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Sasha: Cardiovascular Clinical Assessment > CA Bates info > Flashcards

CA Bates info Flashcards

1
Q

Angina Pectoris

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • Factors that relieve
  • associated symptoms
A
  • Process: temporary mycocardial ischemia, usually secondary to coronary artherosclerosis
  • Location: Retrosternal or across the anterior chest, sometimes radiating to the shoulders, arms, neck, lower jaw or upper abdomen
  • Quality: Pressing, squeezing, tight, heavy, occasionally burning
  • Severity: Mild to moderate, sometimes perceived as discomfort rather than pain
  • Timing: usually 1-3 min but up to 10 min. prolonged episodes up to 20 min
  • Factors that aggravate: Exertion, espeially in the cold; meals; emotional stress. May occur at rest.
  • Factors that relieve: Rest, nitroglycerin
  • associated symptoms: sometime dyspnea, nausea, sweating
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2
Q

Myocardial Infarction

  • Process
  • Location
  • Quality
  • Severity
  • Timing
A
  • Process: prolonged myocardial ischemia, resulting in irreversible muscle damage or necrosis
  • Location: Retrosternal or across the anterior chest, sometimes radiating to the shoulders, arms, neck, lower jaw or upper abdomen
  • Quality: Pressing, squeezing, tight, heavy, occasionally burning
  • Severity: Often but not always a severe pain
  • Timing: 20 min to several hours
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3
Q

Pericarditis

  • Process (2) and then explain on these points for both processes!!!!
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • Factors that relieve
  • associated symptoms
A
  • Process 1: irritation of parietal pleura adjacent to the pericardium
  • Location: Retrosternal or left preordial, may radiate to the tip of eft shoulder
  • Quality: sharp, knifelike
  • Severity:​ often severe
  • Timing: ​perisitent
  • Factors that aggravate: breathing, chaining position, coughing, lying down, sometime swallowing
  • Factors that relieve: sitting forward may relieve it
  • associated symptoms: seen in autoimmune disorders, post-myocardial infarction, viral infection, chest irradiation
  • Process 2: mechanism unclear
  • Location: retrosternal
  • Quality: crushing
  • Severity: Severe
  • Timing: persistent
  • associated symptoms: of the underlying illness
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4
Q

Dissecting Aortic Aneurysm

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • associated symptoms
A
  • Process: a splitting within the layers of the aortic wall, allowing passage of blood to dissect a channel
  • Location: anterior chest, radiating to the neck, back, or abdomen
  • Quality: ripping, tearing
  • Severity: very severe
  • Timing: Abrupt onset, early peak, perisistent for hours or more
  • Factors that aggravate: Hypertention
  • associated symptoms: If thoracic, hoarseness, dysphagia, also syncope, hemiplegia, paraplegia
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5
Q

tracheobronchitits

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • Factors that relieve
  • associated symptoms
A
  • Process: inflammation of trachea and large bronchi
  • Location: upper sternal or on either side of the sternum
  • Quality: burning
  • Severity: mile to moderate
  • Timing: variable
  • Factors that aggravate: coughing
  • Factors that relieve: lying on the involved side may relieve it
  • associated symptoms: cough
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6
Q

Pleuritic Chest Pain

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • Associated symptoms
A
  • Process: Inflammation of the parital pleura, as in pleurisy, pneumonia, pulmonary infarction, or neoplasm
  • Location: chest wall overlying the process
  • Quality: sharp, knifelike
  • Severity: often severe
  • Timing: perisitent
  • Factors that aggravate: deep inspiration, coughing, movements of the trunk
  • Associated symptoms: of the underlying illness
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7
Q

Reflex Esophagitis

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • Factors that relieve
  • associated symptoms
A
  • Process: inflamm of esophageal mucosa by reflux of gastric acid
  • Location: retrosternal, may radiate to abck
  • Quality: bringing, maybe sqeezing
  • Severity: mile-severe
  • Timing: variable
  • Factors that aggravate: large meal, bending over, lying down
  • Factors that relieve: antacids, belching
  • associated symptoms: sometimes regurgitiation, dysphagia
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8
Q

Diffuse esophageal spasm

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • Factors that relieve
  • associated symptoms
A
  • Process: motor dysfunction of the esophageal muscle
  • Location: retro sternal, may radiate toback, arms, jaw
  • Quality: sqeezing
  • Severity: mild-severe
  • Timing: variable
  • Factors that aggravate: swallowing food or cold liquid, emotional stress
  • Factors that relieve: sometimes nitro
  • associated symptoms: dysphagia
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9
Q

Chest wall pain=

COSTOCHONDRITIS

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • associated symptoms
A
  • Process: variable, often unclear
  • Location: below the left breast or along the costal cartilages
  • Quality: stabbing, sticking or dull aching
  • Severity: variable
  • Timing: fleeting to hours or days
  • Factors that aggravate: movements of chest, trunk, arms
  • associated symptoms: often local tenderness
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10
Q

Anxiety

  • Process
  • Location
  • Quality
  • Severity
  • Timing
  • Factors that aggravate
  • associated symptoms
A
  • Process: unclear
  • Location: precordial, below the left breat, or acors the anterior chest
  • Quality: stabbing, sticking, or dull aching
  • Severity: variable
  • Timing: fleeting to hours or days
  • Factors that aggravate: may follow effort, emotional stress
  • associated symptoms: Breathlessness, palpittions, weakness, anxiety
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11
Q

Left-sided Heart Failure

  • Process
  • Timing
  • Factors that aggravate
  • Factors that relieve
  • associated symptoms
  • setting
A
  • Process: Elevated pressure in pulmonary capillary bed with transduction of fluid into intersitial spaces and alveoli, decreased compliance (increased stiffness) of the lungs, increased work of breathing
  • Timing: Dyspnea may progress slowly, or suddenly as ina cute pulmonary edema
  • Factors that aggravate: exertion, lying down
  • Factors that relieve: Rest, sitting up, through dyspnea may become persistent
  • associated symptoms: often cough, orthopnea, paroxysmal nocturnal dyspnea, sometimes wheezing
  • Setting: history of heart disease or its predisposig factors
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12
Q

what ECG pattern and usual resting rate is related with Fast rate ( >100)

A
  • Sinus tachycardia: 100-180
  • Supraventricular (arterial or nodal) tachycardia : 150-250
  • Atrial flutter with a regular ventricular response: 100-175
  • Ventricular tachycardia: 110-250
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13
Q

What is the ECG pattern and usual resting heart rate with a normal rate (60-100)

A
  • normal sinus rhythm: 60-90
  • second degree AV block: 60-100
  • Atrial lutter with a regular ventricular response: 75-100
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14
Q

What is the ECG pattern and usual resting rate of a slow rate ( <60 )

A
  • sinus bradycardia: <60
  • second degree AV block: 30-60
  • complete heart block: <40
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15
Q

Define Sporadic

A

premature or extra beats at random intervals, but normal underlying rhythm: ie. atrial or ventricular premature contractions, sinus arrhythmia

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16
Q

Define: Regularly irregular

A

regular pattern of cadences: ie. ventricular tigeminy

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17
Q

Define: irregularly irregular

A

no discernible regularity: ie. atrial fibrillation, atrial flutter

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18
Q

Sporadic sinus arrhythmia

  • rhythm
  • heart sounds
A
  • rhythm: heart varies cyclically, usually speeding up with inspiration andslowing down with expiration
  • Heart sounds: notmal, although S1 may vary with the heart rate.
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19
Q

Atrial or Nodal Premature Contractions (supraventricular)

  • rhythm
  • heart sounds
A
  • rhythm: beat of atrial or nodal origin comes earlier than the enxt expected normal beat. a pasue follows, and then the rhythm resumes
  • heart sounds: S1 may differ in intensity from the S1 of normal beats, and S2 may be decreased
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20
Q

Sporadic or regularly irrefular Ventricular Premature Contractions (ventricular bigeminy or trigeminy)

  • rhythm
  • heart sounds
A
  • Rhythm: beat of ventricular origin comes earlier than the enxt expected normal beat. a pause follows, and the rhythm resumes
  • Heart sounds: S1 may differ in intensity from the S1 of the normal beats, and S2 may be decreased. Both sounds are likely to be split
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21
Q

irregularly irregular atrial fibrillation and atrial flutter with varying AV block

  • rhythm
  • heart sounds
A
  • Rhythm: ventricular rhythm is totally irregular, although short runs of the irregular ventricular rhythm may seem regular
  • heart sounds: S1 varies in intensity
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22
Q

this picture is relating to the next couple cards. It can be found on page 393 in the Bates book!

