Talley Review Flashcards

1
Q

radiofemoral delay

A

Palpate radial pulse and femoral pulse (situated below the inguinal ligament, 1/3rd of the way up from the pubic tubercle)
A noticeable delay in the arrival of the femoral pulse wave suggests dx of coarctation of the aorta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

radial-radial delay

A

Inequality in timing or volume, usually due to a large arterial occlusion by atherosclerotic plaque or aneurysm or to subclavian artery stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pulse sign in aortic regurgitation

A

collapsing pulse (bounding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pulsus alternans

A

alternating strong and weak pulse

advanced LVF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pulsus paradoxus

A

normal reduction of blood pressure with inspiration is exaggerated.
BP reduce because intrathoracic pressure becomes more negative and blood pools in the pulmonary vessels so left-heart filling is reduced

Chasmal meant by this that there was a fall in bp and a paradoxical rise in PR

Fall in bp on inspiration of more than 10mmHg is abnormal and may occur with constrictive pericarditis, pericardial effusion or severe asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

JVP
What does it tell us about?
What is assessed?

A

Tells us about right atrial and right ventricular function.
Height: JVP of 3cm+ of the zero point indicated right heart filling pressure is raised - sign of RVH, volume overload or of some types of pericardial disease.
Character: assessment of waves
a wave - right atrial systole - coincides with 1st heart sound and precedes the carotid pulsation
v wave - due to atrial filling, in the period when the tricuspid valve remains closed during ventricular systole
X descent - trough caused by atrial relaxation - the x descent is interrupted by the c point which is due to transmitted carotid pulsation and coincides with tricuspid valve closure - no usually visible

Following the v wave, the tricuspid valve opens and rapid ventricular filling occurs this results in the y descent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

JVP clinical sign noted in any condition in which right ventricular filling is limited (e.g.. constrictive pericarditis, cardiac tamponade or right ventricular infarction)

A

Kussmaul’s sign - elevation of the venous pressure which is more marked on inspiration when venous return to the heart increases

Sign is best elicited with the patient sitting up at 90 degrees and breathing quietly through the mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hepatojugular reflux or abdominojugular reflux test

A

Testing for right of left ventricular failure or elevated left atrial pressures
it may remain elevated over 4cm for the duration of the compression

Apply pressure with palm of hand to middle of abdomen for 10 seconds

the sudden fall in the JVP >4cm as the pressure is released ay be easier to see than the initial rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathological JVP waves:
cannon a waves
giant a waves
large v waves

A

Cannon a waves - right atrium contracts against the closed tricuspid valve - occurs intermittently in complete heart block

Giant a waves - large but not explosive a waves with each beat. They occur when right atrial pressures are raised because elevated pressures in the pulmonary circulation or obstruction to outflow (tricuspid stenosis)

large v waves - tricuspid regurgitation should never be missed - visible welling up into the neck during each ventricular systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Checking for pitting pedema

A

palpate behind the medial malleolus of tibia and distal shaft of the tibia by compressing for at least 15 seconds

pitting - skin indented and only slowly refills

oedema due to hypoalbuminaemia often refills more quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

causes of peripheral oedema
Pitting vs non-pitting
and unilateral lower limb oedema

A

Pitting lower limb oedema
Cardiac - CCF, constrictive pericarditis
Drugs - calcium antagonists
Hepatic - cirrhosis causing hypoalbuminaemia
Renal - nephrotic syndrome causing hypoalbuminaemia
GI - malabsorption, starvation, protein-losing enteropathy causing hypoalbuminaemia
Beri-beri
cyclical oedema

Pitting unilateral lower limb oedema
DVT
Compression of large veins by tumour or lymph nodes

Non-pitting lower limb oedema
Hypothyroidism
Lymphoedema
- infections - filariasis
- malignant (tumour invasion of lymphatics)
- congenital (lymphatic development arrest)
- allergy
- milord’s disease - unexplained lymphedema which appears at puberty and is more common in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Definition
Dyspnoea

