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PD Block 2 > Cardiac and Peripheral Vascular > Flashcards

Cardiac and Peripheral Vascular Flashcards

1
Q

pulmonic valve

A
  • semilunar valve
  • between RV and pulmonary artery
  • trileaflet
  • S2 (dub) -> when closes (end of systole)
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2
Q

aortic valve

A
  • semilunar valve
  • between LV and ascending aorta
  • trileaflet
  • S2 (dub) -> when closes (end of systole)
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3
Q

precordium

A

the area of the chest/thorax overlying the heart

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4
Q

tricuspid valve

A
  • right AV valve
  • between RA and RV
  • opens in diastole
  • trileaflet
  • S1 (lub) -> when closes (end of diastole)
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5
Q

mitral valve

A
  • left AV valve
  • between LA and LV
  • bileaflet
  • S1 (lub) -> when closes (end of diastole)
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6
Q

preload

A

end diastolic volume (in LV)

  • amount of ventricular stretch at end of diastole
  • balloon: blow air in, more air blow in, greater the stretch
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7
Q

afterload

A

resistance against which ventricles must pump (indicative of how much effort ventricles must put forth to force blood into systemic circulation (increased by pulmonic/aortic stenosis, ht., high PR)
-balloon: knot at end of balloon (to get air out, balloon must work against the knot)

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8
Q

S3

A
  • gallop

- possible sound of ventricle refilling during diastole

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9
Q

S4

A
  • gallop

- contraction of atria to insurance all blood was drained into ventricles

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10
Q

murmur

A

An ausculatory sound, benign or pathologic, loud or soft. Relatively prolonged extra sounds heard during systole or diastole. Caused by some disruption in the flow of blood into, through, or out of heart.

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11
Q

PMI

A
  • Point of Maximal Impulse
  • The point on the chest where the impulse of the left ventricle is felt most strongly.
  • 5th intercostal space midclavicular line.
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12
Q

Thrill

A

A vibration felt by an examiner on palpation, Fine, palpable murmur, often, but not Always over the base of the heart. Palpable murmur.(grade 4/6)

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13
Q

Heave/lift

A

Are sustained palpable movements of localized areas of the precordium due to increased intensity of systolic contraction o fone or more cardiac chambers.

  • lift: RV hypertrophy
  • heave: more pronounce life
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14
Q

situs inversus

A

condition in which the organs of the chest and abdomen are arranged in a perfect mirror image reversal of the normal positioning.

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15
Q

dextrocardia

A

Location of the heart in the right side of the thorax. The Apex pointing to the right.

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16
Q

gallop

A
  • an auscultatory finding of three or four heart sounds, created by gushes of blood entering resistant or stiffened ventricles.
  • This can happen at two different times during ventricular diastole: either at initial filling or at the time of ventricular contraction. Therefore, gallops occur during early and late ventricular diastole.
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17
Q

rub

A
  • Inflammation of the pericardial sac causes a roughening of the parietal and visceral surface, which produces rubbing “machine-like” sound.
  • This is widely heard sound, though clearest toward the Apex.
  • May occupy all of systole and diastole.
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18
Q

click

A
  • MITRAL VALVE PROLAPSE
  • heard during mid/late systole
  • usually accompanied with late systolic murmur indicative of mitral regurgitation
  • heard best with diaphragm apex (and left sternal boarder)
  • Extra heart sound.
  • Ejection clicks are high-pitched sounds that occur at the moment of maximal opening of the aortic or pulmonary valves.
  • They are heard just after the first heart sound.
  • The sounds occur in the presence of a dilated aorta or pulmonary artery or in the presence of a bicuspid or flexible stenotic aortic or pulmonary valve
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19
Q

snap

A
  • opening of AV values (mitral/tricsupid) usually silent
  • thickening or deformities of the leaflets occur (rheumatic heart disease) a sound generated in diastole = opening of heart valves.
  • opening snap = classic finding in mitral valve stenosis
  • if valve calcifies, may no longer be able to hear opening snap

-a short, sharp, high-pitched click occurring in early diastole and caused by opening of the mitral cusps, a characteristic sound in mitral stenosis.

