Diseases

of the CV
System

CAD
Refers to the variety of pathologic
conditions that cause narrowing
of the coronary arteries
Atherosclerosis- Deposits of
cholesterol and lipids within the
walls of the artery
Risk Factors: Family history,
hyperlipidemia, smoking, DM, HPN,
obesity, sedentary/stressful
lifestyle

Family history,
Hyperlipidemia, DM,HPN

Hyperlipidemia, smoking,
obesity, stressful/sedentary lifestyle
Anti hyperlipidemics
Lifestyle mods

Endothelial Injury
Inflammation
Thromboxane

Permeability
Release of
Adhesion Molecules
Macrophage adhere to
Endothelium

ASA

Foam Cells
Fatty Streaks

Vasoconstriction

Platelet Aggregation

PTCA.
endartherectomy

Release of enzymes
and toxic O2 Radicals
Oxidation

Serotonin, Endothelin

Vessel obstruction
Necrosis of
vessel tissue

Smooth muscle
cells develop

Endothelial Dysfunction
Fibrous Plaque

Metabolism of Fats
Dietary Fats
Stomach
Small Intestines

Bile acid sequestrants

Gall bladder releases bile
Fat emulsification

Bile acids recycled

to liver

Micelles absorbed into intestines

Fibrates

Chylomicrons absorbed into

lymphatics

Gemfibrozil, niacin
Hmg CoA blockers

Enter circulation and

periphery
Liver proceeds fats
Into HDL,LDL

Myocadial
Infarction
Death of myocardial cells from
inadequate oxygenation
Signs and symptoms: Pain, N&V,
dyspnea, cool and clammy skin,
elevated temperature,initial
increase, then drop in
BP,restlessness
Laboratory findings: Elevated WBC,
CPK, AST, LDH
ECG Changes: pathologic
Q wave, ST segment elevation,
inverted T wave

Types of MI
TYPE

Artery
Occluded

Anterior

Location of
ST/Q wave
changes
V1-V4

Inferior

II, III, Avf

RCA

Lateral

I, Avl, V5-V6

LCX

Posterior

V1-V2

RCA

LADA

Types of MI
TYPE

Layer affected

Subendocardial

Inner layer

Subepicardial

Inner and middle

layer

Transmural

All layers

ASHD,CAD, DM, age, gender, HPN,

Stress, thrombosis/embolism

PTCA,CABG,ASA Thrombolytocs
Myocardial Ischemia
CKMB, TROP I, T

O2, CBR,
Laxatives,
NTG,
Lifestyle
Mod

O2 Supply O2 Demand

Leukocytosis,ESR

Cellular Hypoxia

Cellular Necrosis

Anaerobic Metabolism
H Ions
Antiarrythmics

Morphine

Cell membrane permeability

K,Ca,Mg

Lactic Acid
LDH Flipping

Chest Pain

Sympathetic Response N & V

Glucose,
Fatty Acids

Diaphoresis

HR

After Load

Cool,
Clammy Skin

Contractility
Cardiotonics

BP

Disatolic Filling
CO

Rheumatic Heart
Disease
Inflammatory disorder that involves
the heart, joints, muscle and CNS
Assessment findings
Major (Jones Criteria)
Carditis
Aschoff nodules,
valvular insuffucienscy
Cardiomegaly
SOB, hepatomegaly, edema
Polyarthritis
Sunbcutaneus nodules
Chorea/ Sydenhams chorea/St.
Vitus dance
Erythema marginatum

 Minor
History of GAS infection
Fever
Elevated ESR, WBC, ASO titer

GAS infection
(Beta hemolytic Streptococcus)

Fever, elevated
WBC,ESR

Inflammatory
response

Penicillin/
Erythromycin

Activation of T cells
by streptococcal antigens

Anti-inflammatory
ents ( steroids,NSAIDS)

CNS

Binds to receptors
within.

Heart
Positioning
ASA

Chorea
Swelling, heat, pain
arthralgia
Decrease stimulation
Safety precautions

Joints
Polyarthritis

Subcutaneus nodules

Heart
Pericarditis

Endocardial
Inflammation

Friction rub

Chest pain

Inflammation of
valve leaflets
Erosion of leaflet
contact

Valve replacement,
thrombolytics
Murmur

Clumping of vegetation
With platelets & fibrin

Penetrates
myocardium

Scarring/shortening

Fibrin deposits
Develop with area of
necrosis

Decreased elasticity
Mitral/ Tricuspid
regurgitation

Bed rest
CHF

Aschoff nodules

Arrythmias
Disruption in the normal events of
cardiac cycle which may/ may not
lead to decreased cardiac output
(to which the manifestations are
attributed).

Shock, anemia,
respiratory distress,
cellular hypoxia

Exercise, pain,
strong emotions, anxiety
O2, Bed rest
Carotid massage,
identify
effective
coping strategies

Decreased CO

Decreased
arterial pressure

Sympathetic
stimulation

Hyperthyroidism

Increased
Cathecolamines
Ca channel blockers
Increased HR >100BPM

Pathophysiology of Sinus Tachycardia

Hyperkalemia, digoxin,
MI, hypothermia

Late hypoxia

Sleep, valsalva maneuver

vomiting

O2, Bed rest

Symphatomimetics
pacers

Decreased
automaticity

Decreased
ATP

Increased vagal
stimulation

HR <60BPM

Pathophysiology of Sinus Bradycardia

Electrolyte
imbalance

Anterior MI

Hypoxia
Correct
imbalance

2nd deg AVblock

O2, Bed rest

Shortening of
the phases of
cardiac cycle

Circus reentry &

Increased automaticity

Increased cell
permeability

Impulses not
conducted to
the ventricles

Digoxin, Ca channel
Blockers, class Ia, II
antiarrythmics, sychronized
cardiovertion

Atrial rate
200-400BPM
Pathophysiology of Atrial
Fibrillation/Flutter

Electrolyte imbalance, acidosis, hypoxia myocardial ischemia

drug intoxication (cocaine, amphetamines, TCA)
Decreased oxygen demand,
correct electrolyte levels, Class Ib, II
antiarrythmics

Disruption of electrolyte shifts

During depolarization and repolarization

Synchronized cardioversion

Irritability

Ectopic beat/ PVCs

Pathophysiology of Premature Ventricular

Contraction