Transcript Congestive heart failure and Pulmonary Edema

Congestive Heart Failure and
Pulmonary Edema
Mortality/Morbidity
– Approximately 30-40% of
patients with CHF are
hospitalized each year.
Leading diagnosis-related
group over 65. The 5 year
mortality after Dx was
reported as 60% in men and
45% in women in 1971. In
1991, data from the
Farmington heart study
showed the 5 year mortality
rate remaining unchanged,
with a median survival of 3.2
years for men, and 5.4 years
for women, post dx.
– The most common cause of
death is progressive heart
failure, but sudden death may
account for up to 45% of all
deaths.
– Patients with coexisting
IDDM have a significantly
higher mortality rate.
Background
– Effects an estimated 4.9
million Americans
– 1% of adults 50-60
– 10% adults over 80
– Over 550,000 new cases
annually
– $28.7 million committed
in research dollars each
year
– $132 million for lung
cancer, affecting
390,000 Americans
– Responsible for 5-10% of all
hospital admissions
– Causes or contributes to
approximately 250,000 deaths
per year
CHF Defined
– An imbalance in pump function in which the
heart fails to maintain the circulation of blood
adequately.
Pathophysiology
 Summarized as an imbalance in Starlings
forces or an imbalance in the degree of enddiastolic fiber stretch proportional to the
systolic mechanical work expended in the
ensuing contraction.
 Or basically like a rubber band, the more it
is stretched, the greater the releasing
velocity.
– Under normal circumstances, when fluid is
transferred into the lung interstitium with
increased lymphatic flow, no increase in
interstitial volume occurs.
– However, when the capacity of the lymphatic
drainage is exceeded, liquid accumulates in the
interstitial spaces surrounding the bronchioles
and lung vasculature, this creating CHF.
– When increased fluid and pressure cause tracking
into the interstitial space around the alveoli and
disruption of alveolar membrane junctions, fluid
floods the alveoli and leads to pulmonary edema
Etiologies
– Coronary artery disease-chronic
– HTN--both
– Valvular heart disease
(especially aorta and
mitral disease)--chronic
– Infections--acute
– Dysrhythmias--acute
– Alcohol--chronic
– MI--acute
– Diabetes—chronic
Important Terminology
– Preload—
• The amount of blood the heart
must pump with each beat
• Determined by:
– Venous return to heart
– Accompanying stretch of the
muscle fibers
• Increasing preload à increase
stroke volume in normal heart
• Increasing preload à impaired
heart à decreased SV. Blood
is trapped àchamber
enlargement
– Afterload—
• The pressure that must be
overcome for the heart to
pump blood into the arterial
system.
• Dependent on the systemic
vascular resistance
• With increased afterload, the
heart muscles must work
harder to overcome the
constricted vascular bed à
chamber enlargement
• Increasing the afterload will
eventually decrease the
cardiac output.
CAD
– When cholesterol and fatty deposits build up in
the heart’s arteries, less blood reaches the heart
muscle. This damages the muscle, and the healthy
heart tissue that remains has to work harder
Hypertension
– Uncontrolled HTN doubles the chances of failure
– With HTN, the chambers of the heart enlarge and
weaken.
Valvular Heart Disease
– Can result from disease, infection, or be
congenital
– Don’t open and/or close completely à increased
workload à failure
Disrhythmias
– Tachycardias àdecreased diastolic filling time à
decreased SV.
– Atrial dysrhythmias à as much as 30% reduction
in stroke volume
MI--Acute and Past
– The ischemic tissue is basically taken out of the
equation, leaving a portion of the heart to do the
work of the entire heart à decreased SV àCHF.
Diabetes
– Tend to be overweight
– HTN
– Hyperlipidemia
Types of Rhythms Associated with CHF
Types of CHF
–Left Ventricular Failure with Pulmonary Edema
• Aka—systolic heart failure
–Right Ventricular Failure
• Aka—diastolic heart failure
Left Ventricular Failure with PE
– Occurs when the left ventricle
fails as an effective forward
pump
– àback pressure of blood into
the pulmonary circulation
– à pulmonary edema
– Cannot eject all of the blood
delivered from the right heart.