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20
Q

ejection sound

A
  • opening of semilunar valves (aortic/pulmonic) usually silent
  • abnormal dilation or calcification of the aortic and pulmonic valves can cause an abnormal early systolic ejection sound as they open during systole
  • aortic ejection sounds: do not vary with respiration
  • pulmonic ejection sounds: decrease with intensity during inspiration

-click like sounds during ejection from a hypertensive aorta or pulmonary artery or associated with stenosis (particularly congenital) of the aortic or pulmonic valve.

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21
Q

electrical conduction system of heart

A

SA node (right wall of right atrium) -> AV node (atrial septum) ->bundle of HIS ->perkinje fibers (heart cells specialized for electrical condition, located in ventricular myocardium)

-ventricular contraction initiated at the apex and proceeds towards base of heart

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22
Q

where is aortic valve?

A

2nd right ICS

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23
Q

where is pulmonic valve?

A

2nd and 3rd left ICS

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24
Q

where is Erb’s point?

A

3rd left ICS

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25
Q

where is tricuspid valve?

A

4th left ICS/LLSB

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26
Q

where is mitral valve?

A

4th or 5th left IVS in MCL

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27
Q

what 4 things do you listen for in heart?

A

heart sounds, rate, rhythm, regularity

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28
Q

what is tape measure for in heart exam?

A

PMI to sternum, aortic diameter in abdomen

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29
Q

levine’s sign

A

clutching hand in fist over chest

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30
Q

signs of acute cardiac distress

A

cyanosis, diaphoresis, pallor, cool temp, difficulty breathing, anxiety, Levine’s sign

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31
Q

sign of chronic heart issues

A

clubbing, xanthelasma, obesity or correction (underdeveloped lower extremities)

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32
Q

is percussion helpful in cardiac exam?

A

no

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33
Q

cardiac exam: bell vs diaphragm

A
  • bell: bruits

- diaphgram: heart sounds

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34
Q

where can S1 best be heard?

A

over apex of heart (diaphragm)

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35
Q

where can S2 best be heard?

A

left and right ICS (diaphragm)

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36
Q

physiologic splitting

A
  • normal
  • splitting of S2 (A2 and P2)
  • NORMAL: during deep inspiration, the decrease in intrathoracic pressure causes an increase in venous return (This causes the right atrium and ventricle to fill slightly more than normal, and it takes the ventricle slightly longer during systole to eject this extra blood. This delay in ejection forces the pulmonary valve to stay open a bit longer than usual, and the normally small difference between aortic and pulmonary valve closure becomes noticeable as a split S2)

-during expiration, aortic part of second heart sound (A2) and the pulmonic component of second heart sound (P2) are separated by

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37
Q

auscultation of chest (upright or supine?)

A
  • listen with both bell and diaphragm in both upright and supine positions
  • also let lateral decubitus (bell over mitral area: brings hear closer to chest wall to heart S1 and mitral valve murmurs better)
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38
Q

pathologic splitting (name 2 types)

A

fixed and paradoxic splitting

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39
Q

fixed splitting

A

Splitting is fixed when it is unaffected by respiration. This occurs with delayed closure of pulmonic valve when output of the RV is greater then that of left. (causes: atrial septal defects, ventricular septal defect, RV failure)

A splitting of sounds A2 (aortic component of 2nd heart sound) and P2 (pulmonic component of 2nd heart sound) that is wide and
there is no variation between respirations. This could be heard in atrial septal defect and right ventricular failure.

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40
Q

paradoxic splitting

A

When aortic valve is delayed. (Left bundle block) heard during expiration and disappears during inspiration.

During respiration there is a delay in the closure of the aortic valve (A2) creating an inconsistent movement of A2 and P2. The sounds are separate during expiration and sound closer together during inspiration. This could be heard with a left bundle branch block.

