Chapter 14 outline Flashcards by Danielle Hayes

Between what costal cartilage is the heart located?

behind the sternum between 3rd and 6th costal cartilage

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What is the top and bottom of the heart called?

base (top) bottom (apex)

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What is it called when your heart is positioned to the right instead of the left?

dextrocardia

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if the heart and stomach are on the right and liver on the left it is called?

situs inversus (rare)

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What is the double-walled fibrous sac with fluid in between the walls = low friction movement

pericardium

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What is the outermost layer of heart

epicardium

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What is the muscle layer responsible for pumping?

myocardium

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What lines the chambers of heart and covers heart valves?

endocardium

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Name the layers of the pericardium from outermost to inner most?

Epicardium ->Myocardium -> Endocardium

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Name the four chambers of the heart, their thickness and what they do?

2 X atria (thin walled)-house blood returning from veins

2 X ventricles (thick walled) pump blood into arteries

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The left and right chambers of the heart are separated by (blank), which is impenetrable to blood

interventricular septum

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What are the two types of important valves of the heart and what do they do?

Atrioventricular
• Tricuspid = between right atrium and right ventricle
• Bicuspid/Mitral = between left atrium and left ventricle

Semilunar
• Pulmonic = between right ventricle and pulmonary artery
• Aortic = between left ventricle and aorta

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Where is the tricupsid located?

between right atrium and right ventricle

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Where is the bicuspid/mitral valve located?

between left atrium and left ventricle

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Where is the pulmonic valves located?

between right ventrical and pulmonary artery

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Where is the aortic valve located?

between left ventricle and aorta.

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What happens during systole?

ventricles contract to eject blood into arteries ( aortic and pulmonary)

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What happens during diastole?

atria contract to get blood into ventricles

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During the S1 what do you hear and what happens?

lubb, tricuspid and mitral valves CLOSE as ventricle contracts

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During the S2 what do you hear and what happens?

dubb  aortic and pulmonic valves CLOSE when ventricle is empty
• 2 components (not always distinguishable):
o A2 and P2
A2  aortic valve closes = happens first
P2  pulmonic valve closes = happens second

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During the S3 what happens?

sound of blood rushing from atria to ventricles = not always heard

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During S4 what happens?

atria fully contract to make sure no blood is left in atria = also not always heard

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What is the path of impulse for a ECG?

SA (sinoatrial) Node -> AV (atrioventricular) Node -> Bundle of His -> Purkinje Fibers in ventricles

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What does the ECG path of impulse allow for and how does the ventricular contraction move?

Atria contract before ventricles and contraction begins at apex and moves toward the base

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What are ECG waves based on?

 Based on depolarization and repolarization of cardiac myocytes

Describe the ECG waves

 P Wave  atrial depolarization  PR interval  time in between atrial depolarization and ventricular depolarization  QRS complex  ventricular depolarization  ST segment and T wave  ventricular repolarization  U wave  small deflection seen after T wave  QT interval  time between onset of ventricular depolarization and completion of ventricular repolarization=pretty much systole

explain the path of blood flow for infants

• Umbillical cord  Liver  Right Atrium  Right Ventricle OR Left Atrium via foramen ovale

In an infant, if the blood moves to the right ventricle then it will move by way of (blank), cuz lungs arent functional. What if it moves to the left atrium?

o If it goes to right ventricle -> ductus arteriosus instead of pulmonary artery b/c lungs aren’t yet functional -> joins aorta and goes to rest of body o If it goes to the left atrium ->l eft ventricle -> aorta

In an infant, are the atria and ventricles the same size?

yes

when does the ductus arteriosus and foramen ovale CLOSE?

at birth

By age (blank), ventricles are twice the size of the atria

Heart is more (blank) until age 7

horizontal

What type of women have increased plasma volume by 50% until 30 weeks and returns to normal after delivery?

pregnant

Do pregnant women have increased cardiac output? | By how much?

yes | 30-40% and peaks about 30 weeks and returns to normal after delivery

What is significant about heart size in old people? What is significant about the valves and SA node? What happens to the myocardium?

decreases unless there is hypertension or heat disease the left ventricle thickens can fibrose or calcify becomes stiff

What will you see on an ECG of an old person?

o Blocks, wave abnormalities, premature systole, left ventricular hypertrophy, or atrial fibrillation

Overall, what can you say about the heart of an older person?

