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angina pectoris
acute chest pain that occurs when myocardial demand exceeds its o2 supply
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aortic regurgitation
aka aortic insufficiency. incompetent aortic valve that allows backward flow of blood into left ventricle during diastole.
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aortic stenosis
calcification of aortic valve cusps that restricts forward flow of blood during systole
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aortic valve
the L semilunar valve. separates L ventricle and aorta.
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apex of the heart
tip of heart pointing down toward the 5th ICS
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apical impulse
aka point of maximal impulse, PMI. pulsation created as the L ventricle rotates against the chest wall during systole, normally at the 5th ICS in the MCL.
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base of the heart
broader area of the heart's outline located at the 3rd R and L ICS.
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bell (of stethoscope)
cup-shaped endpiece used for soft, low-pitched sound
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clubbing
bulbous enlargement of distal phalanges of fingers and toes that occurs with chronic cyanotic heart and lung conditions.
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coarctation of aorta
severe narrowing of the descending aorta, a congenital defect of the heart
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cor pulmonale
right ventricular hypertrophy and heart failure due to pulmonary hypertension
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cyanosis
dusky blue mottling of the skin and mucous membranes due to excessive amt of reduced hemoglobin in blood
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diaphragm (of stethoscope)
flat endpiece used for hearing relatively high-pitched heart sounds
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diastole
heart's filling phase
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dyspnea
difficult, labored breathing
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edema
swelling of legs or dependent body part due to increased interstitial fluid
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Erb's point
traditional auscultatory area in 3rd L ICS
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first heart sound (S1)
occurs with closure of AV valves, signaling beginning of systole
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fourth heart sound (S4)
aka S4 gallop, atrial gallop. very soft, low-pitched, ventricular filing sound that occurs in late diastole
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gallop rhythm
the addition of a 3rd or 4th heart sound, makes the rhythm sound like cadence of galloping horse
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inching
technique of inching stethoscope across precordium thru auscultatory areas while listening to heart sounds
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LVH (left ventricular hypertrophy)
increase in thickness of myocardial wall that occurs when the heart pumps against chronic outflow obstruction, e.g., aortic stenosis
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mitral regurgitation
aka mitral insufficiency. incompetent mitral valve allows regurgitation of blood back into L atrium during systole
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mitral (L AV valve) stenosis
calcified mitral valve impedes forward flow of blood into L ventricle during diastole
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palpitation
uncomfortable awareness of rapid or irregular heart beat
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paradoxical splitting
opposite of a normal split S2 so that the split is heard in expiration, and in inspiration the sounds fuse to one sound
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pericardial friction rub
high-pitched scratchy extracardiac sound heard when the precordium in inflamed
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physiologic splitting
normal variation in S2 heard as two separate components during inspiration
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precordium
area of chest wall overlying the heart and great vessels
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pulmonic regurgitation
aka pulmonic insufficiency. backflow of blood thru incompetent pulmonic valve into the R ventricle
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pulmonic stenosis
calcification of pulmonic valve that restricts forward flow of blood during systole
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pulmonic valve
R SL valve, separating the R ventricle and pulm artery
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second heart sound (S2)
occurs with closure of the SL valves, and signals the end of systole
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summation gallop
abnormal mid-diastolic heard sound heard when both the pathologic S3 and S4 are present
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syncope
temporary loss of consciousness due to decreased cerebral blood flow (fainting), caused by ventricular asystole, pronounced bradycardia, or ventricular fibrillation
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third heart sound (S3)
soft, low-pitched, ventricular filling sound that occurs in early diastole (S3 gallop) and may be an early sign of heart failure
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thrill
palpable vibration on the chest wall accompanying severe heart murmur
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tricuspid valve.
bicuspid
R AV valve
L AV valve
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precordium
area on anterior chest overlying the heart and great vessels
reminder: the "precordial thump" from CPR
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What is the mediastinum?
Where is it located?
- what: midthoracic cavity that contains the heart and great vessels
- where: 2nd to 5th ICS, R sternal border to L MCL
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Where is the apex of the heart?
What should you suspect if the apex is located more lateral?
- 5th ICS, 7-9 cm L of midsternal line (at approximately MCL)
- If apex extends past MCL (i.e., is more lateral) --> heart is enlarged/hypertrophied; sign of disease.
reminder: apex of heart is inferior to base, apices of lungs are superior.
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How is heart rotated in the chest? (which side posterior, which anterior?)
Right side is mostly anterior, L is mostly posterior
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What are the structures (layers) of the heart tissue?