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41
Q

presentations of chest pain

A
  • Many differential diagnoses for chest pain not just CV!
  • Angina pectoris- pressure or choking sensation sub- sternal &/or into neck, jaw.
  • Levine’s sign= ischemic pain.
  • When assoc w/ breathing= called pleuritic chest pain.
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42
Q

presentation of fatigue

A

-Worse w/ exertion, unable to keep up w/ peers, persistent, chronic hypoxia, body working hard to compensate

43
Q

presentation of dyspnea

A

-difficult and labored breathing with shortness of breath, worse with exertion, better with rest (propped up with pillows), increases with severity of pulmonary and CV disease

44
Q

presentation of diaphoresis

A

-often with anxiety, sympathetic response to stress (seen in MIs)

45
Q

presentation of syncope

A
  • fainting, temporary loss of consciousness, brief lack of blood flow to brain
  • associated with palps, exertion, dysrhymia, etc (commonly seen with hypovolemia, low BP, bradycardia, valve stenosis)
46
Q

presentation of cyanosis

A

-blueness, due to hypoxia, nails first (peripheral cyanosis occurs first then works centrally), periorbital

47
Q

presentation of cough

A

-dry, wet, nighttime, worse lying down, maybe associated with valvular disease

48
Q

presentation of orthopnea

A

-SOB that starts with lying down, relieved by sitting or standing (ask pt if they sleep propped up), associated with HF

49
Q

presentation of claudication

A

-pain, burning, fatigue in legs/butt, occurs with walking and better with rest, symptom of narrowing of artery or blockage-

50
Q

presentation of paroxysmal noctural dyspnea

A

-Sudden onset of shortness of breath after a period of sleep, issues with pulmonary function related to CV disease, congestion, better w/ sitting up

51
Q

presentation of xanthelasma

A

-cholesterol deposits (seen around eyelids and extensor surfaces of joints) or yellowish deposit of fat under skin

52
Q

If patient comes in with CV complaint, what other organ system would need to be examined?

A

CV, respiratory, peripheral vascular systems

  • musculoskeletal (shoulder jt disfunction, etc)
  • GI system (heartburn, ulcer, cholecystitis, etc)
  • Psychoneurotic (anxiety)
53
Q

hypertension

A

> 140/90

54
Q

postural/orthostatic hypotension

A

-abnormal decrease in blood pressure from sitting to standing; decrease >20mmHg systolic or >10mmHg abnormal

55
Q

7 dimensions of heart murmur

A
  • timing/duration
  • pitch
  • intensity
  • pattern
  • location
  • radiation
  • respiratory phase variations
  • it’s a whoosh sound!
  • when valve stenotic or damaged, abnormal turbulent flow of blood produces a murmur, heard during systole or diastole
56
Q

timing and duration of a murmur

A

between S1 and S2 or S2 and S1? short or prolonged?

57
Q

pitch of heart murmur

A

high, medium or low? bell or diaphragm?

58
Q

intensity of a murmur

A

grade 1-6

  • 1-3: no thrill
  • 4-6: thrill
  • 6: don’t need steth to hear
59
Q

pattern of a murmur

A

crescendo: increased blood velocity; decresendo: decreased blood velocity; square/plateau: constant intensity

60
Q

location of murmur

A

where is it auscultated best?