A

just a picture for help

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23
Q

Abnormalities of the Arterial Pulse and pressure waves:

NORMAL

A

the pulse pressure is appox 30-40 mm Hg. pusle contour is smooth and rounded. (notch on descending slope of the pulse wave is not palpable)

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24
Q

Abnormalities of the Arterial Pulse and pressure waves:

small, weak pusle

definition

casues (2)

A

Pulse pressure is diminished, and the pulse feels weak and small. upstroke may feel slowed, peak prolonged.

causes include:

  • decreased stroke volume, as in hart fialure, hypovolemia, and severe aortic stenosis
  • increased peripheral resistance, as in exposure to cold and severe heart failure
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25
Q

Abnormalities of the Arterial Pulse and pressure waves:

Large, bounding pulses

definition

what does the pulse feel like?

causes (3)

A

pulse pressure is increased, and pusle feels strong and bounding. rise and fall may be rapid and peak may be brief

causes include:

  • increased stoke volume, decreased peripheral resistnace, or both, as in fever, anemia, hyperthyroidism, aortic regurg, arteriovenous fistulas, patent ductus arteriosis
  • incresed stroke volume because of slow heart rates, as in bradycardia and complete heart block
  • decreased compliance (increased stiffness) of the aortic walls, as in aging or artherosclerosis
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26
Q

Abnormalities of the Arterial Pulse and pressure waves:

Bisferiens Pulse

definition

causesn (3)

A

Bisferiens Pulse is an increased pulse is an increased arterial pulse with a double systolic peak.

casues include:

  • pure aortic regurg
  • combined aortic stenosis and regurg
  • and, though less commonly palpable, hypertorphic cardiomyopathy
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27
Q

Abnormalities of the Arterial Pulse and pressure waves:

Pulsus Alternans

what can it be detected by?

what does it indicate?

what accompanies it

A

amplitude from beat to beat even though the rhythm is basically regular (must be for you to make this judgment). when the difference between stronger and weaker beats is slight, it can de detected only by sphygmomanometry.

Pulses alternans indicates left ventricular failure and is usually accompanied by a left sided S3.

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28
Q

Abnormalities of the Arterial Pulse and pressure waves:

Bigeminal Pulse

what migh this mimic?

definition?

tell me about the stroke volume?

A

this disorder of rhythm may mimic pulsus alternans.

a bigeminal pulse is caused by a normal beat alternating with a premature contraction.

the stroke volume of the premature beat is diminshed in relation to that of the normal beats, and the pulse varies in amplitude accodingly

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29
Q

Abnormalities of the Arterial Pulse and pressure waves:

Paradoxical pulse

how can it be detected?

when is a blood pressure cuff needed?

what is systolic pressure during inspiration?

what is this found in?

what is it sometimes notd in?

A
  • Paradoxical pulse may be detected by a palpable decrease in the pulse’s amplitude on quiet inspiration.
  • if the sign is less pronounced, a blood pressure cuff is needed
  • systolic pressure decreases by more than 10 mmHg during inspiration
  • a paradoxical pulse is found in pericardial tamponade and frequently in exacerbations of asthma and COPD.
  • sometime noted in constrictive pericaditis
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30
Q

Heart sounds

Normal variations (2 types)

A
  1. S1 is softer than S2 at the base (right and left 2nd interspaces)
  2. s1 is often but not alwys louder than S2 at the apex
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31
Q

Heart sounds

Accentuated S1

(2 types it is accentuated in)

A

S1 is accentuated in:

  1. tachycardia, rhythms with a short PR interval, and high cardiac output states (ie. exercise, anemia, hyperthryoidism)
  2. mitral stenosis

in these conditions the mitral valve is still open wide at the onset of ventricular systole and then closes quicikly

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32
Q

Heart sounds

Diminshed S1

what is is diminshed in?

what has the mitral valve had time for?

what are 2 other conditions the S1 is also diminshed in?

A

S1 is diminshed in first-degree heart block (delayed conduction from atria to ventricles).

here the mitral valve has had time after atrial contraction to float back into an almost closed position before ventricular contraction shuts it. it closes more quietly.

S1 is also diminished:

  1. when the mitral valve is calcified and relatively immobile, as in mital regurg
  2. when left ventricular contractibility is markedly reduced, as in heart failure or coronary heart disease
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33
Q

Heart sounds

Varying S1

2 things that cause varies in the intensity?

which vlave is in carying positions furing these situations?

therefore what varies?

A

S1 varies in intensity

  1. in complete heart block, when atria and ventricles are beating independently of each other
  2. in any totally irregular rhythm (ie. a. fib)
  • in these situations, the mitral valve is in varying positions before being shut by ventriuclar contraction.
  • therefore its closure varies in loudness.
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34
Q

Heart sounds

Split S1

  • Where might the split occur and what happens for it to be heard?
  • where is it heard?
  • what else should you consider?
  • what two conditions would abnormal splitting be heard in?
A
  • S1 may be split normally along the lower left sternal border where the tricuspid componenet, often too faint to be heard, becomes louder
  • split may smoetimes be heard at the apex
  • but consider also an S4, aortic ejection sound, and an early systolic click
  • abnormal splitting of both heart sounds may be heard in right bundle branch block and in premature ventricular contractions.
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35
Q

Heart sounds

Physiologic splitting

Where do you listen for this and in which heart sound?

how does pulmonic component of S2 usually sound?

so then what is S2 usually a single sound derived from?

what accentuated splitting?

when does it disappear?

what about younger patients?

A
  • listen for physiologic splitting of S2 in the 2nd or 3rd intercostal space
  • pulmonic component of S2 is usually too faint to be heard at the apex or aortic area,
    • where S2 is a single sound derived from aortic valve closure alone.
  • normal splitting is accentuated by inspiration and usually disappears on expiration
  • in younger patients, S2 may not become single on expiration… it may merge when the patient sits up
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36
Q

Heart Sounds

Wide splitting

what is this referring to?

what can it be caused by?

what 2 things can it be caused by? and give examples please..

A
  • wide splitting of S2 refers to an increase in the usual splitting that persists throughout the respirtory cycle.
  • can be caused by :
    1. delayed closure of the pulmonic valve
      • ie. pulmonic stenosis, right BBB
      • right bundle branch block can also cause splitting of S1 into its mitral and tricuspid components
    2. caused by early closure of the aortic valve
      • as in mitral regurg
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37
Q

Heart Sounds

Fixed splitting

what is this referring to?

what does it occur in? (2)

A
  • refers to wide spliting that does not vary with respiration.
  • occurs in:
    • atrial spetal defect
    • right ventricular failure
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38
Q

Heart Sounds

Paradoxical or reversed splitting

what does this refer to?

what is abnormally delayed ? and what follows what in expiration?

what makes the split disappear?

what is the most common cause?

