By: Darryl Jamison

Macon County EMS Training

Coordinator
INCIDENCE&MORTALITY
– Approximately 30-40% of – The most common cause of
patients with CHF are death is progressive heart
hospitalized each year. failure, but sudden death
Leading diagnosis-related may account for up to 45%
group over 65. The 5 year
mortality after Dx was of all deaths.
reported as 60% in men and – Patients with coexisting
45% in women in 1971. In IDDM have a significantly
1991, data from the higher mortality rate.
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.
– Effects an estimated – Responsible for 5-10% of
4.9 million Americans all hospital admissions
– 1% of adults 50-60 – Causes or contributes to
approximately 250,000
– 10% adults over 80 deaths per year
– Over 550,000 new
cases annually
– $28.7 million
committed in research
dollars each year
– $132 million for lung
cancer, affecting
390,000 Americans
– An imbalance in pump function in which the
heart fails to maintain the circulation of blood
adequately.
♦ Summarized as an imbalance in Starlings
forces or an imbalance in the degree of end-
diastolic 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
– Coronary artery – Alcohol--chronic
disease--chronic – MI--acute
– HTN--both – Diabetes—chronic
– Valvular heart disease
(especially aorta and
mitral disease)--
chronic
– Infections--acute
– Dysrhythmias--acute
– Preload— – Afterload—
• The amount of blood the • The pressure that must be
heart must pump with each overcome for the heart to
beat pump blood into the
• Determined by: arterial system.
– Venous return to heart • Dependent on the systemic
– Accompanying stretch vascular resistance
of the muscle fibers • With increased afterload,
• Increasing preload  the heart muscles must
increase stroke volume in work harder to overcome
normal heart the constricted vascular
• Increasing preload  bed  chamber
impaired heart  enlargement
decreased SV. Blood is • Increasing the afterload
trapped chamber will eventually decrease
enlargement the cardiac output.
– 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
– Uncontrolled HTN doubles the chances of
failure
– With HTN, the chambers of the heart enlarge
and weaken.
– Can result from disease, infection, or be
congenital
– Don’t open and/or close completely 
increased workload  failure
– Tachycardias decreased diastolic filling time
 decreased SV.
– Atrial dysrhythmias  as much as 30%
reduction in stroke volume
– The ischemic tissue is basically taken out of the
equation, leaving a portion of the heart to do
the work of the entire heart  decreased SV
CHF.
– Tend to be overweight
– HTN
– Hyperlipidemia
Types of Rhythms Associated
with CHF
– Left Ventricular Failure with Pulmonary Edema
• Aka—systolic heart failure

– Right Ventricular Failure

• Aka—diastolic heart failure
The smooth, glistening pleural surface of a lung is shown here. This patient had
marked pulmonary edema, which increased the fluid in the lymphatics that run
between lung lobules. Thus, the lung lobules are outlined in white.
– Occurs when the left – When pressure
ventricle fails as an
effective forward pump becomes to high, the
 back pressure of blood fluid portion of the
into the pulmonary blood is forced into the
circulation alveoli.
  pulmonary edema
– Cannot eject all of the
 decreased
blood delivered from the oxygenation capacity
right heart. of the lungs
– Left atrial pressure rises 
increased pressure in the
– AMI common with
pulmonary veins and LVF, suspect
capillaries
– Severe resp. distress– – Diaphoresis—
• Evidenced by • Results from
orthopnea, dyspnea sympathetic stimulation
• Hx of paroxysmal – Pulmonary congestion
nocturnal dyspnea. • Often present
– Severe apprehension, • Rales—especially at the
bases.
agitation, confusion— • Rhonchi—associated
• Resulting from hypoxia with fluid in the larger
• Feels like he/she is airways indicative of
smothering severe failure
• Wheezes—response to
– Cyanosis— 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
– Etiology— – Pathophysiology—
• Acute MI— • Decreased right-sided
– Inferior MI cardiac output or
• Pulmonary disease increased pulmonary
– COPD, fibrosis, HTN vascular resistance
increased right vent.
• Cardiac disease
Pressures.
involving the left or
• As pressures rise, this
both ventricles
increased pressure in
• Results from LVF
the right atrium and
venous system
• Higher right atrium
pressures  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
– Marked JVD – Often will be on Lasix,
– Clear chest Digoxin,
– Hypotension – Have chronic pump
– Marked peripheral failure
edema
– Ascites, hepatomegaly
– Poor exercise tolerance