- pericardium
- epicardium
- myocardium
- endocardium
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pericardium
attached to vessel, esophagus, sternum and pleura; anchored to the diaphragm. Heart sits in pericardial sac that must be cut through to get to the heart in surgery
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pericardium
outside layer (but deep to pericardium)
heart sits in pericardial sac that must be cut through to get to heart in surgery
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myocardium
middle, muscle layer of heart. Thickest on L ventricle
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endocardium
inside lining of heart, in chambers and valves. Electrical system embedded within
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Valves
-multidirectional or uni?
-active or passive opening and close?
unidirectional, passive open and close
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AV valves
- L: mitral / bicuspid
- R: tricuspid
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Chordae tendinea
attach AV vales to papillary muscles and provide stability to valves during systole (when AV valves are open). rupture of them (as can happen in severe MI) may be life threatening b/c failed valves = immediate death
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Which two systems in the heart work together to pump blood?
- conduction - electrical system that initiates and conducts heart beat (b/c electricity causes muscle contraction)
- hemodynamic - moves blood thru heart and vessels, depends on pressure changes
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Which layer of the heart houses the electrical pathway of the heart?
endocardial
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intrinsic pacemaker of heart? normal rate of firing?
trace route of electrical conduction in heart.
SA node is pacemaker. Normally fires at 60-100 bpm
SA node --> AV node --> Bundle of His --> Perkinje fibers
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Brief description of ECG.
P, PR interval, QRS complex, T, U
- P: depolarization of atria. Spread of stimuli thru atria. Is SA node not firing, no P wave is present.
- PR: time b/w stimulation of atria to stim of ventricles
- QRS: depolarization (i.e., contraction) of ventricles. Spread of stim thru ventricles.
- T: repolarization of ventricles. Resting phase. *Repolarization = *Rest
- U: final ventricular repolarization. Not always seen on ECG
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Trace flow of blood from lower body and from upper body throughout the heart and lungs.
Lower (including abd): inferior vena cava --> RA --> R AV valve / tricuspid valve --> pulmonic / R SL valve --> pulmonic arteries --> lungs/alveoli --> pulmonary veins --> LA --> L AV valve / mitral / bicuspid valve --> LV --> aortic / L SL valve --> aorta --> body
Upper (head and neck): superior vena cava ... rest is same as lower body.
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What causes backflow? Why?
How can you recognize this on the R side of heart? On the L?
Excessively high atrial pressures because no valves between L atrium and pulm veins or between R atrium and venae cavae.
On R: Blood back flows into veins of neck and PV system --> distended neck veins and peripheral edema
On L: Blood back flows into lungs --> pulm congestion (e.g., crackles/rales)
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Normal amt of blood pump thru body / min? What is this called?
Normal stroke volume?
- Cardia output. CO ~= 4-6 L/min.
- SV ~=70 ml/beat
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Factors that could affect stroke volume?
Definition of SV?
- dehydration
- bleeding
- fluid overload
SV: amt of blood ejected by L ventricle with 1 heart beat
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preload
aka LVEDV: L ventricular end diastolic vol
increased LV vol causes more stretch on myocardial muscles fibers at end of diastole. --> > stretch = stronger muscle contraction.
goal is maximize preload (vol) in order to maximize LV contraction and CO. But excessive preload leads to decreased CO and HF.
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Frank Starling's Law
the greater the stretch of muscle fibers (compliance), the stronger the contraction. why preload is a good thing (up to a point).
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afterload
aka?
def'n?
problems of excess?
causes?
aka SVR (systemic vascular resistance) or PVR (peripheral vascular resistance)
definition: opposing pressure the ventricle must generate to open aortic valve during systole.
excessive afterload increases myocardial workload and O2 consumption
causes: arteriosclerosis, HTN, SNS stim, excess ETOH intake
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What produces heart sounds?
On which side of the heart are they loudest? Why?
- Produced by closing of valves.
- Louder on side of heart (mitral > tricuspid, aortic > pulmonic) b/c takes more force to move blood to periphery from L side
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Valve sites (sites for clearest auscultation of valves)
- aortic - 2nd ICS, R sternal border
- pulmonic - 2nd ICS, L sternal border
- erb's - 3rd ICS, L sternal border (good location for referred sounds, for picking up on murmurs)
- tricuspid - 4th ICS, L sternal border
- mitral - 5th, MCL
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How to auscultate for heart sounds
- 1. listen to all sites with diaphragm AND bell
- 2. listen for aortic murmurs (with pt sitting and leaning forward is best
- 3. listen for extra heart sounds (L lateral decubitus (i.e., sidelying) position is best)
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S1
- AV valves close (mitral and tricuspid)
- SL valves open (aortic, pulmonic)
- diastole ends, systole begins
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S2
- aortic/pulmonic valves close
- mitral/tricuspid valves open. begins with rapid filling phase, then atrial kick.
