By: Darryl Jamison

Macon County EMS Training

Coordinator

 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.

 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

 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 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

 Coronary artery
disease--chronic
HTN--both
Valvular heart disease
(especially aorta and
mitral disease)-chronic
Infections--acute
Dysrhythmias--acute

Alcohol--chronic
MI--acute
Diabeteschronic

 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
increase stroke volume in
normal heart
Increasing preload
impaired heart
decreased SV. Blood is
trapped chamber
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 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

ventricle fails as an
effective forward pump
back pressure of blood
into the pulmonary
circulation
pulmonary edema
Cannot eject all of the
blood delivered from the
right heart.
Left atrial pressure rises
increased pressure in the
pulmonary veins and
capillaries

When pressure
becomes to high, the
fluid portion of the
blood is forced into the
alveoli.
decreased
oxygenation capacity
of the lungs
AMI common with
LVF, suspect

 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
Ralesespecially at the
bases.
Rhonchiassociated
with fluid in the larger
airways indicative of
severe failure
Wheezesresponse 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.
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
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
increased right vent.
Pressures.
As pressures rise, this
increased pressure in
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
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

 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 few hours

Often within 1
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 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
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

 Aimed at diminishing the compensatory

mechanisms of low cardiac output and also
improving contractility
VasodilatorsACE inhibitors
Diuretic agents
Inotropic agents

 Dilate blood vessels

Often constricted due
to activation of the
sympathetic nervous
system and the reninangiotensinaldosterone system.
AkaACE inhibitors

Common ACE
inhibitors

Captopril
Lisinopril
Vasotec
Monopril
Accupril

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
Diltiazem
Verapamil
Amlodipine
Felodipine

Used to dilate blood

vessels
Used mostly with CHF
in the presence of
ischemia

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 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