Transcript SAED Recert - Hamilton Health Sciences

PULMONARY
EDEMA
Prepared by:
South West Education
Committee
Congestive Heart Failure
or
Acute Pulmonary Edema
SWEC Base Hospitals
Credit: W.A. (Bill) Penhallurick Southeastern Regional BH
OUTLINE
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Review the pathophysiology and
etiology of Congestive Heart Failure
Review the pathophysiology, etiology
and emergency treatment of Acute
Pulmonary Edema
Review cardio-respiratory assessments
Review the Acute Pulmonary Edema
protocol and the use of Nitroglycerin
OBJECTIVES
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Describe the possible causes of
pulmonary edema.
Explain the indications for NTG
treatment
Describe the limitation to treatment
Explain the treatment procedure.
INTRODUCTION
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Congestive Heart Failure (CHF)??? :
A syndrome resulting from an imbalance
in pump function in which the heart fails
to maintain an adequate circulation of
blood.
Results in retention of fluid “congestion”.
PULMONARY CIRCULATION
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Blood flows from the right ventricle
through the pulmonary artery
Blood reaches the capillaries
surrounding alveoli where gas
exchange occurs
Oxygenated blood returns by pulmonary
veins to the left ventricle where it is
pumped into systemic circulation
ETIOLOGY AND
PATHOPHYSIOLOGY
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Syndrome usually results from LV
dysfunction and compensatory
mechanisms
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Cardiac performance is a function of 4
primary factors. What are they?
4 FACTORS DETERMINING
CARDIAC PERFORMANCE
1.
2.
3.
4.
Preload (define)
Afterload (define)
Contractility
Heart Rate
Compensatory Mechanisms to
Maintain Cardiac Output:
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The Frank-Starling mechanism
– Myocardial hypertrophy

Increased sympathetic tone
– All result in increased myocardial O2 demand!

Kidneys
CAUSES OF
Congestive Heart Failure
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Conditions that increase preload, e.g. aortic
regurgitation, ventricular septal defects, fluid
overload
Conditions that increase afterload, e.g. aortic
stenosis, systemic hypertension
(vasoconstriction),
Conditions that decrease myocardial
contractility, e.g. MI, cardiomyopathies,
pericarditis, tamponade
SIGNS &SYMPTOMS OF
Congestive Heart Failure
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Exertional dyspnea usually with Crackles
- fatigue may be the first sign
Increased respiratory rate and effort
Orthopnea and/or PND
Cyanosis and pallor
Tachycardia
JVD
Dependant edema
CATEGORIZING FAILURE
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Left or Right sided heart failure
Forward or Backward ventricular failure
– Backward failure is secondary to elevated
systemic venous pressures.
– Forward ventricular failure is secondary to
left ventricle failure and reduced flow into
the aorta and systemic circulation
LV BACKWARD EFFECTS
Decreased emptying of the left ventricle

Increased volume and end-diastolic
pressure in the left ventricle
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Increased volume (pressure) in the left
atrium
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Increased volume in pulmonary veins

LV BACKWARD EFFECTS con’t
Increased volume in pulmonary capillary
bed = increased hydrostatic pressure
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Transudation of fluid from capillaries to
alveoli
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Rapid filling of alveolar spaces

Pulmonary edema
LV FORWARD EFFECTS
Decreased cardiac output

Decreased perfusion of tissues of body

Decreased blood flow to kidneys and glands

Increased reabsorption of sodium and water and
vasoconstriction

LV FORWARD EFFECTS con’t
Increased secretion of sodium and
water-retaining hormones

Increased extracellular fluid volume

Increased total blood volume and
increased systemic blood pressure
RV BACKWARD EFFECTS
Decreased emptying of the right ventricle

Increased volume and end-diastolic pressure in
the right ventricle
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Increased volume (pressure) in right atrium
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Increased volume and pressure in the great veins
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RV BACKWARD EFFECTS con’t
Increased volume in the systemic venous
circulation
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Increased volume in distensible organs
(hepatomegaly, splenomegaly)
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Increased pressures at capillary line
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Peripheral, dependant edema and serous
infusion
RV Forward Effects
Decreased volume from the RV to the
lungs
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Decreased return to the left atrium and
subsequent decreased cardiac output

