PATHOPHYSIOLOGY Etiologic Factors Predisposing Factors Factors Increasing age Present Justifications Age influences both the risk

and the severity of CHD. Symptomatic CHD appears predominantly in people older than 40 years of age, and 4 of 5 people who die of CHD are age 65 years and older. Our patients age is 72 years old so he is consider being at risk to have severe CHD.

Heredity

Children whose parents had heart disease are at higher risk of CHD.

Gender

Coronary artery disease is the number one killer of both men and women. Men are at higher risk for heart attacks at younger ages, the risk for women increases significantly at menopause. Our patient is a male.

Precipitating Factors Factors Hypertension Present Justification High blood pressure increases the workload of the heart by increasing afterload, enlarging and weakening the left ventricle over time.

Elevated serum cholesterol level

The risk of CHD increases as blood cholesterol levels increase. Cholesterol circulates in the blood in combination with triglycerides and proteinbounded phospholipids called lipoprotein.

Cigarette smoking

Both active smoking ang passive smoking have been strongly implicated as a risk factor in the development of CHD. Tar contains hydrocarbons and other carcinogenic substances. Nicotine increases the release of epinephrine and norepinephrine, which results in peripheral vasoconstriction, elevated blood pressure and heart rate, greater oxygen consumption, and increased likelihood of dysrhythmias. Carbon monoxide reduces the amount of blood available to the intima of the vessel wall and increases the permeability of the endothelium.

Obesity

Obesity places an extra burden on the heart, requiring the muscle to work harder to pump enough blood to support added tissue mass.

Diabetes

Fasting blood glucose of more

than 126 mg/dl or a routine blood glucose level of 180 mg/dl and glucosuria signal the presence of diabetes and represents an increased risk for CHD. Clients with diabetes have a two- to four-fold higher prevalence, incidence, and mortality from all forms of CHD.

Physical Inactivity

There is an inversely relationship between exercise and the risk of CHD. Those who exercise reduce the risk of CHD because they have higher HDL levels, lower LDL cholesterol, triglyceride, and blood glucose levels, greater insulin sensitivity, lower blood pressure, and lower BMI.

Homocysteine level

Researchers have reported that elevated levels of plasma homocysteine ( an amino acid produced by the body) are associated with an increase risk of CHD

Symptomatology Symptoms Exertional dyspnea Justification Dyspnea due to heart disease is generally precipitated or exacerbated by exertion and usually results from elevated left atrial and pulmonary venous pressures or form hypoxia. Dyspnea commonly caused by LV systolic dysfunction Chest pain is usually described as dull, aching, and sense of pressure. The sensation may be tightness or squeezing chest pain. It is due to the occluded blood flow in the coronary arteries in which other parts of myocardium are deficit in oxygen Increase in JVP usually due to the right-sided heart failure in which there is pressure of the left ventricle blood flow Rales heard at the lung bases are a sign of CHF but may be caused by similarly localized pulmonary disease. Cardiac rales tend to occur late in inspiration and be fine in nature, while pulmonary rales tend to be more coarse and appear in early or mid inspiration. Rales are loudest at the bases in heart failure, and the examiner should note how far up from the diaphragm they are audible. Wheezing suggests obstructive pulmonary disease and only rarely occurs in left heart failure Subcutaneous fluid collections appear first in the lower extremities in ambulatory patients or in the sacral region

Chest pain

Distended jugular vein

Rales

Wheezing

Edema

of bedridden individuals. In heart disease, edema primarily results from elevated RA pressures or associated peripheral venous disease. Orthopnea Orthopnea is dyspnea that occurs in recumbency and results from an increase in central blood volume when supine. It may also result from pulmonary disease and obesity. Paroxysmal nocturnal dyspnea is shortness of breath that occurs abruptly 30 minutes to 4 hours after going to bed and is relieved after 10 or 20 minutes by sitting up or standing up; this symptom is more specific for cardiac disease. Cyanosis may be central, due to arterial desaturation, or peripheral, reflecting impaired tissue delivery of adequately saturated blood in low-output states, polycythemia, or peripheral vasoconstriction. Left-sided heart failure is usually the cause of pulmonary congestion because of the pressure or regurgitation of blood flow from the myocardium to the lungs. Cardiac enlargement may happen because both ventricles are hypertrophied due to the increase workload If pain is felt at the RUQ, it is indicated because of the righsided heart failure due (hepatomegaly) to increase pressure and volume in systemic venous circulation.

