Macon County EMS Training Coordinator

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• By Darryl Jamison
• Macon County EMS Training Coordinator

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• 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.

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• 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
  

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• An imbalance in pump function in which the heart
  fails to maintain the circulation of blood
  adequately.

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• 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.

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• 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

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

• Alcohol--chronic
• MI--acute
• Diabeteschronic

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• 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.

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• 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

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• Uncontrolled HTN doubles the chances of failure
• With HTN, the chambers of the heart enlarge and
  weaken.

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• Can result from disease, infection, or be
  congenital
  
• Dont open and/or close completely ? increased
  workload ? failure

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• Tachycardias ?decreased diastolic filling time ?
  decreased SV.
  
• Atrial dysrhythmias ? as much as 30 reduction in
  stroke volume

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• 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.

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• Tend to be overweight
• HTN
• Hyperlipidemia

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Types of Rhythms Associated with CHF
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• Left Ventricular Failure with Pulmonary Edema
• Akasystolic heart failure
• Right Ventricular Failure
• Akadiastolic heart failure

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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.
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• 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

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• 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

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• 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

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• LOC
• may vary.
• Depends on the level of hypoxia
• Chest Pain
• May in the presence of MI
• Can be masked by the RDS.

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• REMEMBER LEFT VENTRICULAR FAILURE IS A TRUE LIFE
  THREATENING EMERGENCY

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• 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

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• 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

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• 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

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• Neurohormonal system
• Renin-angiotensin-aldosterone system
• Ventricular hypertrophy

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• Stimulated by decreased perfusion ? secretion of
  hormones
  
• Epi
• Increases contractility
• Increases rate and pressure
• Vasoconstriction ? SVR
• Vasopressin
• Pituitary gland
• Mild vasoconstriction, renal water retention

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• 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

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• Long term compensatory mechanism
• Increases in size due to increase in work load ie
  skeletal muscle

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• Aimed at diminishing the compensatory mechanisms
  of low cardiac output and also improving
  contractility
  
• VasodilatorsACE inhibitors
• Diuretic agents
• Inotropic agents

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• Dilate blood vessels
• Often constricted due to activation of the
  sympathetic nervous system and the
  renin-angiotensin-aldosterone system.
  
• AkaACE inhibitors

• Common ACE inhibitors
• Captopril
• Lisinopril
• Vasotec
• Monopril
• Accupril
• Nitrates

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• Lasix
• Hydrochlorothiazide(HCTZ)
• Spironolactone
• These inhibit reabsorption of Na into the
  kidneys
  

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• Digoxin
• Lanoxin
• Increases the contractility of the heart ?
  increasing the cardiac output

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• Nifedipine
• Diltiazem
• Verapamil
• Amlodipine
• Felodipine

• Used to dilate blood vessels
• Used mostly with CHF in the presence of ischemia

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• 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

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• The prehospital goals for managing CHF
• Promotion of rest
• Relief of anxiety
• Decreasing cardiac workload
• Attainment of normal tissue perfusion

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• 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

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• 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

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• NTG
• MS
• Lasix
• O2High flow O2

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• ACE Inhibitors
• Digitalis
• Diuretics
• Hydralazine
• Nitrates

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• Prevent the production of the chemicals that
  causes blood vessels to narrow
  
• Resulting in blood pressure decreasing and the
  heart pumping easier

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• Inotropic effects on the heart
• Negative chronotropic effects

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• Decrease the bodys retention of salt and water
• Reduces blood pressure
• Probably will be on potassium

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• Widens the blood vessels, therefore allowing more
  blood flow

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• Relaxation of smooth muscle
• Widens blood vessels
• Lowers systolic blood pressure

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• Particularly difficult in elderly
• Atypical presentations
• Predominant symptoms include
• Anorexia
• Generalized weakness
• Fatigue
• Mental disturbances
• Anxiety

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• Bubbling Rhonchi
• Coarse Crackles
• Fine Crackles
• Gurgling Rhonchi
• Rales

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