Cardiomyopathy, Raynaud's And Perfusion

Apical hypertrophic cardiomyopathy is a disease that mainly affects the apex of the heart and does not cause any obstruction. [1] These abnormalities in the heart muscle can cause a wide variety of symptoms. As the heart becomes stiff it increases the pressure in the left ventricle which can push blood back into the lungs, causing shortness of breath in exercise. Chest pain can occur as there is not enough oxygen available to the cardiac muscle due to insufficient blood supply. Palpitations and lightheadedness, along with other conditions can occur as a result of HCM. In addition to these discomforting symptoms, the patient may develop an arrhythmias that often goes unnoticed. An arrhythmia takes place as the electrical conduction of the heart is disturbed by the abnormal scattering of myocytes. The two most common arrhythmias are atrial fibrillation causing palpitations, and ventricular tachycardia that can be life threatening causing sudden death. Both conditions can be controlled with medication. [4]

Systolic heart failure is characterized by enlarged ventricles that are unable to fully contract to pump enough blood into circulation to adequately perfuse tissues. The enlargement in ventricles is due to an increased end-systolic volume. If the heart is not able to sufficiently pump the expected volume of blood with each contraction, which in a normal healthy heart is 50-60%, there will be a residual volume left in the heart after every pump (Heart Healthy Women, 2012). With the next period of filling, the heart will receive the same amount of blood volume from the atria combined with that residual volume from the previous contraction. This causes the ventricles to have to dilate to accommodate this increase in volume. The dilation causes the walls of the ventricles to stretch and become thin and weak. Also the myocardium, the muscle layer of the heart, will stretch and not be able to adequately make a full and forceful enough contraction to push blood from the ventricles (Lehne, 2010).

As this disease progresses and the workload of the heart is consistently increased, ventricular hypertrophy occurs. At first, the hypertrophied heart muscles will increase contractility, thus increasing cardiac output; however, as hypertrophy of the ventricular myocardial cells continues, it begins to have poor contractility, requires more oxygen to perform, and has poor circulation from the coronary arteries. This can result in heart tissue ischemia and lead into cardiac dysrhythmias (Lewis et al. 2014, 768).

This causes the ventricles to dilate in order to maintain adequate stroke volume. Usually, this will improve over the next 7-10 days.

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.

Dyspnea and decreased exercise tolerance- which contributes to diastolic dysfunction with an increase in left ventricular filling pressures with exercises.

However, it can also result from certain neurologic disorders — especially life-threatening increased intracranial pressure (ICP) — or from cardiovascular disorders that cause blood backflow into the heart with each contraction such as aortic insufficiency. Widened pulse pressure can easily be identified by monitoring arterial blood pressure and is commonly detected during routine sphygmomanometer recordings (Lippincott, 2005, pg 527-528).

Contractility is the pumping of the heart muscle. It is measured as the ejection fraction. Contractility directly influences stroke volume. Increased contractility will increase stroke volume with any amount of preload. Diseases that disrupt myocyte activity reduce contractility. Myocardial infarction is the most common. Others include, but are not limited to, cardiomyopathies, degenerative valve disease, and myocarditis (Francis & Tang, 2003). Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to neurohumoral , immune, and inflammatory changes and can cause ventricular remodeling. Ventricular remodeling occurs when the size, shape, and function of the affected chamber is distorted. Ventricular remodeling causes hypertrophy and dilation of the heart muscle and causes progressive myocyte contractile dysfunction over a period of time. When contractility is decreased, stroke

The article is published in a peer-reviewed, scholarly and evidence-based journal. The sources are valid and five of the seven references are current within five years of the date of the article. The fact that the article is looking for EBP, also lends to validity, in that the authors were seeking best practice and what is appropriate care available to the CHF patient.

Right ventricular hypertrophy is where the muscle of the right ventricle is thicker than usual and causes the heart to work harder than normal to move blood through the narrowed pulmonary valve.

As previously mentioned, the left ventricle is no longer as compliant and therefore cannot fill with blood without encountering resistance. The use of diuretics decreases overall volume, which as a result decreases overall pressure. This lost pressure may be needed in order for blood to pump with added pressure against the resistance into the ventricle. Once pressure is lost the patient is said to have hypotension and is at risk for blood not being able to perfuse to vital tissues (Burchum et al., 2016, pg.

Mr. Steward’s priority problems include impaired cardiac tissue perfusion, impaired gas exchange, and pain. We are concerned about impaired cardiac tissue perfusion because the pt. is exhibiting signs of myocardial ischemia including chest pain and shortness of breath (Gillespie, 2012). Although we acknowledge that impaired cardiac tissue perfusion can decrease the function of the heart and will have the potential to affect the perfusion and delivery of oxygen to other end organs, our primary focus will be a focused cardiovascular assessment (House-Kokan, 2012). At 1800, Mr. Steward was SOB, had shallow and rapid breathing (RR = 44), and a SaO2 of 72% on RA. Due to the fluid buildup in his lungs, Mr. Steward has impaired gas exchange, and requires supplemental oxygen to maintain his SaO2; this warrants a focused respiratory assessment.

Congestive heart failure (CHF) is a condition that affects the pumping ability of your heart

The major causes of diastolic heart failure are hypertension-induced myocardial hypertrophy and myocardial ischemia-induced ventricular transformation (coronary artery disease). Hypertrophy and ischemia cause a decreased ability of the myocytes to actively pump calcium from the cytosol, resulting in impaired relaxation. Some of the other causes are aortic valvular disease and cardiomyopathies. Diabetes can also lead to diastolic heart failure (Huether and McCune 2012). Other risk factors for this disease are chronic kidney disease, obstructive sleep apnea, and older age. There are two types of the heart failure: systolic heart failure and diastolic heart failure. In systolic heart failure, the left ventricle has difficulty contracting and ejecting blood into the circulation, which causes reduced left ventricular fraction. On the other hand, diastolic heart failure has a slow and delayed relaxation and increased chamber rigidity, which then causes inadequate filling of blood and

Arteriolar vascular constriction, heart rate increases, and renal retention of sodium and water all help to regulate cardial output. Ventricular dilatation is commonly seen. A large amount of ventricular myocardium is lost, contractility may be greatly compromised, and cardiogenic shock may ensue.