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Diseases of the Cardiovascular System
Circulation/Transport:
◦ Nutrients
◦ Oxygen
◦ Hormones
◦ Drugs
◦ Waste products
Major Functions of the Heart
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
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
Clinical Manifestations of Cardiovascular Diseases
TACHYCARDIA/PALPITATION
ABNORMAL HEART
SOUNDS/MURMURS
OEDEMA/ASCITES
CARDIOMEGALY
HEPATOMEGALY
VENOUS ENGORGEMENT
HYPER/HYPOTENSION
SHOCK
SUDDEN DEATH
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
Major Cardiovascular Disorders
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
Cardiovascular Diseases
Risk FactorsModifiable
Unhealthy lifestyle
◦ Junk food/obesity
◦ Smoking
◦ Stress
◦ Physical inactivity
Socioeconomic status
Systemic diseases:
◦ Diabetes
◦ Hypercholesterolemia
◦ hypertension
Non-modifiable
Age
Gender
Congenital anomalies
Genetic
Family History
Ethnicity
AtherosclerosisA 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.
Stable Angina
◦ Collateral blood supply
Unstable Angina
◦ Disruption of a plaque
Variant Angina
◦ Cyclic attacks at rest
Silent Ischemia
◦ Diabetic patients
Types of Angina Pectoris
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
β-blockers, reduce myocardial oxygen demand by decreasing the force of contraction and heart rate◦ β adrenergic receptors are found in peripheral blood
vessels, the bronchial tree (β1) and the myocardium (β2).
◦ They may precipitate bronchospasm in individuals with underlying asthma thus cardio selective β-blockers should be prescribed to asthmatics
◦ All β-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).
Lewis’s 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