Thrombophlebitis

Thrombophlebitis
- is swelling (inflammation) of a vein caused by a blood clot
- refers to thrombus formation on the wall of a vein with resulting inflammation

Hypertension

Hypertension (HPN) or high blood pressure is a chronic medical condition in which the blood pressure in the arteries is elevated. It is classified as either primary (essential) or secondary. Primary hypertension which refers to high blood pressure for which no medical cause can be found. The Secondary hypertension are caused by another conditions that affect the kidneys, arteries, heart, or endocrine system.
People can live with hypertension for many years without having any symptoms. That's why high blood pressure is frequently known as "The Silent Killer". High blood pressure is a condition in which the patient has higher than normal blood pressure. It's currently defined as a BP of above 140/90 mmHg. Basically there are three types of hypertension namely Primary, Secondary & White Coat Hypertension.

Primary Hypertension, may lead to worse conditions. It's not easy to find the cause of the primary hypertension. some say that primary hypertension is linked to genetic, poor diet, overweight, etc.

Secondary Hypertension, is an effect of other medical conditions. It means there are several conditions that may cause high blood pressure. the disorder of an organ in the body may lead high pressure. Kidneys disorder is an example of the condition that may cause the secondary hypertension.

Tension & Anxiety are known to cause temporary increases in blood pressure, which is known as White Coat Hypertension. If a person is having white coat hypertension, he is asked to monitor his blood pressure by wearing a device called an ambulatory blood pressure device. This device is usually worn for 24 hours& can take blood pressure every 30 minutes.

It is very important to know the type of hypertension one is having. The treatment is also essential because if it's not treated it causes the heart to work very hard & ultimately damages it. The American Medical Association notifies that serene cases of untreated hypertension can double the chance of a heart attack & a temperate case triples it.
Stages of Hypertension
Pre-hypertension – Systolic blood pressure (SBP) 120-139 or diastolic blood pressure(DBP) 80-89
Stage I HTN – SBP 140-159 or DBP 90-99
Stage II HTN – SBP >160 or DBP >100
Signs and Symptoms

• Tiredness
• Irregular Heartbeat
• Blurred Vision
• Confusion
• Headache
• High blood pressure

Risk Factors

• Diabetes Mellitus
• Family History
• Advance age
• Obesity
• Sedentary Lifestyle
• Stress
• Smoking
• High intake of Na, saturated fats
• Alcohol

Prevention

• One can control hypertension or blood pressure by adopting healthy lifestyle options like quit smoking, healthy eating habits like little salt, ample of fruits & vegetables & an active lifestyle involving daily cycling or walking.
• Exercise is an important treatment for hypertension.
• Practices like yoga, meditation also help in reducing high blood pressure.
• Only people with severe uncontrolled hypertension, which is very rare, need to be careful about exercise.

Pathophysiology of Hypertension
Nursing Care Plan of Hypertension

Medications and Treatment

Thiazide diuretics. Diuretics, sometimes called "water pills," are medications that act on your kidneys to help your body eliminate sodium and water, reducing blood volume. Thiazide diuretics are often the first — but not the only — choice in high blood pressure medications. If you're not taking a diuretic and your blood pressure remains high, talk to your doctor about adding one or replacing a drug you currently take with a diuretic.
Beta blockers. These medications reduce the workload on your heart and open your blood vessels, causing your heart to beat slower and with less force. When prescribed alone, beta blockers don't work as well in blacks or in the elderly — but they're effective when combined with a thiazide diuretic.

Angiotensin-converting enzyme (ACE) inhibitors. These medications help relax blood vessels by blocking the formation of a natural chemical that narrows blood vessels.
Angiotensin II receptor blockers. These medications help relax blood vessels by blocking the action — not the formation — of a natural chemical that narrows blood vessels.

Calcium channel blockers. These medications help relax the muscles of your blood vessels. Some slow your heart rate. Calcium channel blockers may work better for blacks and older adults than do ACE inhibitors or beta blockers alone. A word of caution for grapefruit lovers, though. Grapefruit juice interacts with some calcium channel blockers, increasing blood levels of the medication and putting you at higher risk of side effects. Talk to your doctor or pharmacist if you're concerned about interactions.

