Learning Outcomes
Alterations of the Cardiovascular System
Describe the normal structure and function of the cardiovascular systems (review).
Describe the alterations in vascular flow (including thrombus formation, emboli, traumatic injury, atherosclerotic plaques, vasospastic disease and varicosities) that result in outcomes such as deep venous thrombosis (DVT), stasis ulcers, chronic insufficiencies and superior vena cava syndrome.
Define and characterize primary, secondary, isolated, complicated, malignant and orthostatic hypertension.
Describe the differences between true and false aneurysms.
Distinguish between a thrombosis, embolus, thromboembolism, and describe conditions contributing to this pathology.
Distinguish between arteriosclerosis and atherosclerosis and explain the pathophysiology and complications of atherosclerosis.
Describe peripheral artery disease (PAD).
Describe the cardiovascular risk factors and pathology of acute myocardial infarction.
Describe the progression of coronary artery disease from ischemia to infarction, including clinical symptoms, diagnostic evaluation of myocardial infarction and critical timing for intervention.
Distinguish between myocardial ischemia and myocardial infarction.
Describe the association between dyslipidemia and coronary artery disease.
Describe the clinical symptoms, evaluation and pathophysiology of pericardial disease.
Define and differentiate the disorders of the myocardium: myocarditis and cardiomyopathy.
Compare and contrast valvular stenosis and regurgitation.
Describe the pathophysiology and manifestations of rheumatic heart disease including infective endocarditis.
Define heart failure and compare the pathophysiology and manifestations of right-sided and left-sided heart failure.
Define and classify dysrhythmia and describe common causes, types, hemodynamic effects and clinical presentations.
Chambers, valves and great vessels (review)
Pulmonary and systemic circulation (review)
Layers of the heart: pericardium, myocardium, endocardium
Endocardium continues with endothelium lining blood vessels
There is a space between visceral and parietal pericardium that contains fluid. This is where pericardial effusion occur
Electrical conduction system of the heart is responsible for stimulating contraction of the muscle
– Impulse begins in the SA node (also termed the ‘pacemaker’ of the heart’) located in the right atrium
– The impulse progress through the RA, then left-atrium (LA) to reach AV node where there is a slight delay
– The impulse pass through the septum to the left and right
bundle branches (left and right ventricles)
– The last phase of the impulse is passing via Purkinje fibers, which are small branches that distribute the impulse throughout the thickness ventricular walls
Oxygen deprivation to the heart muscle may cause conduction issues and subsequent dysrhythmias.
Disorders of the Cardiovascular System
Arteriosclerosis:
Stiffness, loss of elasticity, and thickening of the arterial wall
Leads to narrowing and subsequent obstruction of the lumen resulting in decreased blood flow
Atherosclerosis:
Most common form of arteriosclerosis
Can affect any vessel
A chronic inflammatory response to lipid accumulation in the intimal layer of the arterial walls
– Over time there is progressive hardening of the artery, loss of elasticity, and
plaque formation (atheromas)
– Narrowing of the artery leads to low blood supply
– The process starts from birth and continues throughout the lifespan
– Lifestyle (i.e. diet, activity, substance use) impacts the rate and severity of plaque build-up 
Manifestations:
When atherosclerosis develops in a coronary artery this leads to coronary artery disease (CAD), which can progress to angina and MI
Non-modifiable Risk Factors
Age
Gender
Family history
Modifiable Risk Factors
Lifestyle
Obesity
Physical inactivity
Smoking
Diseases that Increase Risk for Atherosclerosis
Type 2 DM (can be reversed)
– Those with poor diabetes management are at increased risk
Hyperlipidemia
Hypertension
Atherosclerosis Pathophysiology:
Endothelial damage
– Multiple causes for endothelial cell damage (e.g. smoking, HTN, diabetes, high LDL, inactivity, etc.)
– Damaged endothelium lose its protective antithrombic vasodilating mechanisms
– Damaged endothelium evokes inflammation with attraction of inflammatory cells including macrophages and generation of oxygen free radicals
– Oxidized LDL in the intima recruits monocytes that differentiate into macrophages
o These engulf oxidized LDL to form foam cells 
Fatty streaks/plaque
– Lots of foam cells creates what’s known as a fatty streak
– Fatty streaks produce more free radicals and inflammatory mediators
– Macrophages also release growth factors that stimulate smooth muscle proliferation
Fibrous plaque
– Collagen grows over the streak to make a fibrous cap fibrous plaque
– Can calcify and then protrude into the lumen to obstruct blood flow
Complicated plaque and thrombus formation
– Some plaques can become “unstable” and can rupture
– A plaque that ruptures is a ‘complicated plaque’
– Exposure of the underlying tissue
o Results in platelet adhesion, initiation of the clotting cascade, and thrombus formation
– Thrombus can occlude a vessel
o Partial occlusion leads to ischemia
o Complete occlusion leads to infarction
Summary of atherosclerosis pathophysiology:
– Stage 1: Scratch and damage to the endothelium
– Stage 2: Inflammation, collection of macrophages and other inflammatory cells
– Stage 3: This makes it easy to generate a thrombus on top of plaque or exposed suburothelium
Coronary Artery Disease (CAD)
Atherosclerosis of the coronary arteries
Narrowing or blocking of coronary arteries → decreased blood flow→ low O2 supply to the heart → low tissue perfusion→ myocardial ischemia.
Clinical manifestations:
Asymptomatic
Angina pectoris
Myocardial infarction
Cardiac complications
Dysrhythmia
Heart failure
Sudden death