• Efficient at resting levels BUT poor response during stress/exercise

What should you ask your patient if he/she complains about chest pain?

``` onset and duration character location severity symptoms treatment fatigue cough difficulty breathing loss of consciousness ```

If a child complains of chest pain what should you look for? pregnant woman? old person?

* With children specifically  look for fatigue, shortness of breath, joint pain, and preferring to squat instead of sitting * With pregnant women specifically  look for dizziness when standing, shortness of breath (dyspnea), fainting (syncope) * With old people specifically  look for confusion, dizziness, palpitations, coughs and wheezes, chest tightness, leg edema

If a pnt complain of chest pain, ask about PMH for what?

 Cardiac surgery?  Any rhythm disorder of the heart?  Any rheumatic fever or swollen joints?  Any chronic illnesses such as hypertension, hyperlipidemia, diabetes, thyroid problems, coronary artery disease, congenital heart issues?

What are common differential diagnoses of chest pain?

 Angina Pectoris  pressure or choking pain that relays to neck, happens more after strenuous exercise or in the cold, specific time of onset, relief with nitroglycerin  Musculoskeletal  history of trauma, vague onset, relief with NSAID’s  Gastrointestinal  history of indigestion, vague onset, relief with antacids

When you are inspecting the heart, where do you look for the apical impulse?

chest moves up at 5th intercostal space on left side | • Harder to see when obese or have large breasts

If you cannot find heart sounds then what problems could result?

could be extracardiac problem = problem with pleural or pericardial fluid

You should inspect skin and nail bed for (blank)

cyanosis

What is the normal capillary refill time?

2 seconds

When you palpate, where should you start?

at the apex, move up left border, move towards sternum, move down toward right border

When you palpate, what should you feel for?

apical impulse (if too forceful, could be increased cardiac output or left ventricle hypertrophy)

If the apical impulse is displaced to the right, it may be signs of (blank)

dextrocardia

If the apical impulse is faint it may be a sign of (blank)

pericardial or pleural fluid problem

What is the apical impulse indicative of?

What else should you palpate for other than the apical impulse?

Feel for the thrill -> fine, rushing vibration in 2nd intercostal space • If you can feel it = aortic or pulmonary stenosis, pulmonary hypertension, or atrial septal defect

While feeling for the apical impulse, you should also feel for pulse in (blank)

carotid artery (medial neck region)

Why do you percuss the heart?

to find the borders of heart (sound will change to resonant to dull at border)

What 5 areas should you ausucultate?

* aortic valve (2nd right intercostal space along sternum) * Pulmonic Valve  second left intercostal space along sternum * Second pulmonic area  third left intercostal space along sternum * Tricuspid area  fourth left intercostal space along sternum * Mitral area  fifth left intercostal space along midclavicular line

It is always louder at the (blank) of the heart and softer at the (blank)

apex, base

This is for which S? Ask patient to hold breath upon expiration • Louder at apex, quieter at base • Possible for splitting to occur (because there are 2 valves – tricuspid and mitral) but RARE • If too loud  blood velocity is increased o Anemia, fever, hyperthyroidism, anxiety, exercise • If too soft  possible blockage o Increased overlying fat, systemic or pulmonary Htn, fibrosis and calcification of mitral valve

This is for which S? Ask patient to inhale deeply and try to hear split S2 (best heard in pulmonic valve area) o With the splitting, A2 (aortic) is before P2 (pulmonic) o Easier to detect in young patients o Possible Pathology  Wide Splitting  delay in split = pulmonic stenosis or pulmonary Htn  Fixed Splitting  unaffected by respiration = septal defects  Reversed Splitting  P2 before A2 = heard during expiration instead of inspiration • Louder at base, quieter at apex • If too loud  o Systemic or pulmonary Htn • If too soft  o Increased overlying fat, aortic or pulmonic stenosis

This is for which S's Here it sometimes, don’t hear it other times = it just depends • S3 is very quiet b/c it is atrium passively filling the ventricle o Sounds like Ken-TUCK-y • S4 is the atrium forcefully contracting to fill ventricle o Often times confused with a Split S1 because it occurs at the end of diastole (right before S1 is supposed to occur) o Sounds like TEN-nes-see o When loud  ALWAYS indicative of pathology • Both are louder in left lateral decubitus position

 For S3 and S4