61
Q

radiation of murmur

A

do you hear it only over the specific valve or elsewhere? sound generally transmitted in direction of blood flow

62
Q

respiratory phase variations

A

impacted by inspiration/expiration? variation of intensity, quality, timing? if venous return issue, variations increase with insp, decrease with exp

63
Q

external clues to circulatory status

A
  • hair pattern (loss starts at toes and goes up)
  • venous pattern
  • varicosities
  • color (rubor, pallor, brown)
  • pigmentation
  • dermatologic findings (rash, scars, ulcerations, gangrene)
  • temperature: cold
64
Q

issues with circulation: toes vs ankles

A
  • toes: arteries

- ankles: veins (where valves are so stasis occurs here)

65
Q

what different color changes mean with circulatory status

A
  • brown: venous issues
  • pallor/rubor: arterial issues (rubor, specifically, poor circulation and increased levels of toxic metabolites in tissues)
66
Q

pain (arterial vs venous)

A
  • arterial: intermittent claud, progressing to rest pain

- venous: none to aching on dependency

67
Q

pulses (arterial vs venous)

A
  • arterial: decreased/absent

- venous: normal, through may be hared to feel through edema

68
Q

color (arterial vs venous)

A
  • arterial: pale, esp on elevation, red on dependency

- venous: normal to cyanotic on dependency, petechiae then brown pigment appear with chronicity

69
Q

temperature (arterial vs venous)

A
  • arterial: cool

- venous: normal

70
Q

edema (arterial vs venous)

A
  • arterial: absent or mild; may develop as patient tries to relieve rest pain by lowering leg
  • venous: present
71
Q

skin changes (arterial vs venous)

A
  • arterial: thin, skiny, atrophic skin; loss of hair over foot and toes; nails thickened and ridged (trophic changes)
  • venous: often brown pigmentation around ankles, stasis dermatitis, possible thickening skin,and narrowing of leg as scarring develops
72
Q

ulceration (arterial vs venous)

A
  • arterial: if present, involves toes or points of trauma on feet
  • venous: if present, develops on side of ankle, esp medially
73
Q

gangrene (arterial vs venous)

A
  • arterial: may develop

- venous: does not develop

74
Q

arterial pain

A
  • come on quick during exercise
  • relieve fast by rest
  • degree of pain correlates to intensity and duration of exercise
75
Q

venous/musculoskeletal pain

A
  • comes on during or after exercise
  • relieved by rest, but after hours or days
  • pain tends to be constant
  • greater variability in pain than in arterial area
76
Q

arterial pulse

A

ventricular systole (produces a pressure was through out arterial system)

77
Q

arterial pressure

A

force exerted by blood against the wall of an artery as result of bolus of blood exiting left ventricle as heart contracts

78
Q

characteristics to consider when examining arterial bp and pulse

A
  • stroke volume: amount of blood ejected (if SV lessened, pulse would be lessened)
  • viscosity of blood
  • peripheral resistance
  • dispensability of aorta and large arteries
  • rate of cardiac emptying
  • forceful wave that is smooth and more rapid on ascending part of wave
  • becomes domed, less steep and slower on descending part
  • *grade of pulse: 0-4
79
Q

JVD

A
  • jugular venous distention
  • distention of EXTERNAL jugular vein = poor right heart function (may be present in athletes)
  • if blood backs up into jugular vein, right side CHF (look for edema in extremities as well)
80
Q

hepatojugular reflux

A
  • exaggerated when right HF present (its measurement is used to evaluate that condition)
  • use your hand to apply firm and sustained pressure to the abdomen in the mid-epigastric region and instruct patient to breath normal.
  • Observe the neck for an elevation in JVP followed by an abrupt fall in JVP as the hand pressure is released
  • The JVP quickly equilibrates to its true level between the positions it achieved with and immediately after removal of the abdominal hand pressure.
  • If the JVP is not obvious with this maneuver, the pressure is either much higher of much lower (repeat maneuver with patient more supine if you suspect the pressure to be lower and position patient more upright if you suspect the JVP to be higher)
81
Q

JVP

A
  • jugular venous pressure
  • looks at INTERNAL jugular vein
  • look at area over this vein for fluttering movement (it’s closest to the right atrium) -> not a true pulse (different from the carotid pulse)
  • position patient with head at 30-45 degree angle, observe jugular venous pulsation, measure from sternal angle to top of visible oscillations over internal jugular vein

*measure of 3-4cm or more (or a total of 9 cm is indicative of increased central venous pressure)

