Cardiac Adaptation For Chronic Hypoxia

The cardiovascular and the respiratory system both work toward the same goal: getting oxygen to tissues and getting carbon dioxide out. Every cell in the body requires oxygen in order to carry out its job correctly. The body cannot survive without oxygen for more than a few minute. If the body is starved of oxygen for longer than 6 minutes it will result in death ( Tortora & Derrickson 2006)

Hypoxia is one of the major problems associated with this increase in altitude. This is due to the fact that the partial pressure of oxygen decreases proportionately with increases in altitude. Carbon dioxide that is continually excreted from the pulmonary blood to the alveoli along with water vaporizing in the inspired air from the respiratory surfaces dilute the oxygen in the alveoli which cause the oxygen concentration to decrease.

The same happens with Carbon Dioxide (CO2). The blood in the surrounding capillaries has a higher concentration of CO2 than the inspired air due to it being a waste product of energy production. This is when O2 and CO2 pass each other going back around the body systems to the heart. Once this is done the flow goes from Deoxygenated blood to Oxygenated blood.

The altitude that this stage could happen in is between 5000 to 11400 ft.(3) "The body generally has the ability to stave off further effects of hypoxia by increasing the rate and depth of ventilation and cardiac output ".(1) The respiration rate, blood pressure, and the heart rate can rise up in this stage.(2) the arterial oxygen saturations in this stage is between 80 and 90 percent.(1)

If there aren't enough red blood cells to carry oxygen, the heart will try to move the small number of cells at a faster rate and overtax itself.

Long-term hypertension can result in a variety of consequences. These consequences are the result of the heart having to adapt and work harder, i.e. against an increased afterload due to the increased systolic pressure. The heart adapts via hypertrophy of the smooth muscle. Chronic hypertension can also lead to a disruption of the endothelium, thus increasing the

There are many causes of heart failure. Among them is a reduction in the contractile ability of the heart due to mechanical problems or any problem that limits the filling capacity of the heart chambers with blood due to any form of cardiomyopathy. Whatever the cause, the patient’s tissues are compromised because they cannot receive an adequate amount of oxygen necessary to perform optimally (Bui, Horwich, & Fonarow, 2010).

When there is insufficient amount of blood due to blood loss, organs do not obtain the amount of blood that is needed. As a result, the organs do not receive enough nutrients and oxygen; hypoxia. A decrease of blood pressure also decreases in perfusion of the carotid and aortic bodies, “several clusters of chemoreceptors” (Boron).This decline in perfusion, increases the rate of the chemoreceptors which increases the firing of the sympathetic vasoconstriction (Boron).

In the American Heart Association (AHA)/American College of Cardiology guidelines1, heart failure (HF) is defined as a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood. A normal healthy heart is a muscular organ with four chambers, two on the right and two on the left, that pumps blood to the lungs and rest of the body2. The two upper chambers are called atria and the two lower chambers are called ventricles. The right atria take in oxygen-poor blood from the rest of the body and sends it back out to the lungs through the right ventricle where the blood becomes oxygenated. Oxygen-rich blood travels from the lungs to the left atrium, then on to the left ventricle, which pumps it to the rest of the body. In a patient with heart failure, the heart muscle has been progressively weakened and unable to pump enough blood through to the body.

Vascular remodeling of the vessel layers of the pulmonary arteries from smooth muscle cell proliferation and inflammation results in reducing the size of the arterial lumen (Lundgren & Ladegran, 2014). As pulmonary hypertension progresses, this vascular remodeling leads to a further reduction in the size of the arterial lumen, increased peripheral vascular resistance, increased right ventricular load, and right ventricular hypertrophy (Lundgren & Ladegran, 2014). Eventually, the right ventricle is unable to compensate for the increased pressure causing it to dilate resulting in the symptoms associated with the disease and eventual death (Lundgren & Ladegran, 2014; Weber et al.

In most tissues of the body, ATP production primarily occurs through mitochondrial oxidative phosphorylation of reduced intermediates, which are in turn derived from substrates such as glucose and fatty acids. In order to maintain ATP homeostasis, and cellular function, the mitochondria requires a constant supply of fuels and oxygen. In many individuals at altitude, tissue oxygen levels fall and the cell must meet this hypoxic challenge to maintain energetic and limit oxidative stress. Varying on protocols, the body can adapt to the lack of oxygen which can be increasing the mass of red blood cells and haemoglobin or changes in muscle metabolism. Depending very much on the protocols used, the body may adapt to the relative lack of oxygen in one

The lack of oxygen in the body causes the heart to attempt to pump more blood, forcing the ventricles to work even harder. Should the

Heart failure is a condition where the heart is unable to pump insufficient amount of blood to supply the rest of the body. This is a consequence of ventricular remodelling. Ventricular remodelling is a term that refers to alterations in structure, shape and function of the left ventricle. (1) The activation of neuro-hormonal systems such as RAAS and the sympathetic nervous system are predominantly linked to the pathophysiology of heart failure. Therefore, interrupting this system is vital to delaying the progression of heart failure. (2)

These effects which make your heart work harder to pump blood through your pulmonary arteries and lungs. For a long time, the pressure on arteries inclines. Surely, the

lactate paradox may only be a transient feature of hypoxic adaptation at altitude, disappearing in