APO Flashcards

(15 cards)

1
Q

Define APO

A

Sudden accumulation of serous Transexudate into the interstitial space between the capillaries and the alveoli, Bronchioles and bronchi

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2
Q

Describe the reasons for left ventricular failure

A
AMI
Cardiomyopathy 
ACS
Hypertension 
Valvular disease
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3
Q

What compensatory mechanisms arise as a result of left ventricular failure

A
  • starlings regulation
  • sympathetics
  • ventricular remodelling
  • Renal Compensation
  • Atrial Natriuretic peptide
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4
Q

Describe the fluid movement in the alveoli under normal pressures

A

Normal pressure
Artery side - hydrostatic pressure forces fluid out of the capillaries into the interstitial space

Vein side - colloid osmotic pressure forces fluid back into the capillary

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5
Q

Describe fluid movement in lungs with APO

A

Extra pressure build up leads to increased hydrostatic pressure forcing more fluid into interstitial space

Colour osmotic pressure is not enough to force fluid back into capillaries therefore fluid fills alveoli and gas exchange is compromised

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6
Q

Describe the vicious cycle of APO

A

Increased hydrostatic pressure - fluid accumulation in alveoli

Reduced gas exchange = hypoxia ^ Work of breathing

Increased Catecholamine release and renin, angiotensin, aldosterone activation

Increased systemic vascular resistance
Increased preload and afterload
Increased cardiac work and O2 demand

Decreased Ventricular emptying, relaxation
decreased cardiac output

Increased end diastolic volume/pressure
Increased LA pressure
Increased pulmonary vascular pressure

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7
Q

Patient presentation of APO

A

Cardiovascular

  • increase hr
  • arrhythmias
  • orthostatic hypotension
  • decreased peripheral pulses
  • pale/cyanosic, cool clammy

Respiratory

  • dyspnoea on exertion
  • orthopnoea (sob on lying down)
  • tachypnoea
  • dry cough
  • adventitious sounds (crackles, wheezes, decreased breath sounds)

subclavian retraction
V/Q mismatch

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8
Q

Ddx for APO

A
  • acute episode of COPD or asthma
  • acute pneumonia
  • pulmonary embolism
  • arrythmia
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9
Q

Patient management APO

A
- GTN 
rest and recovery 
Posture 
Oxygen
cpap 
Diuretics 
Opiates 

IV access
12 Lead ecg

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10
Q

Describe a diuretic drug

A

Frusemide

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11
Q

Describe starlings regulation

When does it happen?

A

Pooling if blood in the LV increased LVEDP leading to lengthening of myocardial fibres

  • resulting in
    Increased inotropy, preload, SV, myocardial oxygen consumption

APO mechanism

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12
Q

Describe sympathetic regulation

A

Detected by baroreceptors

  • increased force of contraction (inc. sympathetic tone)
  • inc. catecholamine release
  • tachycardia, vasoconstriction, redistribution of blood

APO mechanism

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13
Q

Describe ventricular remodeling

A

Changes to structure (muscle mass) and function (impaired systolic function)

Injury to the myocardium > hypertrophy

APO mechanism

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14
Q

Describe Renal Compensation

When it’s seen?

A

APO mechanism

Activation of
Renin - angiotensin - aldosterone RAA system

Decreased Renal blood flow > sodium and water retention

Angiotensin - peripheral vasoconstriction
Aldosterone > promotes sodium retention, SNS activation, baroreceptor dysfunction > stretch ventricle walls (good) but leads to neg outcome

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15
Q

Atrial Natriuretuc Peptide describe

A

Potent diuretic
Release from Syria in response to stretch

Inhibit
RAA system
Sympathetic ns system

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