– The first three are for

an inferior MI,
describe cardiac
tamponade.
– Neurohormonal system
– Renin-angiotensin-aldosterone system
– Ventricular hypertrophy
– Stimulated by decreased perfusion  secretion of
hormones

• Epi—
– Increases contractility
– Increases rate and pressure
– Vasoconstriction  SVR
• Vasopressin—
– Pituitary gland
– Mild vasoconstriction, renal water retention
– Decreased renal blood flow secondary to low
cardiac output triggers renin secretion by the
kidneys
• Aldosterone is released  increase in Na+ retention
 water retention
• Preload increases
• Worsening failure
– Long term compensatory mechanism
– Increases in size due to increase in work load ie
skeletal muscle
 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 Rare
few hours hour
Smoking Common Less common Less common
Pedal edema Occasional Common with none
chronic
 COPD CHF Pneumonia

Onset Often URI with Orthopnea at night Gradual with

cough fever, cough
Chest Pain pleuritic Substernal, Pleuritic, often
crushing localized
Clubbing Often Rare Rare

Cyanosis Often and severe Initially mild but May be present

progresses
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 Mild to severe Rare

with RVF
BP Usually normal Often high Normal

Dysrhythmia Occasional May precipitate Common

CHF
Wheeze Common Less common Common

Crackles Coarse, diffuse Fine to coarse, Localized to

begin in gravity diffuse, coarse
dependent areas
– Aimed at diminishing the compensatory
mechanisms of low cardiac output and also
improving contractility

– Vasodilators—ACE inhibitors
– Diuretic agents
– Inotropic agents
– Dilate blood vessels – Common ACE
– Often constricted due inhibitors
to activation of the • Captopril
sympathetic nervous • Lisinopril
system and the renin- • Vasotec
angiotensin- • Monopril
aldosterone system. • Accupril
– Aka—ACE inhibitors – Nitrates
 – Lasix
– Hydrochlorothiazide(HCTZ)
– Spironolactone

♦ These inhibit reabsorption of Na+ into the

kidneys
 – Digoxin
– Lanoxin

♦ Increases the contractility of the heart 

increasing the cardiac output
– Nifedipine – Used to dilate blood
– Diltiazem vessels
– Verapamil – Used mostly with CHF
– in the presence of
Amlodipine
ischemia
– Felodipine
– Metoprolol – Useful by blocking the
– Atenolol beta-adrengergic
– receptors of the
Propanolol
sympathetic nervous
– Amiodarone system, the heart rate
and force of
contractility are
decreased could
actually worsen CHF
– The prehospital goals for managing CHF
– Promotion of rest
– Relief of anxiety
– Decreasing cardiac workload
– Attainment of normal tissue perfusion
– 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
– 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
– NTG
– MS
– Lasix
– O2—High flow O2
– ACE Inhibitors
– Digitalis
– Diuretics
– Hydralazine
– Nitrates
– Prevent the production of the chemicals that
causes blood vessels to narrow
– Resulting in blood pressure decreasing and the
heart pumping easier
– Inotropic effects on the heart
– Negative chronotropic effects
– Decrease the body’s retention of salt and water
– Reduces blood pressure
– Probably will be on potassium
– Widens the blood vessels, therefore allowing
more blood flow
– Relaxation of smooth muscle
– Widens blood vessels
– Lowers systolic blood pressure
– Particularly difficult in elderly
– Atypical presentations
– Predominant symptoms include:
• Anorexia
• Generalized weakness
• Fatigue
• Mental disturbances
• Anxiety
– Bubbling Rhonchi
– Coarse Crackles
– Fine Crackles
– Gurgling Rhonchi
– Rales
NURSING MANAGEMENT