By: Darryl Jamison

Macon County EMS Training

Coordinator
 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 Diabeteschronic
Valvular heart disease
(especially aorta and
mitral disease)--
chronic
Infections--acute
Dysrhythmias--acute
 Preload Afterload
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
increase stroke volume in
normal heart
Increasing preload
impaired heart
decreased SV. Blood is
trapped chamber
enlargement
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 chamber
enlargement
Increasing the afterload
will eventually decrease
the cardiac output.
 When cholesterol and fatty deposits build up in
the hearts 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
Dont 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
Akasystolic heart failure

Right Ventricular Failure

Akadiastolic 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 blood decreased
delivered from the right oxygenation capacity
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, Ralesespecially at the
bases.
agitation, confusion Rhonchiassociated
Resulting from hypoxia with fluid in the larger
Feels like he/she is airways indicative of
smothering severe failure
Wheezesresponse to
Cyanosis airway spasm
 Jugular Venous
Distentionnot directly
related to LVF.
Comes from back pressure
building from right heart
into venous circulation
Vital Signs
Significant increase in
sympathetic discharge to
compensate.
BPelevated
Pulse rateelevated to
compensate for decreased
stroke volume.
Respirationsrapid 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
both ventricles As pressures rise, this
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 Often within 1 Rare
a 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 Gradual with

cough night 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

VasodilatorsACE 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
AkaACE 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
Amlodipine in the presence of
ischemia
Felodipine
 Metoprolol Useful by blocking the
Atenolol beta-adrengergic
Propanolol receptors of the
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 patients 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
O2High 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 bodys 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