Cardiovascular diseases (CVDs) are a group of disorders of the heart and blood vessels

and include:

• Coronary heart disease – disease of the blood vessels supplying the heart muscle
• Cerebrovascular disease – disease of the blood vessels supplying the brain
• Peripheral arterial disease – disease of blood vessels supplying the arms and
legs
• Rheumatic heart disease – damage to the heart muscle and heart valves from
rheumatic fever, caused by streptococcal bacteria
• Congenital heart disease – malformations of heart structure existing at birth.
• Deep vein thrombosis and pulmonary embolism – blood clots in the leg veins,
which can dislodge and move to the heart and lungs.

Heart attacks and strokes are usually acute events and are mainly caused by a blockage
that prevents blood from flowing to the heart or brain. The most common reason for this
is a build-up of fatty deposits on the inner walls of the blood vessels that supply the heart
or brain. Strokes can also be caused by bleeding from a blood vessel in the brain or from
blood clots.

FACTS ABOUT CARDIOVASCULAR DISEASES

• CVDs are the number one cause of death globally: more people die annually from
CVDs than from any other cause;
• An estimated 17.5 million people died from CVDs in 2005, representing 30% of
all global deaths. Of these deaths, an estimated 7.6 million were due to coronary
heart disease and 5.7 million were due to stroke.
• Over 80% of CVD deaths take place in low- and middle-income countries and
occur almost equally in men and women;
 • By 2015, almost 20 million people will die from CVDs, mainly from heart
disease and stroke. These are projected to remain the single leading causes of
death.

CAUSES OF CARDIOVASCULAR DISEASES

• The causes of CVDs are well established and well known. The most important
causes of heart disease and stroke are unhealthy diet, physical inactivity and
tobacco use. These are called ‘modifiable risk factors’.
• The effects of unhealthy diet and physical inactivity may show up in individuals
as raised blood pressure, raised blood glucose, raised blood lipids, and overweight
and obesity; these are called ‘intermediate risk factors’.
• The major modifiable risk factors are responsible for about 80% of coronary heart
disease and cerebrovascular disease.
• There are also a number of underlying determinants of chronic diseases, or, if you
like, "the causes of the causes". These are a reflection of the major forces driving
social, economic and cultural change – globalization, urbanization, and population
ageing. Other determinants of CVDs are poverty and stress.

COMMON SYMPTOMS OF CARDIOVASCULAR DISEASES

• Often, there are no symptoms of the underlying disease of the blood vessels. A
heart attack or stroke may be the first warning of underlying disease.
• Symptoms of a heart attack include: pain or discomfort in the centre of the chest;
pain or discomfort in the arms, the left shoulder, elbows, jaw, or back. In addition
the person may experience difficulty in breathing or shortness of breath; feeling
sick or vomiting; feeling light-headed or faint; breaking into a cold sweat; and
becoming pale.
• Women are more likely to have shortness of breath, nausea, vomiting, and back or
jaw pain.
• The most common symptom of a stroke is sudden weakness of the face, arm, or
leg, most often on one side of the body. Other symptoms include sudden onset of:
numbness of the face, arm, or leg, especially on one side of the body; confusion,
difficulty speaking or understanding speech; difficulty seeing with one or both
eyes; difficulty walking, dizziness, loss of balance or coordination; severe
headache with no known cause; and fainting or unconsciousness.
• People experiencing these symptoms should seek medical care immediately.

POTENTIAL NURSING DIAGNOSIS FOR SEVERE HYPERTENSION:

1. Risk for decreased cardiac output

2. Activity intolerance
3. Acute headache pain
4. Imbalanced nutrition more than body requirements
5. Ineffective coping
6. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs
VIEW SAMPLE NURSING CARE PLAN FOR HYPERTENSION

POTENTIAL NURSING DIAGNOSIS FOR CHRONIC HEART FAILURE (CHF)

1. Decreased Cardiac output

2. Activity intolerance
3. Excess fluid volume
4. Risk for impaired gas exchange
5. Risk for impaired skin integrity
6. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs

VIEW SAMPLE NURSING CARE PLAN FOR CHRONIC HEART FAILURE

(CHF)

POTENTIAL NURSING DIAGNOSIS FOR ANGINA (CORONARY ARTERY

DISEASE)

1. Acute pain
2. Risk for decreased cardiac output
3. Anxiety
4. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs

POTENTIAL NURSING DIAGNOSIS FOR MYOCARDIAL INFARCTION

1. Acute pain
2. Activity intolerance
3. Anxiety/ Fear
4. Risk for decreased cardiac output
5. Ineffective tissue perfusion
6. Risk for excess fluid volume
7. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs

VIEW SAMPLE NURSING CARE PLAN FOR MYOCARDIAL INFARCTION

POTENTIAL NURSING DIAGNOSIS FOR DYSRHYTHMIAS (INCLUDING

DIGITALIS TOXICITY)

1. Risk for decreased cardiac output

2. Risk for poisoning, digitalis toxicity
3. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs
POTENTIAL NURSING DIAGNOSIS FOR CARDIAC SURGERY:
POSTOPERATIVE CARE – CORONARY ARTERY BYPASS GRAFT (CABG),
MINIMALLY INVASIVE DIRECT CORONARY ARTERY BYPASS (MIDCAB),
CARDIOMYOPLASTY, VALVE REPLACEMENT

