Professional Documents
Culture Documents
Arteriosclerosis:
Type:
1. Hyaline Arteriolosclerosis (essential Hypertension, DM)
- Hardening of small vessel due to HTn and DM
- High pressure cause Protein built up cause stiffen
- Hyaline material cause thick wall
- Blood flow reduced
- O2 decreases
- Kidney, glomerulus scar ( arteriolonephrosclerosis ) may lead to chronic renal failue
Diabetes
- High blood sugar damage endothelium (by altering carbohydrat & fat metabolism)
- Dmaged basement membrane
Sign
1. Chest pain (angina)
2. Leg pain
3. Stroke like symtom(brain)
4. Renal Failure (kidney)
Risk
1.
2. Hypertension ( BP> 169/95mm)
3. Diabtetes : AGEs trap LDL and prevent its efflux
4. Inflammation : C-reactive protein
5. Obesity
6. Homocystinurea
7. High lipoprotein (Lp(a)): altered form LDL increase ischaemic heart disease
8. Type A personality : lack exercise, stressful
9. Diet: high carbohydrate, high fat intake
Pathogenesis
1. Increase LDL cause deposition in tunica intima and become oxidised
2. Damaged endothelial wall activate endothelial cell
3. Cause adhesion of blood leukocytes and monocytes move to
4. Macrophages eat LDL33 , foam cell formed
5. Foam cell cause migration of smooth muscle proliferation from tunica media to tunica intima
6. Increase smooth muscle proliferation increase collagen synthesis & ECM deposition
7. Cause hardening of plaque
8. Foam cell release lipid (lipid accumulation)
9. Thromboplastic plaque rupture, blood coagulation cause reduced blood flow
Details...
- Endothelium protects vessel wall and prevents clotting
- Damaged wall due to low density lipoprotein ,high blood pressure and smoking
- Hyperlipidemia, homocysteine, toxins
- Damaged wall cause LDL to go in
- Monocyte go in too , adhere to endothelial wall and break LDL down by oxidation
- Macrophage eat LDLP
- Dead monocyte = FOAM CELL
- cytokines & VCAM (vascular cell adhesion molecule) released
- More monocyte and leukocyte bind and adhere, eat more LDLP
- As more foam cell built up, fatty streak (blood can clot on it)
- Platelet gather at damaged endothelium and release platelet-derived groeth factor
- Encourogage smooth muscle ( at tunica media) growth – migrate to tunica intima
- Secrete collagen& ECM that cause formation wall around fatty streak and prevent blood clot
- These extracellular wall = fibrous cap
- Fibrous cap + fatty streak = ?
- Ca deposited into plaque create crystal (normally deposited by LDL, removed by HDL)
- But plaque stop removal of ca by HDL
- These cause artery to stiffen
- Time to time, fibrous cap crack , exposed downward stuff
- Blood clot form on partially occluded artery, even less blood flow
Complications
1. Calcifications
2. Rupture/ fissure/ ulcer
3. Thrombosis
4. Atheroembolism : rupture plaque deposit atherosclerotic debris into blood , produce microemboli
5. Haemorrhage into plaque
6. Anuerysmal Dilatation: atrophy of underlying media with loss elastic tissue cause weakness and may rupture
7. Renal arteries --> kidney think blood pressure low, activated RAAS, so increase blood volume cause HTN
Prevention
- maintain normal blood pressure
- Dont smoke
- Avoid sugary and fatty food
Diagnosis
1. Blockage
2. Weaken pulse
3. Stethoscope: bruits ‘whoosh whoosh’
4. Imaging – angiogram : narrowing
Treat
1. Lifestyle change : dont smoke, good diet and exercise
2. Medicine:
- Cholesterol medication : statin
- Antiplatelet medication: Aspirin
- Blood pressure medication : Beta blocker, diuretics, ACE inhibitors
3. Surgery
- Angio[plasty and stent ( balloon)
- Endarterectomy ( remove fatty streak)
- Bypass
Aneruysm
Definition: A localised abnormal dilatation of blood vessel or the heart (especially in abdominal aorta )
- Thoracic : 40%
- Abdominal : 60%
- Aorta
Types
1. Normal
2. True aneurysm ( fusiform) : symmetrical
3. True Aneurysm (saccular-berry ): assymmetrical (one side high pressure or weaker)
4. False Aneurysm (Pseudoaneurysm): Defect in arterial wall, hole
Cause
1) Atheroscleorosis
2) Hypertension
3) Trauma
4) Congenital defect
o Berry aneurysm typically in circle of Wills)
o Marfan syndrome ( intrinsic quality of vascular wall connective tissue is poor)
Weaken wall: because elastic propeties compromised in fibrillin
