

The two most important disease of the peripheral arteries are atherosclerosis of large arteries and microvascular disease. The most common cause of peripheral arterial occlusive disease is atherosclerosis affecting medium and large vessels of the extremities. The abdominal aorta is a common site of aneurysm. An aneurysm larger than 5 cm has a 20% chance of rupture in 1 year and 50% chance of rupture in 5 years.

Microvascular disease is common to people with diabetes. Peripheral neuropathy is often a sequelae.

Peripheral venous disease can progress to venous stasis and thrombotic disorders.

Structure and Physiology

Upright posture = Venous pressure in the LE is highest.

Dilation of the veins occurs as a result of weakening of the walls of the veins. This affects venous closing. Blood pools and the venous pump is impaired. This mechanism causes venous stasis which leads to chronic venous insufficiency. Complications of venous insufficiency are: pigmentation, dermatitis, cellulitis, ulceration, and thrombus formation.

The most important clinical symptoms of lymphatic obstruction are lymphedema and lymphangitis.

Review of Specific Symptoms

Symptoms include: pain, changes in skin temp and skin color, edema, ulceration, emboli, stroke, and dizziness

Pain

Pain is a principal symptom of atherosclerosis.

Intermittent Claudication = Pain in the LE during exercise. Pain is often distal to the site of occlusion. Progression of the problem produces pain at rest. Pain at rest is worsened by cool temperatures and elevation.

Leriche’s Syndrome = Chronic aortoiliac obstruction presenting with intermittent claudication, buttock or thigh pain while walking and erectile dysfunction. The problem is usually an atherosclerotic plaque at the terminal aorta and iliac arteries.

Pseudocladification = Bilateral leg pain or numbness that occurs while walking or at rest. The problem is usually due to musculoskeletal problems in the lumbar area.

Skin Changes

Types:

A). Chronic Arterial Insufficiency = Causes cool, pale extremity

B). Chronic Venous Insufficiency = Makes extremities warmer than normal, erythematous, increased pigmentation, swelling, aching or heavy extremities, and dependent edema

C). Deep Vein Thrombosis = Warmth, redness, fever, pain, swelling (greater than 2 cm compared to the other side)

Edema

Lymphedema = Firm, non-pitting edema that is painless and often is attributed with “heaviness” of the extremity.

Ulceration

Persistent ischemia of a limb is associated with ischemic ulceration and gangrene.

A). Arterial insufficiency ulcers are painful, discrete edges and show a “punched out” appearance, crusted over and are rapidly developing

B). Venous Insufficieny Ulcers = Causes stasis ulcers that are painless, reddened, “cobblestone appearance”, slowly developing and typically located near the medial malleolus.

Emboli

Thrombus formation occurs because of stasis and hypercoagulability. The most important cause is thrombus formation.

Causes of Emboli and Thrombi: 1). Bed rest 2). CHF 3). Obesity 4). Pregnancy 5). Plane Travel 6). Oral contraceptives

Other Emboli and Symptoms:

1). Pulmonary Emboli = SOB

2). Splenic, Intestinal, Renal Artery Emboli = Abdominal Pain

3). Carotid or Vertebrobasilar Artery Emboli = Neurological Symptoms

4). Peripheral Artery Emboli = Pain and paresthesia

Neurologic Symptoms

Cerebrovascular Occlusive Disease = Strokes, Dizziness, Changes in consciousness

A). Internal Carotid Artery Occlusion = Contralateral hemiplegia, contralateral sensory deficits, and dysphasia

B). Vertebrobasilar Artery Occlusion = Diplopia, Cerebellar dysfunction, change in consciousness and facial paresis

Physical Exam

Inspection, Exam of arterial pulses, Exam of lymphatics, Other special techniques

Inspection – Inspect for Symmetry of the Extremities

Size, color, temperature, venous patterns

Inspection -- Inspect the Lower Extremity

Pigmentary abnormalities, ulcers, edema, venous patterns, cyanosis, pitting, bilateral color changes, swelling of legs

Inspection – Assess the Skin Temperature

Coolness = Commonly found with arterial insufficiency

Inspection – Inspection for Varicosities

Performed in standing…Inspect the femoral ring and distal legs

Examination of Arterial Pulses

The most important finding is an absent or decreased pulse. Radial, brachial, femoral, popliteal, dorsalis pedis and post tib are evaluated

Palpate the Radial Pulse

Timing and Strength

Palpate the Brachial Pulse

Should normally be stronger than the distal pulses….Waveform is assessed

Auscultate the Carotid Artery

Auscultation for bruits is performed with the diaphragm of the stethoscope with the patient supine, head slightly elevated and head turned opposite the side being examined. The arteries are palpated after the auscultation

Presence of murmur should be noted. A murmur can indicate atherosclerosis of the carotid.