All the forward effects of left heart failure
Congestive Heart Failure
Can Be Defined Based on:
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How rapid the symptoms onset
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Which ventricle is primarily involved
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Overall cardiac output
Left Heart Failure and
Pulmonary Edema
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LVF occurs when the left ventricle fails to
function as an effective forward pump,
causing a back-pressure of blood into the
pulmonary circulation
May be caused by a variety of forms of heart
disease including ischemic, valvular, and
hypertensive heart disease
Untreated, significant LVF culminates in
pulmonary edema
Left Heart Failure and
Pulmonary Edema
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Signs and symptoms
– Severe respiratory distress
– Severe apprehension, agitation, confusion
– Cyanosis (if severe)
– Diaphoresis
– Adventitious lung sounds
– JVD
– Abnormal vital signs
Right Heart Failure
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Occurs when the right ventricle fails as an
effective forward pump, causing backpressure of blood into the systemic venous
circulation
Can result from:
– Chronic hypertension (in which LVF usually
precedes RVF)
– COPD
– Pulmonary embolism
– Valvular heart disease
– Right ventricular infarction

RVF most commonly results from LVF
Right Heart Failure
Signs and symptoms
– Tachycardia
– Venous congestion
• Engorged liver, spleen, or both
• Venous distention; distention and pulsations
of the neck veins
– Peripheral edema
– Fluid accumulation in serous cavities
– History-common signs and symptoms of acute
right-sided heart failure include chest pain,
hypotension, and distended neck veins
CARDIOGENIC SHOCK
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The most extreme form of pump failure
Occurs when left ventricular function is
so compromised that the heart cannot
meet the metabolic needs of the body
Usually caused by extensive myocardial
infarction, often involving more than
40% of the left ventricle, or by diffuse
ischemia
MAP drops below 70mmHg
New York Heart Association’s
functional classification of
CHF
CLASS I
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A patient who is not limited with normal
physical activity by symptoms but has
symptoms with exercise.
CLASS II
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Ordinary physical activity results in
fatigue, dyspnea, or other symptoms.
CLASS III
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Characterized by a marked limitation in
normal physical activity.
CLASS IV
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Defined by symptoms at rest or with any
physical activity.
Three Stages of Pulmonary
Edema
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Stage 1 - Fluid transfer is increased into the lung
interstitium; because lymphatic flow also
increases, no net increase in interstitial volume
occurs.
Stage 2 - The capacity of the lymphatics to drain
excess fluid is exceeded and liquid begins to
accumulate in the interstitial spaces that
surround the bronchioles and lung vasculature
(which yields the roentgenographic pattern of
interstitial pulmonary edema).
Three Stages of Pulmonary
Edema
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Stage 3 - As fluid continues to build up,
increased pressure causes it to track into
the interstitial space around the alveoli.
Fluid first builds up in the periphery of the
alveolar capillary membranes and finally
floods the alveoli .
During stage 3 the x-ray picture of alveolar
pulmonary edema is generated and gas
exchange becomes impaired.
Three Stages of Pulmonary
Edema
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Stage 3 cont. Additionally gravity exerts an
important influence on the fluid mechanics of
the lung.
Blood is much denser than air and aircontaining tissue
Under normal circumstances more perfusion
occurs at the lung bases than at the apices;
however, when pulmonary venous pressures
rise and when fluid begins to accumulate at
the lung bases the blood flow begins to be
redistributed toward the apices.
Acute Pulmonary Congestion/
Pulmonary Edema
Mechanisms to Keep
Interstitium and Alveoli Dry
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Plasma oncotic pressure
Connective tissue and cellular barriers
relatively impermeable to plasma
proteins
Extensive lymphatic system
Acute Pulmonary Edema
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May be CARDIAC or NON-CARDIAC in origin.
Results from conditions such as:
– Increased pulmonary capillary pressure
– Increased pulmonary capillary permeability
– Decreased oncotic pressure
– Lymphatic insufficiency
– mixed or unknown mechanisms
Differential Diagnosis for APE:
Cardiac causes of acute CHF
 COPD exacerbation
 Non-cardiac pulmonary edema:
Tansudate vs. Exudate
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– fluid overload
– infection
– ARDS
– High altitude
– Pulmonary Embolism
– Pneumonia
CLINICAL
PRESENTATION:
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History
Physical Exam
EKG
• This should provide enough
information to establish a cardiac
etiology, if one exists!
HISTORICAL
INFORMATION
