CONGESTIVE HEART

FAILURE
(CHF)

APPROACH TO DIAGNOSE
HEART DISEASE
1. ANAMNESIS
2. PHYSICAL EXAMINATION
3. ELECTROCARDIOGRAM
4. CHEST X RAY
5. ANOTHER SUPPORTING
EXAMINATION
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Heart Failure

An imbalance in pump function in which the

heart fails to maintain the circulation of blood
adequately.

Basic Definition
Heart failure is a
medical term that
describes an
inability of the heart
to keep up its work
load of pumping
blood to the lungs
and to the rest of
the body.

Kep up: m lnjutkangdvy

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http://danilhammoudimd_1.tripod.com/cardio1/id57.htm

CLASSIFICATION OF HEART
FAILURE
NEW YORK HEART ASSOCIATION FUCTIONAL
CLASSIFICATION :
I. Pts with cardiac disease but without resulting
limitation
II. Pts with cardiac disease resulting slight
limitation of physical activity.
III. Pts with cardiac disease resulting in marked
limitation on physical activity.
IV. Pts with cardiac disease resulting in inability
to carry on any physical activity without discomfort.
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Congestive heart failure is a syndrome that

can be caused by multiple underlying
diseases such as:
Congenital heart disease
Atherosclerosis
Rheumatic fever
Cardiomyopathy
Valve disorders
Ventricular failure
Left or right-sided failure
Hypertension
Prolonged alcohol or drug addiction
Previous heart attack
Diabetes
Chronic rapid heartbeats

PATHOPHYSIOLOGY
HEART DIVIDED INTO 2 PUMPING SYSTEMSRIGHT AND LEFT VENTRICLES/CARDIAC
FUNCTIONING REQUIRES EACH VENTRICLE
TO PUMP OUT EQUAL AMOUNTS OF BLOOD
CONDITIONS THAT CAUSE HEART FAILURE
MAY AFFECT ONE OR BOTH OF THE HEARTS
PUMPING SYSTEMS.
LEFT SIDE FAILS 1ST BECAUSE OF
GREATEST WORKLOAD. ONE SIZE USUALLY
LEADS TO FAILURE OF THE OTHER SIDE.

RIGHT-SIDED HEART
FAILURE
JUGULAR VEIN
DISTENSION
DEPENDENT
PERIPHERAL
EDEMA
ASCITES
WEIGHT GAIN
FATIGUE
WEAKNESS

SPLENOMEGALY
HEPATOMEGALY
GI DISCOMFORT
NOCTURIA
TACHYCARDIA

LEFT-SIDED HEART FAILURE

DYSPNEA
DRY COUGH
CRACKLES
WHEEZES
ORTHOPNEA
HEMOPTYSIS
Paroxysmal
NOCTURNAL
DYSPNEA

CHEYNE-STOKES
RESPIRATIONS
FATIQUE
WEAKNESS
CYANOSIS
NOCTURIA
TACHYCARDIA
Serious: life threatening
Pulmonary Edema

ACUTE VS CHRONIC

ACUTE
RAPID RESPIRATIONS
SEVERE DYSPNEA
CRACKLES/WHEEZE
COUGHING
FROTHY SPUTUM
ANXIOUS/RESTLESS
CLAMMY SKIN/COOL

CHRONIC
S/S INFLUENCED BY
PATIENTS:
AGE
UNDERLYING CAUSE
VENTRICLE THAT IS
FAILING

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

Alcohol--chronic
MI--acute
Diabeteschronic

 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

Heart - Pathology
Ischemic Heart Disease

Pnylamatanthy

 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.

