Definisi

Heart Failure

• Sindrom klinis yang terjadi pada pasien karena kelainan struktur dan/atau fungsi jantung, sehingga menimbulkan gejala sehingga pasien mengalami rawat inap yang sering, kualitas hidup yang buruk, dan usia harapan hidup yang berkurang

COPD

• Emphysema– Destruksi dan pembesaran alveoli paru-paru

• Bronkitis Kronis– Ciri khas yaitu batuk kronis dengan obstruksi jalan

nafas irreversibel

Asma

Etiology

Heart Failure• Penurunan Ejeksi Fraksi (<40%)

CAD Nonischemic dilated

cardiomyopathy Chronic pressure overload Toxic/drug-induced damage Chronic volume overload Disorders of rate and rhythm

• Preserved Ejection Fraction (>40–50%) Pathological hypertrophy Restrictive cardiomyopathy Aging Fibrosis Endomyocardial disorders

• Pulmonary Heart Disease Cor pulmonale Pulmonary vascular disorders

• High-Output States Metabolic disorders Excessive blood-flow

requirements

Asthma• Atopy• Intrinsic Asthma • Infections • Environmental Factors

– Hygiene Hypothesis– Diet low in antioxidants, such as vitamin C and vitamin A, magnesium,

selenium, and omega-3 polyunsaturated fats (fish oil), or high in sodium and omega-6 polyunsaturates

– Air Pollution such as sulfur dioxide, ozone, and diesel particulates, may trigger asthma symptoms, cities with a high ambient level of traffic pollution

– Allergens house dust mites– Occupational Exposure

Anamnesa

Heart Failure

• Fatigue and shortness of breath• Orthopnea • Exertional dyspnea• Nocturnal cough• Paroxysmal Nocturnal Dyspnea (PND)• Cheyne-Stokes Respiration – Hyperventilation and hypocapnia, followed in turn by

recurrence of apnea.• Acute Pulmonary Edema

COPD• Cough• Sputum production• Exertional dyspnea. • Many patients have such symptoms for months or years before seeking medical

attention• Activities involving significant arm work, particularly at or above shoulder level, are

particularly difficult for patients with COPD• Conversely, activities that allow the patient to brace the arms and use accessory muscles

of respiration are better tolerated. Examples of such activities include pushing a shopping cart, walking on a treadmill, or pushing a wheelchair. As COPD advances, the principal feature is worsening dyspnea on exertion with increasing intrusion on the ability to perform vocational or avocational activities. In the most advanced stages, patients are breathless doing simple activities of daily living.

• Accompanying worsening airflow obstruction is an increased frequency of exacerbations (described below). Patients may also develop resting hypoxemia and require institution of supplemental oxygen.

Asma• Wheezing, dyspnea, and coughing which are variable, both

spontaneously and with therapy.• Symptoms may be worse at night, and patients typically

awake in the early morning hours.• Patients may report difficulty in filling their lungs with air.• There is increased mucus production in some patients, with

typically tenacious mucus that is difficult to expectorate. There may be increased ventilation and use of accessory muscles of ventilation. Prodromal symptoms may precede an attack, with itching under the chin, discomfort between the scapulae, or inexplicable fear (impending doom).

PE

PE Heart Failure• General Appearance and Vital Signs

– Shortness of breath– Systolic blood pressure may be normal or high– Pulse pressure may be diminished, reflecting a reduction in stroke volume

• Peningkatan Jugular Veins Pressure• Pulmonary Examination

– Pulmonary crackles (rales or crepitations)– Pleural effusions

• Cardiac Examination – Cardiomegaly– third heart sound (S3) is audible and palpable at the apex. Patients with enlarged or hypertrophied right ventricles

may have a sustained and prolonged left parasternal impulse extending throughout systole. An S3 (or protodiastolic gallop) is most commonly present in patients with volume overload who have tachycardia and tachypnea, and it often signifies severe hemodynamic compromise. A fourth heart sound (S4) is not a specific indicator of HF but is usually present in patients with diastolic dysfunction. The murmurs of mitral and tricuspid regurgitation are frequently present in patients with advanced HF.

