Presentation Transcript
Congestive Heart Failure :Congestive Heart Failure Developed by: Russell K. Miller Jr. MD, FACEP
Assistant Professor of Surgery and Internal Medicine The University of Texas Medical Branch Galveston Lynn K. Wittwer, MD, MPD
Clark County EMS
Objectives :Objectives Overview of CHF
Review cardiac physiology and pathophysiology
Early recognition of CHF
Early and aggressive management of CHF
Heart Failure :Heart Failure The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body.
Pulmonary Edema :Pulmonary Edema An abnormal accumulation of fluid in the lungs.
CHF :CHF Pulmonary Edema due to Heart Failure (Cardiogenic Pulmonary Edema)
Statistics :Statistics US Health and Human Services.
5 million Americans suffer from CHF.
$17.8 billion spent annually.
400,000 new cases reported each year.
Etiology :Etiology Arteriosclerotic Cardiovascular Ischemia
Hypertension
People Live with Atherosclerosis – But Die of Thrombosis! :People Live with Atherosclerosis – But Die of Thrombosis! The formation, progression and rupture of an atherosclerotic plaque
Slide 9:Occlusion of Proximal Cx
RAO view - Baseline During Rotational Ablation Rotastenting of Proximal Cx
RAO view - Baseline Patient with recent Non Q Wave MI
If randomized to the Invasive Arm
Would have been pushed toward
Early CABG
Slide 10:Patient with Non Q Wave MI
Cath showing degenerated vein
graft anastomosis and distal LAD
High risk for intervention because
depressed EF and occluded native
coronary arteries Angiographic results post
Rotablator assisted stenting
of the anastomosis and distal LAD.  ïƒ
Hypertension :Hypertension Hypertrophic Cardiomyopathy
Morbidity & Mortality :Morbidity & Mortality Dramatically Affects: Quality & Length of Life
5 Year Mortality: Males 62%
Females 42%
6 Year Mortality: Both Sexes 75%
Physiology :Physiology Frank-Starling
Length: Tension Ratio
Ejection Fraction
End diastolic volume/end systolic volume
Cardiac Output
Stroke volume x heart rate
Preload
Volume of blood delivered to heart during diastole
Afterload
Peripheral vascular resistance
: Infiltration of Interstitial Space Normal Micro- anatomy
Micro-anatomy with fluid movement.
Preload :Preload Primarily a venous and diastolic function
Afterload :Afterload Primarily arterial and systolic function
Three Pathophysiological Causes of Failure :Three Pathophysiological Causes of Failure Increased work load (HTN)
Myocardial Dysfunction (ASCVD)
Decreased Ventricular Filling (Misc.)
Decompensation :Decompensation Increased Pulmonary Venous Pressure (PAWP)
Interstitial Edema
Alveolar Edema
Compensatory Mechanisms to Failure :Compensatory Mechanisms to Failure Increased Heart Rate
(Sympathetic = Norepinephrine)
Dilation
(Frank Starling = Contractility)
Neurohormonal
(Redistribution of Blood to the Brain)
CHF Vicious Cycle :CHF Vicious Cycle Low Output
Increased Preload Increased Afterload Norepinephrine
Increased Salt Vasoconstriction Renal Blood Flow
Renin
Angiotension I
Angiotension II
Aldosterone
Symptoms :Symptoms Fatigue
Nocturia
DOE
PND GI Symptoms
Chest Pain
Orthopnea
Profound Dyspnea
Slide 22:Acute Pulmonary Edema is a true Life Threatening Emergency for which the clinical picture is hard to forget!