paroxysmal nocturnal dyspnea

Cyanosis

pulmonary congestion

cardiac enlargement

right upper quadrant pain (RUQ)

Hypertension

Hypertension or increase in Blood pressure may due to increase stimulation of the sympathetic nervous system for the release of catecholamine or may be due to the Angiotensin II in RAAS in which it is a potent vasoconstrictor. Increase in heart rate usually occurs when SNS release epinephrine and norepinephrine Dysrhythmias usually happens because of the changes in the heart rate every time there is a problem occurs in the impulse conduction or contractility in the myocardium. Due to the increase residual of blood in the ventricles, blood will regurgitate back to the mitral valve, left atrium, and towards the lungs leading to pulmonary congestion. Obstruction in the gasexchange like pulmonary congestion secondary to congestive heart failure leads to increase RR because of the oxygen demand needed by the lungs. Decrease blood flow that will be distribute in the blood means that there will also be a decrease in oxygen distribution that will lead to fatigue.

Tachycardia

Dysrhythmias

Pulmonary congestion

Tachypnea

Fatigue and weakness

Schematic Diagram

Predisposing Factors: Increase age Male gender Family history

Precipitating Factors: Hypertension Elevated serum cholesterol level

atherogenesis

Rx: Dyslipidemic Agent

Atherosclerosis (formation of plaque in the blood vessels) in the heart

Rx: Anticoagulant/ Thrombin inhibitors Thrombolytics Surgical Management

Stable atherosclerosis

Unstable atherosclerosis

Occlude the vessel lumina

Thrombus formation

Surgical management: Percutaneous transluminal coronary angioplasty Intravascular stenting Atherectomy Coronary Artery Bypass Graft

B A
Limited blood supply in coronary arteries Obstruction in the coronary arteries

Limited blood supply

Myocardial O2 deficit

Cut off blood supply

S/s: Angina pectoris Depressed ST segment

Less than 20 mins: Ischemic attack/ Myocardial Ischemia

If treated: Nitrates Anticoagulant and thrombolytics O2 administration Antihypertensive Vasodilators

If not treated: Myocardial Infarction (greater than 20 mins.)

Release of lysosomal enzymes

Trop I (+)

Anaerobic metabolism

C
S/s: Chest pain Hydrogen ions and lactic acid accumulation

acidosis

S/s: ECG changes, dysrhythmias

Suppressed impulse conduction

Decreased myocardial contractility

Decrease in cardiac rate

Decreased left ventricular function

Decreased stroke volume

Decrease cardiac output

F
Increase SNS stimulation

G
Decrease renal blood flow S/s: Fatigue Weakness dizziness

S/s: Tachycardia hypertension

Increase catecholamines

Decrease perfusion of tissues

Vasoconstriction

Rx: ACE inhibitors

RAAS activation

S/s: Increase BP

Increase cardiac output

Increase afterload and increase heart workload

Angio II: potent vasoconstrictor

Angio II: increase aldosterone and antidiuretic hormone

Hypertrophy of the myocardium

F
Decrease myocardial contractility Rx: Diuretics Fluid and Na restriction Electrolyte replacement

G
Sodium and water retention

Ventricular remodeling

Increase ECF volume

Increase preload

Increase BNP

Increase osmotic pressure

Stretched the myocardium and constrict the coronary arteries

Hypoxia of the myocardium

Decrease contractility

Increase residual of blood in the left ventricles

F
Regurgitation of blood in to the lungs S/s: Dyspnea Decrease 02 sat Increase RR orthopnea frothy sputum tachycardia

Venous pulmonary congestion

Right-sided failure

Increase pulmonary pressure

Pulmonary edema

Rx: Oxygen administration diuretics

If treated: Diuretics, decrease OFI Sodium restriction

If not treated: Shock and suffocation

Death GOOD PROGNOSIS

BAD PROGNOSIS

I
Increase left ventricular pressure in the lungs

Increase resistance of the blood from the right ventricle

Increase afterload Decreased oxygen supply (Deoxygenated blood)