1. Risk for decreased cardiac output

2. Acute pain
3. Ineffective role performance
4. Risk for ineffective breathing pattern
5. Impaired skin integrity
6. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs

POTENTIAL NURSING DIAGNOSIS FOR THROMBOPHLEBITIS: DEEP VEIN

THROMBOSIS (INCLUDING PULONARY EMBOLI CONSIDERATIONS)

1. Ineffective tissue perfusion

2. Acute pain
3. Impaired gas exchange (in presence of pulmonary embolus)
4. Deficient knowledge (Learning Need) regarding condition, treatment plan,
self-care, and discharge needs
Pathophysiology

Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the
ischemic cascade.[22] Brain tissue ceases to function if deprived of oxygen for more than
60 to 90 seconds and after approximately three hours, will suffer irreversible injury
possibly leading to death of the tissue, i.e., infarction. (This is why TPA's (e.g.
Streptokinase, Altapase) are given only until three hours since the onset of the stroke.)
Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels
leading to a reduction of blood flow, by causing the formation of blood clots within the
vessel, or by releasing showers of small emboli through the disintegration of
atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the
circulatory system, typically in the heart as a consequence of atrial fibrillation, or in the
carotid arteries, break off, enter the cerebral circulation, then lodge in and occlude brain
blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low
in energy, and thus it resorts into using anaerobic respiration within the region of brain
tissue affected by ischemia. Unfortunately, this kind of respiration produces less
adenosine triphosphate (ATP) but releases a by-product called lactic acid. Lactic acid is
an irritant which could potentially destroy cells since it is an acid and disrupts the normal
acid-base balance in the brain. The ischemia area is referred to as the "ischemic
penumbra".[23]

Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of
high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to
failure of energy-dependent processes (such as ion pumping) necessary for tissue cell
survival. This sets off a series of interrelated events that result in cellular injury and
death. A major cause of neuronal injury is release of the excitatory neurotransmitter
glutamate. The concentration of glutamate outside the cells of the nervous system is
normally kept low by so-called uptake carriers, which are powered by the concentration
gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the
supply of oxygen and glucose which powers the ion pumps maintaining these gradients.
As a result the transmembrane ion gradients run down, and glutamate transporters reverse
their direction, releasing glutamate into the extracellular space. Glutamate acts on
receptors in nerve cells (especially NMDA receptors), producing an influx of calcium
which activates enzymes that digest the cells' proteins, lipids and nuclear material.
Calcium influx can also lead to the failure of mitochondria, which can lead further toward
energy depletion and may trigger cell death due to apoptosis.

Ischemia also induces production of oxygen free radicals and other reactive oxygen
species. These react with and damage a number of cellular and extracellular elements.
Damage to the blood vessel lining or endothelium is particularly important. In fact, many
antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the
endothelium and not in the brain per se. Free radicals also directly initiate elements of the
apoptosis cascade by means of redox signaling.[20]

These processes are the same for any type of ischemic tissue and are referred to
collectively as the ischemic cascade. However, brain tissue is especially vulnerable to
ischemia since it has little respiratory reserve and is completely dependent on aerobic
metabolism, unlike most other organs.

Brain tissue survival can be improved to some extent if one or more of these processes is
inhibited. Drugs that scavenge reactive oxygen species, inhibit apoptosis, or inhibit
excitatory neurotransmitters, for example, have been shown experimentally to reduce
tissue injury due to ischemia. Agents that work in this way are referred to as being
neuroprotective. Until recently, human clinical trials with neuroprotective agents have
failed, with the probable exception of deep barbiturate coma. However, more recently
NXY-059, the disulfonyl derivative of the radical-scavenging spintrap
phenylbutylnitrone, is reported to be neuroprotective in stroke.[24] This agent appears to
work at the level of the blood vessel lining or endothelium. Unfortunately, after
producing favorable results in one large-scale clinical trial, a second trial failed to show
favorable results.[20]

In addition to injurious effects on brain cells, ischemia and infarction can result in loss of
structural integrity of brain tissue and blood vessels, partly through the release of matrix
metalloproteases, which are zinc- and calcium-dependent enzymes that break down
collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also
contribute to this process. The loss of vascular structural integrity results in a breakdown
of the protective blood brain barrier that contributes to cerebral edema, which can cause
secondary progression of the brain injury.

As is the case with any type of brain injury, the immune system is activated by cerebral
infarction and may under some circumstances exacerbate the injury caused by the
infarction. Inhibition of the inflammatory response has been shown experimentally to
reduce tissue injury due to cerebral infarction, but this has not proved out in clinical
studies.

[edit] Hemorrhagic

Head CT showing deep intracerebral hemorrhage due to bleeding within the cerebellum,
approximately 30 hours old.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an
expanding hematoma or hematomas. This can distort and injure tissue. In addition, the
pressure may lead to a loss of blood supply to affected tissue with resulting infarction,
and the blood released by brain hemorrhage appears to have direct toxic effects on brain
tissue and vasculature.[20]