CARDIOVASCULAR SYSTEM
CONGESTIVE CARDIAC FAILURE
• Multisystem derangement that occurs when
the heart can’t eject blood delivered to it
• Left heart
– Systemic HTN
– Mitral/aortic valve disease
– Ischaemic HD
• Right heart
– Left ventricular failure
– Intrinsic lung parenchyma disease
• Entire heart
CONGESTIVE CARDIAC FAILURE CONT’D
Adaptive changes
• Neurohormonal
– ↑ed activity of the sympathetic nervous system
• More forceful contraction & ↑ in HR
• Molecular
• Morphologic
• Hypertrophy & Dilatation
– Initially positive
– ↑oxygen demand
• Vulnerability to ischaemia
CONGESTIVE CARDIAC FAILURE CONT’D
Dilatation/chamber enlargement
• Dilated chamber is meeting the needs of the body
= compensated HF
• Decompensated HF
Clinical feature
• Dyspnoea
– Exertional
• Orthopnoea
• Paroxymal nocturnal dyspnoea
– Severe SOB, Coughing, Choking sensation & wheezing
CONGESTIVE CARDIAC FAILURE CONT’D
Clinical Features Cont’d
• Fatigue
• Third heart sound
• Atrial fibrillation
• Cyanosis
• Acidosis
ATHEROSCLEORSIS (ATH)
• Characterized by atheromas, atheromatous, or
fibrofatty plaques that obstruct the vascular
lunmina
• Intimal thickening
• Lipid accumulation
• Primarily affects elastic arteries
– Aorta
– Carotid
– Iliac
ATHEROSCLEORSIS (ATH) CONT’D
Risk Factors
• Age
• Men affected > women
• Women protected by oestrogen
• Diet / Lifestyle
• Hyperlipidemia
• Familial predisposition
– DM, HTN, deranged lipoprotein metabolism,
hypercholesterolemia
ATHEROSCLEORSIS (ATH) CONT’D
• Cigarette smoking
• DM induces hypercholesterolemia
• Homocystinuria
– Inborn error of metabolism – premature vascular
disease
• Hyperhomocystinemia
– Low folate, B6 & B12 intake
• Type A personality
• Uncontrolled weight gain
ATHEROSCLEORSIS (ATH) CONT’D
Pathogenesis
• Chronic endothelial injury
• ↑ed permeability, leucocyte adhesion,
>thrombotic potential
• Insudation of lipoproteins
• Oxidation and free radicle generation
• Adhesion of monocytes
– Transformation into macrophages and foam cells
• Smooth muscle cell proliferation
ISCHAEMIC HEART DISEASE
• Syndromes characterized by imbalance
between myocardial oxygen demand and
blood supply
• Commonest cause is narrowing of the lamina
of the coronary arteries
– Coronary heart /coronary artery disease
ISCHAEMIC HEART DISEASE CONT’D
Syndromes
• Angina pectoris
• Acute myocardial infarction (MI)
• Sudden Cardiac Death
• Chronic Ischaemic HD with CCF
• All are late manifestations of coronary
atherosclerosis
• Acute Coronary Syndrome
– Unstable angina
– Acute MI
– Sudden Cardiac Death
ISCHAEMIC HEART DISEASE CONT’D
• Occur at any age
– Older adults
• Peak incidence after 60 in men and 70 in women
• Men more common than females until after the ninth
decade
Contributing factors
• HTN
• DM
• Smoking
• ↑LDL
• Genetics
ISCHAEMIC HEART DISEASE CONT’D
Pathogenesis
• ≥ 75% luminal narrowing = critical stenosis
• Symptoms and prognosis depend on above
but also on the dynamic changes in the plaque
– Acute plaque changes
– Coronary artery thrombosis
– Coronary artery vasospasm
ISCHAEMIC HEART DISEASE CONT’D
Acute Plaque Changes
• Fissuring
• Hemorrhaging into the plaque
• Plaque rupture with embolization
• Platelet aggregation and thrombosis
ISCHAEMIC HEART DISEASE CONT’D
Coronary artery thrombosis
• Plaque rupture exposes thrombogenic lipids and
subendothelial collagen
• Sets in motion platelet aggregation & thrombin generation
/formation
– ACS
– Vessel completely occluded
» MI
– Incompletely occluded
» Unstable angina
» Lethal arrythmias
» Sudden cardiac death
ISCHAEMIC HEART DISEASE CONT’D
Coronary artery vasospasm
• Incompletely understood
• At point of rupture
– Release of vasospastic mediators e.g.