– Left atrial pressure rises à
increased pressure in the
pulmonary veins and
capillaries
– When pressure becomes
to high, the fluid portion
of the blood is forced
into the alveoli.
– àdecreased oxygenation
capacity of the lungs
– AMI common with LVF,
suspect
Signs and Symptoms of LVF
–
Severe resp. distress–
• Evidenced by orthopnea,
dyspnea
• Hx of paroxysmal
nocturnal dyspnea.
– Severe apprehension,
agitation, confusion—
• Resulting from hypoxia
• Feels like he/she is
smothering
– Cyanosis—
– Diaphoresis—
• Results from sympathetic
stimulation
– Pulmonary congestion
• Often present
• Rales—especially at the
bases.
• Rhonchi—associated with
fluid in the larger airways
indicative of severe failure
• Wheezes—response to
airway spasm
– Jugular Venous Distention—
not directly related to LVF.
• Comes from back pressure
building from right heart into
venous circulation
– Vital Signs—
• Significant increase in
sympathetic discharge to
compensate.
• BP—elevated
• Pulse rate—elevated to
compensate for decreased
stroke volume.
• Respirations—rapid and
labored
– LOC—
• may vary.
• Depends on the level of hypoxia
– Chest Pain
• May in the presence of MI
• Can be masked by the RDS.
 REMEMBER LEFT VENTRICULAR
FAILURE IS A TRUE LIFE
THREATENING EMERGENCY
Right Heart Failure
– Etiology—
• Acute MI—
– Inferior MI
• Pulmonary disease
– COPD, fibrosis, HTN
• Cardiac disease involving
the left or both ventricles
• Results from LVF
– Pathophysiology—
• Decreased right-sided
cardiac output or increased
pulmonary vascular
resistance àincreased right
vent. Pressures.
• As pressures rise, this
àincreased pressure in the
right atrium and venous
system
• Higher right atrium
pressures à JVP
– In the peripheral veins, pressures rise and the
capillary pressures increase, hydrostatic pressure
exceeds that of interstitial pressure
– Fluid leaks from the capillaries into the
surrounding tissues causing peripheral edema
– Lungs are clear due to left ventricular pressures
are normal
Signs and Symptoms
– Marked JVD
– Clear chest
– Hypotension
– Marked peripheral
edema
– Ascites, hepatomegaly
– Poor exercise tolerance
– The first three are for an
inferior MI, describe
cardiac tamponade.
– Often will be on Lasix,
Digoxin,
– Have chronic pump
failure
Compensatory Mechanisms in CHF
– Neurohormonal system
– Renin-angiotensin-aldosterone system
– Ventricular hypertrophy
Neurohormonal System
–Stimulated by decreased perfusion à secretion of
hormones
• Epi—
– Increases contractility
– Increases rate and pressure
– Vasoconstriction à SVR
• Vasopressin—
– Pituitary gland
– Mild vasoconstriction, renal water retention
Renin-Angiotensin Mechanism
– Decreased renal blood flow secondary to low
cardiac output triggers renin secretion by the
kidneys
• Aldosterone is released à increase in Na+ retention à
water retention
• Preload increases
• Worsening failure
Ventricular Hypertrophy
– Long term compensatory mechanism
– Increases in size due to increase in work load ie
skeletal muscle
Comparison of COPD, CHF Pneumonia
COPD
CHF
Pneumonia
Cough
Frequent
Occasional
Frequent
Wheeze
Frequent
Occasional
Frequent
Sputum
Thick
Thin/white
Thick/yellow/
brown
Hemoptysis
Occasionally
Pink frothy
occasionally
PND
Sometimes after a Often within 1
few hours
hour
Rare
Smoking
Common
Less common
Less common
Pedal edema
