2. – 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.
3. – 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
4. – An imbalance in pump function in which the
heart fails to maintain the circulation of blood
adequately.
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— – 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.
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
• Aka—systolic heart failure
– Right Ventricular Failure
• Aka—diastolic heart failure
17.
18. – 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
19. – 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
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— – 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
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 – 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.
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 Often within 1 Rare
a few hours hour
Smoking Common Less common Less common
Pedal edema Occasional Common with none
chronic
31. 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
32. 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
33. – Aimed at diminishing the compensatory
mechanisms of low cardiac output and also
improving contractility
– Vasodilators—ACE inhibitors
– Diuretic agents
– Inotropic agents
34. – 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
35. – Lasix
– Hydrochlorothiazide(HCTZ)
– Spironolactone
♦ These inhibit reabsorption of Na+ into the
kidneys
36. – Digoxin
– Lanoxin
♦ Increases the contractility of the heart
increasing the cardiac output
37. – Nifedipine – Used to dilate blood
– Diltiazem vessels
– Verapamil – Used mostly with CHF
– Amlodipine in the presence of
ischemia
– Felodipine
38. – 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
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
45. – Prevent the production of the chemicals that
causes blood vessels to narrow
– Resulting in blood pressure decreasing and the
heart pumping easier
