Presentation on theme: "Prepared by: South West Education Committee"— Presentation transcript:
1 Prepared by: South West Education Committee PULMONARY EDEMAPrepared by:South West Education Committee
2 “The Power of 7” Base Hospital Programs CambridgeGrey BruceHamiltonLambtonLondonNiagaraWindsorSouthWestEducationCommittee
3 SWEC MEMBERS Cambridge – Lori Smith Grey Bruce – Andy Whittemore Hamilton – Ken Stuebing, Tim DoddLambton – Judy PotterLondon – Tre RodriguezNiagara – Greg SotoWindsor – Cathie HedgesRTN – Peter Deryk
4 Congestive Heart Failure or Acute Pulmonary Edema SWEC Base HospitalsCredit: W.A. (Bill) Penhallurick Southeastern Regional BH1
5 OUTLINEReview the pathophysiology and etiology of Congestive Heart FailureReview the pathophysiology, etiology and emergency treatment of Acute Pulmonary EdemaReview cardio-respiratory assessmentsReview the Acute Pulmonary Edema protocol and the use of Nitroglycerin
6 OBJECTIVES Describe the possible causes of pulmonary edema. Explain the indications for NTG treatmentDescribe the limitation to treatmentExplain the treatment procedure.
7 Congestive Heart Failure (CHF)??? : INTRODUCTIONCongestive 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”.
8 PULMONARY CIRCULATION Blood flows from the right ventricle through the pulmonary arteryBlood reaches the capillaries surrounding alveoli where gas exchange occursOxygenated blood returns by pulmonary veins to the left ventricle where it is pumped into systemic circulation
14 Compensatory Mechanisms to Maintain Cardiac Output: The Frank-Starling mechanismMyocardial hypertrophyIncreased sympathetic toneAll result in increased myocardial O2 demand!Kidneys6
15 CAUSES OF Congestive Heart Failure Conditions that increase preload, e.g. aortic regurgitation, ventricular septal defects, fluid overloadConditions that increase afterload, e.g. aortic stenosis, systemic hypertension (vasoconstriction),Conditions that decrease myocardial contractility, e.g. MI, cardiomyopathies, pericarditis, tamponade
16 SIGNS &SYMPTOMS OF Congestive Heart Failure Exertional dyspnea usually with Crackles- fatigue may be the first signIncreased respiratory rate and effortOrthopnea and/or PNDCyanosis and pallorTachycardiaJVDDependant edema
17 CATEGORIZING FAILURE Left or Right sided heart failure Forward or Backward ventricular failureBackward 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
18 LV BACKWARD EFFECTS Decreased emptying of the left ventricle Increased volume and end-diastolic pressure in the left ventricleIncreased volume (pressure) in the left atriumIncreased volume in pulmonary veins
19 LV BACKWARD EFFECTS con’t Increased volume in pulmonary capillary bed = increased hydrostatic pressureTransudation of fluid from capillaries to alveoliRapid filling of alveolar spacesPulmonary edema
20 LV FORWARD EFFECTS Decreased cardiac output Decreased perfusion of tissues of bodyDecreased blood flow to kidneys and glandsIncreased reabsorption of sodium and water and vasoconstriction
21 LV FORWARD EFFECTS con’t Increased secretion of sodium and water-retaining hormonesIncreased extracellular fluid volumeIncreased total blood volume and increased systemic blood pressure
22 RV BACKWARD EFFECTS Decreased emptying of the right ventricle Increased volume and end-diastolic pressure in the right ventricleIncreased volume (pressure) in right atriumIncreased volume and pressure in the great veins
23 RV BACKWARD EFFECTS con’t Increased volume in the systemic venous circulationIncreased volume in distensible organs (hepatomegaly, splenomegaly)Increased pressures at capillary linePeripheral, dependant edema and serous infusion
24 RV Forward Effects Decreased volume from the RV to the lungs Decreased return to the left atrium and subsequent decreased cardiac outputAll the forward effects of left heart failure
25 Congestive Heart Failure Can Be Defined Based on: How rapid the symptoms onsetWhich ventricle is primarily involvedOverall cardiac output3
26 Left Heart Failure and Pulmonary Edema LVF occurs when the left ventricle fails to function as an effective forward pump, causing a back-pressure of blood into the pulmonary circulationMay be caused by a variety of forms of heart disease including ischemic, valvular, and hypertensive heart diseaseUntreated, significant LVF culminates in pulmonary edema
27 Left Heart Failure and Pulmonary Edema Signs and symptomsSevere respiratory distressSevere apprehension, agitation, confusionCyanosis (if severe)DiaphoresisAdventitious lung soundsJVDAbnormal vital signs
28 Right Heart FailureOccurs when the right ventricle fails as an effective forward pump, causing back-pressure of blood into the systemic venous circulationCan result from:Chronic hypertension (in which LVF usually precedes RVF)COPDPulmonary embolismValvular heart diseaseRight ventricular infarctionRVF most commonly results from LVF
29 Right Heart Failure Signs and symptoms Tachycardia Venous congestion Engorged liver, spleen, or bothVenous distention; distention and pulsations of the neck veinsPeripheral edemaFluid accumulation in serous cavitiesHistory-common signs and symptoms of acute right-sided heart failure include chest pain, hypotension, and distended neck veins
30 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 bodyUsually caused by extensive myocardial infarction, often involving more than 40% of the left ventricle, or by diffuse ischemiaMAP drops below 70mmHg
31 New York Heart Association’s functional classification of CHF
32 CLASS IA patient who is not limited with normal physical activity by symptoms but has symptoms with exercise.
33 CLASS IIOrdinary physical activity results in fatigue, dyspnea, or other symptoms.
34 CLASS IIICharacterized by a marked limitation in normal physical activity.
35 CLASS IVDefined by symptoms at rest or with any physical activity.
36 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).
