PULMONARY EDEMA

Prepared by:

South West Education Committee

Congestive Heart Failureor

Acute Pulmonary Edema

SWEC Base Hospitals

Credit: W.A. (Bill) Penhallurick Southeastern Regional BHCredit: W.A. (Bill) Penhallurick Southeastern Regional BH

OUTLINE 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

Describe the possible causes of pulmonary edema.

Explain the indications for NTG treatment

Describe the limitation to treatment Explain the treatment procedure.

INTRODUCTION

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

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

Syndrome usually results from LV dysfunction and compensatory mechanisms

Cardiac performance is a function of 4 primary factors. What are they?

4 FACTORS DETERMINING CARDIAC PERFORMANCE

1. Preload (define)

2. Afterload (define)

3. Contractility

4. Heart Rate

Compensatory Mechanisms to Maintain Cardiac Output:

The Frank-Starling mechanism– Myocardial hypertrophy

Increased sympathetic tone– All result in increased myocardial O2 demand!

Kidneys

CAUSES OF Congestive Heart Failure

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

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

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 EFFECTSDecreased emptying of the left ventricle

Increased volume and end-diastolic

pressure in the left ventricle

Increased volume (pressure) in the left atrium

Increased volume in pulmonary veins

Increased volume in pulmonary capillary bed = increased hydrostatic pressure

Transudation of fluid from capillaries to alveoli

Rapid filling of alveolar spaces

Pulmonary edema

LV BACKWARD EFFECTS con’t

LV FORWARD EFFECTSDecreased cardiac output

Decreased perfusion of tissues of body

Decreased blood flow to kidneys and glands

Increased reabsorption of sodium and water and

vasoconstriction

Increased secretion of sodium and water-retaining hormones

Increased extracellular fluid volume

Increased total blood volume and increased systemic blood pressure

LV FORWARD EFFECTS con’t

RV BACKWARD EFFECTSDecreased emptying of the right ventricle

Increased volume and end-diastolic pressure in

the right ventricle

Increased volume (pressure) in right atrium

Increased volume and pressure in the great veins

Increased volume in the systemic venous Increased volume in the systemic venous circulationcirculation

Increased volume in distensible organs Increased volume in distensible organs (hepatomegaly, splenomegaly)(hepatomegaly, splenomegaly)

Increased pressures at capillary lineIncreased pressures at capillary line

Peripheral, dependant edema and serous Peripheral, dependant edema and serous infusioninfusion

RV BACKWARD EFFECTS con’t

RV Forward Effects

Decreased volume from the RV to the lungs

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:

How rapid the symptoms onset

Which ventricle is primarily involved

Overall cardiac output

Left Heart Failure andPulmonary Edema

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 andPulmonary Edema

Signs and symptoms– Severe respiratory distress– Severe apprehension, agitation, confusion– Cyanosis (if severe)– Diaphoresis– Adventitious lung sounds– JVD– Abnormal vital signs

Right Heart Failure Occurs when the right ventricle fails as an

effective forward pump, causing back-pressure 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 FailureSigns 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

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

A patient who is not limited with normal physical activity by symptoms but has symptoms with exercise.

CLASS II

Ordinary physical activity results in fatigue, dyspnea, or other symptoms.

CLASS III

Characterized by a marked limitation in normal physical activity.

CLASS IV

Defined by symptoms at rest or with any physical activity.

Three Stages of Pulmonary Edema

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

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

Stage 3 cont. Additionally gravity exerts an important influence on the fluid mechanics of the lung.

Blood is much denser than air and air-containing 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

Plasma oncotic pressure Connective tissue and cellular barriers

relatively impermeable to plasma proteins

Extensive lymphatic system

Acute Pulmonary Edema

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

– fluid overload– infection– ARDS– High altitude– Pulmonary Embolism– Pneumonia

CLINICAL PRESENTATION:

History Physical Exam EKG

• This should provide enough information to establish a cardiac etiology, if one exists!

HISTORICAL INFORMATION

Maintain a high clinical suspicion for ischemia or infarction – [# 1 cause of CHF (think ASA)]

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 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 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

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

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

Crackles Wheezing (Cardiac Asthma) Tachypnea Coughing (Dry cough may be med related) Retractions, accessory muscle use Frothy pink-tinged sputum

Physical Findings

Varying degrees of pulmonary and systemic vascular congestion and hypoperfusion

Classic patient with APE presents sitting “bolt” upright

Physical Findings ( cont. )

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:

Search for evidence of infarction or ischemia

Non-specific findings may include:– hypertrophy– chamber enlargement– conduction disturbances

CHEST XRAY:

Usually demonstrates increased heart size

Progression of pulmonary congestion:– first: Cephalization– second : Interstitial edema– third: Pulmonary (alveolar) edema

Treatment of APE:

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:

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

Patient in moderate to severe respiratory distress

Patient is assessed by the paramedic as being in Acute Pulmonary Edema

Acute Pulmonary Edema Protocol - Conditions

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

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

Patient in sitting position

100% oxygen via NRB or BVM

Cardiac monitor

Limitations

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

Q: If the patient is in Pulmonary Edema with crackles, can I give Salbutamol?

Answer

A. Continue with oxygen administration and NTG. Salbutamol is not the drug of choice.

Frequently Asked Questions

Q: What if I can only hear wheezing but suspect the patient is in Pulmonary Edema. Should I give Salbutamol?

Answer

A. Continue with oxygen administration. Consider the Acute Pulmonary Edema protocol and consult a BHP before administering Salbutamol if still uncertain.

QUESTIONS?