Renin inhibitors. Aliskiren (Tekturna) slows down the production of renin, an enzyme produced by your kidneys that starts a chain of chemical steps that increases blood pressure. Tekturna works by reducing the ability of renin to begin this process. Due to a risk of serious complications, including stroke, you shouldn't take aliskiren with ACE inhibitors or ARBs.

If you're having trouble reaching your blood pressure goal with combinations of the above medications, your doctor may prescribe:

Alpha blockers. These medications reduce nerve impulses to blood vessels, reducing the effects of natural chemicals that narrow blood vessels.
Alpha-beta blockers. In addition to reducing nerve impulses to blood vessels, alpha-beta blockers slow the heartbeat to reduce the amount of blood that must be pumped through the vessels.
Central-acting agents. These medications prevent your brain from signaling your nervous system to increase your heart rate and narrow your blood vessels.
Vasodilators. These medications work directly on the muscles in the walls of your arteries, preventing the muscles from tightening and your arteries from narrowing.

Once your blood pressure is under control, your doctor may have you take a daily aspirin to reduce your risk of cardiovascular disorders.

To reduce the number of daily medication doses you need, your doctor may prescribe a combination of low-dose medications rather than larger doses of one single drug. In fact, two or more blood pressure drugs often work better than one. Sometimes finding the most effective medication — or combination of drugs — is a matter of trial and error.

Lifestyle changes to treat high blood pressure
No matter what medications your doctor prescribes to treat your high blood pressure, you'll need to make lifestyle changes to lower your blood pressure. These changes usually include eating a healthier diet with less salt (the Dietary Approaches to Stop Hypertension, or DASH, diet), exercising more, quitting smoking and losing weight.

DIABETES MELLITUS

DIABETES MELLITUS

-      is a group of metabolic disease characterized by increased levels of glucose in the blood (HYPERGLYCEMIA) resulting from defects in insulin secretion, insulin action, or both. Normal Range for blood glucose 80-120 mg/dL.

CLASSIFICATION OF DIABETES MELLITUS

1. Type 1 Diabetes

         

a.   Onset any age, but usually young (< 30 years old)

b.   Usually thin at diagnosis recent weight loss

c.   Etiology includes genetic, immunologic, and environmental factors.

d.   Insulin Dependent

2. Type 2 Diabetes

a.   occurs more commonly among people who are older than 30 years old

b.   Obese

c.   Two main problems related to insulin in type 2 diabetes are Insulin resistance and Impaired insulin secretion.

Insulin resistance refers to decreased tissue sensitivity to insulin. While, impaired insulin secretion, refers lack of supply of insulin.

Signs and Symptoms of Type 2 diabetes

1.   Fatigue

2.   Irritability’

3.   Polyuria

4.   Polydipsia

5.   Poorly healing skin wounds

6.   Vaginal Infection

7.   Blurred Vision

This may indicate that glucose level is very high.

3. Gestational Diabetes

a.   Onset during pregnant, usually in the second or third trimester.

b.   Due to hormones secreted by placenta, which inhibit secretion of insulin

RISK FACTORS for DIABETES MELLITUS

1.   Family History of Diabetes (ex. Parents or siblings with diabetes).

2.   Obesity (ex. ≥20% over desired body weight or BMI ≥27 KG/M2)

3.   Race/ethnicity

4.   Age ≥45 years old

5.   Previously identified impaired fasting glucose or impaired glucose tolerance.

6.   Hypertension

7.   HDL cholesterol level ≤35 mg/dL

8.   History of Gestational Diabetes.

PREVENTION of DIABETES MELLITUS

1.   Change in lifestyle

2.   Drink Maintenance Medicine all the time.

3.   Always see your Doctor for follow-up check up.

4.   Exercise

5.   Proper Diet

CLINICAL MANIFESTATION of DIABETES MELLITUS

The Three (3) P’s SYMPTOMS of diabetes:

1.   Polyuria, refers to increased in urination,

2.   Polydipsia, refers to increased in thirst.

3.   Polyphagia, refers to increased in appetite.

Other symptoms:

a.   Weakness

b.   Sudden vision changes

c.   Tingling or numbness in the hands and feet

d.   Dry skin

e.   Skin lesions or wounds that are slow to heal

f.     Recurrent infection.