``` What occupies both systole and diastole • 3 distinct components contribute to sound: o Atrial systole o Ventricular systole o Ventricular diastole  More distinct at APEX  Cause? • Inflammation of pericardial sac causes roughening of parietal and visceral surfaces ```

pericardial friction rub

 CLICK sound early in diastole |  More distinct at APEX

Prosthetic mitral valve

 CLICK sound early in systole

prosthetic aortic valve

(blank) is a term used to define the failure of the mitral and tricuspid valvs or the pulmonic and aortic valves to close simulataneously.

splitting

fixed splitting is unaffected by (blank)

respiration

fixed splitting is unaffected by (blank)

respiration

paradoxic splitting occurs when closure of the aortic valve is (blank)

delayed

paradoxic splitting occurs when closure of the aortic valve is (blank)

delayed

o For the valves, sound depends on material used for prosthetic  Animal tissue =  Pacemaker = NO SOUND

QUIET

o For the valves, sound depends on material used for prosthetic  Animal tissue =  Pacemaker = NO SOUND

QUIET

What are heart murmurs?

 Prolonged heart sounds that usually sound like “whooshing”  Could have backflow of blood due to faulty valve  regurgitation

What are heart murmurs?

 Prolonged heart sounds that usually sound like “whooshing”  Could have backflow of blood due to faulty valve  regurgitation

What is the most common cause of heart murmurs?

anatomic disorder of heart valves

What is the most common cause of heart murmurs?

anatomic disorder of heart valves

What are these causes of? • 1) Increased speed of blood flow (could be from anemia or pregnancy) • 2) Structural defects that reroute blood flow (myocardial septum defect) • 3) Weak contraction • 4) Blockage in blood flow of vessels near heart (such as aorta) • 5) Aortic valve stenosis • 6) Ruptured chordae tendineae in mitral valve • 7) Forceful left ventricle contraction (more common in children) • 8) Obstructive diseases in cervical arteries  atherosclerotic carotids OR fibromuscular hyperplasia

heart murmurs

What is the difference between benign and innocent heart murmurs?

innocent, particularly in children or young athletes = NO structural anomaly at all even though benign may have one

What is the difference between benign and innocent heart murmurs?

innocent, particularly in children or young athletes = NO structural anomaly at all even though benign may have one

How are heart murmurs characterized?

 1) Timing and Duration  ex: Early systolic = begins with S1, decrescendos, and ends before S2  2) Pitch  can be high, medium, or low  High pitch = use diaphragm, low pitch = use bell  3) Intensity  5 Grades of “loudness”  4) Pattern  Crescendo or decrescendo  5) Quality  what does it sound like?  6) Location and Radiation  sound usually transmitted in direction of blood flow from the affected valve!  7) Respiratory  does breathing change it?

How are heart murmurs characterized?

• Narrowed mitral valve = obstructed flow from left atrium to left ventricle • Often seen with mitral regurgitation • Causes? Rheumatic fever OR cardiac infection • Findings o Low-frequency diastolic o Heard at apex o Palpable thrill o S1 is increased  makes sense because this valve needs to close to produce S1 sound!

mitral stenosis

• Narrowed aortic valve due to calcification • Causes? Rheumatic heart disease OR atherosclerosis • Findings o Mid-frequency midsystolic o Heard at left sternal border o Palpable thrill o S2 is very quiet or absent  make sense because this valve needs to close to produce S2 sound and it can’t close properly due to calcification 

aortic stenosis

``` • Fibrous ring inferior to aortic valve • Can become worse with time • HARD to differentiate this from aortic stenosis • Findings o Fills systole o Heard at apex o Palpable thrill o Multiple waves felt at apical impulse o Split S2, hear S3 and S4 ```

Subaortic Stenosis