82
Q

pulsus alternans

A
  • “alternating pulse” = alternation of pulsation of small amplitude with the pulsation of a large amplitude while the rhythm is regular
  • indication of left ventricular failure (more significant if pulse slow)
  • small then big
83
Q

pulsus bigeminus

A
  • “bigeminal pulse” -> result from normal pulsation followed by a premature contraction (the amplitude of the pulsation of the premature contraction is less than that of the normal pulsation
  • indication of disorder of rhythm
  • big then small
84
Q

pulsus bisferiens

A
  • best detected by palpation of carotid artery -> characterized by 2 main peaks (first is termed percussion wave and second is tidal wave)
  • indication of aortic stenosis combine with aortic insufficiency
85
Q

pulsus paradoxus

A
  • an exaggerated decrease (>10mmHg) in amplitude of pulsation during inspiration and increased amplitude during expiration
  • indication:
  • premature cardiac contraction
  • tracheobronchial obstruction
  • bronchial asthma
  • emphysema
  • pericardial effusion
  • constrictive pericarditis
86
Q

pulse deficit

A

difference between apical pulse and peripheral pulse

-indication: a fib

87
Q

venous insufficiency

A
  • hx of phlebitis, leg injury, chronic stasis
  • manifests with brawny ankle edema and induration (hardening), stasis pigmentation, varicosities, ankle ulcers
  • issue with valve, so get stasis (end up swelling vessels and go to edematous state)
  • would want to examine patient standing and supine (particularly with suspected chronic venous occlusion)
88
Q

acute superficial thromophlebitis

A
  • partial or complete occlusion of vein by a thrombus with secondary inflammatory reaction causing scarring of vascular wall (mini trauma when bang leg into table)
  • tender, swollen, erythematous area overlying a corded superficial vein (usually lower)
  • inspect extremities for signs of venous insufficiency (thrombosis, varicose veins or edema) -> examine patient in standing and supine positions
  • thrombosis: note redness, thickening and tenderness along superficial vein
89
Q

DVT

A
  • -pain and swelling in ankle, calf or thigh associated with blood clot in deep venous system (SWELLING AND PAIN IN ONE LEG, NOT BOTH -> difference from superficial)
  • associated with OCPs, immobilization and bed rest
  • may progress to PE
  • pain, swelling and tenderness occur OVER a vein
  • check for HOMAN sign (dorsiflex foot)
90
Q

arterial insuffficiency

A
  • inadequate arterial circulation
  • may be manifested by pain, intermittent claudication (pain in lower extremities), rest pain, absent or diminished pulses, pallor on elevation (body cannot fight gravity), rubor on dependency, ulceration, coldness, gangrene, pain with exercise
  • patient not getting good circulation (also clogging up coronary/carotid arteries), so look at lower legs
91
Q

arterial obstruction

A
  • manifests as pain, numbness, tingling, weakness, pallow, mottling, superficial vasculature collapse (not enough O2 in blood getting into lower extremities so nothing to bring back on other side)
  • distal pulses are absent
  • associated with atherosclerotic disease
92
Q

varicosities

A
  • dilated, tortuous alterations in the saphenous veins and tributaries
  • dull, aching pain and heaviness (“my legs ache when I stand all day”)
  • hereditary and exacerbated by pregnancy and obesity
  • from book: dilated and swollen, with diminished rate of blood flow and increased intravenous pressure (due to incompetence of vessel wall, venous valves or obstruction in more proximal vein)
  • inspect patient for these standing; palpate legs to feel venous distention (would maintain itself for longer than a few seconds if venous insufficiency is suspected)
93
Q

