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