ACUTE CORONARY SYNDROME

ST Elevation

No ST Elevation

NSTEMI

Unstable Angina
N Qw Myocardial
Infarction

Qw Myocardial
Infarction
AHA Guidelines, 2000

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 Tend to be overweight
HTN
Hyperlipidemia

 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
Appr ktakutankny
Smoth mncekikgky

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/sukarthy

 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

Leakbcorthy

 Marked
JVD/JVDistended
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

Symptoms
(involving gravity/exhaustion of heart
Swelling of the
ankles, legs, and
hands
Orthopnea, or the
shortness of breath
when lying flat
Shortness of breath
during exertion

Grav:k gawtansdry
Invlv m lputibvgth

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Symptoms
(involving circulation)
Cyanosis, or a bluish color that is seen in the lips
and fingernails from a lack of oxygen
Fatigue or weakness
Rapid or irregular heart beat
Changes of behavior such as restlessness,
confusion, and decreased attention span

Span: hyjangka wkthdphsrty

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Symptoms
(involving congestion)

Unexplained or unintentional weight gain

Chronic cough
Increased urination
Distended neck veins
Loss of appetite or indigestion

Uninten : tdkd sngajarwey

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Left-sided/Right-sided Failure
Blood backs up causing congestion and
thus swelling of extremities and internal
organs

Backupmnggenangthy
Congest:konjesen

32

Chest X-ray
Size and shape of heart
Evidence of pulmonary venous congestion
(dilated or upper lobe veins perivascular
edema)
Pleural effusion

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Congestive Heart
Failure
Increased heart
size: cardiothoracic
ratio >0.5

Large hila
with indistinct
markings
Fluid in
interlobar
fissures
Pleural
effusions,
alveolar
Indsting: kburdry

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Differential diagnosis
(Congestive Heart Failure)

Pericardial diseases
Liver diseases
Nephrotic syndrome
Protein losing enteropathy

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Progression to Heart Failure

from Risk Factors
Smoking

MI

Dyslipidemia
Diabetes
Hypertension

Normal LV
structure and
function

LVH

LV
remodeling
Years

Systolic
dysfunction

Diastolic
dysfunction

Subclinical
LV
dysfunction

HEART
FAILURE

Clinical Heart Failure

Years/months

Levy et al. JAMA, 275:1557, 1996

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MANAGEMENT
MAIN GOALS OF THERAPY :
Identification and correction of the
underlying conditions
Elimination of the acute precipitating
cause of symptoms.
Treatment of the acute symptoms of
congestive heart failure
Improvement in longterm survival.
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Treatment
When a treatable underlying cause of
congestive heart failure exists,
correcting the cause may resolve, or at
least greatly improve, the degree of
heart failure
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Diet and Activity

Salt restriction
Fluid restriction
Daily weight (tailor therapy)
Gradual exertion programs

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How much Salt is too much?

Limit is 2000 mg of salt per day. This
equals 1 teaspoon of salt all day.
Stay away from salty snacks- potato
chips; salted crackers; pretzels.
No salt shaker.

Pot.chip:k ripikthy
Krack : kuetry
Pretz kue krghyng asinthy

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How much can I drink?

Do not drink more than 1.5 litres to 2 litres
of fluid per day.
That equals 6-8 cups of fluid all day.

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Daily Weights
Weigh yourself daily.
Use the same scale, and weigh yourself
first thing in the morning before breakfast.
Call the clinic if weight increases by two
pounds overnight or five pounds in a few
days.

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COPD

CHF

Pneumonia

Cough

Frequent

Occasional

Frequent

Wheeze

Frequent

Occasional

Frequent

Sputum

Thick

Thin/white

Thick/yellow/
brown

Hemoptysis

Occasionally

Pink frothy

occasionally

PND/Par.Nock.
Dispneu

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.
ACE 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/pncpaianthy of normal tissue perfusion

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

Relaxation of smooth muscle

Widens blood vessels
Lowers systolic blood pressure

Eras of Heart Failure

Management
NonPharmacological

Pharmacological

Bed rest

Digitalis

Inactivity

Diuretics

Fluid restriction

Neuro-hormonal
interventions

(Digitalis, diuretics)

Pre-1980s

1980s

Pharmacological
Digitalis
Diuretics
Vasodilators
Inotropes

1990s

Cellular/Genes
Gene therapies
Cell implantation
Xenotransplantation

2000s

2020s

Device/alt br
CRT
ICDs
LVADs
Others

THE END

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