A
  • refers to splitting that appears on expiration and disappears on inspiration
  • closure of aortic valve is abnormally delayed as that A2 follows P2 in expiration.
  • normal inspiratory delay of P2 makes the split disapear
  • most common cause:
    • left bundle branch block
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39
Q

Where is increased intensity of A2 heard?

what does it occur in (2)? WHY?

Why would you have decreased or absent A2?

What about if A2 is inaudible?

A

A2 is usually heard in the right 2nd interspace

WHAT DOES IT OCCUR IN?

  1. systemic hypertension
    • because of increased pressure load
  2. aortic root is dilated
    • because the aortic valve is then closer to the chest wall

Decreased or absent A2 in right 2nd interspace noted in calcific aortic stenosis because of valve immobility

IF A2 IS INAUDIBLE? no splitting is heard

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40
Q

Increased intensity of P2

what do you suspect?

and other causes?

what is the meaning of “accentuated”?

Dereased intensity of P2

what is is from?

what else?

what if P2 is inaudible?

A

INCREASED INTENSITY OF P2

  • When P2 is equal or louder than A2, suspect PULMONARY HYPERTENSION
  • other causes: dilated pulmonary artery, atrialseptal defect
  • Accentuated: when a split in S2 is heard widely, even at the apex and the right base, P2 is accentuated.

DECREASED INTENSITY OF P2

  • from the increased anteroposterior diameter of the chest assoicated with aging
  • result from: pulmonic stenosis
  • if P2 is inaudible, no splitting is heard
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41
Q

Extra Heart sounds in Systole

Early systolic ejection sounds

when does it occur? with opening of what?

what does it sound like (3 qualities to hit on)?

what is it better heard with

what does this indicate?

A
  • occur shortly after S1, coincident with opening of the aoritc and pulmonic valves
  • high pitch, have a sharp, clicking quality
  • better heard with the diaphragm of the stethoscope
  • ejection sound indicated cardiovascular disease
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42
Q

Extra Heart sounds in Systole

Aortic ejection sound

where do you listen for this?

where is it louder?

what does it vary with?

what may it be accompanied with?

A
  • listen for it at the base and apex
  • louder in apex
  • does not vary with respiration
  • may accompany:
    • dilated aorta, or aortic valve disease from congenital stenosis or a bicuspid aortic valve
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43
Q

Extra Heart sounds in Systole

Pulmonic ejection sound

when is this heard best?

what may you be hearing when this is loud?

when does intensity decrease?

what are the causes (3)?

A
  • heard best in the 2nd and 3rd interspaces
  • when S1, usually relativly soft in this area, appears to be loud, you may be hearing a pulmonic ejection sound
  • intensity often decreases with inspiration
  • casues include:
    • dilatation of the pulmonary artery
    • pulmonary hypertension
    • pulmonic stenosis
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44
Q

Extra Heart sounds in Systole

Systolic clicks

  1. what is this caused by?
  2. what is Mitral valve prolapse?
    • how many people does it effect in population?
    • men or women?
  3. when are the clicks heard during systole?
  4. how many clicks
  5. where are they heard?
  6. what is their pitch
  7. what part of the stethoscope do you use?
  8. what is the click followed by?
    • and what is that from?
  9. what does the murmur do conscerning S2?
  10. are the findings consistent with this?
  11. squatting vs. standing?
A
  1. usually caused by MITRAL VALVE PROLAPSE
  2. mitral valve prolapse: abnormal systolic ballooning of part of the mitral valbe into the left atrium from both leaflet redundancy and elongation of the chordae tenineae
    • affects about 2-3% of the general popilation
    • equal prevelance in men and women
  3. clicks are usually mid or late systolic
  4. clicks are usually single
  5. heard medical to the apex (or at the apex) but also at the lower left sternal border
  6. high pictched
  7. listen with diaphragm
  8. click is followed by late systolic murmur fromm mitral regurgitation
  9. murmur usually crescendos up to S2
  10. finding usually varies from time to time and often changes with body position
  11. squatting delays the click and murmur VERSUS standing moves them closer to S1
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45
Q

Extra Heart sounds in Diastole

opening snap

  1. what type of sound
  2. what is is produced by?
  3. where is it heard best?
  4. what happens when it is loud?
  5. what is it mistaken with ?
  6. what will help distinguish it from S2?
  7. what part of the stethoscope is used?
A
  1. very early diastolic sound
  2. produced by the opening of a stenotic mitral valve
  3. heard best just medial to the apex and along the lower left sternal border
  4. when loud= an opening snap raadiates to the apex and to the pulmonic area
  5. may be mistaken for the pulmonic component of a split S2
  6. high pitch and snapping quality help distinguish it from S2
  7. use diaphragm
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46
Q

Extra Heart sounds in Diastole

physiologic S3

  1. who is it frequently in, what age?
  2. what about pregnancy?
  3. when does it occur?
  4. what is it later than?
  5. what does it sound like/pitch? (2 words)
  6. where is it heard best?/ and in what position?
  7. what part of the stethoscope?
A
  1. frequently in children and in young adults to the age of 35-40
  2. common during last trimester of pregnancy
  3. occuring early in diastole during rapid ventricular filling
  4. later than an opening snap
  5. dull and low in pitch
  6. heard best at the apex in left lateral decubitis position
  7. bell of the sethoscope should be used with very light pressure
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47
Q

Extra Heart sounds in Diastole

Pathologic S3

  1. what is another name for this?
  2. what does it sound like?
  3. what do you need to have S3 be pathologic?
  4. what does it arise from?
  5. when does it occur in diastole?
  6. what are the causes (3)
  7. where is left sided S3 heard? What position?
  8. where is right sided S3 heard? what position? and what position is it louder in?
  9. what does the term gallop mean/come from? what does it sound like?
A
  1. also called ventricular gallop
  2. sounds similar to physiologic S3
  3. S3 in adults over the age of 40 is usually pathologic
  4. arises from high pressure and abrupt decleration of inflow across the mitral valve
  5. occurs at the end of rapid filling phase of diastole
  6. causes include:
    • decreased myocardial contactility
    • heart failure
    • volume overloading of a ventricle, as in mitral or tricuspid regurgitation
  7. Left sided S3 is heard typically at the apex in the left lateral decubitis position
  8. Right sided S3 is heard along the lower left sternal border or below the xiphoid with the patient supine, and is louder on inspiration
  9. Term gallop comes from the cadence of 3 heart sounds, especially at rapid heart rates, and sounds like “kentucky”
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48
Q

Extra Heart sounds in Diastole

S4

  1. another name for S4
  2. what does this sound come right before?
  3. what does it sound like/pitch (2 characteristics)
  4. what part of the stethoscope do you use?
  5. what is this normal in (2 groups)
  6. what is this due to ?
  7. what is increased resistance related to?
  8. LEFT sided S4
    • causes (4)
    • where is it heard best? what position
    • what does it sound like (specifc word)
  9. RIGHT sided S4
    • is it common?
    • where is it heard
    • what does it get louder with?
    • causes (2)
  10. what else is S2 associated with? (hint: relating to atria and ventricles)
  11. what does a delat seperate? and what does this cause?
  12. when is S4 never heard? and when does this occur?
A
  1. atrial sound or atrial gallop
  2. just before S1
  3. dull, low pitch
  4. use the bell
  5. normal in trained athletes and older age groups
  6. due to increased resistance to ventricular filling following atrial contraction
  7. increased resistance is related to decreased compliance (increased stiffness) of the ventricular myocardium
  8. LEFT SIDED S4:
    • ​​causes of left-sided s4 include:
      • _​​_hypertensive heart disease
      • myocardial ischemia
      • aortic stenosis
      • cardiomyopathy
    • Left sided S4 is heard best at apex in the left lateral position ….
    • sounds like Tennessee
  9. RIGHT SIDED S4:
    • ​​Right sided S4 is less common
    • heard along the lower left sternal border or below the xiphoid
    • right sided S4 gets louder with inspiration
    • causes of right sided S4:
      • pulmonary hypertension
      • pulmonic stenosis
  10. S4 may also be associated with delayed conduction between the atria and ventricles
  11. Delay seperates the normally faint atrial sound from the louder S1 and makes it audible
  12. S4 is never heard in the absence of atrial contraction, which occurs in atrial fibrillation
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49
Q

