Cardiovascular System Flashcards
Primary hypertension
Idiopathic
95% of cases
Secondary hypertension
Secondary to: renal disease, vascular disease, endocrine disorders, adrenal disorders, alcohol intake, hyperthyroidism, coarctation of aorta etc etc
5% of cases
Blood pressure results from:
Cardiac output (CO) + peripheral vascular resistance (TPR)
What predicts cardiovascular events better, systolic or diastolic BP?
Systolic BP (measures how hard heart is working)
What is a common consequence of inadequately treated hypertension?
Stroke
Relationship between artherosclerosis and BP
High bp accelerates development of atherosclerosis
Hypertension
Persistent elevation of diastolic (>90 mmHg) and/or systolic (>140 mmHg) blood pressure.
Measured twice, two weeks apart
Hypertensive vascular disease
Aka hypertension
Incidence
Rate of new cases; probability of occurrence
Prevalence
Proportion of cases in a population in a given time.
Congenital heart disorders develop
In utero during 1st trimester
Septal defects
Most common form of congenital heart disease (40%)
Defect in septum between left and right side of heart
Ventricular septal defect more common and more serious
Pathogenesis of Ventricular Septal Defect
Higher left chamber pressure than right Left-to-right shunt Hypertrophy of right side of heart Pulmonary hypertension Narrowing of pulmonary artery Increased pressure in right side Right to left shunt Deoxygenated blood leaving heart Cyanosis
Left to right shunt
In VSD
Higher pressure in left chamber causes blood to flow from left to right through defect
Right to left shunt
In VSD
Pulmonary hypertension and narrowing of pulmonary artery causes increase in pressure in right chamber
Blood then flows from right to left through defect.
Tetralogy of Fallot
- Stenosis of pulmonary artery or valve
- Ventricular septal defect
- Dextroposition of aorta
- Hypertrophy of right ventricular.
Most common congenital heart defects
Septal defect
Most common cause of infant cyanosis
Tetralogy of Fallot
Patent ductus arteriosis
Failure to form ligamentum arteriosum
Ductus arteriosis between pulmonary trunk and aorta remains open.
Usually occurs in preterm infants.
Aortic blood flows into pulmonary trunk, increasing pulmonary BP and overworking both ventricles.
Coarctation of the aorta
Local congenital malformation.
Decreased flow of oxygenated blood, left ventrical works harder, hypertension develops.
Hypertrophic of left ventricle.
Rheumatic Fever and heart disease
Systemic, immunologically mediated disease related to streptococcal infection
Usually two weeks after strep throat
10% cases result in scarring a deformity of heart valves (pancarditis)
Can manifest with: chorea, poly arthritis, SOB, cough, rash …
Endocarditis
Inflammation of endocardium. Usually includes valvular defects.
From bacterial infection, especially staphylococcal and streptococcal.
Men 2x women
Variable manifestation. Difficult to diagnose. Heart murmurs, failure.
Poor prognosis. Untreated always fatal.
Myocarditis
Inflammation of myocardium. Often viral (but also bacterial and parasitic). Can also result from sarcoidosis, SLE, drugs, radiation.
HIV, rheumatic fever, Chagas disease
Common.
Vague symptoms: chest pain, mild fever, SOB and other signs of heart failure.
Can include arrhythmia, cardiac conduction problems
Chronic – can lead to cardiomyopathy
Pericarditis
Inflammation of pericardium
May be isolated by most often associated with other infections of the heart. Primary or secondary
RHD, LSE, uremia, radiation, trauma
Thickened layers of pericardium (parietal and visceral, aka epicardium) rub against each other and the heart.
Chest pain.
Fibrous exudate.
Two predisposing factors required for endocarditis
- Predisposing abnormality of endocardium
2. Microorganisms in the bloodstream
Pathogenesis of endocarditis
Bacteria damages surface of valves
Inflammation
Fibrin and platelet thrombi form and create nidus for more thrombogenic material
Grow into wartlike structures (verrucous endocarditis)
Inflammation and scarring cause deformities and/or ulcerations
Valves may rupture and create septic emboli (kidney, brain, extremities)
Nidis
“Nest” of bacteria, parasites, and other agents of disease.
