2. – 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.
3. – Effects an estimated
4.9 million Americans
– 1% of age 50-59
– 10% age over 80 89
years
– In the UK most
patients admitted to
hospital with heart
failure are >70 years
and remain
hospitalised for a
week or more.
4. – Heart failure describes the clinical syndrome
that develops when the heart can not maintain
an adequate cardiac output,or can do so only at
the at the exposure of an elevated filling
pressure.
– In mild to moderate form of heart failure
,cardiac output is adequate at rest and only
becomes inadequate when the metabolic
demand increases during exercise or some other
forms of stress
5. ♦ 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.
6. – 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
8. – 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.
9. – 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
10. – Uncontrolled HTN doubles the chances of
failure
– With HTN, the chambers of the heart enlarge
and weaken.
11. – Can result from disease, infection, or be
congenital
– Don’t open and/or close completely
increased workload failure
12. – Tachycardias decreased diastolic filling time
decreased SV.
– Atrial dysrhythmias as much as 30%
reduction in stroke volume
13. – 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.
14. – Tend to be overweight
– HTN
– Hyperlipidemia
16. – Left Ventricular Failure with Pulmonary Edema
– Right Ventricular Failure
17. 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.
18. – 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
19. – Severe resp. distress–
• Evidenced by
orthopnea, dyspnea
• Hx of paroxysmal
nocturnal dyspnea.
– Severe apprehension,
agitation, confusion—
• Resulting from hypoxia
– 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
20. – 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
21. – LOC—
• may vary.
• Depends on the level of hypoxia
– Chest Pain
• May in the presence of MI
• Can be masked by the RDS.
22. ♦ REMEMBER LEFT VENTRICULAR
FAILURE IS A TRUE LIFE
THREATENING EMERGENCY
23. – 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
24. – 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
25. – Marked JVD
– Clear chest
– Hypotension
– Marked peripheral
edema
– Ascites, hepatomegaly
– Often will be on Lasix,
Digoxin,
– Have chronic pump
failure
27. – Stimulated by decreased perfusion secretion
of hormones
• Epi—
– Increases contractility
– Increases rate and pressure
– Vasoconstriction SVR
• Vasopressin—
– Pituitary gland
– Mild vasoconstriction, renal water retention
28. – 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
29. – Long term compensatory mechanism
– Increases in size due to increase in work load ie
skeletal muscle
30. 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
31. 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
32. 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
34. – Aimed at diminishing the compensatory
mechanisms of low cardiac output and also
improving contractility
– Vasodilators—ACE inhibitors
– Diuretic agents
– Inotropic agents
35. – Dilate blood vessels
– Often constricted due
to activation of the
sympathetic nervous
system and the renin-
angiotensin-
aldosterone system.
– Aka—ACE inhibitors
– Common ACE
inhibitors
• Captopril
• Lisinopril
• Vasotec
• Monopril
• Accupril
– Nitrates
37. – Digoxin
– Lanoxin
♦ Increases the contractility of the heart
increasing the cardiac output
38. – 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
39. – The prehospital goals for managing CHF
– Promotion of rest
– Relief of anxiety
– Decreasing cardiac workload
– Attainment of normal tissue perfusion
40. – 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
41. – 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
43. – Prevent the production of the chemicals that
causes blood vessels to narrow
– Resulting in blood pressure decreasing and the
heart pumping easier