COMPLICATION of DIABETES MELLITUS

1.   Cardiovascular Disease (Myocardial infarction, stroke)

2.   Peripheral Disease

3.   Gas gangrene

4.   Kidney Disease

5.   Eye Disease

6.   Disease of the nerve.

7.   Macrovascular Complication (coronary artery disease)

NURSING CARE PLAN

• Diabetes Mellitus
• Hemodialysis - Complication of DM Type II can lead to Renal Failure
  

Myocardial Infarction

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to part of the heart, causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).

Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom). Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue.[1] Approximately one quarter of all myocardial infarctions are silent, without chest pain or other symptoms.

People will receive a number of diagnostic tests, such as an electrocardiogram, a chest X-ray and blood tests to detect heart muscle damage. The most often used markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. On the basis of the ECG, a distinction is made between ST elevation MI (STEMI) or non-ST elevation MI (non-STEMI). Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual nitroglycerin. If further pain relief is needed morphine sulfate is typically used.[2] A 2009 review about the use of high flow oxygen for treating myocardial infarction found high flow oxygen administration increased mortality and infarct size, calling into question the recommendation for its routine use.[3] Most cases of STEMI are treated with thrombolysis or percutaneous coronary intervention (PCI). NSTEMI is managed with medication, although PCI is often performed during hospital admission. In people who have multiple blockages and who are relatively stable, or in a few emergency cases, bypass surgery maybe an option.

Heart attacks are the leading cause of death for both men and women worldwide.[4] Important risk factors are previous cardiovascular disease, older age, tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein) and low levels of high density lipoprotein (HDL), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress levels

Anatomy and Physiology

The heart is a hollow, muscular organ located in the center of the thorax, where it occupies the space between the lungs (mediastinum) and rests on the diaphragm. It weighs approximately 300 g (10.6 oz), although heart weight and size are influenced by age, gender, body weight, extent of physical exercise and conditioning, and heart disease. The heart pumps blood to the tissues, supplying them with oxygen and other nutrients. The pumping action of the heart is accomplished by the rhythmic contraction and relaxation of its muscular wall. During systole (contraction of the muscle), the chambers of the heart become smaller as the blood is ejected. During diastole (relaxation of the muscle), the heart chambers fill with blood in preparation for the subsequent ejection. A normal resting adult heart beats approximately

60 to 80 times per minute. Each ventricle ejects approximately 70 mL of blood per beat and has an output of approximately 5 L per minute.

ANATOMY OF THE HEART

The heart is composed of three layers (Fig. 26-1). The inner layer, or endocardium, consists of endothelial tissue and lines the inside of the heart and valves. The middle layer, or myocardium, is made

up of muscle fibers and is responsible for the pumping action. The exterior layer of the heart is called the epicardium. The heart is encased in a thin, fibrous sac called the pericardium, which is composed of two layers. Adhering to the epicardium is the visceral pericardium. Enveloping the visceral pericardium is the

parietal pericardium, a tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral column and supports the heart in the mediastinum. The space between these two layers (pericardial space) is filled with about 30 mL of fluid, which lubricates the surface of the heart and reduces friction during systole.

Heart Chambers

The four chambers of the heart constitute the right- and leftsided pumping systems. The right side of the heart, made up of the right atrium and right ventricle, distributes venous blood (deoxygenated blood) to the lungs via the pulmonary artery (pulmonary circulation) for oxygenation. The right atrium receives

blood returning from the superior vena cava (head, neck, and upper extremities), inferior vena cava (trunk and lower extremities), and coronary sinus (coronary circulation). The left side of the heart, composed of the left atrium and left ventricle, distributes oxygenated blood to the remainder of the body via