Seen in endocarditis
“Vegetation”
Abnormal growth (seen in endocarditis)
Excrescence
Distinct outgrowth on a body, especially one that results in disease or abnormality
Acute bacterial endocarditis: presentation
May present as an acute febrile illness
Subacute bacterial endocarditis: presentation
Mild temperature that waxes and wanes
Pathogenesis of Myocarditis
Involves three stages (1. active 2. healing 3.healed) that are characterized by inflammatory cell infiltrates leading to intersitial edema, focal necrosis and fibrosis.
Pericardial effusion
Exudation of fluid into pericardial sac. Associated with pericarditis
Cardiomyopathy
Group of conditions impairing contraction of and relations between cardiac muscle fibres.
Can be primary or secondary.
Dilated, hypertrophic, restrictive
Dilated cardiomyopathy
Occurs most commonly in middle aged black men
Idiopathic or secondary
Fatigue, weakness, chest pain.
Risk factors: obesity, alcohol, hypertension, smoking, infections, pregnancy
Hypertrophic cardiomyopathy
Appears to be an autosomal dominant condition
Frequently asymptomatic
Most common cause of sudden cardiac death in young athletes
Restrictive cardiomyopathy
Occurs as a result of myocardial fibrosis
amyloidosis, sarcoidosis, etc.
Rigid, noncompliant cardiovascular tissue
Exercise intolerance, SOB, fatigue, edema, ascites
Amyloidosis
Rare condition involving buildup of amyloid (inappropriately folded proteins).
Can cause restrictive cardiomyopathy
Sarcoidosis
Collection of inflammatory cells in nodules, within tissues
Can cause restrictive cardiomyopathy
Mitral Regurgitation
Incompetency of the mitral valve.
Back flow from left ventricle to left atrium
Mitral Stenosis
Narrowing of mitral valve impeding blood flow from left atrium to left ventricle
Aortic regurgitation
Incompetency of aortic valve
Backflow from aorta to left ventricle
Aortic stenosis
Narrowing of aortic valve obstructing blood flow from left ventricle to aorta.
Valvular disease
Stenosis or incompetency
Usually mitral or aortic valves.
RDH, endocarditis, congential valve disease, autoimmune disorders
Backflow –> overburdened chamber –> hypertrophy
Hypertension
Decreased blood flow
Variable manifestation: angine, dyspnea, heart failure, arrhythmia, palpations, heart murmur
… of asymptomatic
Arteriosclerosis
Hardening of the arteries
Atherosclerosis
A form of arteriosclerosis in which fatty plaque deposits build up in arteries
Ischemic Heart Disease
AKA coronary heart disease (CHD) or coronary artery disease (CAD)
Major disorder of myocardium due to insufficient blood supply
Gradual ischemic heart disease can lead to
Hypofusion if myocardium and congestive heart failure
Angina pectoralis
Chest pain, which may radiate (especially down left arm)and lasts 3-20 minutes.
Typically precipitated by effort
Relieved by rest and nitroglycerin
Most common in men over 65
Causes of angina pectoralis
Anything that alters blood supply to myocardium, or blood requirements of myocardium
Categories of angina
- Chronic stable
- New-onset
- Nocturnal
- Postinfarction
- Preinfarction
- Prinzmetal’s
- Decubitus
Chronic stable angina
Classic exertional angina
Predictable and constant
New-onset angina
Unstable. Developed within the lasts two weeks.
Prinzmetal’s angina
Symptoms similar to typical
Caused by coronary artery spasm (not blockage)
Occurs early in morning, so not exercise related
Decubitus angina
Atypical
More common in women
Occurs at rest
Relieved by sitting or standing
Myocardial infarction
Development of ischemia with resultant necrosis of myocardial tissue
Heart attack.
Due to sudden occlusion of a coronary artery (anterior descending branch of LCA most common)
Congestive heart failure
Heart unable to pump sufficient blood
Predominantly the failure is on left.
Blood flow slows
Blood returning to heart backs up in veins
Edema in tissues, lungs
Decreased blood to kidneys leads to Na and H2O retention, which increases load on heart
Heart has to work harder –> LV hypertrophy
Poor prognosis. Not really reversible
Cor pulmonale
Right ventricle enlargement secondary to lung disorder.
