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Flashcards in Cardiovascular Deck (81):

Bisferiens Pulse

Increased arterial pulse with a double systolic peak. Causes include AR, combined AS/AR, and HOCM.


Pulsus Alternans

Amplitude from beat to beat even though the rhythm is basically rregular, with stronger alternating with weaker beat. Indicates LVF usually accompanied by left sided S3. Felt best with light pressure to radial or femerol arteries. Use BP cuff, pump up, lower slowly to systolic level, initial Korotkoff sounds strongest beats, as you lower cuff, weaker alternating beats heard. Upright position may accentuate alternans.


Paradoxical Pulse

Palpable decrease in pulse's amplitude on quiet inspiration. SBP decrease of more than 10mmHg. Causes include pericardial tamponade( inc JVP, rapid/dim pulse, dyspnea), constrictive pericarditis, and obstructive lung disease( most commonly).


Semilunar valves

Aortic and Pulmonic


Atrioventricular valves

Mitral and Tricuspid


PMI/ Apical Impulse

Diameter 1-2.5cm. Greater than 2.5cm is evidence of LVH or enlargement. Displacement of PMI lateral to MCL or greater than 10cm lateral to the MSL also suggests LVH or enlargement.



ventricular contraction
AP open, MT closed



ventricular relaxation
AP closed, MT open


Electrical conduction

SA-AV-bundle of His-purkinje fibers- myocardium


Electrical vectors

positive- approaching lead, + deflection
negative- traveling away from lead, - deflection
isoelectric- straight line


P wave

atrial depolarization: P 80ms, PR 120-200 ms


QRS complex

ventricular depolarization, up to 100ms
Q wave- downward deflection- septal depolarization
R wave upward deflection- ventricular depolarization
S wave, downward deflection following R wave.


T wave

ventricular repolarization or recovery


Cardiac Output

amount of blood ejected in 1 minutes time from each ventricle. Product of HR and stroke volume. Stroke volume is amount of blood ejected with each beat.



;load that stretches cardiac muscle before contraction. Volume of blood left in RV at end of diastole= preload for next beat. RV preload is increased by increasing venous return to right heart. Increased blood volume in a dilated RV of CHF also causes increased preload. Physiologic causes of increased preload are inspiration and increased blood volume that ensues from exercising muscles. Decreased RV preload include exhalation, decreased LV output, pooling of blood in capillary bed o the venous system.


Myocardial contractility

ability of cadiac muscle, when given a load, to shorten. Contractility increases when SNS stimulated. Contractility decreased when blood flow or oxygen delivery to myocardium impaired.



degree of vascular resistance to ventricular contraction. Sources of ventricular resistance include aortic wall tone, large arteries, peripheral vascular tree as well as volume already in aorta.


Heart Failure

increased preload- volume overload
increased afterload- pressure overload



estimates RA pressure= CVPand RVED pressure. Estimated from RIJ vein. JVP affected by volume status, R/L ventricular function, patency of T/P valves, pressure in pericardium, arrhythmias(Jx, AV blocks). Elevation causes: RHF, constrictive pericarditis, TS, SVC obstr.


JVP measurement

HOB 30 degrees. highest oscillation point of RIJ, extend ruler from this point to sternal angle and measure. JVP above 4cm, or 9cm above RA. If hypovolemic, may need to check flat and if hypervolemic, may need to check at 60-90 degrees.


Health History

CP, SOB, Palpiatation, Edema


Health Promotion

HTN, CHD/Stroke, HPL, promote lifestyle modifications and risk factor reduction.


Chest Pain

signals angina. Classic CP is exertional, pain/pressure, discomfort in chest/shoulder/back/neck/arm- seen 50% of AMI. Atypical CP: cramping, grinding, prickling, jaw/tooth pain.



Acute myocaridal ischemia, USA, NSTEMI, STEMI.


Acute Aortic dissection

Tearing ripping chest pain radiating to back/neck.