Quadruple rhythm

A

patient has both an S3 and an S4 produces a Quadruple rhythm of 4 heart sounds

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50
Q

summation gallop

A

at rapid heart rates, the S3 and S4 may merge into one loud extra heart sound : Summation gallop

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51
Q

Pansystolic (Holosytolic) murmurs

A

pathologic arising from blood flow from a chamber with high pressure to one of lower pressure, through a valve or other structure that should be closed. Murmur begins immediatly with S1 and continues up to S2

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52
Q

MITRAL REGURGITATION

  1. location?
  2. radiation?
  3. intensity? what is it associated with?
  4. pitch?
  5. Quality (2)?
  6. what does this not become louder in?
  7. what extra heart sound is in this? what does it reflect?
  8. how is ampical impulse affected (3)?
  9. Mechanism behind mitral regurgitation?
A
  1. location: apex
  2. Radiation: to left axilla, less often to the left sternal border
  3. Intensity: soft to loud; if loud associated with an apical thrill
  4. Pitch: medium-high
  5. Quality: Harsh, holosystolic
  6. does NOT become louder in inspiration
  7. apical S3, reflects volume overload of the left ventricle
  8. Apical impulse is increased in amplitude, laterally displaced, and may be sustained
  9. MECHANISM: when mitral valve fails to close fully in systole, blood regugitates from left ventricle to left atrium, causing murmur. this leakage creates volume overload on the left ventricle, with subsequent dilatation. several structural abnormalities cause this condition and finding may vary accordingly
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53
Q

TRICUSPID REGURGITATION

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. quality (2 words)
  6. when will the intensity increase
  7. how is right ventricular impulse affected
A
  1. location: lower left sternal border
  2. Radiation: to the right of the sternum, to the xiphoid area, and perhaps to the left midclavicular line, but not into axilla
  3. intensity: variable
  4. Pitch: medium
  5. Quality: blowing, holosystolic
  6. the intensity may increase slightly with inspiration
  7. right ventricular impulse is increased in amplitude and may be sistained
  8. S3 may be audible along the lower left sternal border.
  9. jugular venous pressure is often elevated
  10. MECHANISM: tricuspid valve fails to close fully in systole, blood regurgitates from right ventricle to right atrium, prodicing murmur. most common cause is right ventricular failure and dilatation, with resulting enlargement of the tricuspid orifice, often initiated by pulmonary hypertension or left ventricula failure.
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54
Q

VENTRICULAR SEPTAL DEFECT

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. quality
  6. how is S2 obscured
  7. what causes findings to vary (2)
  8. Mechanism
A
  1. location: 3rd, 4th, 5th left interspaces
  2. radiation: often wide
  3. intensity: often very loud, with a thrill
  4. pitch: high, holosystolic
  5. quality: often harsh
  6. S2 may be obscured by the loud murmur
  7. findings vary with the severity of the defect and with associated lesions
  8. MECHANISM: ventricular spetal defect is a congenital abnormality in which blood flows from the relatively high pressure left ventricle into the low pressure right ventricle through a hole. the defect may be accompanied by other abnormalities, but an uncomplicated lesions is described here.
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55
Q

Midsystolic murmur

common?

3 types?

when do they peak?

crecendo-decrescendo

A
  • midsystolic ejection mururs are the most common kinda of heart murmur

TYPES:

  1. innocent: without any detectable physiologic or structural abnormality
  2. Physiologic: from physiologic changes in body metabolism
  3. pathologic: arising from a structural abnormality in the heart or great vessels
  • midsystolic murmurs tend to peak near midsystole and usually stop before S2.
  • The crecendo-decrescendo or “diamond” shape is not always audible but the gap between the murmur and S2 helps to distinguish midsystolic from pansystolic murmurs
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56
Q

Midsystolic Murmurs

INNOCENT MURMUR

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. quality
  6. when does it decrease or disappear
  7. associated findings? if not, what is found (4)?
  8. what can sometimes be present?
  9. mechanism
A
  1. location: 2nd to 4th left interspaces between the left sternal border and the apex
  2. radiation: little
  3. intensity: Grade 1 to 2, possibly 3
  4. pitch: soft to medium
  5. quality: variable
  6. usually decreases or disappears on sitting
  7. no associated findings:
    • normal splitting
    • no ejection sounds
    • no diastolic murmurs
    • no palpable evidence of ventricular enlargement
  8. sometimes a innocent and pathologic murmur are present
  9. MECHANISM: turbulent blood flow, probably generated by ventricular ejection of blood into the aorta from the left and occasionally the right ventricle.
  10. very common in children and young audlts- may also be heard in older people.
  11. no underyling cardiovascular disease
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57
Q

Midsystolic Murmurs

PHYSIOLOGIC MURMURS

  1. murmur
    • location
    • radiation
    • intensity
    • pitch
    • quality
    • what makes it decrease/disappear?
A
  1. Murmur is similar to innocent murmurs
    • location: 2nd to 4th left interspaces between the left sternal border and the apex
    • radiation: little
    • intensity: Grade 1 to 2, possibly 3
    • pitch: soft to medium
    • quality: variable
    • usually decreases or disappears on sitting
  2. MECHANISM: turbulence due to a temporary increase in blood flow in predisposing conditions such as anemia, pregnancy, dever, hyperthryoidism
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58
Q

AORTIC STENOSIS

  1. location
  2. radiation
  3. intensity
  4. ptich (3 things to touch on) / where is it heard
  5. quality
  6. where is it best heard
  7. associated findings
    • what if aortic stenosis worsens?
    • what is A2 is delayed?
    • carotid upstroke
    • hypertrophied left ventricle
  8. mechanism
  9. causes
  10. conditions that mimic aortic stenosis w/out obstructing flow (4)
A
  1. Location: right 2nd interspace
  2. Radiation: often to the carotids, down the left sternal border, even to the apex
  3. Intensity: sometimes soft but often loud, with a thrill
  4. Pitch: medium, harsh; crescendo-decrescendo may be higher at the apex
  5. Quality: often harsh, may be more muscial at the apex
  6. Heard best with the patient sitting and leaning forward
  7. Associated findings
    • if aortic stenosis worsens, A2 decreases and then murmur peaks later in diastole.
    • A2 may be delayed and merge with P2​ –> single S2 on expiration or paradoxical S2 split.
    • carotid upstroke may be delayed, with slow rise and small amplitude
    • Hypertrophied left ventricle may –> sustained apical impulse and an S4 from decreased compliance
  8. MECHANISM:
    • signif. aortic valve stenosis impairs blood flow acorss valce, causing turbulance, and increases left ventricular afterload.
  9. Causes:
    • congenital, rhuematic and degenerative calcification of the leaflets
  10. Conditions mimic aortic stenosis without obstructing flow:
    • aortic sclerosis: stiffening of aortic valve leaflets associated with aging
    • bicuspid aortic valve: congenital condition that may not be recognized until adulthood
    • dilated aorta: as in arteriorsclerosis, syphilis, Marfan’s syndrome
    • pathologically increased flow across the aortic valve during systole can accompany aortic regurgitation
59
Q

