The document discusses the cardiovascular system, including the structure and function of the heart and circulatory system. It covers several cardiovascular conditions in depth such as atherosclerosis, myocardial infarction, congestive heart failure, rheumatic heart disease, infective endocarditis, and atrial fibrillation. Diagnostic tests and treatments for various cardiovascular diseases are also summarized.

1. Dr. Suhail S. Kishawi
Consultant in Endocrinology and Diabetes
Consultant in internal Medicine
Cardiovascular Disorders

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Understanding the Cardiovascular System
 The Heart: A Mighty Machine
• Four chambers
• Two upper chambers are called atria
• Two lower chambers are called
ventricles
• Valves regulate the flow of blood

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Anatomy of the Heart

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lungs
head & arms
liver
digestive system
kidneys
legs
pulmonary artery
aorta
pulmonary vein
main vein
LeftRight
How does this system work?
Circulatory System

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Lungs
Body cells
Our circulatory system is a double circulatory system.
This means it has two parts parts.
The right side of
the system
deals with
deoxygenated
blood.
The left side of
the system
deals with
oxygenated
blood.

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Structure of the Heart
 Consists of three layers:
• Endocardium (inner lining of heart
chambers and valves).
• Myocardium (thickest part of the
heart; consists of cardiac muscle).
• Epicardium (inner layer of a double
walled sac called the pericardium
that surrounds the heart).

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 2 coronary arteries
branch from the main
aorta just above the
aortic valve.
 They divide and
encircle the heart to
cover its surface like
crown.
Blood Supply To The Heart

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Conduction System
 For the heart to beat regularly in a rhythmic
sequence, electrical impulses follow a set
pattern through the conduction system of the
heart.
 The conduction system consists of the
sinoatrial node, atrioventricular node, bundle
of His, bundle branches and Purkinje fibers.

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Electrical System of Heart

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Components of a NSR ( Normal Sinus Rhythm )

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• Hypertension.
• Stroke (CVA).
• Arteriosclerosis.
• Aneurysm.
• Coronary artery disease (CAD).
• Heart attack.
• Congestive heart failure (CHF).
• Arrhythmias
• Congenital and Rheumatic Heart Disease
• Anemia, hemophilia, and leukemia.
Diseases And Disorders Of The
Cardiovascular System

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Diagnostic Tests for Cardiovascular Function
 ECG
• Monitors arrhythmias, MI, infection, pericarditis
• Studies conduction activation and systemic abnormalities
 Ausculation
• Studies heart sounds using stethoscope
 Exercise stress test
• Assess general cardiovascular function
• Checks for exercise-induced problems
 Chest X-ray Film
• Shows shape, size of heart
• Evidence of pulmonary congestion associated with heart
failure
• Nuclear imaging

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Diagnostic Tests
 Cardiac Catheterization
• Visualize inside of heart,
measure pressure, assess
valve and heart function
• Determine blood flow to and
from heart

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Diagnostic Tests
 Angiography
• Visualization of
blood flow in
coronary artery
• Obstruction
assessed and
treated
• Basic catheterization
• Balloon angioplasty

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Atherosclerosis

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Lipoproteins and Transport

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Atherosclerosis--Pathophysiology
 Analysis of serum lipids:
• Total cholesterol, triglycerides, LDL, HDL
 LDL
• High cholesterol content
• Transports cholesterol liver  cells
• Dangerous component
 HDL
• “good”
• Low cholesterol content
• Transports cholesterol cells  liver

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Consequences of Atherosclerosis

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Atherosclerosis—Etiology
 Age
 Gender
 Genetic factors
 Obesity, diet high in cholesterol, animal fats
 Cigarette smoking
 Sedentary life style
 Diabetes mellitus
 Poorly controlled hypertension
 Combo of BC pills and smoking

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CAD: Myocardial Infarction
 Coronary artery completely obstructed
• Prolonged ischemia and cell death of myocardium
 Most common cause is atherosclerosis with
thrombus
 3 ways it may develop:
• Thrombus obstructs artery
• Vasospasm due to partial occlusion
• Embolus blocks small branch of coronary artery
 Majority involve L ventricle
• Size and location of infarction determine severity of
damage

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Myocardial Infarction

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MI—Signs and Symptoms
 Pain
• Sudden, substernal area
• Radiates to L arm and neck
• Less severe in females
 Pallor, sweating, nausea, dizziness
 Anxiety and fear
 Hypotension, rapid and weak pulse (low CO)
 Low grade fever