Hypertrophy of right ventricle

Narrowing of right coronary artery

Increase right ventricular oxygen demand

Right ventricle hypoxia

Decrease force of right ventricle contraction

I
Increase volume and pressure in systemic venous circulation

Increase pressure in great veins and distensible organs

Increase peritoneal pressure

S/s: Ascites

Jugular vein distention

S/s: Anorexia, nausea

Venous congestion of GI

Hepatospleenomegaly

S/s: RUQ pain

S/s: Peripheral edema Cool, pale extremities

Venous congestion in the peripheries

Narrative Pathophysiology The underlying etiologic factors will cause atherogenesis or plaque formation due to the deposition of lipids into the blood vessel walls causing to obstruct the passageway of blood. There are two types of atherosclerosis: stable atherosclerotic plaque produce fixed obstruction of coronary blood flow and unstable atherosclerotic plaques tend to fissure or rupture causing platelet aggregation forming into a thrombus. The thrombus will become an embolus and will occlude the atherosclerotic coronary arteries and will block the myocardial blood flow. Myocardial oxygen deficit will occur because the blood that carries oxygen will not be distributed in the arteries of the myocardium and a condition of myocardial ischemia is called. Myocardial ischemia is an imbalance between the blood supply and the demands of the heart for oxygenated blood. Angina pectoris is the common symptom of myocardial ischemia due to the deprivation of the myocardium for oxygen. Nitrates, antihypertensive, thrombolytics, and anticoagulants are the medications prescribed while percutaneous translucent angioplasty, atherectomy, intravascular stenting, and coronary artery bypass graft (CABG) are the common surgical management to treat myocardial ischemia that focuses more on the atherosclerotic arteries. If not treated after 20 minutes or radiating pain can be felt after taking 3 doses of nitrates, the myocardial tissues are necrotized and myocardial infarction (MI) or heart attack will happen. For after how many seconds of the decrease blood flow in the myocardium, it will become cyanotic and myocardial reserves tend to used quickly. Anaerobic metabolism or breakdown of fats and lactic acid will occur and glycogen stores decrease of oxygen demand in the heart that is needed for adenosine triphosphate (ATP). But because the heart has a poor buffering capabilities and sensitive to low pH, myocardium may result to acidosis and it may suppress impulse conduction. If there is decrease in contractility, therefore there will be a decrease in the heart rate. Decrease stroke blood volume is due to the decrease in contractility of the myocardium as well as decrease left ventricular function, thereby leading to heart failure. Decrease cardiac output stimulates the SNS to release more catecholamines to increase heart rate and blood pressure. There will be an increase in afterload because the ventricles will continue to pump to overcome the systemic pressure and increase the workload of the left ventricles. Too much increase in afterload and workload of the ventricles will hypertrophy and in this condition the ventricles cannot eject the whole blood anymore because contractility of the heart was reduced. Decrease in myocardial contractility will activate the neurohormones to contribute in ventricular modeling. It can cause of dilation in the heart and an increase in preload. Increase in preload actually improve cardiac output, but if preload continues to rise, the myocardium will be stretched and will constrict the lumen of coronary arteries and hypoxia of the heart may happen leading again to reduce its contractility. Myocardium at this time loses its elasticity and decreases its contractility. Chambers especially the left ventricles was hypertrophied and it cannot pump the whole blood towards the body system. Residual of blood can be found in the ventricles. Regurgitation will follow because the left atrium was also affected due to the inability of the left ventricle to eject the blood into the system. The blood will flow back into the lungs that will cause venous pulmonary congestion or pulonary edema or it can cause increase pulmonary pressure that can lead to right-sided failure.

In the right-sided heart failure, the same pathophysiology follows except that it only affects the great veins and organs unlike in left-sided heart failure it complicates in the lungs and sometimes peripheries. On the other hand, as the cardiac output decreases there will be decrease renal blood flow. Therefore, there is no enough oxygen distributed in the kidneys. Because of the decrease blood flow in the kidneys, Renin-Angiotenisn-Aldosterone System will be activated and the Angiotensin II, the potent vasoconstrictor, will stimulate the adrenal gland to release aldosterone and stimulate hypothalamus to release antidiuretic hormone. ADH and Aldosterone causes water and sodium reabsorption and secretion of potassium. Common management for sodium and water retention are medications such as diuretics and beta-blockers. ACE inhibitors are given to inhibit the conversion of Angiotensin I to Angiotesin II by the Angiotensin-converting enzyme. As the fluid and sodium is retained, extracellular fluid volume will increase as well as osmotic pressure increases and as expected there will be an edema due to the retention. If left untreated, pulmonary edema will lead to suffocation and DEATH.