Orthopnoea

Paroxysmal nocturnal dyspnoea

A

the awareness that an abnormal amount of effort is required for breathing

Orthopnoea - SOB when supine

PND - severe dyspnoea that wakes pt from sleep so that he or she is forced to get up grasping for breath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NY Heart classification - Dyspnoea

A

Class I - disease present by no dyspnoea or dyne only on heavy exertion
Class II - dyspnoea on moderate exertion
Class III - dyspnoea on minimal exertion
Class IV - dyspnoea at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ddx of dyspnoea based on time course of onset

A
Seconds to minutes 
- asthma
- PE
- pneumothorax
- pulmonary oedema
- anaphylaxis
- foreign body causing airway obstruction
Hours or days 
- COPD -exacerbation
- CF
- Ashtma
- respiratory infection
- pe
- metabolic acidosis
Weeks++
- pulmonary fibrosis
- COPD
- PE
- Anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cardiac dyspnoea

A

typically chronic and occurs with exertion because of failure of LV output to rise with exercise - this leads to an acute rise in LV ED Pressure, raised pulmonary venous pressure, interstitial fluid leakage and thus reduced lung compliance

Orthopnoea - when upright pt interstitial oedema is redistributed to lower zones of the lungs and become worse and upper zones better.

Note absence of orthopnoea suggest that LVF is unlikely to be the cause of a pats dyspnoea

PND - sudden failure of LV output with an acute rise in pulmonary venous and capillary pressures - leads to transudation of fluid into the interstitial tissues which increased the work of breathing. The sequence may be precipitated by resorption of peripheral oedema at night while supine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When you are assessing a patient with shortness of breath, you need to recognize the signs and symptoms consistent with severe respiratory distress.

A

Inability to speak
Diaphoresis (sweating)
Tripod positioning - this is where the patient stands or sits leaning forwards, supporting the upper body with the hands on the knees or another surface. This position optimises the mechanics of respiration by taking advantage of the accessory muscles of the neck and upper chest to get more air into the lungs.
Extreme tachypnoea (respiratory rate greater than 30 breaths per minute)
Hypoxaemia (Pulse Oximetry

17
Q

Muscles used in quiet respiration:

A

The diaphragm and, to a lesser extent, the intercostal muscles drive respiration during quiet breathing.

18
Q

Accessory Muscles of respiration

Seen in respiratory distress..

A

sternocleidomastoid and the scalene muscles (anterior, middle and posterior scalene) are typically considered accessory muscles of breathing. Both assist in elevating the rib cage.

Apart from these neck muscles, the following muscles have also been observed contributing to respiration: serratus anterior, pectoralis major and pectoralis minor, trapezius, latissimus dorsi, erector spinae, iliocostalis lumborum, quadratus lumborum, serratus posterior superior, serratus posterior inferior, levatores costarum, transversus thoracis, subclavius

19
Q

Muscles of expiration

A

During quiet breathing, there is little or no muscle contraction involved in exhalation; this process is simply driven by the elastic recoil of the thoracic wall. When forceful exhalation is required, or when the elasticity of the lungs is reduced (as in emphysema), active exhalation can be achieved by contraction of the abdominal wall muscles (rectus abdominus, transverse abdominus, external oblique muscle and internal oblique muscle). These press the abdominal organs cranially (upward) into the diaphragm, reducing the volume of the thoracic cavity.

The internal intercostal muscles have fibres that are angled obliquely downward and backward from rib to rib. These muscles can therefore assist in lowering the rib cage, adding force to exhalation

20
Q

Renal artery bruits
Where best heard?
Systolic vs diastolic renal bruit.. ?significance

A
  1. above umbilicus 2cm to left or right of midline
  2. A diastolic component makes the bruit more likely to be haemodynamically significant. Presence suggest renal artery stenosis due to fibromuscular dysplasia or atherosclerosis - approx 50% of patients with renal artery stenosis will have a bruit. soft systolic bruit - half of these puts will not have any significant renal artery stenosis.