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MI—Diagnostic Tests
 ECG
 Serum enzyme and
isoenzyme test
 High serum levels of
troponin
 Abnormal electrolytes
 Leukocytosis
 Arterial blood gases

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MI—Complications
 Arrhythmias
• 25% pts sudden death after MI
• Due to ventricular arrhythmias and
fibrillation
• Heart block
• Premature ventricular contraction (PVCs)
 Cardiogenic shock
 CHF

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CHF—Pathophysiology
 Heart unable to pump sufficient blood to
meet metabolic needs of body
 Acute or chronic
 Results from
• Problem in heart itself
• Increased demands placed on heart
• Combo
 One side usually fails 1st

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CHF—Etiology
 Causes of failure on affected side:
• Infarction that impairs pumping ability
or efficiency of conduction system
• Valve defects
• Congenital heart defects
• Coronary artery disease

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CHF—Etiology
 Increased demands on heart cause failure
• Depends on ventricle most adversely
affected
• Ex: Hypertension increases diastolic BP
• Requires L ventricle to contract more
forcibly to open aortic valve
• Ex: Pulmonary disease
• Damages lung capillaries, increases
pulmonary resistance
• Increase work load to R vent

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CHF—Signs and Symptoms
 Forward effects
• Similar with failure on either side
• Decrease blood supply to tissue and
general hypoxia
• Fatigue, weakness, dyspnea
(breathlessness), cold intolerance,
dizziness
 Compensation mechanism
• Indicated by tachycardia, pallor, daytime
oliguira

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CHF—Treatment
 Underlying problem should be treated
 Decrease work load on heart
 Prophylactic measures
 Other methods
• Diet
• Drugs

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CHF—Signs and Symptoms
 Systemic backup effects of R-sided
failure
• Edema in feet, legs
• Hepatomegaly, splenomegaly
• Ascites

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Rheumatic Fever And Valvular Heart
Disease
 Rheumatic fever is an acute immunologically
mediated multisystem inflammatory disease
that occurs a few weeks following an episode
of group A streptococcal pharyngitis.
 Acute rheumatic carditis, during active phase
 May progress to Chronic rheumatic heart
disease.

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Morphology
ACUTE RH. FEVER  Pancarditis
 Pericarditis- serofibrinous
 Myocarditis  Aschoff bodies
 Endocarditis 
• Verrucous vegetations (1-2mm) at lines of closure of valves
• Fibrinoid necrosis along cusps and teninous cords

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Pathogenesis
vegetations Aschoff body,
myocardium
Fibrinous
pericarditis

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Morphology of chronic RHD
 Mitral valve is most
often affected with
rheumatic heart
disease, followed by
mitral and aortic
together, then aortic
alone, then mitral,
aortic, and tricuspid
together.
 Mitral stenosis (99%
cases)
 Fishmouth/ buttonhole
stenosis

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Clinical features of ARF
Major criteria :
 Migratory polyarthritis
 Carditis,
 Subcutaneous nodules,
 Erythema marginatum, and
 Sydenham chorea.
Minor criteria:
 Fever, arthralgias, increased blood levels of acute phase reactants
( ESR/C-reactive) , leukocytosis and prolonged PR interval on
ECG.
Plus evidence of antecedent streptococcal infection, e.g. positive
throat cultures for group A streptococci, elevated antistreptolysin
O titre (> 250 U) or a history of recent scarlet fever

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DIAGNOSIS
Jones criteria:
 Evidence of preceding group A strept.
infection
 Presence of two major or more
 or one major and two minor or more criteria

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Clinical features of chronic rheumatic
carditis
 Valvular disease and its sequelae (yrs later)
 Murmurs
 Cardiac hypertrophy, dilatation, heart failure
 Arrythmias esp Atrial fibrillation
 Thromboembolic complications
 Infective endocarditis

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Atrial Fibrillation

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Infective Endocarditis
 Infection of heart valve or mural
endocardium by a microbe leading to
formation of bulky friable vegetations and
destruction of underlying tissue.
 Vegetations are composed of thrombotic
debris and organisms

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Infective endocarditis
 Turbulent blood flow (from congenital or acquired heart
disease)Endothelial trauma
 Platelets and fibrin deposit on damaged endothelium
 Nonbacterial Thrombotic Endocarditis (NBTE)
 Bacteremia Colonization of NBTE  Bacterial
Vegetation

