Bahan Kuliah Gagal Jantung

Basis of Cardiac Failure

Abnormalities in energy metabolism. Relative subendocardial myocardial

ischemia Reduced high-energy (eg. Creatine

phosphate / CRP) stores. Mitochondrial abmormalities Reduced creatine kinase activity

Alteration in expression or activity of contractile proteins (ie. reversion to the “fetal gene pattern)

Alterations in myosin heavy chain (MHC), troponin T, and myosin light chain-I

Abnormalitiesin excitation-contraction coupling.

Prolongation of intracellular Ca+

transient Increased diastolic Ca+ concentrations

Cytoskeletal abnormalities

Excessive microtubular polymerization

Increased cytoskeletal protein (eg. tubulin, dystrophin)

Decreased cytoskeletal proteins (eg. α-actinin, tinin)

Cytoskeletal gene mutations in desmin, dystrophin, sarcoglycans and laminin A and C.

Aterations in β-adrenergic signaling.Characteristic of Cardiac Remodeling Initiated by damage to the heart, such

as myocardial injury of increased pressure or volume load.

Often continues even after resolution of initiating event.

Tends to progress over time. Results in increased cardiac chamber

volumes and muscle mass (eccentric hypertrophy),as well as increased ECM deposition.

Compensatory Mechanisms to Support the Failing Heart.

Mechanism Benefecial Effect Deleterious Consequences

Immediate Salt/water retention Increased intravascular Increased wall stress

Volume resulting in in – Pulmonary and sys- Creased CO and BP temic congestion

Peripheral Increased venous return Increased wall stressvasoconstriction to the heart and augmen - Pulmonary conges-

ted BP tionIncreased heart rate Increased CO Increased myocardial

O2 consumptionIncreased myocardial Increased CO Increase mypcardialcontractility O2 consumption

Long-termMyocardial hyper- Increased force genera- Abnormalities in struc-trophy tion caused by an increa- tural and functional

sed number of contractile proteins within the units (ie, sarcomeres) myocyte.

Normalization of the wall Energy supply/demand stress mismatch

Increased fibrosisChamber dilation Increased stroke volume Increased wall stress

20valvular insufficiency

Heart Failure Risk Factors

Aging

Coronary Artery Disease Hypertension Left ventricular hypertrophy Diabetes Mellitus Obesity

Systolic & Diastolic HF Comparison Dysfunction

Systolic Diastolic - EF < 40% > 40%- LV cavity Increased Normal- Age of pts All ages elderly- Gender of pts Male (I) Female (I)- S 3 Frequently Uncommon- Ass with Hyp. Sometimes Frequently- Ass with DM Sometimes Frequently- Ass with CAD 50-60% Unclear>50%- Freq Hospital Yes Yes- Ventr Arrh Common Unclear- Atrial Arrh Common Common

Congestion at rest

NO Yes

Warm & dry Warm & wetNO A B

Cold & dry Cold & WetYES

L C

Low

per

fusi

onat

res

t?

Evidence for congestion

OrthopneaHigh jugular venous

pressureEdemaPulsatile

hepatomegalyAscites

Radiation of P2 leftRales (rarely)

Valsalva square wave

Abdomino-jugular reflex

Evidence for low perfusionNarrow pulse pressureCool extremitiesMay be sleepy, obtundedSuspect from ACEI hypotensionSubject from declining serum NaOne cause of worsening renal fn

WARM & dryThe goal of acute therapy for stabilization

during decompensation.Allows eventual estabhlisment of effective

chronic neurohormonal therapy

DRY WETWARM A B

COLD L C

NlSVR High SVR

New York Heart Association Function

COLD & dryUncommon profile.Usually comfortable at restNo lasting benefit from

inotropic therapy.May benefit from beta

blockers

WET & warmDiuretics often adequate

to treat congestionCan usually maintain

previous beta blocker doses.

WET & coldUsually need to “warm up” before “drying out”

Inotropic drugsDobutamineMilrinoneCalcium sensitive

VasodilatorNitroprussideNitroglycerinNatriuretic peptides

Classification of Chronic Heart Failure

Class SymptomsI No perceived limitation of Physical activity

II A / B Symptoms with moderate Physical activity

III A / B Symptoms with low levels of physical exertion (ie, those for activities of daily living )

IV Resting symptoms

A = early stage; B = late stage

Common Symptoms of Chronic Heart Failure

Congestive

Dyspnea (rest or exertional) Paroxysmal Nocturnal Dyspnea Abdominal or epigastric discomfort Nausea or anorexia Pedal / leg edema Sleep disturbance (anxiety or air

hunger) Orthopnea Cough (recumbent or exertional) Abdominal bloating (ascites) Early satiety Weight gain (rapid) Chest tightness or discomfort)

Common Symptoms of Chronic Heart Failure

Low Cardiac Output. Easy fatigability Nausea or anorexia Poor energy level or endurance Weight loss, unexplained Impaired concentration or memory Malaise Early satiety Decreased exercise tolerance Muscle wasting or weakness Daytime oliguria with recumbent

nocturia

Physical Examination Finding and Typically Associated

Hemodynamic Pertubations in Chronic Heart Failure.

Reduced Cardiac Output. Resting tachycardia Pulsus alternans Cachexia Cheyne-Stokes respiration (with or without apnea) Low carotid pulse volume Cool / vasoconstricted extremities Altered mentation (somnolence,

confusion)

Volume and/or Diastolic Overload. Jugular venous distention

Abdomino-jugular reflux Ascites S3 Hepatomegaly Pleural effusion Dependent edema Loud pulmonic closure sound Pulmonic rales.

Nonspecific Hemodynamic Correlation Cardiomegaly S4 Accessory respiratory muscle use Wheezing Subxiphoid impulse Abnormal apical impulse Tachypnea Parasternal lift

When Should Patients Be Admitted to the Hospital for

Acute Decompensation of Heart Failure ?

- Onset of acute myocardial ischemia- Pulmonary edema or increasing res- piratory distress- Oxygen saturation below 90% not caused by pulmonary disease- Complicating medical illnesses

- Symptomatic hypotension with fluid overload. - Syncope - Heart failure refractory to out- patient treatment - Anasarca - Inadequate outpatient social support system