COPD (chronic) Pulmonary embolism (acute)
Pulmonary embolism
Occlusion of one or more pulmonary arteries by thrombi
Cause DVT in 50% of cases
Atelectasis
Total or partial collapse of lung
Possible consequence of pulmonary embolism
Rales
Crackly, rattling lung sounds
Possible sign of pulmonary embolism
Dysthymia
Disturbance in rate or rhythm of heartbeat
Atrial fibrillation
Most common chronic arrhythmia
Inefficient pumping, Usually secondary to heart disease
Ventricles don’t fill properly, so heart races but blood flow diminishes
Fibrillation
Rapid uncoordinated heart beats
Ventrical fibrillation
Electrical problem
Involuntary uncoordinated contractions
Frequent cause of cardiac arrest
“Clear!”
Heart block
AV block
Dysrrhythmia caused by interruption in cardiac conduction
1st, 2nd and 3rd degree blocks.
Can be caused by meds or disease
Treated with meds or pacemaker
Ectopic beats
Electrical activation of heart that originates outside SA node
Paroxysmal tachycardia
Abnormal rapid heart rate that begins and ends suddenly
Arteriosclerosis
Group of disorder characterized by thickening and loss of elasticity in the arterial walls.
Hardening of the arteries.
Three types of arteriosclerosis
- Athlerosclerosis
- Monckeberg’s artiosclerosis
- Artiolosclerosis
Athlerosclerosis
Plaques/fatty deposits form in the intima of arteries, blocking lumen
Athero=gruel (lipids, macrophages, T cells, smooth muscle cells, ECM, calcium, necrotic debris).
Simultaneous hardening and softening.
Monckeberg’s Arteriosclerosis
Age-related (senile) arteriosclerosis
Destruction of muscle and elastic fibres in middle layer of endothelial wall (tunica media), and formation of calcium deposits.
Arteriolosclerosis
Arteriolar sclerosis
Thickening of walls of small arteries
Hypertension related
Not atheroma-related.
Atheroma
Accumulation of degenerative material in the tunica interna.
Mostly macrophage cells containing lipids, calcium, and fibrous connective tissue.
Occur in atherosclerosis.
Pathogenesis of atherosclerosis
Normal endothelium: smooth and non-reactive.
But endothelium gets damaged – often from LDLs that get corrupted by free radicals (from booze and ciggies), or by bacteria, or wear and tear from high blood pressure.
Damage allows macromolecules (esp cholesterol) to slip through to underlying muscle.
Collagen, platelets, proliferation, obstruction.
Three categories of atherosclerosis
- Coronary artery disease
- Peripheral vascular disease
- Cerebrovascular disease
Peripheral Vascular Disease
Any disease of the circulatory system outside the brain or the heart.
Lower extremities more commonly affected than upper extremities
Most commonly a result of atherosclerosis
Symptoms include intermittent claudication, pain, cyanosis, fatigue, gangrene, cold
Vasculitis
A form of peripheral vascular disease.
Inflammation of a blood vessel, affecting either an organ or a system
Arteritis
A vasculitis; Inflammation of an artery
Infective arteritis
Arteritis due to infection
Rheumatoid arteritis
Arteritis associated with Rheumatoid Heart Disease
Giant Cell Arteritis (GCA)
A form of Arteritis
AKA cranial or temporal arteritis
Vasculitis primarily involving multiple sites of temporal and cranial arteries, sometimes aortic arch
More often in older women
Left untreated, may lead to stroke, blindness, aortic dissection
Symptoms of Giant Cell Arteritis
Severe, continuous, unilateral, throbbing headache and temporal pain.
May also include: flu-like symptoms, visual disturbance, radiating pain, blindness, shoulder paralysis, claudication of the arm with cold hands, absent radial pulse.
Claudication
Angina of the legs/jaw/arm
Thromboangiitis Obliterans
Buerger’s Disease
A vasculitis affecting peripheral blood vessels, primarily in extremities (hands and feet).
Inflammatory lesions in peripheral blood vessels, accompanied by thrombus formation and vasospasm.
Small and medium blood vessels occluded and obliterated.
More common in men who smoke
Symptoms of Thromboangiitis Obliterans
Episodic and segmental pain
Plantar, tibial and digital vessels most commonly affected
Polyarteritis Nodosa
Multiple sites of inflammatory and digestive lesions in the arterial system.
Often comorbid with Hep B; frequently found in IV drug users
Affects small and medium sized vessels.
Good prognosis with treatment
Which systems are more often involved with polyarteritis nods?
Kidneys Heart Liver GI tract Muscles Testes
Aneurysm
Stretching of blood vessel wall at least 50% beyond its normal diameter.