the aorta (systemic circulation). The left atrium receives oxygenated blood from the pulmonary circulation via the pulmonary veins.  The varying thicknesses of the atrial and ventricular walls relate to the workload required by each chamber. The atria are thin-walled because blood returning to these chambers generates low pressures. In contrast, the ventricular walls are thicker because they generate greater pressures during systole. The right ventricle contracts against low pulmonary vascular pressure and has thinner walls than the left ventricle. The left ventricle, with walls two-and-a-half times more muscular than those of the right ventricle, contracts against high systemic pressure. Because the heart lies in a rotated position within the chest cavity, the right ventricle lies anteriorly (just beneath the sternum) and the left ventricle is situated posteriorly. The left ventricle is responsible for the apex beat or the point of maximum impulse (PMI), which is normally palpable in the left midclavicular line of the chest wall at the fifth intercostal space.

Heart Valves

The four valves in the heart permit blood to flow in only one direction. The valves, which are composed of thin leaflets of fibrous tissue, open and close in response to the movement of blood and pressure changes within the chambers. There are two types of valves: atrioventricular and semilunar.

ATRIOVENTRICULAR VALVES

The valves that separate the atria from the ventricles are termed atrioventricular valves. The tricuspid valve, so named because it is composed of three cusps or leaflets, separates the right atrium

from the right ventricle. The mitral, or bicuspid (two cusps) valve, lies between the left atrium and the left ventricle. Normally, when the ventricles contract, ventricular pressure rises, closing the atrioventricular valve leaflets. Two additional structures, the papillary muscles and the chordae tendineae, maintain valve closure. The papillary muscles, located on the sides of the ventricular walls, are connected to the valve leaflets by thin fibrous bands called chordae tendineae. During systole, contraction of the papillary muscles causes the chordae tendineae to become taut, keeping the valve leaflets approximated and closed.

SEMILUNAR VALVES

The two semilunar valves are composed of three half-moon-like leaflets. The valve between the right ventricle and the pulmonary artery is called the pulmonic valve; the valve between the left ventricle and the aorta is called the aortic valve.

Coronary Arteries

The left and right coronary arteries and their branches (Fig. 26-2) supply arterial blood to the heart. These arteries originate from the aorta just above the aortic valve leaflets. The heart has large metabolic requirements, extracting approximately 70% to 80%of the oxygen delivered (other organs consume, on average, 25%). Unlike other arteries, the coronary arteries are perfused during diastole. An increase in heart rate shortens diastole and can decrease myocardial perfusion. Patients, particularly those with

coronary artery disease (CAD), can develop myocardial ischemia (inadequate oxygen supply) when the heart rate accelerates. The left coronary artery has three branches. The artery from the point of origin to the first major branch is called the left main coronary artery. Two bifurcations arise off the left main coronary artery. These are the left anterior descending artery, which courses down the anterior wall of the heart, and the circumflex artery, which circles around to the lateral left wall of the heart.

The right side of the heart is supplied by the right coronary artery, which progresses around to the bottom or inferior wall of the heart. The posterior wall of the heart receives its blood supply by an additional branch from the right coronary artery called the posterior descending artery. Superficial to the coronary arteries are the coronary veins. Venous blood from these veins returns to the heart primarily

through the coronary sinus, which is located posteriorly in the right atrium.

Cardiac Muscle

The myocardium is composed of specialized muscle tissue. Microscopically, myocardial muscle resembles striated (skeletal) muscle, which is under conscious control. Functionally, however,

myocardial muscle resembles smooth muscle because its contraction is involuntary. The myocardial muscle fibers are arranged in an interconnected manner (called a syncytium) that allows for coordinated

myocardial contraction and relaxation. The sequential pattern of contraction and relaxation of individual muscle fibers ensures the rhythmic behavior of the myocardium as a whole and

enables it to function as an effective pump.

Pathophysiology Narrative

CK-MB

CK catalyses the conversion of creatine and consumes adenosine triphosphate (ATP) to create phosphocreatine and adenosine diphosphate (ADP). Elevated CK-MB signifies damage to muscle tissue including the heart.

LDH

Damage to heart tissues releases heart LDH, which is rich in LDH-1, into the bloodstream.

Angiography

A catheter is inserted into an artery (usually the femoral artery) and pushed to the vessels supplying the heart to determine narrowing of blood vessels.