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Endocarditis Classification
 Acute
• Virulent! Staph aureus, GNR
• Normal valves
• Acute course with rapid valve destruction, HF
 Subacute (SBE)
• Strep, Enterococcus, Staph epi
• Underlying cardiac dz
• More indolent presentation: low-grade fever, murmur
 New classification
• Native valve, addict, prosthetic valve, culture-neg

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Diagnosis of IE
 Fever, new murmur or heart failure,
bacteremia
 Systemic findings of emboli
 Neurologic impairment
 EKG
• New AV block or BBB suggests
perivalvular invasion
 CXR
• Septic pulmonary emboli

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Major Duke’s Criteria
Definite IE: 2 major, 1 major + 3 minor, or 5 minor
 (+) blood cultures with appropriate organism
 Evidence of Coxiella burnetii infection
 New Valvular regurgitation
 + Echo findings

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Minor Duke’s Criteria
 High-risk for IE, or h/o IVDU
 Temperature > 38o
C
 Vascular Phenomena
• Arterial embolism, septic pulm infarcts, mycotic
aneurysm, intracranial hemorrhage, Janeway lesions
 Immunologic phenomena
• Osler’s nodes, Roth spots, GN, Rheumatoid factor
 Serologic studies
 Blood cultures or echo results not meeting the
major criteria

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Clinical features
Splinter hgs
Petechiae Janeway lesions
Osler’s nodes

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Septic Emboli

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Pale retinal lesions surrounded by hemorrhage, usually near optic disk
Roth Spots

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Janeway Lesions
Non tender, erythematous, hemorrhagic or pustular lesions
on palms, soles

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Osler Nodes
●
Tender, subcutaneous
nodules
●
Pulp of the digits or
thenar eminence
4 P’s:
Pink
Painful
Pea-sized
Pulp of fingers/toes

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Endocarditis:
Prophylaxis and Infection

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Frequency of Transient Bacteremia
 Tooth extraction 10-100%
 Periodontal surgery 36-88%
 Teeth cleaning 40%
 Tooth brushing, flossing 20-68%
 Using wooden toothpicks 20-40%
 Chewing food 7-51%

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Risk of IE from dental procedures?
 No prospective, randomized, placebo-
controlled studies exist on efficacy of Abx
ppx in preventing IE after dental procedure
 The evidence linking bacteremia from dental
procedures with IE is largely circumstantial
• Case reports used time periods as long as
3-6mos from dental procedure to onset of
IE overestimation of cases

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2007: Who gets prophylaxis?
Only patients with the highest risk of adverse
outcomes (heart failure, surgery, death) from
endocarditis:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplant recipients who develop
cardiac valvulopathy
4. Congenital Heart Disease

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Dental Procedures
 “If it bleeds, give prophylaxis”
 High-risk pts undergoing all dental procedures
that involve manipulation of gingival tissues
OR periapical region of teeth OR perforation of
oral mucosa
• i.e. biopsies, suture removal, placing orthodontic
bands
 NO PROPHYLAXIS:
• Xray, anesthetic injections, fluoride treatments
• Shedding of deciduous teeth
• Placement/adjustment of removable prosthodontic
or orthodontic appliances

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Summary: IE prophylaxis
 Need high-risk pt PLUS high-risk procedure
 High-risk pts:
1. Prosthetic cardiac valve
2. Previous IE
3. Cardiac transplants w/ valvulopathy
4. Congenital Heart Disease
 High-risk procedures:
1. Dental: “If it bleeds, give prophylaxis”
2. Respiratory: Consider if pt will be cut or biopsied
3. GI/GU: never

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Prophylaxis for Dental Procedures
 Goal: cover Strep Viridans
 Single dose, 30-60 min prior to procedure
PO Amoxicillin 2g
PO,
PCN-
allergic
Cephalexin 2g
OR Clinda 600mg OR Azithro 500mg
**Don’t use Cephalexin if anaphylaxis, angioedema, or
urticaria w/PCNs or ampicillin
IV: Ampicillin 2gm IV/IM
OR Cefazolin 1g IV/IM OR Ceftriaxone 1g IV/IM
IV, PCN-
allergic
Cefazolin 1g IV/IM
OR Ceftriaxone 1g IV/IM OR Clinda 600mg
IV/IM

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No Prophylaxis
 Endotracheal intubation
 Cardiac cath/stent
 Pacer/ICD implantation
 EGD, Colonoscopy
 Barium Enema
 TEE
 Incision/Bx of surgically scrubbed skin
 Circumcision
 Vaginal delivery
 Hysterectomy

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