Skipping, racing, fluttering, pounding, stopping of heart beat. Causes irregular heart beat, Not with VT.Can happen with AFib, PVC's, SVT, ST greater than 120 BPM.



dyspnea- difficult breathing
orthopnea- dyspnea while supine, improves when sits up. Causes- LV HF, MS, Obst. LD.
PND- suddenly awakens dypneic, usually 1-2 hrs after going to bed. A/w wheezing, coughing. Recurs nghtly. PND in LV HF or MS may be mimicked by noctural asthma attacks.



Accumulation of excessive fluid in EV IS space. Dependent edema occurs in renal and hepatic disease. Periorbital puffiness, tight rings with nephrotic syndrome, enlarged waistline from ascites and liver failure.
IS tissue can absorb several liters of fluid, accomodates up to 10% weight gain before pitting edema appears.



Normal- less than 120/80
Pre HTN- SBP 120-139, DBP 80-89- lifestyle modification
Stage 1- SBP 140-159, DBP 90-99- initiate anti-HTN drug.
BP target for pts with DM and CKD is less than 130/80.


HTN risk factors

physical inactivity, microalbuminuria, GFR less than 60mL/min, family Hx of premature CHD, excess dietary Na, insufficient dietary K, excess ETOH.


CAD/stroke screening

start screening at age 20. Screen before first event because any event could be fatal. Family Hx CHD, Smoker, diet, ETOH, physical activity, BP, BMI, waist circumference, pulse, fasting lipid and glucose.


Dyslipidemia risk factors

smoker, BP above 140/90, on anti-HTN, HDL less than 40 mg/dL, family Hx CHD.


Metabolic syndrome indicators

Trig above 150 mg/dL
HDL M less than 40 mg/dL
F less than 50 mg/dL
BP above 130/85
Glucose above 110 mg/dL
Waist M above 40 in, F above 35 in


HTN lifestyle modifications

optimal wt, BMI 18.5-24.9, Salt less than or 2.4 grm Na/day, Regular aerobic exercise 30 minutes almost daily, Moderate ETOH- 2drinks M, 2 drink F. 3500 dietary K. Diet rich in fruits, vegetables, low fat dairy, reduced sat fat and total fat.


CHD/stroke prevention

smoking cessation, BP control, healthy diet, lipid mngmt, regular aerobic, DM mngmt, convert afib.


elevated JVP

Increased LVED pressure and low LVEF.


JVP pulsations

a wave- precedes S1. x descent seen with systolic collapse. v wave almost coincides with S2. y descent follows. Look for absent/prominent waves.
prominent a wave- increased resistance to RA contraction- TS, 1st degree AV bock, SVT, Jx, Pulm HTN, PS.
absent a waves= afib
large v waves= TR, constrictive pericarditis


Murmur timing

Systolic/Diastolic, when loudest, positioning to hear best, shape of murmur(crescendo etc), Intensity(1-6), quality of S1, S2, or extra sounds: S3, S4, snap.


Midsystolic murmur

after S1 and stops before S2. Brief gap audible between M and heart sounds. Usually M across semilunar valves(A/P)


Pansystolic/Holosystolic murmur

Starts with S1, stops at S2, no gaps between murmur and heart sound. Often with regurg(backward flow) across AV valves(M/T)


Late Systolic murmur

starts mid- or late systolic and continues to S2. M of mitral valve prolapse- often preceded by systolic click


Early Diastolic murmur

starts immediately after S2, no gap, fades into silence before next S1. Usually accompany regurg flow across incompentant semilunar valves


Middiastolic murmur

starts after S2, may fade away or merge into late diastolic murmur. Middiastolic and presystolic murmurs refelct turbulent flow AV valves


Late Diastolic(Presystolic) murmur

starts late diastolic and typically continues up to S1



grows louder.
Ex presystolic murmur of MS



grows softer
Ex. early diastolic murmur of AR



first intensity rises, then falls
Ex. midsystolic murmur of AS and innocent flow murmur.