Laboratory Findings :Laboratory Findings CXR - Single most useful clinical tool
EKG - Non Specific
Lab - Non Specific
Physical Exam :Physical Exam Anxious
Pale
Clammy
Dyspnea
Tachypnea
Confusion
Edema
Hypertension
Diaphoretic Rales
Ronchi
Tachycardia
S3 Gallop
JVD
Pink Frothy Sputum
Cyanosis
Displaced PMI
Precipitating Causes :Precipitating Causes Non Compliance with Meds and Diet
Acute MI
Arrhythmia
Pneumonia
Increased Sodium Diet (Holiday Failure)
Anxiety
Pregnancy
EMS Management :EMS Management Sit upright
High Flow O2
NTG (If SBP > 100)
Diuretics (Lasix)
Rotating Tourniquets (Controversial)
Ventilatory Support
CPAP
intubation/ventilation
Emergency Dept. ManagementEMS Therapy Plus: :Emergency Dept. ManagementEMS Therapy Plus: Morphine
Dopamine
Dobutrex
Antihypertensives
Digitalis
Antihypertensives :Antihypertensives Nitroprusside
ACE Inhibitors (Enalapril)
Calcium Channel Blockers (Nefedipine)
Beta Blockers (With Caution)
Hydralazine
Phosphodiesterase Inhibitors (Amrinone)
Chronic CHF TreatmentAdjunctive Treatment: :Chronic CHF TreatmentAdjunctive Treatment: Lifestyle changes
Weight loss
Decrease dietary salt
Increase O2
Drugs :Drugs Treat cause
Diuretics
Digitalis
NTG
Antihypertensives
Introduction :Introduction CPAP is a non-invasive procedure that is easily applied and can be easily discontinued without untoward patient discomfort.
CPAP is an established therapeutic modality, recently introduced into the prehospital setting.
In the primary phase CPAP application in cardiogenic pulmonary edema, thus far, appears to be beneficial to patient outcome.
Key Points of CPAP :Key Points of CPAP CPAP has been successfully demonstrated as an effective adjunct in the management of pulmonary edema secondary to congestive heart failure.
CPAP may prove to be a viable alternative in many patients previously requiring endotracheal intubation by prehospital personnel.
CPAP Mechanism :CPAP Mechanism Increases pressure within airway.
Airways at risk for collapse from excess fluid are stented open.
Gas exchange is maintained
Increased work of breathing is minimized
Prehospital Indications :Prehospital Indications Congestive Heart Failure
Pulmonary Edema associated with volume overload ( renal insufficiency, iatrogenic volume overload, liver disease , etc)
Near Drowning
Absolute Contraindications :Absolute Contraindications Respiratory Arrest
Agonal Respirations
Unconscious
Shock associated with cardiac insufficiency
Pneumothorax
Facial Anomalies e.g. burns, fractures, etc.
Facial trauma
Relative Contraindications :Relative Contraindications Decreased L.O.C.
COPD
Asthma
Claustrophobia
Patient Intolerance to equipment (e.g. mask)
Tracheostomy (If lacking the adaptor)
Hazards :Hazards Gastric Distention (19 cm H2O pressure)
Corneal Drying
Hypotension
Pneumothorax
Important Points :Important Points Pulmonary edema patients, properly selected, quickly improve with CPAP in a matter of minutes.
CPAP is to CHF like D50 is to insulin shock.
Visual inspection of chestwall movement reveals improved respiratory excursion.
Important Points (Continued) :Important Points (Continued) COPD and Asthmatic patients do not respond predictably to CPAP.
They have a higher risk of complications such as pneumothorax, and thus should not be treated in the field with CPAP
Study Introduction :Study Introduction IRB approval through UTMB.
6 hours didactic instruction
Recognize CHF
Differentiate CHF, COPD, Asthma & Bronchitis.
2 hours clinical training.
Instruction on assessment most important reason for success.
Slide 43:Data Summary 1996 – 1997
September – May
Total Intubations 22
Hospital Stay 14.8 Days
ICU Admission 100%
Slide 44:Data Summary 1997 – 1998
September – May
CPAP 50
Total Intubations 8 (15%)
- Primary Intubations 4 (8%)
- CPAP Failures 4 (8%)
Hospital Stay 8 days
ICU Admission 48%
Slide 45:Data Comparison 1996 – 1997 1997 – 1998
Intubated 22 8
CPAP 0 50
Hospital Stay 14.8 8
ICU Admission 100% 48%
CPAP vs. Intubation :CPAP vs. Intubation CPAP
Non-invasive
Easily discontinued
Easily adjusted
Use by EMT-B
Does not require sedation
Comfortable Intubation
Invasive
Usually don’t extubate in field
Potential for infection
Requires highly trained personnel
Can require sedation
Traumatic
Summary :Summary CPAP provides an adjunct between oxygen by NRB and endotracheal intubation.
Reduces length of hospital admission.
Reduces trauma of intubation
Reduces costs