HYPERTROPHIC CARDIOMYOPATHY

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. quality
  6. assoicated findings
    • what is it decreased and increased with and from what
    • what heart sound is present
    • what other heart sound is present and where
    • apical impulse
    • carotid pulse
  7. mechanism
A
  1. location: 3rd and 4th left interspaces
  2. radiation: down the left sternal border to the apex, possibly to the base, but not to the neck
  3. intensity: variable
  4. pitch: medium
  5. quality: harsh
  6. associated findings:
    • decreases with squatting, increases with straining down from Valsalva and standing
    • S3 may be present
    • S4 present at apex (unlike mitral regurg)
    • apical impulse may be sustained and have two palpable components
    • Carotid pulse rises quickly, unlike the pulse in aortic stenosis
  7. MECHANISM: massive ventricular hypertrophy is assoicated with unusually rapid ejection of blood from the left ventricle during systole. Outflow tract obstruction of flow may coexist. Accompanying distortion of the mitral valve may cause mitral regurgitaiton
60
Q

Pulmonic stenosis

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. quality
  6. associated symptoms
    • in severe stenosis what is split and what is diminished
    • what sound is common
    • what may you hear
    • what is often icnreased
  7. Mechanism
  8. usually found in who?
  9. what about atrial septal defect ? what may mimic pulmonic stenosis..?
A
  1. location: 2nd and 3rd left interspace
  2. Radiation: if loud, toward the left shoulder and enck
  3. intensity: soft to loud; if loud assoicated with a thrill
  4. Pitch: medium; crescendo-decrescendo
  5. quality: often harsh
  6. Associated symptoms:
    • in severe stenosis: S2 is widely split, and P2 is diminished or inaudible.
    • an early pulmonic ejection sound is common
    • may hear a right-sided S4.
    • right ventricular impulse often increased in amplitude and sustained
  7. Mechanism: pulmonic valve stenosis impairs flow across the valve, increasing right ventricular afteroad.
  8. congenital and usually found in children
  9. in an atrial septal defect: the systolic murmur from pathologically increased flow across the pulmonic valve may mimic pulmonic stenosis
61
Q

Diastolic murmur

  1. what does this usually indicate
  2. what are the two types?
  3. what murmur is less common and which can be difficult to hear… diastolic or systolic?
A
  1. almost always indicates heart disease
  2. two basic types:
    • Early decrescendo diastolic murmurs: signify regurgitant flow through an incompetent semilunar valve, more commonly the aortic
    • Rumbling diastolic murmurs in mid- or late diastole: suggest stenosis of an atrioventricular valve, usually the mitral.
  3. Diastolic murmurs are far less common than systolic murmurs and are often more difficult to hear
62
Q

Diastolic murmur

AORTIC REGURGITATION

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. quality
  6. how is murmur best heard
  7. what sound may be present
  8. what sound(s) would suggest severe regurgitation
  9. changes in the apicla impulde (4)
  10. pulse pressure are____? and arterial pulses are _____?
  11. Mechanism
  12. 2 other murmurs associated?
A
  1. location: 2nd to 4th left interspaces
  2. radiation: if loud, to the apex, perhaps to the right sternal border
  3. intensity: grade 1 to 3
  4. pitch: high….. use diaphragm
  5. quality: blowing decrescendo; may be mistaken for breath sounds
  6. murmur heard best with patient sitting, leaning forward, with breath held after exhalation
  7. ejection sound may be present
  8. S3 and S4 (if present) suggest severe regurgitation
  9. progresive changes in apical impusle include increased amplitude, displacement laterally and downward, widened diameter, and increased duration
  10. pulse pressure increases, and arterial pulses are often bounding.
  11. MECHANISM: the leaflets of the aortic valve fail to close completely during diastole, and blood regurgitates from the aorta back into the left ventricle. Volume overload on the left ventricle results.
  12. 2 other murmurs may be associated:
    • mitral diastolic (Austin flint) murmur: attributed to diastolic impingement of the regurgitation flow on the anterior leaflet of the mitral vave
    • midsystolic murmur: from the resulting increased forward flow across the aortic valve
63
Q

Diastolic Murmur

MITRAL STENOSIS

  1. location
  2. radiation
  3. intensity
  4. pitch
  5. which part of stethoscope do you listen with
  6. what are positions and factors to make murmur audible? heard best in ________?
  7. what heart sound is accentuated and where is it palpable?
  8. what often follows S2 and intialted the murmur?
  9. what happens when pulmonary hypertension develops
  10. what is associated with mitral stenosis (2)
  11. mechanism
  12. 2 componenents of resulting murmur
A
  1. location: usually limited to the apex
  2. Radiation: little or none
  3. intensity: grade 1 to 4
  4. pitch: decrescendo low pitched rumble
  5. use bell of stethoscope
  6. placing bell exactly on the apical impulse, turning the patient into a left lateral position and mild exercise all help to make murmur audible. heard better in EXHALATION
  7. S1 is accentuated and may be palpable at the apex
  8. opening snap (OS) often follows S2 and initiates the murmur
  9. pulmonary hypertension develops=p2 is accentuated=right ventricular impulse become palpable
  10. assoiated with mitral stenosis:
    • mitral regurgitation
    • aortic valve disease
  11. Mechanism: when the leaflets of the mitral valve thicken, stiffen, and become distorted from the effects of rheumatic fever, the mitral valve fails to open sufficiently in diastole.
  12. resulting murmur has 2 componenets:
    • presystolic (during atrial contraction)
    • middastolic (during rapid ventricular filling)
64
Q

Cardiovascular sounds with both systolic and diastolic compenents

  • 3 examples
  • continous murmurs
  • arteriovenous fistulas
A
  • some cardiovascular sounds extend beyond one phase of the cadiac cycle
  • 3 examples all nonvalvular in origin
    1. venous hum: benign sound prodiced by turbulence of blood in the jugular veins (common in children)
    2. Pericardial friction rub: produced by inflammation of the pericardial sac
    3. patent ductus arteriosous: congenital abnormality in which an open chanel persists between the aorta and pulmonary artery
  • Continous murmurs: begin in systole and extend through S2 into all or part of diastole, as in Patent Ductus Arteriosus
  • Arteriovenous fistulas (common in dialysis patients) also produce continous murmurs.
65
Q

Cardiovascular sounds with both systolic and diastolic compenents

VENOUS HUM

  1. timing
  2. location
  3. radiation
  4. intensity
  5. quality
  6. pitch
  7. heard best with
A
  1. timing: continous murmur without a silent interval. Loudest in diastole
  2. location: above the medial third of the clavicles, especially on the right
  3. radiation: 1st and 2nd interspaces
  4. intensity: soft to moderate: can be obliterated by pressure on the jugular veins
  5. quality: humming, roaring
  6. pitch: Low
  7. heard with the bell
66
Q

Cardiovascular sounds with both systolic and diastolic compenents

PERICARDIAL FRICTION RUB

  1. timing (3 components) what is each associated with?
  2. what is usually present? what makes the diagonsis? what makes confusion?
  3. location
  4. radiation
  5. intensity
  6. quality (2)
  7. pitch
  8. heard best with?
A
  1. Timing: 3 short componenets, each asscociated with friction from cardiac movements in the pericardial sac
    1. arterial systole
    2. ventricular systole
    3. ventricular diastole
  2. usually first two components are present, all three makes diagnosis easy, only one (usually systolic) invites confusion with a murmur
  3. location: variable, but usually heard bst in the 3rd interspace to the left of the sternum
  4. radiation: little
  5. intensity: variable. may increase when the patient leans forward, exhales, and hold breath (in contrast to pleural rub)
  6. quality: Scratchy, scraping
  7. Pitch: high
  8. heard best with diaphragm
67
Q

Cardiovascular sounds with both systolic and diastolic compenents

PATENT DUCTUS ARTERIOSUS

  1. timing
  2. loudest when? what does it obscure? when does it fade?
  3. location?
  4. radiation?
  5. intensity? what is it associated with?
  6. quality (2 words)
  7. pitch?
A
  1. Timing: continous murmur in both systole and distole, often a silent interval in late diastole
  2. loudest in late systole, obscures S2, fades in diastole
  3. Location: left 2nd interspace
  4. radiaton: toward left clavicle
  5. intensity: usually loud, sometimes associated with a thrill
  6. quality: harsh, machinery-like
  7. Pitch: medium
68
Q

PMI greater then what is evidence of Left ventricular hypertrophy (LVH), or enlargement, seen in hypertension and aortic stenosis

A

gret than 2.5 cm

69
Q

displacement of the PMI __________ to the miclavicular line or greater than _____cm __________to the mitdsternal line also suggests LVH

A

displacement of the PMI lateral to the miclavicular line or greater than 10 cm lateral to the mitdsternal line also suggests LVH

70
Q

when are heart sounds S3 and S4 pathologic?

correlated with what?