dependent edema

A

fluid build up in legs or sacral area

94
Q

pitting edema

A
  • press index finger over bony prominence of the tibia or medial malleolus for several seconds.
  • orthostatic (pitting) edema: a depression that does not rapidly refill and resume its original contour
  • right sided heart failure leads to an increased fluid volume, which in turn elevates the hydrostatic pressure in vascular space = edema in dependent parts of body
  • graded 1+ - 4+
    • if edema is unilateral, suspect occlusion of major vein; bilateral = CHF
    • if occurs without pitting, suspect arterial insufficiency or lymphedema
    • if occurs with some thickening and ulceration of skin = venous obstruction
95
Q

non pitting edema

A
  • non pitting: brawning edema
  • someone had edema for so long that the inflammatory response has caused edema to scar down; it’s solid, can push and not make a pit
96
Q

claudication

A
  • pain in extremities from insufficient arterial flow (angina = pain in heart)
  • when walking, don’t get enough blood to legs and there is pain (pain from muscle ischemia)
  • dull ache associated with muscle fatigue and cramps (usually a few minutes of rest will relieve it)
97
Q

capillary refill

A
  • inspect nail bed for cyanosis
  • should be less than 2 seconds
  • greater = poor perfusion
  • allows fluid exchange between the vascular and interstitial spaces, determined by the hydrostatic pressures of the blood and interstitial tissues and the colloid osmotic pressures of plasma and interstitial fluids. In the healthy person the dominance of hydrostatic pressure at the arterial end of the capillary bed (pushing fluid out) and of the colloid osmotic pressure at the venous end (pulling fluid in) maintains the balance of fluids in intravascular and extravascular spaces.
  • if system compromised, can indicate PAD, hypovolemic shock, hypothermia
  • environmental influences (cool temps) can prolong capillary refill time
98
Q

abnormal splitting of S2 heart sound

A

hearing 2 distinct sounds during EXPIRATION = ABNORMAL!

  • reversed of paradoxical splitting
  • wide splitting
  • fixed splitting
99
Q

physiologic murur

A
  • high flow through a normal valve (normal murmurs are produced by normal blood flow through a stenotic valve)
  • ex: pregnancy, thyrotoxicosis, anemia (high metabolic, high output states)
  • not pathologic itself, but indicates underlying disease process
100
Q

S3 and S4, systolic or diastolic sounds?

A

-both diastolic sounds

101
Q

S3

A
  • occurs right after S2
  • in first stage of diastole there is a period of rapid ventricular filling where approx 80% of blood is transferred to ventricles from atria
  • at end of this stage of rapid filling, an S3 may be heard if the volume of blood that has been transferred is abnormally large (as in mitral regurg)
  • S3 gallop thought to be sound ventricle makes when its forced to dilated beyond its normal range due to volume overload in atria (eg. heart failure, decreased ventricle compliance)
  • conditions of high cardiac output (thyrotoxicosis, anemia) can also cause S3 gallop
  • heard best with bell
  • note: one would not hear S3 gallop in a person with significant mitral stenosis, because mitral stenosis prevents rapid filling of ventricles!
  • physiologic S3 can be heard normally in children and young adults (less than 40 years) and third term of pregnancy
102
Q

S4

A
  • gallop
  • late stage of diastole
  • marked by atrial contraction or “kick” where final 20% of atrial output is delivered to ventricle
  • if ventricle is stiff and non compliant (left vent hypertrophy secondary to longstanding sever ht., MI, or cardiomyopathy) then the pressure wave gradient generated as the atria contract generates an S4 sound
  • best heard with bell

-TIP: atril contract is required to produce and S4 sound, so one would never heard this during AFIB

  • S4 gallop can sometimes be heard (normally) in well conditioned, trained athlete
  • usually, however, S4 gallop is pathologic finding due to increased resistance to ventricular filling following atrial contraction
103
Q

pericardial rub

A
  • dx of pericarditis
  • produced by heart beating against an inflamed pericardium or fluid build up
  • usually continuous, heard diffusely over chest
  • typically has 3 components (one systolic and 2 diastolic)
  • accentuated when patient sits up and leans forward (also maybe during inspiration)
  • leather, creaking sound

PD Block 2 (5 decks)

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