thromboxane A2
– ↓Endothelial cell derived relaxing factors
– ↑ adrenergic activity & smoking implicated
ANGINA PECTORIS
• Intermittent chest pain
– Transient
– Reversible myocardial ischaemia
Types
• Stable
– Crushing/squeezing substernal
– Radiate down the left arm
– Relieved by rest and the administration of GTN
ANGINA PECTORIS CONT’D
• Prinzmetal / variant
– Occurs at rest or awakens the patient
– Associated with coronary artery spasm
– Relieved by vasodilators
• Unstable angina / crescendo
– ↑ed frequency of chest pain
– Precipitated by less severe exertion, more intense,
last longer
MYOCARDIAL INFARCTION
• Area of myocardial necrosis caused by local
ischaemia
• Men are 4-5times more likely to have a MI
between the ages of 45 & 54
• Most caused by coronary artery thrombosis
• Typically begins in the subendocardial region
MYOCARDIAL INFARCTION CONT’D
Clinical Features
• Severe, crushing substernal chest pain that radiate
to the neck, jaw, epigastrium, shoulder or left arm
• Pain lasts hours to days
• Not relieved by nitroglycerin
• Pulse
– Rapid
– Weak
• Diaphoretic
MYOCARDIAL INFARCTION CONT’D
• Cardiogenic Shock
• Silent MIs
• Lethal arrhythmias and sudden cardiac death occurs in 25%
• Dying myocardium releases
– Creatine kinase
• CK-MB
– 2-4hrs
– Peak 18hrs
– Disappears 48hrs
• Troponins
• Lactate dehydrogenase
RHEUMATIC FEVER/RHEUMATIC HEART
DISEASE
RF
• Acute immunologically mediated disease
following Group A strep pharyngitis
• 3% affected
• Acute rheumatic carditis
• Chronic valvular deformities
• 10 days to 6 wks after pharyngitis
• Ages 5-15 mainly
RHEUMATIC FEVER/RHEUMATIC HEART
DISEASE
RF Cont’d - Clinical features
• Arthritis
– Large joints
• Migratory polyarthritis
• Carditis
– Pericardial friction rubs
– Weak heart sounds
• CCF
RHEUMATIC FEVER/RHEUMATIC HEART
DISEASE
RHD
• Signs and symptoms dependent on the valves
involved
• Cardiac murmurs
• Cardiac hypertrophy & dilatation
• CCF
• Atrial fibrillation
• Mitral stenosis
INFECTIVE ENDOCARDITIS
• Infection of the cardiac valves or mural surface
of the endocardium
• Acute
– Infection with organisms of high virulence
– Affecting structurally normal valves
• Sub Acute
– Infection of abnormal valves
– Lower virulence organisms
INFECTIVE ENDOCARDITIS CONT’D
• Follows bacteremia
• Post Sx, dental procedure
• Interventional procedures
• Intravenous drug users
• Trivial injuries
↑ed risk
• Preexisting cardiac abnormalities
• Prosthetic valves
• IV drug abuse
INFECTIVE ENDOCARDITIS CONT’D
Clinical features
• Gradual or explosive
• Fever/chills
• Malaise
• Weight loss
• Splenomegaly
• Clubbing
• Neurological, renal, pulmonary deficits
• Mycotic aneurysms
• Renal lesions
PERICARDITIS
• Viruses responsible for most cases
• Usually 2⁰ to MI, radiation & Sx
Sequelae
• Immediate hemodynamic complications
– Large effusion
• Resolve
• Chronic fibrosing process
PERICARDITIS CONT’D
Clinical Features
• Chest pain – worse on reclining
• Fainting
• Distant heart sounds
• Distended neck veins
• Declining cardiac output
SUMMARY
