Diseases of the Cardiovascular

System

Major Functions of the

Heart
Circulation/Transport:
Nutrients
Oxygen
Hormones
Drugs
Waste products

Diseases of the HEART may

interfere with its functions
hugely and can be very serious
and may cause sudden death

Pathophysiology of Heart Diseases in

General

Clinical Manifestations of Cardiovascular

Diseases

Dyspnoea/ S.O.B
Orthopena
Nocturnal dyspnoea
Dyspnoea on exertion

Cough and sputum

Cyanosis
Dizziness
Collapse
Chest pain

Severe
Squeezing/tightness
Stabbing
Radiation of pain

TACHYCARDIA/PALPITATION
ABNORMAL HEART
SOUNDS/MURMURS
OEDEMA/ASCITES
CARDIOMEGALY
HEPATOMEGALY
VENOUS ENGORGEMENT
HYPER/HYPOTENSION
SHOCK
SUDDEN DEATH

Major Cardiovascular Disorders

Congenital heart Diseases

ASD
VSD
PDA

Infection
Rheumatic fever
Carditis/pericarditis

Lipid metabolism and blood vessels:

Hyperlipidemia
Atherosclerosis
Hypertension

Ischemic heart diseases (IHDs)

Angina pectoris
Myocardial infarction

Inflammatory angiopathy

Cardiovascular Diseases

Leading cause of death in New Zealand

40% of all deaths from CVD in NZ occur in people
under the age of 70 years
The disease begins in youth, especially so in cultures
(like ours) where there is a diet containing a large
proportion of saturated fats
Lifestyle choices are the main factors that determine
prevalence of CVD

Risk Factors
Modifiable

Unhealthy lifestyle
Junk food/obesity
Smoking

Non-modifiable

Age

Physical inactivity

Gender

Socioeconomic status

Congenital anomalies

Systemic diseases:

Genetic

Family History

Ethnicity

Stress

Diabetes
Hypercholesterolemia
hypertension

Atherosclerosis
A disease of the
muscular arteries in
which the inner layer
becomes thickened by
fatty deposits and
fibrous tissue
Most harmful in the
coronary and cerebral
vessels
Leading cause of
myocardial infarction
and CVA

Angina Pectoris

Origin:
Angina: strangling or tightness
Pectoris: chest

Uncomfortable sensation in the chest and surrounding

structures due to lack of oxygen supply to the cardiac
tissues produced by narrowing or partial blockage of
coronary arteries.

Types of Angina Pectoris

Stable Angina
Collateral blood supply

Unstable Angina
Disruption of a plaque

Variant Angina
Cyclic attacks at rest

Silent Ischemia
Diabetic patients

Diagnosis of CVD is made

by
ECG...

T wave inversion
ST-segment elevation or depression

Coronary Angiography
The most direct means to identify coronary artery
stenosis
Atherosclerotic plaques can be visualised radiographically
following injection of contrast into an artery
Angiography does not reveal the stability of the plaque or
its composition

ECG changes in IHDs

ST segment elevation or depression

If Jen has no treatment she may

go on
to have an MI

Serum Markers for MI

As myocardial cells become necrotic their
components and enzymes diffuse in to the
interstitium and then the blood
Troponin
Part of the actin filament of cardiac muscle
Rises within 3 hours of an MI and may remain elevated
for 7-10 days

Creatine kinase
An enzyme found in muscle cells
Exceeds normal levels 4-8hours post MI and returns to
normal within 2-3 days

Treatment

Goal: improve quality of life by decreasing the

frequency of anginal attacks and to prevent
acute MI
Organic nitrates (e.g. nitroglycerin)
Dilation of coronary vasculature and subsequent
augmentation of blood flow
Venodilation, decreased venous return and thus
decreases demand for oxygen by the myocardium
Used most commonly for an acute attack

Treatment

Antiplatelet therapy with aspirin (150mg) is a

standard addition to a drug regime used to
treat CVD
Platelet aggregation and thrombosis have been
implicated in acute MI and unstable angina
Aspirin inhibits platelet aggregation and thus
reduces the subsequent release of platelet derived
coagulants and vasoconstrictors
Unless contraindications are present (gastric
irritation, allergy) aspirin is a continuous treatment
for individuals with known CVD and/or post MI

Treatment

-blockers, reduce myocardial oxygen

demand by decreasing the force of
contraction and heart rate

adrenergic receptors are found in peripheral

blood vessels, the bronchial tree (1) and the
myocardium (2).
They may precipitate bronchospasm in individuals
with underlying asthma thus cardio selective blockers should be prescribed to asthmatics
All -blockers should be avoided in individuals with
obstructive airway disorders
Names end in the suffix lol

Treatment

Statins
HMG-CoA reductase is a key enzyme in
cholesterol synthesis in the liver
Statins inhibit the action of HMG-CoA and
therefore block the hepatic synthesis of
cholesterol
Statins also reduce triglyceride levels
The cornerstone of lipid lowering treatment
Lipitor/Lipex

Treatment
A Aspirin & Antianginal therapy
B B blocker & Blood pressure
C Cigarette smoking & Cholesterol
D Diet and Diabetes
E Education an Exercise

References
Brown, D. & Edwards, H.(Eds). (2008).
Lewiss medical-surgical nursing:
Assessment &management of clinical
problems (2nd ed). Sydney, Australia:
Elsevier-Mosby.
Craft, J., Gordon, K.L., & Tiziani, A.(2011).
Understanding Pathophysiology. Sydney,
Australia: Elsevier-Mosby