S3 corresponds with?

S4 corresponds with?

A

adults over 40

highly correlated with heart failure and acute myocardial ischemia

S3 corresponds with abrupt decleration of inflow acorss the mitral valve

S4 corresponds with an increased left ventricular and diastolic stiffnesss which decreases compliance

71
Q

closure of mitral valve produces

A

S1 first heart sound

72
Q

maximal left ventricular pressure corresponds with

A

systolic blood pressure

73
Q

aortic valve closure produces

A

S2 second heart sound

74
Q

what is usually silent but may have an audible pathologic opening snap

A

mitral valve opening

75
Q
  • P wave
  • QRS complex
    • Q wave
    • R wave
    • S wave
  • T wave
A
  • P wave: atrial depolarization (80 milliseconds; PR interval 120 to 200 milliseconds
  • QRS complex: ventricular depolarization (up to 100 milliseconds)
    • Q wave: downward deflection from septal depolarization
    • R wave: upward deflection from ventricular depolarization
    • S wave: downward deflection following R wave
  • T wave: ventriuclar repolarization or recovery (duration relates to QRS)
76
Q

volume of blood ejected from each ventricle during 1 min

A

cardiac output

77
Q

load that stretches the cardiac muscle before contraction.

volume of blood in the right ventricle at the end of diastole

increases with increased venous return

decreased during exhalation

A

preload

78
Q

ability of the caridac muscle, when given a load, to shorten

increases when stimulated by action of the sympathetic nervous system and decreases when blood flow or oxygen dleivery to the myocardium is imparied

A

myocardial contractility

79
Q

degree of vascualr reisitance to ventricular contraction.

sources of reisitance to left ventricular contraction include the tone in the walls of the aorta, the large arteries, and the peripheral vascular tree, as well as the volume of blood already in the aorta

A

afterload

80
Q

factors influencing aeterial pressure

A
  1. left ventricular stroke volume
  2. distensibility of aorta and large veins
  3. peripheral vascular reistance, particularly at the arteriolar level
  4. volume of blood in the arterial system
81
Q

JVP

A
  • index of right heart pressure and cardiac function
  • reflect right atrial pressure, which in turn equals central venous pressure and right ventricular end iastolic pressure.
  • right internal jugular vein has direct channel into the right atrium

an elevated JVP is 98% specifc for an increased left ventricular end diastolic pressure and low left ventricular ejection fraction, and increases risk of death from heart fialure

82
Q

Major Cardiovascular risk factors

A
  • family history pr pre mature CVD
  • cigarette smoking
  • poor diet
  • physical inactivity
  • obesity (central adiposty)
  • hypertension
  • dyslipidemias
  • diabetes
  • pulse
83
Q

when do you see prominent a waves?

absent a waves?

large v waves occur in?

A

prominent a waves: occur in increased resistance to right atrial contraction, as in tricupid stenosis; also in first degree atrioventricular block, supraventricular tachycardia, jumctional rhythems, pulmonary hypertension and pulmonic stneosis

absent a waves: occur in atrial fibrillation.

large v waves occur in tricuspid regurgitation and contrictive pericaridits

84
Q

pulsus alernans vs paradocixal pulse

A

pulsus alternas and bigeminal pulse vary beat to beat

pardoxical pusle varies with respiration

85
Q

pulsus alternans

A

rhythm of the pulse remians regular, but for the force of the arterial pulse alternates because of alternatign strong ans weak ventricular contractions.

always indictes severe left sided heart fialure and is usually best felt by applying light pressure on the radial or femoral arteries.

use blood pressure cuff to confirm you findings. after riasing the cuff pressure, lower it slowly to the systolic level

inital kortokoff sounds are the strong beats.

as you lower the cuff you will hear the softer sounds of the alternating weak beats.

86
Q

alternating loud and soft korotkoff sounds or a sudden doubling of the apparent heart rate a the cuff pressure declines indicated

A

pulsus alternans

87
Q

the level identified at first hearing Korotkoff sounds is the highest systolic pressure during respiratory cycle. the level identified at hearing sounds throughout the cycle is the lowerst systolic pressure. a difference between these levels or more than 10 mm Hg indicates a _________________ and suggests pericardial tamponade, possible constrictive pericarditis, but most commonly obstructive airway disease

A

paradoxical pusle

88
Q

usually caused by atherosclerotic narrowing of the internal carotid artery

also can arise from a totuour carotid artery with intraluminal turbulance, external carotid arterial disease, aortic stenosis, the hypervascularity of hyperthyroidism, and external compression from thoracic outlet syndrome

A

Thrill and bruits

thrills: palpation…humming vibrations
bruit: murmurlike sounds arising from tubulent blood flow

89
Q

when is there a palpable S2

A

increased pressure in the pulmonary artery (pulm hypertension)

and

systemic hypertension

pulsation here suggests a dilated or aneurysmal aorta

90
Q

left lateral decubitis accentuates

A

peft sided s3 s4 and mitral murmurs

especially mitral stenosis

91
Q

sit up, lean forward, exhle completly and stop breathing in expiration

this accentuates?

A

aortic murmurs

aortic regurg

92
Q

begins after s1 and stops before s2. brief gaps are audible between the murmur and the heart sounds.

A

midsystolic mirmur

93
Q

starts with s1 and stops at s2 with out a gap between murmur and heart sounds

A

pansystolic (holosystolic) murmur

94
Q

starts in mid or late systole and persists up to s2

A

late systolic murmur

95
Q

starts immed. after s2 without a discernible gap, and then usually fades into silence before the next s1

A

early diastolic murmur

96
Q

starts a short time after s2. it may fade away, or merge into a late diastolic murmur

A

middiastolic murmur

97
Q

starts late in diastole and typically continues up to S1

A

a late diastolic (presystolic) murmur

98
Q

begins in systole and extends into all or part of diastole

A

continous murmur

99
Q

murmur that grows louder

A

crescendo murmur

100
Q

murmur grows softer

A

decrescendo murmur

101
Q

murmur first rises in intensity, then falls

A

crescendo-decrescendo murmur

102
Q

murmur has the same intensity throught

A

plateau murmur

103
Q

grades of murmurs

A
104
Q

maneuvers to identify systolic murmurs

squatting

standing

p. 384 bates

A
105
Q

begins in the intima as lipid filled foam cells and then becomes fatty streaks

A

atheroma

106
Q

thickened asymmetric plaques that narrow the lumen reducing blood flow and weaken the underlying media. they have a soft lipid core and a fibrous cap of smooth muscle ceels an a collagen rich matrix. plaque rupture may preceded thrombisis

A

complex atheromas

107
Q

hair loss over the anterior tibiae and dry or brown black ulcers from gangrene may ensure

A

decreased arterial perfusion

108
Q

symptom location suggests the site of arterial ischemia:

A
  • buttock, hip: aortoiliac
  • erectyle dysfunction: iliacpudendal
  • thigh: common femoral or aortoiliac
  • upper calf: superficial demoral
  • lower calf: popliteal
  • foot: tibial or peroneal
109
Q

abdominal pain, “food fear”, and weight loss may suggest

A

intestinal ischemia of the celiac or superior or inferior mesenteric arteris

110
Q

prominent veins in an edematous arm suggest

A

venous obstruction

111
Q

wrist pulses typically normal

spasm of more distal arteries casues episodes of sharly demarcated pallor of the fingers

A

raynaud’s disease

112
Q

if an artery is widely dilated it is:

A

aneurysmal

113
Q

bounding carotid radial and femoral pusles are present in

A

aorti insufficiency

114
Q

assymetric diminshed pulses occur in

A

arterial occlusion from atherosclerois or embolism

115
Q

what may arise from a local or distal infection and may be associated wth general lymphadenopathy?