• Abdomen and Extremities – Hepatomegaly– Ascites– Jaundice

• Peripheral edema symmetric

PE Asma

• Pemanjangan inspirasi sampai ekspirasi • Ronki pada seluruh area paru• Hiperinflasi dada

Diagnosis

Heart Failure• Routine Laboratory Testing • Complete blood count, a panel of electrolytes, blood urea nitrogen, serum creatinine, hepatic enzymes, and a urinalysis. Selected patients should have assessment for

diabetes mellitus (fasting serum glucose or oral glucose tolerance test), dyslipidemia (fasting lipid panel), and thyroid abnormalities (thyroid-stimulating hormone level).

• Electrocardiogram (ECG) • LV hypertrophy or a prior MI (presence or absence of Q waves)• Chest X-Ray • Assessment of Lv Function • Noninvasive cardiac imaging (Chap. 222) is essential for the diagnosis, evaluation, and management of HF. The most useful test is the 2-D echocardiogram/Doppler,

which can provide a semiquantitative assessment of LV size and function as well as the presence or absence of valvular and/or regional wall motion abnormalities (indicative of a prior MI). The presence of left atrial dilation and LV hypertrophy, together with abnormalities of LV diastolic filling provided by pulse-wave and tissue Doppler, are useful for the assessment of HF with a preserved EF. The 2-D echocardiogram/Doppler is also invaluable in assessing RV size and pulmonary pressures, which are critical in the evaluation and management of cor pulmonale (see below). MRI also provides a comprehensive analysis of cardiac anatomy and function and is now the gold standard for assessing LV mass and volumes.

• The most useful index of LV function is the EF (stroke volume divided by end-diastolic volume). Because the EF is easy to measure by noninvasive testing and easy to conceptualize, it has gained wide acceptance among clinicians. Unfortunately, the EF has a number of limitations as a true measure of contractility, since it is influenced by alterations in afterload and/or preload. For example, the LV EF is increased in mitral regurgitation as a result of ejection of the blood into the low-pressure left atrium. Nonetheless, with the exceptions indicated above, when the EF is normal (50%), systolic function is usually adequate, and when the EF is significantly depressed (<30–40%), contractility is usually also depressed.

• Biomarkers • Natriuretic peptides, Troponin T and I, C-reactive protein, TNF receptors, and uric acid

Asma• Lung Function Tests• Reduced FEV1, FEV1/FVC ratio, and PEF. Reversibility is demonstrated by a >12% or 200 mL increase in FEV1 15 min after an

inhaled short-acting 2-agonist or, in some patients, by a 2- to 4-week trial of oral glucocorticoids (prednisone or prednisolone 30–40 mg daily). Measurements of PEF twice daily may confirm the diurnal variations in airflow obstruction. Flow-volume loops show reduced peak flow and reduced maximum expiratory flow. Further lung function tests are rarely necessary, but whole body plethysmography shows increased airway resistance and may show increased total lung capacity and residual volume. Gas diffusion is usually normal but there may be a small increase in gas transfer in some patients.

• Histamin challenge untuk mengetahui hiperresponsifitas jalur nafas (Penurunan FEV1 20%)• Blood tests are not usually helpful. Total serum IgE and specific IgE to inhaled allergens (RAST) may be measured in some

patients.• Chest roentgenography is usually normal but may show hyperinflated lungs in more severe patients• Skin prick tests

Treatment

COPD

• Stable Phase COPDOnly three interventions—smoking cessation, oxygen therapy in chronically hypoxemic patients, and lung volume reduction surgery in selected patients with emphysema—have been demonstrated to influence the natural history of patients with COPD.

