APO Flashcards
(15 cards)
Define APO
Sudden accumulation of serous Transexudate into the interstitial space between the capillaries and the alveoli, Bronchioles and bronchi
Describe the reasons for left ventricular failure
AMI Cardiomyopathy ACS Hypertension Valvular disease
What compensatory mechanisms arise as a result of left ventricular failure
- starlings regulation
- sympathetics
- ventricular remodelling
- Renal Compensation
- Atrial Natriuretic peptide
Describe the fluid movement in the alveoli under normal pressures
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
Describe fluid movement in lungs with APO
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
Describe the vicious cycle of APO
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
Patient presentation of APO
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
Ddx for APO
- acute episode of COPD or asthma
- acute pneumonia
- pulmonary embolism
- arrythmia
Patient management APO
- GTN rest and recovery Posture Oxygen cpap Diuretics Opiates
IV access
12 Lead ecg
Describe a diuretic drug
Frusemide
Describe starlings regulation
When does it happen?
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
Describe sympathetic regulation
Detected by baroreceptors
- increased force of contraction (inc. sympathetic tone)
- inc. catecholamine release
- tachycardia, vasoconstriction, redistribution of blood
APO mechanism
Describe ventricular remodeling
Changes to structure (muscle mass) and function (impaired systolic function)
Injury to the myocardium > hypertrophy
APO mechanism
Describe Renal Compensation
When it’s seen?
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
Atrial Natriuretuc Peptide describe
Potent diuretic
Release from Syria in response to stretch
Inhibit
RAA system
Sympathetic ns system