Effects of Cardiogenic Pulmonary Edema

• Interference with oxygen transfer in the lungs
• Depression arterial oxygen tension
• Sense of suffocation and oppression in the chest
• Elevates heart rate and blood pressure further restricting ventricular filling.

The increased work of breathing place an additional load on the heart, and cardiac function becomes depressed further by the hypoxia leading to a vicious. Development of acute pulmonary edema is a terrifying experience with extreme breathlessness developing suddenly, and the patient becomes extremely anxious, coughs, and expectorates pink, frothy liquid, with a feeling of drowning. The patient sits upright, or may stand, exhibits air hunger, respiratory rate is elevated, the alae nasi are dilated, and there is inspiratory retraction of the intercostal spaces and supraclavicular fossae that reflects the large  negative intrapleural pressures required for inspiration. The patient often grasps the sides of the bed to allow use of the accessory muscles of respiration. Respiration is noisy, with loud inspiratory and expiratory gurgling sounds that are often easily audible across the room. Sweating is profuse, and the skin is usually cold, ashen, and cyanotic, reflecting low cardiac output and increased sympathetic drive.

Auscultation reveals crepitations and occasionally rhonchi, which appear initially over the lung bases but then extend upward with worsening of the condition. An S3 gallop and loud pulmonic component of the second heart sound are frequently present. Arterial pressure is usually elevated as a result of excitement and discomfort, which cause adrenergically mediated vasoconstriction. And this usually does not represent chronic systemic hypertension. Optic fundus examination may be useful in differentiating the two conditions. Sometimes it may be difficult to differentiate between acute pulmonary edema and acute exacerbation of bronchial asthma.