Cardiovascular Flashcards
Bate's Book
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.
Systole
ventricular contraction
AP open, MT closed
Diastole
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.
Preload
;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.
Afterload
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
JVP
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.
ACS
Acute myocaridal ischemia, USA, NSTEMI, STEMI.
Acute Aortic dissection
Tearing ripping chest pain radiating to back/neck.
Palpitations
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.
SOB
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.
Edema
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.
HTN
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 inHTN lifestyle modifications
optimal wt, BMI 18.5-24.9, Salt less than 6grm.day 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
Crescendo
grows louder.
Ex presystolic murmur of MS
Decrescendo
grows softer
Ex. early diastolic murmur of AR
Crescendo-decrescendo
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.
Intensity
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
- quiet, heard immediately
- moderately loud
- load with thrill
- Very loud, thrill, may be heard with stethescope partly off chest
- Very loud, thrill, heard with stesthescope off chest.
Pitch
high, medium, low
Quality
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
Diastasis
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.
S3
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.
S4
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.
PDA
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
AR
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.
AS
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
MR
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).
MVP
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
MS
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.