CABG

Arteries or veins from elsewhere in the patient's body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the coronary circulation supplying the myocardium (heart muscle).

Angioplasty

Angioplasty is the technique of mechanically widening a narrowed or obstructed blood vessel; typically as a result of atherosclerosis. An empty and collapsed balloon on a guide wire, known as a balloon catheter, is passed into the narrowed locations and then inflated

Cardiogenic Shock

Cardiogenic shock is defined as a hemodynamic state in which the heart cannot produce enough of a cardiac output to supply an adequate amount of oxygenated blood to the tissues of the body.

Myocardial Rupture

Myocardial rupture (or heart rupture) is a laceration or tearing of the walls of the ventricles or atria of the heart

Heart attack risk factors include:

    * Age. Men who are 45 or older and women who are 55 or older are more likely to have a heart attack than younger men and women.

    * Tobacco. Smoking and long-term exposure to secondhand smoke damage the interior walls of arteries — including arteries to your heart — allowing deposits of cholesterol and other substances to collect and slow blood flow. Smoking also increases the risk of deadly blood clots forming and causing a heart attack.

    * Diabetes. Diabetes is the inability of your body to adequately produce or respond to insulin properly. Insulin, a hormone secreted by your pancreas, allows your body to use glucose, which is a form of sugar from foods. Diabetes can occur in childhood, but it appears more often in middle age and among overweight people. Diabetes greatly increases your risk of a heart attack.

    * High blood pressure. Over time, high blood pressure can damage arteries that feed your heart by accelerating atherosclerosis. The risk of high blood pressure increases as you age, but the main culprits for most people are eating a diet too high in salt and being overweight. High blood pressure can also be an inherited problem.

    * High blood cholesterol or triglyceride levels. Cholesterol is a major part of the deposits that can narrow arteries throughout your body, including those that supply your heart. A high level of the wrong kind of cholesterol in your blood increases your risk of a heart attack. Low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol) is most likely to narrow arteries. A high LDL level is undesirable and is often a result of a diet high in saturated fats and cholesterol. A high level of triglycerides, a type of blood fat related to your diet, also is undesirable. However, a high level of high-density lipoprotein (HDL) cholesterol (the "good" cholesterol), which helps the body clean up excess cholesterol, is desirable and lowers your risk of heart attack.

    * Family history of heart attack. If your siblings, parents or grandparents have had heart attacks, you may be at risk, too. Your family may have a genetic condition that raises unwanted blood cholesterol levels. High blood pressure also can run in families.

    * Lack of physical activity. An inactive lifestyle contributes to high blood cholesterol levels and obesity. People who get regular aerobic exercise have better cardiovascular fitness, which decreases their overall risk of heart attack. Exercise is also beneficial in lowering high blood pressure.

    * Obesity. Obese people have a high proportion of body fat (a body mass index of 30 or higher). Obesity raises the risk of heart disease because it's associated with high blood cholesterol levels, high blood pressure and diabetes.

Angina Pectoris

·         Angina pectoris, commonly known as angina, is severe chest pain due to ischemia (a lack of blood, hence a lack of oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Latin angina ("infection of the throat") from the Greek ἀγχόνη ankhone ("strangling"), and the Latin pectus ("chest"), and can therefore be translated as "a strangling feeling in the chest".

·         There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle (i.e., there can be severe pain with little or no risk of a heart attack, and a heart attack can occur without pain).

·         Worsening ("crescendo") angina attacks, sudden-onset angina at rest, and angina lasting more than 15 minutes are symptoms of unstable angina (usually grouped with similar conditions as the acute coronary syndrome). As these may herald myocardial infarction (a heart attack), they require urgent medical attention and are generally treated as a presumed heart attack.

Classifications:

1.       Stable angina

Also known as effort angina, this refers to the more common understanding of angina related to myocardial ischemia. Typical presentations of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest. Symptoms typically abate several minutes following cessation of precipitating activities and resume when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms.

2.       Unstable angina

Unstable angina (UA) (also "crescendo angina;" this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens.