Occasional
Common with
chronic
none
COPD
CHF
Pneumonia
Onset
Often URI with
cough
Orthopnea at
night
Gradual with
fever, cough
Chest Pain
pleuritic
Substernal,
crushing
Pleuritic, often
localized
Clubbing
Often
Rare
Rare
Cyanosis
Often and severe
Initially mild but
progresses
May be present
Diaphoresis
May be present
Mild to heavy
Dry to moist
Pursed Lips
Often
Rare
Rare unless
COPD
COPD
CHF
Pneumonia
Barrel Chest
Common
Rare
Rare unless
COPD
JVD
May be present
with RVF
Mild to severe
Rare
BP
Usually normal
Often high
Normal
Dysrhythmia
Occasional
May precipitate
CHF
Common
Wheeze
Common
Less common
Common
Crackles
Coarse, diffuse
Fine to coarse,
begin in gravity
dependent areas
Localized to
diffuse, coarse
Drug Therapy
–Aimed at diminishing the compensatory
mechanisms of low cardiac output and also
improving contractility
–Vasodilators—ACE inhibitors
–Diuretic agents
–Inotropic agents
Vasodilators
– Dilate blood vessels
– Often constricted due to
activation of the
sympathetic nervous
system and the reninangiotensin-aldosterone
system.
– Aka—ACE inhibitors
– Common ACE
inhibitors
•
•
•
•
•
Captopril
Lisinopril
Vasotec
Monopril
Accupril
– Nitrates
Diureti
cs
–Lasix
–Hydrochlorothiazide(HCTZ)
–Spironolactone
These inhibit reabsorption of Na+ into the
kidneys
Inotropic Agents
–Digoxin
–Lanoxin
 Increases the contractility of the heart à
increasing the cardiac output
Calcium Channel
Blockers
–
–
–
–
–
Nifedipine
Diltiazem
Verapamil
Amlodipine
Felodipine
– Used to dilate blood
vessels
– Used mostly with CHF
in the presence of
ischemia
Beta Blockers
– Metoprolol
– Atenolol
– Propanolol
– Amiodarone
– Useful by blocking the
beta-adrengergic
receptors of the
sympathetic nervous
system, the heart rate
and force of contractility
are decreased àcould
actually worsen CHF
Prehospital Treatment
– The prehospital goals for managing CHF
–
–
–
–
Promotion of rest
Relief of anxiety
Decreasing cardiac workload
Attainment of normal tissue perfusion
Promotion of Rest
– DO NOT make these patient’s walk
– Could start a fluid “rush” into the alveoli
– Try to get them to sit still if they appear agitated
and hypoxic
Relief of Anxiety
– Often experienced
– Leads to increase in O2 demand and cardiac
workload
– Explain what you are doing
– MS 2 mg for treatment of anxiety and for
decreasing preload
Decreasing Cardiac Workload
– NTG
– MS
– Lasix
– O2—High flow O2
Common Heart Failure Medications
– ACE Inhibitors
– Digitalis
– Diuretics
– Hydralazine
– Nitrates
ACE Inhibitors
– Prevent the production of the chemicals that
causes blood vessels to narrow
– Resulting in blood pressure decreasing and the
heart pumping easier
Digitalis
– Inotropic effects on the heart
– Negative chronotropic effects
Diuretics
– Decrease the body’s retention of salt and water
– Reduces blood pressure
– Probably will be on potassium
Hydralazine
– Widens the blood vessels, therefore allowing
more blood flow
Nitrat
es
– Relaxation of smooth muscle
– Widens blood vessels
– Lowers systolic blood pressure
Diagnostic Challenges
– Particularly difficult in elderly
– Atypical presentations
– Predominant symptoms include:
•
•
•
•
•
Anorexia
Generalized weakness
Fatigue
Mental disturbances
Anxiety
Lung Sounds Associated with CHF
– Bubbling Rhonchi
– Coarse Crackles
– Fine Crackles
– Gurgling Rhonchi
– Rales