Farmakoterapi• Smoking Cessation • Bronchodilators• Anticholinergic Agents• Beta Agonists• Inhaled Glucocorticoids• Oral Glucocorticoids• Theophylline• Oxygen• Other Agents

– N-acetyl cysteine

Acute Exacerbations• Bronchodilators• Typically, patients are treated with an inhaled agonist, often with the addition of an anticholinergic agent. These may be administered separately or together, and the frequency of

administration depends on the severity of the exacerbation. Patients are often treated initially with nebulized therapy, as such treatment is often easier to administer in older patients or to those in respiratory distress. It has been shown, however, that conversion to metered-dose inhalers is effective when accompanied by education and training of patients and staff. This approach has significant economic benefits and also allows an easier transition to outpatient care. The addition of methylxanthines (such as theophylline) to this regimen can be considered, although convincing proof of its efficacy is lacking. If added, serum levels should be monitored in an attempt to minimize toxicity.

• Antibiotics• Patients with COPD are frequently colonized with potential respiratory pathogens and it is often difficult to identify conclusively a specific species of bacteria responsible for a

particular clinical event. Bacteria frequently implicated in COPD exacerbations include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. In addition, Mycoplasma pneumoniae or Chlamydia pneumoniae are found in 5–10% of exacerbations. The choice of antibiotic should be based on local patterns of antibiotic susceptibility of the above pathogens as well as the patient's clinical condition. Most practitioners treat patients with moderate or severe exacerbations with antibiotics, even in the absence of data implicating a specific pathogen.

• Glucocorticoids• Among patients admitted to the hospital, the use of glucocorticoids has been demonstrated to reduce the length of stay, hasten recovery, and reduce the chance of subsequent

exacerbation or relapse for a period of up to 6 months. One study demonstrated that 2 weeks of glucocorticoid therapy produced benefit indistinguishable from 8 weeks of therapy. The GOLD guidelines recommend 30–40 mg of oral prednisolone or its equivalent for a period of 10–14 days. Hyperglycemia, particularly in patients with preexisting diagnosis of diabetes, is the most frequently reported acute complication of glucocorticoid treatment.

• Oxygen• Supplemental O2 should be supplied to keep arterial saturations 90%. Hypoxic respiratory drive plays a small role in patients with COPD. Studies have demonstrated that in patients

with both acute and chronic hypercarbia, the administration of supplemental O2 does not reduce minute ventilation. It does, in some patients, result in modest increases in arterial PCO2, chiefly by altering ventilation-perfusion relationships within the lung. This should not deter practitioners from providing the oxygen needed to correct hypoxemia.

• Mechanical Ventilatory Support• The initiation of noninvasive positive pressure ventilation (NIPPV) in patients with respiratory failure, defined as PaCO2 >45 mmHg, results in a significant reduction in mortality, need

for intubation, complications of therapy, and hospital length of stay. Contraindications to NIPPV include cardiovascular instability, impaired mental status or inability to cooperate, copious secretions or the inability to clear secretions, craniofacial abnormalities or trauma precluding effective fitting of mask, extreme obesity, or significant burns.

• Invasive (conventional) mechanical ventilation via an endotracheal tube is indicated for patients with severe respiratory distress despite initial therapy, life-threatening hypoxemia, severe hypercapnia and/or acidosis, markedly impaired mental status, respiratory arrest, hemodynamic instability, or other complications. The goal of mechanical ventilation is to correct the aforementioned conditions. Factors to consider during mechanical ventilatory support include the need to provide sufficient expiratory time in patients with severe airflow obstruction and the presence of auto-PEEP (positive end-expiratory pressure) which can result in patients having to generate significant respiratory effort to trigger a breath during a demand mode of ventilation. The mortality of patients requiring mechanical ventilatory support is 17–30% for that particular hospitalization. For patients age >65 admitted to the intensive care unit for treatment, the mortality doubles over the next year to 60%, regardless of whether mechanical ventilation was required.

Prognosis Heart Failure

• 30–40% within 1 year of diagnosis• 60–70% die within 5 years, mainly from

worsening HF or as a sudden event (probably because of a ventricular arrhythmia)

• [New York Heart Association (NYHA) class IV] have a 30–70% annual mortality rate, whereas patients with symptoms with moderate activity (NYHA class II) have an annual mortality rate of 5–10%