It has at least one of these three features:

1. it occurs at rest (or with minimal exertion), usually lasting >10 min;
2. it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or
3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina (other than symptoms) is the pathophysiology of the atherosclerosis. The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms or coronary thrombosis. The process starts with atherosclerosis, and when inflamed leads to an active plaque, which undergoes thrombosis and results in acute ischemia, which finally results in cell necrosis after calcium entry. Studies show that 64% of all unstable anginas occur between 10 PM and 8 AM when patients are at rest.

In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity.

3.       Microvascular angina

Microvascular Angina or Angina Syndrome X is characterized by angina-like chest pain, but have different causes.The cause of Microvascular Angina is unknown, but it appears to be the result of poor function in the tiny blood vessels of the heart, arms and legs. Since microvascular angina isn't characterized by arterial blockages, it's harder to recognize and diagnose, but its prognosis is excellent.

Signs and symptoms

·         Most patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in the epigastrium (upper central abdomen), back, neck area, jaw, or shoulders. This is explained by the concept of referred pain, and is due to the spinal level that receives visceral sensation from the heart simultaneously receiving cutaneous sensation from parts of the skin specified by that spinal nerve's dermatome, without an ability to discriminate the two. Typical locations for referred pain are arms (often inner left arm), shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating and nausea in some cases. In this case, the pulse rate and the blood pressure increases. The pain usually lasts for about 3 to 5 minutes but the symptoms actually starts 15 to 20 minutes before the cardiac arrest and the pain is relieved by rest or specific anti-angina medication. Chest pain lasting only a few seconds is normally not angina

·         Myocardial ischemia comes about when the myocardia (the heart muscles) receive insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardia or by decreased supply to the myocardia. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients is directly correlated to blocked or narrowed blood vessels.

·         Some experience "autonomic symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting and pallor.

·         Major risk factors for angina include cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle and family history of premature heart disease.

·         A variant form of angina (Prinzmetal's angina) occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women.

Cause

Major risk factors

·         Age (≥ 55 yo for men, ≥ 65 for women)

·         Cigarette smoking

·         Diabetes mellitus (DM)

·         Dyslipidemia

·         Family History of premature Cardiovascular Disease(men <55 yo, female <65)

·         Hypertension (HTN)

·         Kidney disease (microalbuminuria or GFR<60 mL/min)

·         Obesity (BMI ≥ 30 kg/m2)

·         Physical inactivity

Conditions that exacerbate or provoke angina

·         Medications

·         vasodilators

·         excessive thyroid replacement

·         vasoconstrictors

Smoking

One study found that smokers with coronary artery disease had a significantly increased level of sympathetic nerve activity when compared to those without. This is in addition to increases in blood pressure, heart rate and peripheral vascular resistance associated with nicotine which may lead to recurrent angina attacks. Additionally, CDC reports that the risk of CHD, stroke, and PVD is reduced within 1–2 years of smoking cessation. In another study, it was found that after one year, the prevalence of angina in smoking men under 60 after an initial attack was 40% less in those who had quit smoking compared to those who continued. Studies have found that there are short term and long term benefits to smoking cessation.

Other medical problems

·         profound anemia

·         uncontrolled HTN

·         hyperthyroidism

·         hypoxemia

Other cardiac problems

·         tachyarrhythmia

·         bradyarrhythmia

·         valvular heart disease

·         hypertrophic cardiomyopathy

Myocardial ischemia can result from:

1.       a reduction of blood flow to the heart that can be caused by stenosis, spasm, or acute occlusion (by an embolus) of the heart's arteries.

2.       resistance of the blood vessels. This can be caused by narrowing of the blood vessels; a decrease in radius,. Blood flow is inversely proportional to the radius of the artery to the fourth power

3.       reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration. This decreases the ability to of hemoglobin to carry oxygen to myocardial tissue .

Atherosclerosis is the most common cause of stenosis (narrowing of the blood vessels) of the heart's arteries and, hence, angina pectoris. Some people with chest pain have normal or minimal narrowing of heart arteries; in these patients, vasospasm is a more likely cause for the pain, sometimes in the context of Prinzmetal's angina and syndrome X.

