Indication for oxygen therapy

Indication for oxygen therapy:
- Oxygen therapy is indicated in any acute condition causing inadequate tissue oxygenation like pulmonary embolism, severe pneumonia, pneumothorax, acute severe asthma, MI
- Cyanosis and acute dyspnea are obvious signs of severe hypoxia but, in many patients requiring oxygen, the signs, if any, may be much less specific, e.g. tachycardia or mild confusion.
- If the arterial oxygen saturation, as measured by pulse oximetry (SpO2) is less than 90%.
- Prophylactic oxygen therapy is required postoperatively (at least 4 hours following major surgery and following minor surgery until the patient is stable.).
- Hypoxemia is common during heavy sedation: If verbal contact with the patient is lost due to sedation, the airway must be protected and oxygen should be administered.

congestive cardiac failure

 
Definition: Heart failure is a clinical syndrome that results from the progressive process of remodeling, in which mechanical and biochemical factors alter the size, shape, and function of the ventricle’s ability to pump enough oxygenated blood to meet the metabolic demands of the body.

Pathophysiology:
 Heart failure results from a variety of cardiovascular conditions including chronic HTN, coronary artery disease and valvular disease. These conditions can result in decreased contraction (systole), decreased filling (diastole) or both. Significant myocardial dysfunction most often occurs before the patient experiences the signs and symptoms of heart failure such as shortness of breath, edema and fatigue.
 As heart failure develops, the body activates neurohormonal compensatory mechanisms. Systolic heart failure results in decreased blood volume being ejected from the ventricles. The decreased ventricular stretch is sensed by baroreceptors in the aortic and carotid bodies. The sympathetic nervous system is then stimulated to release epinephrine and nor epinephrine. The purpose of this initial response is to increase heart rate and contractility and support the failing myocardium, but the continued response had multiple negative effects. Sympathetic stimulation causes vasoconstriction to the skin, GI tract and the kidneys. A decrease in renal perfusion causes the release of rennin. Rennin promotes the formation of angiotensin I.Angiotensin converting enzyme in the lumen of pulmonary blood vessels converts the angiotensin I to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin II also stimulates the aldosterone from the adrenal cortex, resulting in sodium and fluid retention by renal tubules and stimulating the thirst centre. This leads to the fluid over load commonly seen in heart failure.
 As heart workload increases, contractility of the myocardial muscle fibers decreases. Decreased contractility results in an increase in an end diastolic blood volume in the ventricle, stretching the myocardial muscle fibers and increasing the size of the ventricles. The increased size of the ventricles further increases the stress on the ventricular wall, adding to the workload of the heart. One way the heart compensates the workload is by increasing the thickness of the heart muscles. However this hypertrophy results in an abnormal proliferation of myocardial cells, a process known as ventricular remodeling. 
 Diastolic heart failure results because of continued increased workload in the heart, which responds by increasing the number and size of myocardial cells. The responses cause resistance to ventricular filling, which increases ventricular filling pressures despite a normal or reduced blood volume.

Etiology:
Caused by disorders of heart muscles resulting in decreased contractile properties of the heart; MI, HTN, valvular heart disease; congenital heart disease; cardiomyopathies; dysarrythmias.


Other causes include:
a) Pulmonary embolism, chronic lung disease
b) Hemorrhage and anemia
c) Anesthesia and surgery
d) Transfusions or infusions
e) Increased body demands( fever, infection, pregnancy)
f) Drug induced
g) Physical and emotional stress
h) Excessive sodium intake
Risk factors:
a) Hypertension
b) Hyprelipidemia
c) diabetes
d) CAD
e) Family history
f) Smoking
g) Alcohol consumption
h) Use of cardio toxic drugs