A

epitrochlear node

116
Q

refers to enlargement of nodes with or without tenderness.

distinguish between local and gernalized by finding eithr a causative lesion in the drainage area or enlraged nodes in at least two other noncontagious lymph node regions

A

lymphadenopathy

117
Q

widened popliteal pulse suggests

A

aneruysm of the popliteal artery

118
Q

commonly obstructs arterial cicrulation in the thigh. femoral pusle is normal, the popliteal decreasd or absent

A

atherosclerosis

119
Q

absent or diminshed pulses at the wrist are found in

persisting palow of hand indicates

marked pallor on elevation

A

acute embolic occlusion

occlusion ulnar artery

arterial insufficnency

120
Q

rapid filling of the superficial veins while the saphenous vein is occluded indicated

A

incompetent valces in the communicating veins

bllood flows quickly retrograde direection form the deep to the saphenous system

sudden additional filling of superdicial veins after release of compresion indicates incompetent valves in the saphenous vein

121
Q
  • edema is soft, bilateral, with pitting after 1-2 seconds of thumb pressure on the anterior tibiae and feet
  • no skin thickening, ulceration, pugmentation
  • results from seceral conditions:
    • when legs are dependent from prolonged standing or sitting (leads to increased hyprostatic pressure in the veins and capillaries)
    • heart failure: leading to decreased caridac output)
    • nephrotic syndomre
    • cirrhosis
    • malnutrition leading to low albumin and decreased intravasular colloid oncotic pressure
    • selected meds
  • pitting reflcts viscosity of the edema fluid, usually low in protein concentration
A

pitting edema

122
Q
  • edema is soft, with pitting on pressure, occasionally bilateral
  • brawny changes and skin thickening near ankle
  • ulceration, brownish pigmentation, edema in the feet are common
A

chronic venous insuffieciency

arises from chronic obstruction and from incompetent valves in the deep venous system

123
Q
  • edema is soft in the early stages, then becomes indurated, hard, and nonpitting
  • skin is thickened, ulceration is rare
  • no pigmentation
  • edema is found in the feet and toes, often bilaterally
  • develops in lymph channels when obstructed by tumor, fibrosis, and in cases of axillary node dissection and radiation
A

lymphedema

124
Q

Chronic Arterial insufficiency

  1. pain
  2. mechanism
  3. pusles
  4. color
  5. temp
  6. edema
  7. skin changes
  8. ulceration
  9. gangrene
A
  1. pain: intermittent claudication, progrressing to pain at rest
  2. mechanism: tissue ischemia
  3. pusles: decreased or absent
  4. color: pale, especially on elevation, dusky red on dependency
  5. temperature: cool
  6. edema: absent or mild, may develop as the patient tries to relieve rest pain by lowering legs
  7. skin chnages: trophic chages: thin shiny atrophic skin; loss of hair over food and toes; nails thickened and riged
  8. ulceration: if present involved toes or points of trauma on feet
  9. gangrene: may develop
125
Q

Chronic venous insufficiency

  1. pain
  2. mechanism
  3. pusles
  4. color
  5. temp
  6. edema
  7. skin changes
  8. ulceration
  9. gangrene
A
  1. pain: often painful
  2. mechanism: venous hypertension
  3. pusles: normal though may be difficult to feel through edema
  4. color: normal, or cyanotic on dependency Petechiae and then brown pigmentation appear with chroniciity
  5. temp: normal
  6. edema: persent, often marked
  7. skin changes: often brown pigmentation around ankles, stasis dermatitis, and possible thickening of the skin and narrowing of the leg as scarring develops
  8. ulceration: if present develops at sides of ankles (medial)
  9. gangrene: does NOt DEVELOP
126
Q

CHRONIC VENOUS INSUFFICIENCY ULCER

A
  • meidal malleolus
  • ulcer contains small painful granulation tissue and fibrin
  • necorsis or exposed tendons are rare
  • borders are irreg., flat, or slightly steep
  • pain affects quality of life in 75% of pt
  • associated findings:
    • edma
    • reddish pigmentation
    • purapura
    • venous varicosities
    • eczematous changes of stasis dermatitis (redness, scaling, pruritis)
    • cyanosis at times
    • gangrene rare
127
Q

arterial insufficieny ulcers

A
  • occurs in toes feet or possibly areas of tauma (shins)
  • surrounding skin shows no callus or excess pigment, although it may be atrophic
  • pain often is severe unless neuropathy masks it
  • gangrene can be assoicated
  • decreased pusles
  • trophic changes
  • foot pallow on elevation
  • dusy rubor on dependency
128
Q

neuropathic ulcer

A
  • pressure points of areas with diminshed sensation
  • seen in diabetic neuropathy, neurologic disorders, Hansen disease
  • surrounding skin is calloused
  • no pain, so the ulcer may go unnoticed
  • uncomplicated cases: no gangrene
  • assoicated signs:
    • decreased sensation
    • absent ankle jerks
129
Q

ankle-brachial index

A
  1. pt rests supine in warm room for at least 10 min before testing
  2. place cuff on both arms and ankles then apply ultra sound gel over brachial, dorsalis pedis and posterior tibial arteries
  3. measure the systolic pressures in the arms
    • use vascular doppler to locate brachial pulse
    • inflate cudd 20mm Hg above last audble pulse
    • deflate duff slowly and record pressure at which oulse become audible
    • obtain 2 measures in each arm and record the average as the brachial pressure in that arm
  4. measure systolic pressures in ankles
    • use vascular doppler to locate dorsalis pedis pulse
    • inflate cuff 20 mm Hg above last audble pulse
    • deflate cuff slowly and record pressure at which pulse becomes audible
    • obtain 2 measures in wach ankle and record the average as the dorsalis pedis presure in that leg
    • repeat steps for post. tibial arteries
  5. calculate ABI

Right ABI= (highest right average ankle pressure)/(highest average arm pressure)

interpretation:

>0.90 (range 0.90-1.30)= normal lower extremity blood flow

<0.89 to >0.60= mild PAD

<0.59 to >0.40= moderate PAD

< 0.39=severe PAD

130
Q

Arterial disorders

Atherosclerosis

intermittent claudication

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process: episodic muscular ischemia induced by exericise, due to atheroscerlosis of large or medium sized arteries
  2. location of pain: usually calf muscle, but also mmay be in the buttock, hip, thigh, foot depending on the level of obstruction
  3. timing: fairly brief; pain usually forces the patient to rest
  4. factors that aggrevate: exercise such as walking
  5. factors that relieve : rest usually stops the pain in 1-3min
  6. associated manifestations:
    1. Local fatigue
    2. numbness
    3. diminshed pulses
    4. often signs of arterial insufficiency
131
Q

