Seguerra, Kirch Jaina C.

BSN IV

ANGINA PECTORIS CARDIAC FAILURE (LEFT & RIGHT)

Location of Pain: Substantial

Radiation of pain: Neck, jaw or arms Backup of blood to the pulmonary
circulation
Dull or heavy discomfort with a
pressure Increase Pulmonary Circulation
Fluid shifting (Pulmonary Edema)
Heart unable to pup oxygen rich
blood from lungs to heart
Risk for Myocardial Infarction

MYOCARDIAL INFARCTION Right

Back up into systematic Circulation
Increase in central venous pressure

CONGESTIVE FAILURE
Limits its ability to fill with blood
Blood returns to the heart faster
that it can
Becomes congested
Risk for Myocardial Infarction
The blockage is caused by a buildup of plaque in the arteries (atherosclerosis). Plaque
is made up of deposits, cholesterol, and other substances. When a plaque breaks
(ruptures), a blood clot quickly forms. The blood clot is the actual cause of the heart
attack.

If the blood and oxygen supply is cut off, muscle cells of the heart begin to suffer
damage and start to die. Irreversible damage begins within 30 minutes of blockage. The
result is heart muscle affected by the lack of oxygen no longer works as it should.

Angina pectoris is the result of myocardial ischemia caused by an imbalance between

myocardial blood supply and oxygen demand. It is a common presenting symptom
(typically, chest pain) among patients with coronary artery disease (CAD). 

The right ventricle (RV) receives its arterial blood supply primarily from the right
coronary artery (RCA), which arises from the right coronary cusp of the aorta. The
division produces the conus artery, which supplies blood flow to the right ventricular
outflow tract. The RCA from the second division also supplies the sinoatrial node (SA).
Coursing in the atrioventricular groove, the RCA then gives off multiple, small branches
to supply the anterior RV before dividing terminally into the acute marginal branch (AM)
that runs anteriorly along the diaphragm and the posterior descending artery (PDA) that
runs posteriorly. 
Heart failure developing after MI hospitalization is a consequence of cardiomyocyte
death and scar formation, which triggers chronic neurohumoral activation (renin–
angiotensin–aldosterone and sympathetic nervous system up-regulation) and
ventricular remodeling
Left heart failure occurs when there is dysfunction of the left ventricle, resulting
insufficient delivery of blood to vital organs. Left ventricular failure can be further
subdivided into heart failure with preserved ejection fraction (HFpEF) with ejection
fraction over 50 percent, heart failure with reduced ejection fraction (HFrEF) with
ejection fraction less than 40 percent, or heart failure with mid-range ejection fraction,
with ejection fraction between 41 and 49 percent.