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Maintain a high clinical suspicion for
ischemia or infarction
– [# 1 cause of CHF (think ASA)]
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Search for cardiac etiology
A study of circadian patterns for
Cardiogenic acute pulmonary edema
shows a significant peak for progressive
symptoms and AMI between 06:00 - 11:59
(D.D. Buff, M.D. et all)
HISTORY
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Why did you call? What has changed?
How long has the dyspnea been present?
Was the onset gradual or abrupt?
Is the dyspnea better or worse with position?
Is there associated orthopnea?
Has the patient been coughing?
- If so, was the cough productive?
- What was the character and colour?
- Is there any hemoptysis?
- recent fever?
HISTORY
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Is there pain associated with the dyspnea?
- OPQRST for the pain
Pt’s past history?
Allergies
Current Medications (pay close attention to
O2 therapy, oral bronchodilators,
corticosteriods,Beta Blockers, Digitalis, ACE
Inhibitors, Diuretics)
HISTORY
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What is the patients normal level of
activity?
How has the patient changed his/her
environment to adjust to the disease?
- Pillow props
- Strategically placed chairs
- Meds within easy reach
Symptoms Suspicious of
Pulmonary Congestion
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Any complaint of dyspnea/ decreased
exercise tolerance
PND/ Orthopnea
Feeling of “suffocation” or air-hunger
Restlessness and anxiety
Cyanosis/Diaphoresis
Pallor
Symptoms Suspicious of
Pulmonary Congestion
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Crackles
Wheezing (Cardiac Asthma)
Tachypnea
Coughing (Dry cough may be med related)
Retractions, accessory muscle use
Frothy pink-tinged sputum
Physical Findings
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Varying degrees of pulmonary and
systemic vascular congestion and
hypoperfusion
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Classic patient with APE presents sitting
“bolt” upright
Physical Findings ( cont. )
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JVD
Edema - ankle/pretibial vs sacral
Ascites
- Positive Hepato-jugular reflex test
BP and P are often markedly elevated
Cardiac exam
– S3 or intermittent S4 may be present?
– PMI may be shifted left
EKG Analysis:
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Search for evidence of infarction or
ischemia
Non-specific findings may include:
– hypertrophy
– chamber enlargement
– conduction disturbances
CHEST XRAY:
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Usually demonstrates increased heart
size
Progression of pulmonary congestion:
– first: Cephalization
– second : Interstitial edema
– third: Pulmonary (alveolar) edema
Treatment of APE:
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First and foremost is to increase oxygen
saturation
a reasonable approach is to base
therapy on the Systolic Blood Pressure
Decrease the preload on the heart
Shift and then eliminate excess fluids
Prehospital Management:
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Patient sitting with legs dependent
Supplemental O2 provided
Cardiac monitoring/ Pulse oximetry
Initiate necessary supportive therapy
Nitroglycerin for APE if patient matches
protocol
Be prepared to assist ventilations
PPV is an effective treatment
Acute Pulmonary Edema
Protocol - Indications
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Patient in moderate to
severe respiratory distress
Patient is assessed by the
paramedic as being in
Acute Pulmonary Edema
Acute Pulmonary Edema
Protocol - Conditions
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Weight > 40 Kg
Patient has NOT taken
any erectile dysfunction
medication within 48
hours
Heart rate greater then
60 & < 160 bpm
Initial and subsequent
BP > 140 mmHg
systolic
Acute Pulmonary Edema
Protocol - Procedure
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If the systolic blood pressure remains >140
mmHg - administer Nitroglycerin 0.4 mg
spray SL every 5 minutes to a maximum of
6 doses.
Check the vital signs before administering
EACH dose
NOTE: Do not administer further NTG if the
systolic BP drops below 140 mmHg
Treatment Procedure
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Patient in sitting
position
100% oxygen via
NRB or BVM
Cardiac monitor
Limitations
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Max of 6 doses of Nitro
by Paramedic
Stop if
– Systolic BP <140 mmhg
– Drop in SBP by 1/3
– Heart rate <60 or >160
Frequently Asked Questions
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Q: If the patient is in Pulmonary Edema
with crackles, can I give Salbutamol?
Answer
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A. Continue with oxygen administration
and NTG. Salbutamol is not the drug of
choice.
Frequently Asked Questions
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Q: What if I can only hear wheezing but
suspect the patient is in Pulmonary
Edema. Should I give Salbutamol?
Answer
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A. Continue with oxygen administration.
Consider the Acute Pulmonary Edema
protocol and consult a BHP before
administering Salbutamol if still
uncertain.
QUESTIONS?