ARTERIAL DISORDERS

Atherosclerosis

rest pain

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process: ischemia even at rest
  2. location of pain: distal pain, in the toes or forefoot
  3. timing: persistent, often worse at night
  4. factors that aggrevate: elevation of the feet, as in bed
  5. factors that relieve: sitting with legs dependent
  6. associated manifestations:
    1. numbness
    2. tingling
    3. trophic signs
    4. color changes or arterial insufficeny
132
Q

ARTERIAL DISORDERS

Acute arterial occlusion

  1. process
  2. location of pain
  3. timing
  4. associated manifestations
A
  1. process: embolism or thrombosis, possibly superimposed on arterioscelerosis obliterans
  2. location of pain: distal pain, usually involving the food and leg
  3. timing: sudden onset; associated symptoms may occur without pain
  4. associated manifestations:
    1. coldness
    2. numbness
    3. weakness
    4. absent distal pulses
133
Q

ARTERIAL DISORDERS

Raynaud’s disease and phenomenon

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process:
    1. Raynauds disease: episodic spasm of the small arteries and arterioles; no vascular occlusion
    2. Raynauds phenomenon: syndrome secondary to other conditions such as collagen vascular dsease, arterial occlusion, trauma, drugs
  2. location of pain:
    1. Raynauds Disease: distal potion of one or more fingers
    2. Raynaud’s phenomenon: pain is usually not prominent unmless fingertip ulcers develop. numbness and tingling are common
  3. timing: relatively brief (min.) but recurrent
  4. factors that aggrevate: exposure to cold, emotional upset
  5. factors that relieve : warm environment
  6. associated manifestations:
    • color changes in the distal fingers
      • pallor (essential for diagnosis
      • followed by cyanosis and then
      • redness
134
Q

VENOUS DISORDERS

Superficial thrombophlebitis

  1. process
  2. location of pain
  3. timing
  4. associated manifestations
A
  1. process: clot formation and acute inflammation in a superficial vein
  2. location of pain: pain in a local area along the course of a superficial vein, most often in the saphenous system
  3. timing: an acute episode lasting days or longer
  4. associated manifestations:
    • local redness, swelling, tenderness, palpable cord, possible fever
135
Q

VENOUS DISORDERS

Deep venous thrombosis (DVT)

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process: clot formation in a deep vein
  2. location of pain: tight, bursting pain, if present, usually in the calf; may be painless
  3. timing: often hard to determine because of lack of symptoms
  4. factors that aggrevate: walking
  5. factors that relieve : elevation speeds relief
  6. associated manifestations:
    • possible swelling of the foot and calf
    • local calf tenderness
    • propior hx of DVT
136
Q

VENOUS DISORDERS

Chronic venous insufficiency (deep)

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process: chronic venous engorgement secondary to venous occlusion or incompetency of venous valves
  2. location of pain: diffuse aching of the leg(s)
  3. timing: chronic, increasing as the day wears on
  4. factors that aggrevate: prolonged standing
  5. factors that relieve : elevation of legs
  6. associated manifestations:
    • chronic edema
    • pigmentation
    • possibly ulceration
137
Q

THROMBOANGIITIS OBLITERANS (BUERGER’S DISEASE)

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process: inflammatory and thrombotic occlusions of small arteries and also of veins, occurring in smokers
  2. location of pain:
    • intermittent claudication, particularly in the arch of the foot
    • rest pain in the fingers or toes
  3. timing:
    • fairly brief but recurrent
    • chronic, pereisitent, may be worse at night
  4. factors that aggrevate:
    • exercise
  5. factors that relieve:
    • rest
    • permanent cessation of smoking helps both kinds of pain (but pts seldom stop)
  6. associated manifestations:
    • distal coldness, sweating, numbness, cyanosis
    • ulceration and gangrene at the tips of fingers or toes
    • migratory thrombophlebitis
138
Q

COMPARTMENT SYNDOME

  1. process
  2. location of pain
  3. timing
  4. factors that aggrevate
  5. factors that relieve
  6. associated manifestations
A
  1. process: pressure builds from trauma or bleeding into one of the four major muscle compartments between the knee and ankle. each compartment is enclosed by fascia and thus cannot expand to accommodate increasing pressure
  2. location of pain: tight, bursting pain in calf muscles, usually in the anterior tibial compartment, sometimes with underlying dusky red skin
  3. timing:
    • several hours if ACUTE (pressure must be relieved to overt necrosis).
    • during exerise if CHRONIC
  4. factors that aggrevate:
    • Acute: anabolic steriods; surgica complpicaitons, crush injury
    • chronic: occurs with exericise
  5. factors that relieve:
    • acute: surgical incision to relieve pressure
    • chronic: avoiding exericise; ice elvation
  6. associated manifestations
    • tingling, burning sensation in claf
    • muscles may feel tight, full, numbness, paralysis if unrelieved
139
Q

ACUTE LYMPHANGITIS

  1. process
  2. location of pain
  3. timing
  4. associated manifestations
A
  1. process: acute bacterial infection (usually streptococcal) spreading up the lymphatic channels from a portal of entry such as an injured area or an ulcer
  2. location of pain: an arm or a leg
  3. timing: acute episode lasting days or longer
  4. associated manifestations:
    • red streaks on the skin
    • tenderness, enlarged, tender lymph noses
    • fever
140
Q

Mimics (primarily mistaken for acute superficial thrombophlebitis)

ACUTE CELLULITIS

  1. process
  2. location of pain
  3. timing
  4. associated manifestations
A
  1. process: acute bacterial infection of the skin and sucutaneous tissues
  2. location of pain: arms, legs, elsewhere
  3. timing: an acute episode lasting days or longer
  4. associated manifestations:
    • local area of diffuse swelling, redness, and tenderness
    • with enlarged, tender lymph nodes and fever
    • no palpable cord
141
Q

Mimics (primarily mistaken for acute superficial thrombophlebitis)

ERYTHEMA NODOSUM

  1. process
  2. location of pain
  3. timing
  4. associated manifestations
A
  1. process: raised tender bilateral subq lesions seen in systemic conditions such as pregnancy, sarcoidosis, tuberculosis, streptococcal infections, inflammatory bowel disease
  2. location of pain: anterior surfaces of both lower legs
  3. timing: pain associated with a series of lesions over several weeks
  4. associated manifestations:
    • lesions recur in crops
    • often malaise
    • joint pains
    • fever
142
Q

lifestyle change and risk factor modification for prevention of management of hypertension

A
  1. optimal weight (BMI of 18.5-24.9)
  2. intake of <6g of sodium chloride or 2.4 g of sodium per day
  3. regular aerobic exercise such as brisk walking for at least 30 min per day, most days of the week
  4. moderate alcohol cosumption per day of 2 drinks or fewer for men and 1 drink or fewer for women
  5. dietary intake of more than 3,500 mg of potassium
  6. diet rich in fruits, vegetables, and low-fat dairy products with reduced content of saturated and total fat
143
Q

CVD differences in women

A
  • rates for CVD in women have declined 50% since 1980
  • still leading casue of death in woman and men
  • for women stroke accounts for a high proportion of CVD deaths
  • higher lifetime risk of stroke in women
  • women risk factors for stoke: pregnancy, hormone therapy, early menopasue, preeclampsia, afib
  • adverse trends in CVD risk factors for women
  • black women have the highest prevalence of hypertension and are less likely to have their hypertension controlled
  • AHA recomends placing women into one of the 3 cateogries :
    • high risk
    • at risk
    • ideal cardiovascular health
    • (see picture)
144
Q

CVD in african americans

A
  • CVD death rates for black remain inordinetely high compared to whites for both men and women
  • this is from Bates there is a chart in bates saying the specific numbers and values but i dont think it is relevant
  • p. 352

Sasha: Cardiovascular Clinical Assessment (2 decks)

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