CHF by xiaopangnv

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									    By: Darryl Jamison
        NREMT-P
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                – Diabetes—chronic
– Valvular heart disease
  (especially aorta and
  mitral disease)--
  chronic
– Infections--acute
– Dysrhythmias--acute
– 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.
– 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
– 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
– Don’t 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
   • Aka—systolic heart failure



– Right Ventricular Failure
   • Aka—diastolic heart failure
– 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,            • 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
– 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
– 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

– Vasodilators—ACE 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
– Aka—ACE 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 patient’s 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
–   O2—High 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 body’s 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

								
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