Table 15-1 Characteristics of Physical Signs for Detecting an Abdominal Aneurysm

Definite Pulsatile Mass: Sensitivity (28%)….Specificity (97%)

Definite or suggestive pulsatile mass: Sensitivity (50%)…Specificity (91%)

Abdominal bruit: Sensitivity (11%)…Specificity (95%)

Femoral Bruit: Sensitivity (17%)…Specificity (87%)

Femoral Pulse Deficit: Sensitivity (22%)…Specificity (91%)

*** Just know the characteristics present in an AA and that these signs are specific ***

Palpate the Abdominal Aorta

A ruptured AA carries a mortality of nearly 90%. Even in those that reach the hospital, the mortality is 50%. The exam was performed by palpating deeply into the mid-abdomen. The presence of a mass with laterally expansive pulsation suggests an AAA. In AAA, findings can include a bruit, absent or diminished pulse and pain in the abdomen or back.

Rule Out Abdominal Bruits

1). Abdominal Aortic Bruit: Diaphragm of the stethoscope in the midline of the abdomen about 2 inches above the umbilicus.

2). Renal Bruit: A clue of renal artery stenosis…Performed about 2 inches above the umbilicus and 1-2 inches laterally to R and L of umbilicus

Abdominal bruits during systole are typically not important VS. Bruits present during systole and diastole imply Renovascular hypertension (very specific sign).

Palpate the Femoral Pulse

Assessed as the femoral artery runs obliquely through the corner of the pubic hair triangle inferior to the inguinal ligament at a point midway between the pubic tubercle and ASIS.

If one of the femoral pulses is absent or diminished, auscultation for bruit is necessary. The diaphragm is used to auscultate. The presence of a bruit indicate obstructive Aortoiliofemoral disease.

Rule Out Coarctation of the Aorta

Femoral and Radial pulses should peak at the same time. If not, the femoral should slightly precede the radial. A delay in the femoral pulse indicates coarctation of he aorta with hypertension.

Palpate the Popliteal Pulse

Palpate the Dorsalis Pedis Pulse

Best felt by dorsiflexion of the foot. The artery runs near the extensor retinaculum of the ankle to a point just lateral to the extensor tendon of the great toe (felt between the EDL tendon and EHL tendon)

Palpate the Posterior Tibial Pulse

Posterior to the medial malleoli. The pulse can be absent in 15% of normal people. The most sensitive sign of occlusive peripheral arterial disease is patients over 60 is the absence of post. tibial pulse.

Grading of Pulses

0 = Absent, 1 = Diminished, 2 = Normal, 3 = Increased, 4 = Bounding

Examination of Lymphatic System

Examine for palpable Lymph Nodes, Lymphangitis, Lymphedema…Some descriptions of nodes include painless, tender, single, matter.

1). Generalized Lymphadenopathy = Presence of palpable lymph nodes in 3 or more chains and can include lymphoma, leukemia, collagen vascular disorders, systemic bacterial viral or protozoal infection

2). Localized lymphadenopathy = Local infection or neoplasm

3). Lymphantitis = A llymphatic spread with red streaks on the skin

4). Lymphedema = Obstruction to lymphatic flow that creates a backup

Palpate for Epitrochlear Nodes

Elbow flexed to 90 degress and doctor palpates in the fossa bout 3 cm proximal to the medial epicodle of the humerus in the groove between biceps and tricpes. Size, consistency and tnedernssa are noted. Some cuaese of increased node size are acute nfections and non-Hodgkin’s lymphoma.

Other Special Techniques – evaluate Arterial Supply in the Lower Extremity

The most important sign of arterial insufficiency is a decreased pulse. Test Procedures:

1). Patient is supine and doctor elevates the patietn’s legs to 60 degrees.

2). The patient pumps the ankles to drain blood

3). The doctor inspects the foot for pallor at 60 seconds

Signs of Palor

Grade 1 = Definite Pallor in 60 seconds

Grade 2 = Pallor in 30-60 seconds

Grade 3 = Pallor ini less than 30 seconds

Grade 4 = Pallor without elevation

4). The doctor then drops the feet off the side of the table and assesses time for color to return

Time

Normal = 10-15 seconds for color to return with 15 seocnds for the superficial veins

Moderate Occlusive Disease = 15-25 seocnds for superficial veins to fill

Severe Ischemia = More than 40 seconds for color to return

Evaluate Capillary Refill Time n the Lower Extremity

Typically 3-5 seconds…Prologned refill time indicates arterial vascular insufficiency

Evaluate Artieral Supply in the Upper Extremity

Less common to have arterial insufficiency that in the lower extremity…Allen Test is used. The test checks the radial-ulnar loop Pallor of the palm during compression of one artery indicates occlusion of the other.