Plateau murmur

Pansystolic murmur
Ex. MR


Location of Maximum intensity

Site where murmur originates, where is murmur heard best.


Radiation/Transmission from point of max intensity

Not only radiation from site of origin but intensity of murmur and direction of blood flow, explore area around murmur and determine where else heard.
Ex. Loud AS often radiated to neck(direction of blood flow), esp right side.



6 point graded scale. Influenced by chest wall thickness, intervening tissue. Degree of turbulence may make murmur louder in a thin person vs muscular/obese person. CPOD- may diminish intensity of murmurs


Grade of murmur

1- faint, may not be heard in all positions
2. quiet, heard immediately
3. moderately loud
4. load with thrill
5. Very loud, thrill, may be heard with stethescope partly off chest
6. Very loud, thrill, heard with stesthescope off chest.



high, medium, low



blowing, harsh, rumbling, musical
Murmurs originiating on right side of heart vary more with respirations than left sided murmurs,


Squatting vs standing

Identify MVP, distinguish CMO from AS
When standing venous return to heart, PVR, BP, SV, volume blood in LV- all decrease. when squatting pressures reversed. P393 Bates


HOCM murmur

only systolic murmur that increase intensity during Valsalva- strain phase- squatting.


LV Impulse: Hyperkinetic

Cause: Anxiety, Hyperthyroid, sev anemia
location: normal
diameter: abt 2 cm, may inc amplitude- may it seem larger
amplitude: more forceful tapping
duration: <2/3 systole


LV Impulse: Pressure Overload

Causes: AS, HTN
location: norm
diameter: >2cm
amplitude: more forceful tapping
duration: sustained- up to S2


LV Impulse: Volume Overload

causes: AR, MR
location: displaced to left, maybe downward
diameter: >2cm
amplitude: diffuse
duration: often slightly sustained


RV Impulse: Hyperkinetic

causes: anxiety, Hyperthyroid, sev anemia
location: 3-5 LICS
diameter; not useful
amplitude: slightly more forceful
duration: normal


RV Impulse: Pressure Overload

causes: PS, pulm HTN
location: 3-5 LICS, also subxiphoid
diameter: not useful
amplitude: more forceful
duration: sustained


RV Impulse: Volume Overload

causes: AS defect
location: left sternal border- extending to left cardiac border, also subxiphoid
diameter: not useful
amplitude: slightly to markedly more forceful
duration: norm to slightly more sustained.


Early Diastole

SL valves closure, followed by isovolumetric relaxation ( Normally no flow)


Mid Diasdtole

AV valves open, rapid passive flow



pause between periods of rapid flow, minimal inflow


Atrial Systole

active atrioventricular transport, retrograde pulmonary venous flow


Early Systole

AV valves close followed by isovoulmetric contraction (normally no flow), LV depolorarized and contracts before RV


Mid Systole

SL valves open, Systolic ejection, LA filing


Pathological split S1

Delayed closure of tricuspid valve with RBBB


Pathological split S2

P2 closure is delayed d/t reduced back pressure on valve during inspiration and increased ventricular filling volume causing longer systole. Conduction changes- LBBB. Pressure changes- PS, Pulm HTN, massive PE, AS defect, adv AS(delayed LV emptying, also paradoxical loss of physiologic split)
A2 loud, P2 soft.



Low pitched 3rd heart sound, large volume late vent filling before systole. Best heard left lat decub, with bell at apex.
Causes: LV dysfunction, MR, normal.



Low pitched passive filling on a stiff noncompliant ventricle during late diastole as atria start to contractin systole. Best heard with bell at apex in LLD position.
Causes : HOCM, bicuspid Ao valve.



Continuous flow from Ao to pulm artery.