37 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.
38 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 tissueUnder 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.
40 Mechanisms to Keep Interstitium and Alveoli Dry Plasma oncotic pressureConnective tissue and cellular barriers relatively impermeable to plasma proteinsExtensive lymphatic system
41 Acute Pulmonary Edema May be CARDIAC or NON-CARDIAC in origin. Results from conditions such as:Increased pulmonary capillary pressureIncreased pulmonary capillary permeabilityDecreased oncotic pressureLymphatic insufficiencymixed or unknown mechanisms7
42 Etiology of Pulmonary Edema Increased fluid in lung interstitiumInterstitial edemaPulmonary hydrostatic pressure exceeds colloid osmotic pressureFluid tracks into interstitial spaces around alveoliFluid enters alveoli
43 Differential Diagnosis for APE: Cardiac causes of acute CHFCOPD exacerbationNon-cardiac pulmonary edema:Tansudate vs. Exudatefluid overloadinfectionARDSHigh altitudePulmonary EmbolismPneumonia8
44 CLINICAL PRESENTATION: HistoryPhysical ExamEKGThis should provide enough information to establish a cardiac etiology, if one exists!10
45 HISTORICAL INFORMATION Maintain a high clinical suspicion for ischemia or infarction[# 1 cause of CHF (think ASA)]Search for cardiac etiologyA study of circadian patterns for Cardiogenic acute pulmonary edema shows a significant peak for progressive symptoms and AMI between 06: :59 (D.D. Buff, M.D. et all)11
46 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?
47 HISTORY Is there pain associated with the dyspnea? - OPQRST for the painPt’s past history?AllergiesCurrent Medications (pay close attention to O2 therapy, oral bronchodilators, corticosteriods,Beta Blockers, Digitalis, ACE Inhibitors, Diuretics)
48 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
49 Symptoms Suspicious of Pulmonary Congestion Any complaint of dyspnea/ decreased exercise tolerancePND/ OrthopneaFeeling of “suffocation” or air-hungerRestlessness and anxietyCyanosis/DiaphoresisPallor12
50 Symptoms Suspicious of Pulmonary Congestion CracklesWheezing (Cardiac Asthma)TachypneaCoughing (Dry cough may be med related)Retractions, accessory muscle useFrothy pink-tinged sputum15
51 Physical FindingsVarying degrees of pulmonary and systemic vascular congestion and hypoperfusionClassic patient with APE presents sitting “bolt” upright13
52 Physical Findings ( cont. ) JVDEdema - ankle/pretibial vs sacralAscites- Positive Hepato-jugular reflex testBP and P are often markedly elevatedCardiac examS3 or intermittent S4 may be present?PMI may be shifted left14
53 EKG Analysis: Search for evidence of infarction or ischemia Non-specific findings may include:hypertrophychamber enlargementconduction disturbances18
54 CHEST XRAY: Usually demonstrates increased heart size Progression of pulmonary congestion:first: Cephalizationsecond : Interstitial edemathird: Pulmonary (alveolar) edema19
55 Cephalization on Right - Due to pulmonary hypertension- Pulmonary veins become visible due to increased blood congestion- Decreases or clears after treatment
57 Pulmonary Edema Pulmonary edema is common in congestive heart failure. As pulmonary capillary pressures increase, the initial fluid excess is removed by increased lymphatic drainage.When lymphatic system capacity is exceeded, pulmonary edema occurs. Radiographic signs include septal lines, bronchial wall thickening and subpleural pulmonary edema.Top radiograph illustrates generalized fissural thickening and lack of clarity of intrapulmonary vessels.Figure and description from "Imaging Diseases of the Chest" , p. 388, by Peter Armstrong, Alan G. Wilson, and Paul Dee, Yearbook Medical Publishers, Inc
58 Treatment of APE: First and foremost is to increase oxygen saturation a reasonable approach is to base therapy on the Systolic Blood PressureDecrease the preload on the heartShift and then eliminate excess fluids20
59 Prehospital Management: Patient sitting with legs dependentSupplemental O2 providedCardiac monitoring/ Pulse oximetryInitiate necessary supportive therapyNitroglycerin for APE if patient matches protocolBe prepared to assist ventilationsPPV is an effective treatmentStress DEPENDANT limbsIterate suction vs. PPV21
60 Acute Pulmonary Edema Protocol - Indications Patient in moderate to severe respiratory distressPatient is assessed by the paramedic as being in Acute Pulmonary Edema
61 Acute Pulmonary Edema Protocol - Conditions Weight > 40 KgPatient has NOT taken any erectile dysfunction medication within 48 hoursHeart rate greater then 60 & < 160 bpmInitial and subsequent BP > 140 mmHg systolic
62 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 doseNOTE: Do not administer further NTG if the systolic BP drops below 140 mmHg
63 Treatment Procedure Patient in sitting position 100% oxygen via NRB or BVMCardiac monitor
64 Limitations Max of 6 doses of Nitro by Paramedic Stop if Systolic BP <140 mmhgDrop in SBP by 1/3Heart rate <60 or >160
65 Frequently Asked Questions Q: If the patient is in Pulmonary Edema with crackles, can I give Salbutamol?
66 AnswerA. Continue with oxygen administration and NTG. Salbutamol is not the drug of choice.
67 Frequently Asked Questions Q: What if I can only hear wheezing but suspect the patient is in Pulmonary Edema. Should I give Salbutamol?
68 AnswerA. Continue with oxygen administration. Consider the Acute Pulmonary Edema protocol and consult a BHP before administering Salbutamol if still uncertain.