``` • Narrowed pulmonic valve • Cause? Congenital! • Findings o Mid-frequency Systolic o S1, ejection click, soft or absent S2 o Palpable thrill o Radiates into neck ```

pulmonic stenosis

``` • Narrowed pulmonic valve • Cause? Congenital! • Findings o Mid-frequency Systolic o S1, ejection click, soft or absent S2 o Palpable thrill o Radiates into neck ```

pulmonic stenosis

• Narrowed tricuspid valve due to calcification • Causes? Rheumatic heart disease OR congenital OR endocardial fibroelastosis (thickening of heart chambers b/c of too many elastic fibers = RARE) • Findings o Diastolic o Resembles mitral stenosis BUT louder on inspiration o Palpable thrill over right ventricle

tricuspid stenosis

• Incompetent mitral valve = backflow from left ventricle to left atrium • Causes? Rheumatic fever, myocardial infarction, rupture of chordae tendineae (small tendons that hold heart valves in place) • Findings o High-frequency Holosystolic = hear it throughout whole systole = after S1 until S2 o VERY loud = may mask S2 sound! o Heard best at apex, radiates to left axillary region

mitral regurgitation

• Efficient in early systole BUT prolapses into atrium in late systole = some blood flows back into left atrium! • Can become more severe and lead to mitral regurgitation • Findings o LATE systolic o Often preceded by “clicks” o Heard best at apex when patient is UPRIGHT, not supine

mitral valve prolapse

• Incompetent aortic valve = backflow from aorta to left ventricle • Causes? Rheumatic heart disease, Marfan syndrome, cardiac trauma, syphilis o.O • Findings o High-frequency early diastolic  But can also hear low-frequency version = Austin-Flint murmur o Heard best at apex when patient is sitting upright and leaning forward

Aortic Regurgitation

• Incompetent pulmonic valve = backflow from pulmonary artery to right ventricle • Causes? Pulmonary hypertension OR bacterial endocarditis • Findings o Almost impossible to distinguish from aortic regurgitation with just physical exam

pulmonic regurgitation

• Incompetent tricuspid valve = backflow from right ventricle to right atrium • Causes? Pulmonary hypertension, bacterial endocarditis, cardiac trauma, or congenital • Findings o Holosystolic just like mitral regurgitation!  How to differentiate? • Heard at lower left sternal border rather than apex • Look for pulmonary hypertension by feeling an impulse over second left intercostal space • ALSO P2 (part of split S2) should be accentuated to try and compensate

Tricuspid Regurgitation

if an infant has right sided heart failure it will show signs of an (blank)

enlarged liver that is pushed inferiorly

if an infant has right sided heart failure it will show signs of an (blank)

enlarged liver that is pushed inferiorly

apical impulse shifted to right

diaphragmatic hernia

apical impulse shifted to right

diaphragmatic hernia

murmurs and tachycardia are common for the first 48 hours of infants lifes, they are typicall (blank)

systolic

murmurs and tachycardia are common for the first 48 hours of infants lifes, they are typicall (blank)

systolic

apical impulse shifted to right

dextrocardia

apical impulse shifted to right

dextrocardia

in, infants S2 has a high pitch and splitting is common, S3 and S4 can be heard ... T or F

This is normal in who?  Sinus arrhythmia  fast HR upon inspiration, slow HR upon expiration = NORMAL  Heart rates can change quickly with stress or temperature change

Children

This is normal in who?  Sinus arrhythmia  fast HR upon inspiration, slow HR upon expiration = NORMAL  Heart rates can change quickly with stress or temperature change

Children

Does heart rate decrease or increase with age?

decrease

Does heart rate decrease or increase with age?

decrease

Most heart murmurs in children result from what?

congenital problems or rheumatic fever

Most heart murmurs in children result from what?

congenital problems or rheumatic fever

Who is this heard in?  Increased blood volume and heart rate • Hear split S1 and S2, along with S3 (late in pregnancy) but NO S4  Heart is shifted upwards so apical impulse is also shifted upwards  Systolic murmurs are common in the pulmonic area  Should NOT see cyanosis

pregnant women