Aortic aneurysm
Most common site for an arterial aneurysm
Thoracic (ascending, transverse, first part of descending)
Abdominal (usually between renal and iliac arteries)
Mycotic aneurysm
Bacterial or fungal infection, most often salmonella or syphillis
Artherosclerotic aneurysm
Build up of fatty deposits on the inner wall of the arteries
Plaque formation erodes wall –> stretching –> inflammation –> fibrosis –> rupture
Telangiectasia
Spider veins
Dilation of a small group of blood vessels
Frostbite
Tissue damage caused by exposure to extreme cold (0-2 degrees or colder)
Vasoconstriction –> ice crystals form in tissues and expand –> cell membranes rupture –> digestive enzymes released
Diabetic microangiopathy
Caused by long term, poorly controlled hyperglycemia
Increased inflammation, increased scar tissue, decreased blood supply
Compounded by the immune dysfunction caused by hyperglycemia
Most common manifestations:
- retinopathy
- neuropathy
- nephropathy
Diabetic retinopathy
Most common cause of adult blindness in USA
Retinal capillary microaneurysms –> macular edema –> neovascularization
Diabetic neuropathy
Results from
- nerve ischemia from microvascular disease
- direct effects of hyperglycemia on neurons
- intracellular metabolic changes that impair nerve function
Starts with stocking/glove presentation
Diabetic nephropathy
Glomerular sclerosis and fibrosis caused by metabolic and hemodynamic changes.
Number one cause of renal failure in US
Decompression Sickness
Caisson disease, “the bends”, diver’s disease
Rapid pressure reduction causes gases to form bubbles in blood vessels. Bubbles block vessels, rupture or compress tissue, or activate clotting and inflammatory cascades.
Henry’s Law
80% recover completley
Type 1 Decompression Sickness
Progressive worsening in joints, back and muscles.
Pain worse with movement; deep and boring
Lymphadenopathy, skin mottling, itching, rash
Type 2 Decompression Sickness
Neurologic and maybe respiratory symptoms
Paresis, numbness, tingling, difficulty urinating, loss of bladder and bowel control
Seizures, slurred speech, vision loss, confusion, coma, death.
Varicose Veins
AKA varicosisties
Abnormal dilation of veins leading to tortuosisty of vessel, incompetence of valves, and propensity to thrombosis
Women more than men (70% of women 60-70)
May lead to ulcers, thrombosis, phlebitis
Common sites for varicose veins
Lower extremities Saphenous veins Rectum and anal canal Scrotum (variocele) Esophagus
Venous Thrombosis
Partial or full occlusion of a vein by a clot
Trauma to endothelium makes it stickier for platelets and clotting factors –> thrombosis
Thrombophlebitis
Partial or full occlusion of a vein by a thrombus with a secondary inflammatory reaction in the wall of a vein.
Thrombus –> inflammation
Phlebothrombitis
Inflammation of a vein, which predisposes a person to clot formation
Inflammation –> thrombus
Deep Vein Thrombosis
3rd most common CV disease
Usually in calf.
Often clinically silent and benign, but can lead to pulmonary emboli (especially popliteal, femoral or inferior vena cava)
Possible fates of thrombi
Recanalization (blood carves new pathway)
Dissolution
Organization (new tissue grows in and around it)
Persist as thrombus
Embolus
Chronic Venous Insufficency
AKA postphlebitis syndrome, venous stasis
Inadequate venous return over a long period of time
Follows most sever cases of DVT, but can also be secondary to varicose veins, leg trauma or neoplasm
Damaged valves –> decreased venous return –> increased venous pressure –> venous stasis
–> superficial veins and capillaries dilate –> edema and reddish brown pigmentation
Inadequate oxygenation and waste removal –> cell death —> necrotic tissue –> venous stasis ulcers
Thin, shiny, dry skin. Cellulitis, dermititis
Raynaud’s
Intermittent episodes of small artery or arteriole constriction of the extremities
More common in women
Usually triggered by cold, stress,
Pallor, cyanosis
Can be associated with Buerger’s or CT disorders, or neoplasms, occlusive arterial disease, TOS, frostbite etc.
Raynaud’s phenomenon
secondary Raynaud’s
Raynaud’s disease
primary Raynaud’s, Primary Vasospastic Disorder
Idiopathic