- systole ends, diastole begins
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what is atrial kick?
if there is ventricular resistance to the atrial kick, what will you hear?
- atrial kick: atrial contraction that ejects last 25% of SV into ventricles
- S4
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What's a gallop?
- extra heart sound.
- e.g., S3, S4
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S3
- S1--------S2, S3
- ken-------tuc/ky
- indicates ventricular resistance to early passive filling
- in early diastole
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What could cause an S3?
- decreased ventricular compliance (early sign of HF)
- high output conditions like hyperthyroid, pregnancy
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S4
- S4, S1----------->S2
- ten/nes-----------see
- indicates ventricular resistance to filling during atrial kick
- in late diastole, immediately before S1
- causes: HTN, increased afterload
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summation gallop
having S3 and S4
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murmur
definition?
causes?
- def'n: blowing/swooshing sound that occurs with turbulent flow thru valves or great vessels
- causes:
- -increased velocity (exercise)
- -decreased viscosity (thin blood)
- -decreased volume (anemia)
- -defective valves (forward or back flow)
- -septal defects
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stenotic murmurs
- -occur when valve is open
- -stiff valves prevent adequate forward flow
- -cause harsh murmur
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regurgitant murmurs
- -occur when valve is closed
- -aka insufficiency
- -results in backward flow due to poor valve closure
- -turbulent sound
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2 pss causes of systolic murmurs?
How do you determine which you're hearing?
when are they heard?
- -aortic/pulm stenosis (when SL valves open)
- -mitral/tricuspid insufficiency/regurgitation (when AV valves closed)
- -discern by auscultating for where murmur is loudest
heard in systole, after S1
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2 pss causes of systolic murmurs?
When are they heard?
- -mitral/tricuspid stenosis (AV valves open)
- -aortic/pulm regurgitation (SL valves closed)
heard in diastole, after S2
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holodiastolic
holosystolic
description of murmurs.
holod: b/w S2 and S1
holosys: b/w S1 and S2
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innocent murmur
- aka functional murmur
- not r/t valve, cardiac, or other pathology
- common in childhood d/t increased blood flow
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pss chest pain etiologies
- cardiac - angina, MI, valve prolapse
- pulmonary - pneumonia, pleurisy (inflamed pleura that surround lungs)
- pericardial - pericarditis
- musculoskeletal/chest wall - costochondritis, arthritis
- GI - ulcer, hernia, esophagitis, indigestion
- neurotic - anxiety
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myocardial ischemia
imbalance b/w o2 supply and demand --> therefore, more common with exercise
should resolve in a couple min with rest and/or tx (NTG/nitroglyercin) --> may progress to an MI if not treated
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MI sx
similar to angina/myocardial ischemia, diaphoresis, n/v, palpitations, sense of impending doom
atypical: SOB (esp. in women), sharp chest pain, fatigue
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CAD risk factors
- age (>=45 if male; >=55 or postemenopausal if female)
- HTN or HTN tx
- smoking
- hyperlipidemia
- diabetes
- family history of premature CAD in 1st degree relative (male <55, female <65)
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types of shortness of breath
- dyspnea
- DOE = dyspnea on exertion
- PND = paroxysmal nocturnal dyspnea (classic sx of HF)
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what to ask about re: past hx r/t HF
- cholestrol level
- murmurs
- congenital heart disease
- rheumatic fever
- swollen joints
- heart surgery
- last ECG
- stress test (ETT) results
- family hx (HTN, CAD, DM, obesity, congential heart disease, genetically transmitted diseases)
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personal habits to ask about re: HF
- diet (high fat, sodium)
- smoking (b/c it vasoconstricts)
- ETOH (increases afterload)
- exercise (increases HDL, myocardial muscle tone)
- medications (digitalis, diuretics, beta blockers, Ca channel blockers)
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in assessing jugular venous distension and jugular venous pressure at what angle should the HOB be raised? which side of the neck should you inspect?
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what is normal JVD?
3-4 cm above sternal angle
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why is JVP useful? what is it? what is it normally?
- estimate of RA pressure
- JVP = JVP + 5 cm (distance of RA from sternal angle)
- norm: <= 9 cm H20
p.s. I have no idea what cm h2o means, but it's in the lecture notes.
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where is the PMI? is it always palpable?
4th or 5th ICS, L MCL. palpable in ~1/2 adults
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heave / lift
- sustained forceful thrusting of ventricle during systole
- sign of enlarged heart
- visualized and palpable at apex
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thrill
- palpable vibration
- sign of heart murmur, esp. loud, harsh ones
- palpate across precordium at each valve site
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