``` Who am I describing?  Try not to make them change positions to often  Heart Rate = Low 40’s to low 100’s  Apical impulse is harder to find  S4 is common! ```

old people

 Infection of endothelial layer of heart and valves  Pathology More common with valve defects OR when on IV drugs  Symptoms  fever, fatigue, murmur, CHF  Findings  Neurologic dysfunction, Janeway lesions (small hemorrhaging on palms and soles), Osler nodes (septic emboli on tips of fingers and toes)

bacterial endocarditis

 Decrease in pulmonary or systemic circulation  Pathology -> less flow to tissues, left or right sided, when diastolic -> because of too much glycated collagen = ventricles can’t dilate = happens with older diabetics that has not been well controlled  Symptoms -> fatigue, shortness of breath, edema  Findings ->Systolic = narrow pulse pressure, diastolic = wide pulse pressure

congestive heart failure

 Inflammation of pericardium  Pathology  May lead to cardiac tamponade  Symptoms  Sharp chest pain aggravated by movement  Findings  Hear a friction rub

pericarditis

 Too much fluid in the pericardial sac  Pathology  hard for heart to relax, impairs access of blood into the heart, caused by pericarditis or trauma  Symptoms  anxiety, chest pain, shortness of breath, discomfort when moving, lightheadedness (syncope), pale skin, rapid breathing, palpitations, edema!  Findings  Beck’s triad (heart sounds are muffled, hypotension, jugular venous distention)

cardiac tamponade

 Enlargement of right ventricle b/c of pulmonary malfunction  Pathology  chronic, usually caused by COPD = leads to pulmonary Htn = stress on right ventricle = hypertrophy = BAD!  Symptoms  fatigue, cough  Findings  wheezes and crackles, distended neck veins, cyanosis, loud S2

Cor pulmonale

 Ischemic necrosis caused by blockage in flow to myocardium  Pathology  usually affects left ventricle, caused by atherosclerosis and thrombosis  Symptoms  Deep pain that radiates to neck, jaw, and arm, can be mild in older patients = bad because it goes unnoticed!  Findings  Dysrhythmias, S4 is present, distant heart sounds

myocardial infarction

 Inflammation of the myocardium  Pathology  results from infectious agents, toxins, or autoimmune disorders such as amyloidosis  Symptoms  fatigue, fever, palpitations, shortness of breath  Findings  cardiac enlargement, murmurs, tachycardia

myocarditis

 Problem with conduction of nerve impulses throughout heart  Pathology  Can be ischemic, infiltrative, or rarely neoplastic, can be caused by certain drugs (ex: antidepressants)  Symptoms  transient weakness, syncope (fainting), rapid or irregular heartbeat

