Cardiogenic Pulmonary Oedema

Question 1

define acute cardiogenic pulmonary oedema

Answer 1

Leakage of fluid from the pulmonary capillaries and venules into the alveolar space as a result of increased hydrostatic pressure
Inability of left ventricle to effectively handle its pulmonary venous return

Question 2

causes of ACPO

Answer 2

F - forgot meds
A - arrhythmias and anemia
I - ischemia, infarction, infection
L - lifestyle, sodium diet
U - upregulation of cardiac output like pregnancy and thyroid storm
R - renal failure, retention from steroids and NSAIDS
E - endocardium / valvular pathology

Question 3

clinical features of ACPO

Answer 3

SOB
Orthopnoea
PND
Tachycardia
BP
Wheezing
Crepitations

Question 4

NYHA Classification

Answer 4

Class I : No limitation of physical activity. Ordinary activity causes no undue fatigue, palpitations or dyspnoea.
Class II : Slight limitation of physical activity. Comfortable at rest, symptomatic with ordinary activity.
Class IIIA : Marked limitation of physical activity. Comfortable at rest, symptomatic at less than ordinary activity
Class IIIB : Comfortable at rest, symptomatic with minimal activity.
Class IV : symptomatic at rest, discomfort increased with any activity

Question 5

what is Killip used for ?

Answer 5

Scoring system to assess severity of heart failure in patients with acute myocardial infarction

Question 6

Give the Killip classification

Answer 6

Killip I: no clinical signs of heart failure

Killip II: crackles in the lungs, third heart sound (S3), and elevated jugular venous pressure

Killip III: acute pulmonary oedema

Killip IV: cardiogenic shock or arterial hypotension (measured as systolic blood pressure < 90 mmHg), and evidence of peripheral vasoconstriction

Question 7

evidence of peripheral vasoconstriction

Answer 7

O - oliguria
C - cyanosis
D - diaphoresis

Question 8

physical exam

Answer 8

Assess weight and vital signs, manage accordingly
Presence and severity of crackles, S3 gallop, elevated JVP, hepatic enlargement and tenderness, positive hepatojugular reflex, peripheral oedema and ascites
Thorough clinical examination on cardiovascular and respiratory systems

Question 10

what investigations should be done?

Answer 10

1. Blood
2. ECG
3. Radiology - CXR, echo and bedside ultrasound

Question 11

what bloods should be done?

Answer 11

ABG
FBC - assess anemia or infection
U+E
Troponin - if infarction suspected

Question 12

what might you find on ECG?

Answer 12

ST changes = ischemia or infarction

Arrhythmias

LVH

Prolonged QRS

Question 12

why prolonged QRS

Answer 12

Prolonged QRS duration (QRSd) is an important prognostic indicator in patients with systolic heart failure. 1–4. Prolonged QRSd is due to delayed ventricular electrical activation, most commonly left bundle-branch block. This altered electrical activation sequence may result in mechanical dyssynchrony.

Question 13

Specific ECG Criteria for LVH

Answer 13

Voltage Criteria:
R wave in V5 or V6 greater than 30 mm.
S wave in V1 or V2 greater than 30 mm.
R or S wave in any limb lead greater than 20 mm.
S wave in V1 or V2 plus R wave in V5 or V6 greater than 35 mm (Sokolow-Lyon criterion).

ST-T Wave Changes (Strain Pattern):
Inverted T waves in leads I, aVL, and V5-V6.
Downsloping, asymmetrical ST-segment depression opposite the QRS vector.

Left Axis Deviation:
QRS axis more negative than -30 degrees.

Question 14

CXR findings

Answer 14

• cardiomegaly
• vascular redistribution
• oedema
• effusions

Question 15

in which cases may there be limited CXR findings?

Answer 15

• new dx
• COPD

Question 16

differential diagnosis

Answer 16

Pneumothorax
Neurogenic Pulmonary Oedema
Pulmonary Embolism
Pulmonary Fibrosis

Question 17

management goals in ACPO?