Ao murmurs

Combined stenosis and regurg still have discrete systolic and diastolic components


Physiologic Split S2

After deep breath split can be heard P2 closes later than aortic valve d/t increased pulmonary complaince during inspiration. Inspiration draws more blood into right heart chambers which increases ventricular output into more complaint lungs. Expiration inhibits right heart filing and enhances heart filing by exerting + pressure on lungs



Carotid pule is prominent, wide pulse pressure. Pulse may have mid systolic dip- resulting in bisfeiens pulse. Diastolic backflow through an incompetent AV causes lower diastolic pressure in Ao, and increases diastolic volume in LV, which increases SV and systolic arterial pressure. The increased aortic outflow causes a midsystolic murmur (CD) ending well before S2. The regurgitant flow begins immediately with aortic valve closure, causing a blowing, decrescendo early diastolic murmur (C). Best heard at 3 LICS, leaning forward. Mild AR may early diastolic murmur- holosystolic up to S1- sounds like whispered r.
The visibly bounding arterial pulse (Corrigan's pulse) may also be noted in peripheral sites, such as brachial and femoral arteries. In severe cases, head-bobbing (Musset's sign) and alternate blanching and reddening of the lightly compressed nailbed (Quincke's pulse) may be seen. S1 may be absent.



2 RICS. rough murmur followed by distinct sound(S2). Murmur with pulse upstroke, sounds near peak of pulse, murmur is systolic. Pulse peak delayed (with S2), murmur not holosystolic- ends before S2.
Harsh MSM, diamond shaped (CD). Sounds like knuckles on a table. Murmur ceases as forward flow diminishes before reversing course to close valve. Pause between murmur and S2. Duration o systole in prolonged delaying A2. With more severe AS, LV pressure gradient increases, murmur peaks later. Loud ES/click heard even if AV partially moile. ES may be mistaken for split S1 or S1



Usually well tolerated with miniimal HD effects. Unless valve becomes incompetent suddenly (endocarditis, chordal/papillary rupture, LV fxncompromised by ischemia/HTN) then disabilty ensues. PMI best site to listen with bell. Apex beat displaced to 7th LICS, outward excursion during systole, a/w blowing murmur. Mimicks wow-duh or wow. Occupies all fo systle/holosystolic murmur, obscures S1/S2. The duh sound is seperated from murmur by a pause, therefore is mid diastolic. All of systole, reflecting the driving force of the pressure difference between the LV and atrium that is initiated as the LV pressure rises at the onset of systole and greatly exceeds left atrial pressure throughout systole.
MR results in volume overload in LA/LV. LV needs to increase SV to compensate fro volume lost across incompentant MV. Chamber complaince increased over time, greater volume. Blowing holosystolic murmur, mid diastolic rumble as blood returns to ventricle.
Causes of chronic MR: HYN, LV diastolic dysfunction(hypertrophy, ischemia), LV systolic dysfxn(ischemia, infarction, CMO).



The redundant posterior leaflet moves into the left atrium, causing a click in mid systole from the inflation of the posterior leaflet and a late systolic murmur from trivial mitral regurgitation resulting from loss of apposition of the mitral leaflets.


3 Atrial waves in SR

the a-wave results from atrial contraction
the c-wave results from closure of the A-V valve
the v-wave results from atrial filling during ventricular systole



subtle carotid pule in notch. int/ext JVP, JVP biphasic. A wave prominent- RVH d/t pulm HTN-MS Listen with diaphram at 2LICS. Load S1. Mitral valve closes later in systole. After the 2nd sound, there is a distinct, crisp extra sound which is the opening snap (OS) of the stenotic mitral valve. This sound can be distinguished from a split second sound (A2-P2) by

1) the wider interval between S2 and the opening snap, and

2) the sharper character of the opening snap compared to P2.

The S2-OS interval is approximately 80 milliseconds, and can be emulated saying "lup butter," adding an additional syllable to the normal heart's "lup dup."
At apex can hear OS, MDM, PSM, Load S1. Gap before S2.