conduction disturbances

Syncope is caused by what?

``` CANADA  Cardiac (valve stenosis)  Arteriovenous  Nervous (autonomic problem)  Anemia  Drugs (alcohol, poisons, and diabetes as well)  Altitude ```

o Atrial contraction: ventricular contraction  4:1 (should be 1:1) =too much contraction

atrial flutter

slow heart rate between 50 and 60 bpm -> not necessarily a problem

sinus bradycardia

irregular atrial contraction

atrial fibrillation

slow hear rate b/c disruption of conduction signal between atria and ventricles

heart block

o Usually paroxysmal (transient) and due to some stimulus to the atria that is separate from the SA node  high heart rate

atrial tachycardia

o High heart rate (>200 bpm), usually suggestive of heart failure = BAD prognosis 

ventricular tachycardia

o Irregular ventricular contraction = BAD prognosis = may precede sudden death

ventricular fibrillation

 We’re back to the overall 20 abnormalities!  Arrhythmia caused by malfunction of SA node  Pathology  secondary to hypertension, atherosclerosis, or rheumatic heart disease  Symptoms  fainting, dizzy, seizures, palpitations  Findings  Dysrhythmias as seen above! Can lead to CHF

sick sinus syndrome

 4 cardiac defects  ventricular septal defect, pulmonic stenosis, dextroposition of aorta, right ventricular hypertrophy  Pathology  need surgical correction after first spell  Symptoms  dyspnea (shortness of breath), exercise intolerance, poor growth, can have SPELLS (paroxysmal dyspnea, loss of consciousness, central cyanosis)  Findings  systolic murmur, if not treated can lead to clubbing of fingers and toes, precordial prominence

tetralogy of fallot (infants and children only)

 Infants and children ONLY  Opening between left and right ventricles  Pathology  30-50% close on their own within first 2 years of life  Symptoms  recurrent respiratory infections, if large VSD  poor breathing and growth, can lead to CHF  Findings  arterial pulse is small, holosystolic loud murmur

Ventricular septal defect (VSD) Infants and children

Infants and children ONLY  Failure of ductus arteriosis to close at birth  Pathology  blood destined for pulmonary arteries goes to aorta too = stress on right ventricle  Symptoms  if small, no symptoms. If large, dyspnea (shortness of breath) when exerted  Findings  harsh, continuous murmur, wide pulse pressure

patent ductus anteriosis

 Infants and children ONLY  Congenital defect in division between left and right atria  Symptoms  usually asymptomatic but possible for adults to develop CHF  Findings  brief diastolic murmur, wide split S2

atrial septic defect

 Systemic connective tissue disease occurring after STREPTOCOCCAL infection or skin infection  Pathology  lots of stuff  usually problems with mitral or aortic valve leading to stenosis, most common between age 5 and 15  treatment is antibiotics  Symptoms  fever, inflammation of joints, rash, chest pain, palpitations, fatigue, dyspnea  Findings  murmurs that usually show mitral or atrial regurgitation, friction rub, CHF  Remember that this is the cause of A LOT of murmurs! Detect early and you’re good  • To differentiate this, run an antibody test for the strep bacteria

Infants and children only!!! Acute rheumatic fever

 Infants and children ONLY  Inflammation of arteries throughout the body, including coronary arteries  Pathology  affects lymph nodes, skin, and mucous too, usually affects children under age of 5  Symptoms  high fever, conjunctivitis (inflammation of eyelids), inflamed lips, lymphadenopathy, erythema (redness of skin), joint pain, tachycardia  Findings  diagnosis is made if most of the above symptoms are seen!

kawasaki disease

 Caused by deposition of cholesterol and lipids on arterial walls  Pathology  leads to thickening of vascular wall = narrowing of lumen = less blood flow  Symptoms  angina, dyspnea, palpitations  Findings  family history is common, see dysrhythmias and CHF

atherosclerotic heart disease (old people)

OLD PEOPLE ONLY  Already went over this! Leaky mitral valve = blood flow from left ventricle into left atrium  Symptoms  dyspnea, edema, decreased exercise tolerance  Findings  high pitched murmur radiating to axilla, may hear S3

mitral regurgitation

 Old People!  Pain caused by myocardial ischemia  Pathology  occurs when your cardiac myocytes are receiving less O2 than they require!  Symptoms  pain radiating to neck, jaw, and left arms, dyspnea, fatigue, syncope, diaphoresis (excessive sweating)  Findings  not definitive  see hypertension, tachycardia, and diaphoresis. Look at risk factors and see if patient has them  COPD, HTn, abnormal pulsations

angina

Old People!  Deposition of Amyloid (a fibrillary protein produced by chronic inflammation or a neoplastic disease) into heart  Pathology  reduced heart contraction, possible CHF  Symptoms  palpitations, edema, fatigue, low exercise tolerance  Findings  Arrhythmia, dilated neck veins, hepatomegaly, thickened ventricles

senile cardiac amyloidosis

 Old People!  LAST ONE   Thickening and calcification of aortic valve  Usually asymptomatic except for midsystolic murmur

aortic sclerosis