Cardio diseases.ppt

7/27/2019 Cardio diseases.ppt

http://slidepdf.com/reader/full/cardio-diseasesppt 1/17

Diseases

of the CVSystem



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



Platelet Aggregation

Release of enzymes

and toxic O2 Radicals

Endothelial Injury

Inflammation

Fatty Streaks

Vasoconstriction

Macrophage adhere to

Endothelium

Release of

Adhesion Molecules

Oxidation

Foam Cells

Thromboxane Serotonin, EndothelinPermeability

Vessel obstruction

Fibrous PlaqueSmooth muscle

cells develop

Necrosis of

vessel tissueEndothelial Dysfunction

Family history,

Hyperlipidemia, DM,HPN

Hyperlipidemia, smoking,

obesity, stressful/sedentary lifestyle

Anti hyperlipidemics

Lifestyle mods

ASA

PTCA.

endartherectom



Metabolism of Fats

Dietary Fats

Micelles absorbed into intestines

Gemfibrozil, niacin

Hmg CoA blockers

Fibrates

Fat emulsification

Liver proceeds fats

Into HDL,LDL

Gall bladder releases bile

Bile acid sequestrants

Enter circulation and

periphery

Bile acids recycled

to liver

Small Intestines

Stomach

Chylomicrons absorbed into

lymphatics



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: pathologicQ wave, ST segment elevation,

inverted T wave



Types of MITYPE Location of

ST/Q wave

changes

Artery

Occluded

Anterior V 1-V 4 LADA

Inferior II, III, Avf RCA

Lateral I, Avl, V5-V6 LCX

Posterior V 1-V 2 RCA



Types of MITYPE Layer affected

Subendocardial Inner layer

Subepicardial Inner and middle

layer

Transmural All layers

d



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

Stress, thrombosis/embolism

Myocardial Ischemia

Anaerobic Metabolism

Cellular Hypoxia

O2 Supply ≠ O2 Demand

H Ions Lactic Acid

Chest Pain

LDH Flipping

Cell membrane permeability

Sympathetic ResponseK,Ca,Mg

Glucose,

Fatty Acids BP

After Load

N & V

Cool,

Clammy Skin

Diaphoresis HR

Disatolic Filling

CO

Leukocytosis,ESR

Cellular Necrosis

CKMB, TROP I, T

Contractility

O2, CBR,

Laxatives,

NTG,

LifestyleMod

PTCA,CABG,ASA Thrombolytocs

MorphineAntiarrythmics

Cardiotonics



Rheumatic Heart

Disease

• Inflammatory disorder that involves

the heart, joints, muscle and CNS

• Assessment findings• Major (Jone’s Criteria)

• Carditis

• Aschoff nodules,

• valvular insuffucienscy

• Cardiomegaly

• SOB, hepatomegaly, edema

• Polyarthritis

• Sunbcutaneus nodules• Chorea/ Sydenham’s chorea/St.

Vitus’ dance

• Erythema marginatum



• Minor

• History of GAS infection

• Fever

• Elevated ESR, WBC, ASO titer



GAS infection

(Beta hemolytic Streptococcus)

Binds to receptors

within….

Activation of T cells by streptococcal antigens

Inflammatory

responseFever, elevated

WBC,ESR

Heart JointsCNS

Polyarthritis

Swelling, heat, pain

arthralgiaSubcutaneus nodules

Decrease stimulation

Safety precautions

Chorea

Anti-inflammatory

ents ( steroids,NSAIDS)

Penicillin/

Erythromycin

Positioning

ASA



Heart

Pericarditis

Clumping of vegetation

With platelets & fibrin

Erosion of leaflet

contact

Inflammation of

valve leaflets

EndocardialInflammation

Scarring/shortening

Chest pain

Decreased elasticity

Friction rub

Aschoff nodules

Fibrin depositsDevelop with area o

necrosis

Penetrates

myocardium

Mitral/ Tricuspid

regurgitation

CHF

Murmur

Valve replacement,

thrombolytics

Bed rest



Arrythmias

• Disruption in the normal events of

cardiac cycle which may/ may notlead to decreased c rdi c output

(to which the manifestations are

attributed).



Shock, anemia,

respiratory distress,

cellular hypoxia

Exercise, pain,

strong emotions, anxiety

Carotid massage,

identify

effectivecoping strategies

O2, Bed rest

Ca channel blockers

Increased HR >100BPM

Hyperthyroidism

Increased

Cathecolamines

Sympathetic

stimulation

Decreased

arterial pressure

Decreased CO

Pathophysiology of Sinus Tachycardia



Hyperkalemia, digoxin,

MI, hypothermia

Symphatomimetics

pacers

Late hypoxia

HR <60BPM

Decreased

automaticity

Increased vagal

stimulation

Decreased

ATP

Sleep, valsalva maneuver

vomiting

O2, Bed rest

Pathophysiology of Sinus Bradycardia



Pathophysiology of AtrialFibrillation/Flutter

Electrolyte

imbalance

Circus reentry &

Increased automaticity

Digoxin, Ca channel

Blockers, class Ia, II

antiarrythmics, sychronized

cardiovertion

Correct

imbalance

Atrial rate

200-400BPM

Impulses notconducted to

the ventricles

2nd deg AVblock

Increased cell permeability

Shortening ofthe phases of

cardiac cycle

Anterior MIHypoxia

O2, Bed rest



Pathophysiology of Premature Ventricular

Contraction

Electrolyte imbalance, acidosis, hypoxia myocardial ischemia

drug intoxication (cocaine, amphetamines, TCA)

Disruption of electrolyte shifts

During depolarization and repolarization

Decreased oxygen demand,

correct electrolyte levels, Class Ib, II

antiarrythmics

Synchronized cardioversion

Irritability

Ectopic beat/ PVC’s

Documents

Cardio diseases.ppt