Answer 17

1. ABCs
2. Decrease preload / R-sided filling
3. Increase afterload / L-sided emptying
4. Improve LV contractility

= redistribute fluid out the lungs

Question 18

initial emergency mx

Answer 18

Attach patient to monitors, acute care setting (resus)
Address airway – ensure patency. Apply supplemental oxygen if needed. Consider non-invasive positive pressure ventilation (NPPV) or intubation if necessary
Breathing
Circulation – establish IV access, consider inotropes if clinically shocked or significantly hypotensive (LV contractility)
Disability – may have reduced level of consciousness due to hypoxia

Question 19

supplemental O2

Answer 19

Consider in patients with sats <94% on room air, or with signs of respiratory distress

Titrate oxygen to symptoms

Administer via nasal cannula, facemask or partial non- rebreather mask
Assess efficacy, determine need for NPPV or intubation

Question 20

how is preload reduced?

Answer 20

NITRATES
1. Isordil 5mg s/l or GTN spray (one dose) can be used, repeated every 5-10 minutes

2. Nitrate Infusion: mix 50mg GTN (Tridil) in 200ml normal saline. Rate 0-48ml/hour, start at 20ml/hour and titrte to blood pressure.

Avoid lowering systolic BP <90-100mmHg

Question 21

nitrates MOA

Answer 21

venodilation = decreased preload

higher dose –> arteriolar dilation = decreased afterload

—> decreases pulmonary hydrostatic pressure

Question 22

when should furosemide be considered?

Answer 22

if there is fluid retention, but no benefit in normovolaemic pts

Question 23

dosing of furosemide and MOA

Answer 23

Diuretic naïve: IV furosemide 1mg/kg
Patient already on diuretics: usual dose in IV form

–> decreased preload, but overall effect delayed

Question 24

alternate consideration of drug to be given?

Answer 24

No good evidence to support immediate reduction in preload centrally May provide anxiolysis May reduce BP and respiratory drive If used, titrate in small doses (2,5mg IV as needed, max 0,1mg/kg)

Question 25

what can be give to reduce afterload?

Answer 25

ACE-INHIBITORS

Question 26

MOA and dosing of ACE-I

Answer 26

Sublingual or IV ↓ Afterload ↓ Preload ↓ Pulmonary Capillary Wedge Pressure Down-regulate renin-angiotensin system SBP > 110mmHg: Captopril 25mg s/l crushed SBP 90-110mmHg : Captopril 12,5mg s/l crushed

Question 27

benefits of ACE-I

Answer 27

Decreases need for intubation/ NPPV Combination with nitrates exceeds benefit of either drug used on its own

Question 28

when should inotropic support be given?

Answer 28

Should be used when LV contractility is poor and patient is hypotensive or shocked

Question 29

options for inotropes Options include adrenaline, dopamine, dobutamine, milrinone

Answer 29

Options include adrenaline, dopamine, dobutamine, milrinone

Question 30

the pt has resp failure or an acidosis....what now?

Answer 30

NIPPV - decreases work of breathing, improves oxygenation, CO2 exchange Start with a low PEEP of 5, and slowly increase as needed. Educate patient how to hold mask and breathe, as it is uncomfortable --> If combative or confused, consider intubation

Question 31

when should intubation be considered?

Answer 31

Cardiac arrest Imminent respiratory failure No improvement on NPPV Patient not tolerating NPPV

Question 32

discharge criteria?

Answer 32

No longer hypoxic on room air Vital signs have returned to normal parameters Return to baseline effort tolerance Cause of failure identified and appropriately managed Patient understanding of medication compliance checked Medication adjusted as required Follow up arranged

Question 33

how is vascular re-distribution seen?

Answer 33

upper lobe deviation

Question 34

right diastolic failure seen in...

Answer 34

tamponade

Question 35

markers on CXR of oedema

Answer 35

- upper lobe deviation - Kerly B lines parallel - nodular opacities from alveolar oedema (see other )