Myocardial ischemia also can be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as seen with severe anemia (low number of red blood cells), or long-term smoking.

Pathophysiology

Angina results when there is an imbalance between the heart's oxygen demand and supply. This imbalance can result from an increase in demand (e.g. during exercise) without a proportional increase in supply (e.g. due to obstruction or atherosclerosis of the coronary arteries).

Diagnosis

Suspect angina in people presenting with tight, dull, or heavy chest discomfort which is:

1. Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back. 2. Associated with exertion or emotional stress and relieved within several minutes by rest. 3. Precipitated by cold weather or a meal.

Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort or burping. These atypical symptoms are particularly likely in older people, women, and those with diabetes.

Angina pain is not usually sharp or stabbing or influenced by respiration. Antacids and simple analgesia do not usually relieve the pain. If chest discomfort (of whatever site) is precipitated by exertion, relieved by rest, and relieved by glyceryl trinitrate, the likelihood of angina is increased.

In angina patients who are momentarily not feeling any one chest pain, an electrocardiogram (ECG) is typically normal, unless there have been other cardiac problems in the past. During periods of pain, depression or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test ("treadmill test") may be performed, during which the patient exercises to their maximum ability before fatigue, breathlessness or, importantly, pain intervenes; if characteristic ECG changes are documented (typically more than 1 mm of flat or downsloping ST depression), the test is considered diagnostic for angina. Even constant monitoring of the blood pressure and the pulse rate can lead us to some conclusion regarding the angina. The exercise test is also useful in looking for other markers of myocardial ischaemia: blood pressure response (or lack thereof, particularly a drop in systolic pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram (in patients who cannot exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest) or Stress Echocardiography.

In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG), treatment only with medication, or other treatments. There has been researches which concludes that a freqency is attained when there is increase in the blood pressure and the pulse rate. This frequency varies normally but the range is 45-50 khz for the cardiac arrest or for the heart failure. In patients who are in hospital with unstable angina (or the newer term of "high risk acute coronary syndromes"), those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly.

Treatment

The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that makes more oxygen available to the heart muscle. Beta-blockers and calcium channel blockers act to decrease the heart's workload, and thus its requirement for oxygen. Nitroglycerin should not be given if certain inhibitors such as Viagra, Cialis, and Levitra have been taken by the casualty within the previous 12 hours as the combination of the two could cause a serious drop in blood pressure. Treatments are balloon angioplasty, in which the balloon is inserted at the end of a catheter and inflated to widen the arterial lumen. Stents to maintain the arterial widening are often used at the same time. Coronary bypass surgery involves bypassing constricted arteries with venous grafts. This is much more invasive than angioplasty.

The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and, of course, death. Beta blockers (e.g., carvedilol, propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability and longer life) and short-acting nitroglycerin medications have been used since 1879 for symptomatic relief of angina ^[24]. Calcium channel blockers (such as nifedipine (Adalat) and amlodipine), isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina^{[citation needed]}. A new therapeutic class, called If inhibitor, has recently been made available: ivabradine provides pure heart rate reduction leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and, lastly, statins are the most frequently used lipid/cholesterol modifiers which probably also stabilize existing atheromatous plaque. Low-dose aspirin decreases the risk of heart attack in patients with chronic stable angina, and was previously part of standard treatment, however it has since been discovered that the increase in haemorrhagic stroke and gastrointestinal bleeding offsets this gain so they are no longer advised unless the risk of myocardial infarction is very high.

Exercise is also a very good long term treatment for the angina (but only particular regimens - gentle and sustained exercise rather than intense short bursts), probably working by complex mechanisms such as improving blood pressure and promoting coronary artery collateralisation.

Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension (high blood pressure), encouraging stopping smoking and weight optimisation.

The calcium channel blocker nifedipine prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant.

Suspected angina

Hospital admission for people with the following symptoms, as they may have unstable angina: Pain at rest (which may occur at night), pain on minimal exertion, angina that seems to be progressing rapidly despite increasing medical treatment. Refer urgently all people with suspected angina to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.