Test forIncompetent Saphenous Vein

Procedure:

1).Patient stands

2). Examiner compresses the proximal end of a varicose vein with one hand placing the other 15-20 cm below it at the distal end of the vein

3). Incompetent veins result in transmission of an impulse to the distal fingers.

Test for Retrograde Filling

Trendelenburg Maneuver: Assesses venous valvular competency of the communicating veins in the saphenous system.

Procedure:

1). Tourniquet is wrapped around upper thigh with patietn’s legs elevated 15-20 seconds (this occludes the saphenous vein and does ntot occlude the arterial pulse)

2). Patient stands whiel examiner watches for filling

3). The saphenous vein should fill from below in about 30 seocnds as he femore artery pushes blood through capillary bed into the venous system…Rapid filling fo superficial veins from above indicates retrograde flow through invompenetn valves of communicating veins.

4). After 30 seconds, tourniquet is released…any other filling indicates incompetent valves of the saphenous vein

Clinicopathologic Correlations

Signs of acute arterial occlusion: Pain, pallor, paresthesia, paralysis, pulselessness

Pathology

1). Diabetes Mellitus = Chronic progressive small vessel disease…

a). Necrobiosis Lipoidica Deabeticorum: Skin lesions that can present as waxy, yellow, reddish-bwon, sharply demarcated, plaquelike lesions found on the anterior surface of the lower legs. The lesions are shiny, atrophic and have mareked telangiectacsia with a tendency to ulnceate. The ulncers heal very slowly.

2). DVT = Unilateral swelling, venous distention, erythema, pain, incrased warm, and tenderness. The patient resists ankle dorsiflexion.

a). Femoral or Popliteal DVT = Cause calf or ankle swelling

b). Iliofemoral Thrombosisi = Thigh swelling

Homan’s Sign Squeezing of the calf or dorsiflexion of the ankle that creates pain. The test is linked with DVT’s. 3. Thrombophlebitis; Inflammation of a vein with fever, warmth, and erythema.

4). Pulmonary Embolism = DVT is associated with PE.

5). Raynaud’s = Associated with 3 color changes (white – palor, blue – cyanosis, red – rubor. Color changes are related wo areteirospasm and decreased blood supply (pallor), increased peripheral extraction of O2 (cyanosis), and return of blood supply (rubor). The patient may have numbness due to pallor or cyanosis. During the rubor stage, the patient may complain of burning paresthesia. Between the episodes, ther may be no symptoms or signs of the condition.

6). Gangrene = Necrosis of the deep tissues resulting from a decreased blood

Table 15-2 Precepitating Factors in Thromboembolism

Stasis: Arrhythmia, Heat failure, immobilization, obesity, varicose veins, dehydration

Blood vessel injury = Trauma, fracture

Increased Coagulatbility = Neoplasm, oral contraceptives, pregnancy, polycythemia, prevsiou thromboembolism

Table 15-3 Differential Diagnosis of Raynaud’s Diease and Raynaud’s Phenomenon

Raynaud’s Disease = Sex: Female…Bilaterality: Present (often symmetrical)…Precipitated by cold: Common…Ischemic Changes: Rare…Gangrene: Rare…Disease Association: No

Phenomenon = Sex: Female…Bilaterality: Asymmetrical..Precipitated by cold: Increases Symtpoms…Ischemic Changes: Common…Gangrene: More commonly seen…Disease associtation: Yes

Table 15-4 Differential Diagnosis of the Main Vascular Diseases Causing Gangrene

Diabetes = Age: Any…Sex: Either…Onset: Gradual…Pain: moderate…Distal Pulses: May be absent

Atherosclerosis = Age: Older than 60…Sex: Either…Onset: Gradual…Pain: Moderate…Distal Pulses: May be absent

Thromboangitis Obliterans = Age: Youner than 40…Sex: Male…Onset: Gradual…Pain:Severe…Distal Pulses: May be absent

Raynaud’s = Age: Younger than 40…Sex: Female…Onset: Gradual…Pain: Moderate…Distal Pulses: Present

Arterial Embolism = Age: Any…Sex: Either…Onset: Sudden…Pain: Often Severe…Distal Pulses: Absent

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