5) Tertiary syphillis (syphillitic Aneurysm)
Pathogenesis
1. When ? when structure of connective tissue within vascular wall is compromised
2. Weakness in vessel wall
3. Laplace wall (positive feedback): High Diameter – High pressure
3. Thoracic Aneurysm
o Pulls on Aortic valve
o Blood flows back into ventricle cause aortic insufficiency
o Left recurrent laryngeal nerve strectched by aneurysm
o High pitch cough sound
4. Syphillitic Aneurysm
1. Caused by T.Pallidum
2. Syphillis cause inflammation of vasa vasorum in tunica adventitia --> ENDARTERITIS OBLITERANS
3. Cause thick wall due to inflammation (infiltrate)
4. Cause narrowing of lumen
5. No blood flow
6. Atrophy
7. What to see: Fibrosis, scarring at wall
5. Mycotic Aneurysm
1. Common in cerebaral artery
2. Cause: Infective Endocarditis
3. Bacteria: Bacterioides fragillis, pseudomonas, Salmonella
4. Fungi: Aspergillus, Candida, Mucocytic
5. Embolic bacteria and stuck
6. At intrecranial arteries, visceral arteries, arteries at leg and arm
7. Cause weaken vessel
8. Aneurysm
6. Berry Aneurysm
1. Circle of Wills
2. May be silent for many years
3. Sub Archnoids Haemorrhage
Diagnosis
1. Ultrasound
2. CT Scan
3. MRI
Treat :
1. Surgery
Complications:
1. Rupture
2. Occlusion of branch- due to blood clot
3. Embolism from atheroma
4. Ischaemia
Aortic Dissection
- Blood tunnel between tunica intima and tunica media
- separate 2 layer, create false lumen
*may or may not a/w dilatation
*Mostly because of hypertension, connective tisse disorder, aneurysm
*may lead to cardiac temponae and shock
Cause
1. Chronic Hypertension
o stress, increase blood volume, contraction –narrowing)
2. Weaken aortic wall
o Marfan’s syndrome,
o Ehler’s-Danlos Syndrome
o Decrease blood flow in vasa vasorum
3. Aneurysm < --> aortic disection
Types
1. Type A (Proximal) – ascending aorta
- deBakey I : extensive dissection
- deBakey II : isolation
2. Type B (distal ) – Descending
- deBakey IIIa : isolation
- DeBakey IIIb: extensive
Pathogenesis
1. Tear in tunica intima
2. Blood flow, out into tunica media
3. Blood pool form- false lumen
Complications
1. Blood backs up into pericardial space-> pericardial tamponae
2. Rupture (through tunica media, externa) bleeds into mediastanum
3. May come back into true lumen (Another hole in tunica media)
4. May continue between tunica media and intima
- Till another arteries that branched off aorta: renal artery and subclavian artery
- Compressed by false llumen
- Low blood flow to kidney and arms
Symptoms
1. Sharp chest pain
2. Weak pulse in downstream artery
3. Difference in BP btw left and right arm
4. Hypotension
5. Shock (if rupture)
Test
1. CXR: widen aorta
2. Transesophageall Echocardiogram: true and false lumen at aorta
3. CT angiography
4. Magnetic Resonance Angiiograph
Treat
1. Surgery: remocal of dissected aorta
2. Stent to proped open
3. Blood pressure medications: Beta Blocker
Vasculitis
Vasculitis: Inflammatin of vessel Wall
Pathogenesis
4. Immmunologic
5. Endothelium damaged
6. Blood clot restrict flow
7. Fibrin thickens wall
Symptoms
1. Fever
2. Weight loss
3. fatigue
Types
Large Vessel
1. Giant Cell Arteritis (>50)= >>>ESR
2. Takayasu Arteritis (women <40)= >>> ESR
Medium Vessel (muscular arteries -> organs)
1. Kawasaki Disease: Coronary arteries -> heart
2. Polyarteritis Nodosa (PAN)
a. Immune cell --> Endothelium (confused for hepatitis B)
b. Transmural : All layer (intima, media, adventitia) die
c. Healing, fibrinoid necrosis
d. Prone to aneurysm
e. ** Angiogram: string of beads
Small Vessel (arteriole, cappilary, venules )
1. Wegener’s Granulomatosis / Granulomatosis with polyangitis (GPA)
- B cell produce cANCA (cytoplasmic anti-neutrophilic cytoplasmic antibodies – mainly igG)
- cANCA bind to neutrophil
- cause neutrophil release O2 free radicle, then damage nearby endothelial cell, cause vasculitis
- Biopsy : Granuloma
Nasopharynx: sinusitis-pain, bloody mucus from ulcer, saddle nose deformity
Lung: Difficult breathing, ulcer cause bloody cough
Kidney: Restrict blood to glomeruli, low urind production, high blood pressure
2. Microscopic polyangitis
- Different from GPA
a) Does not affect nasopahrynx
b) No granulomas
c) pANCA (perinuclear)- react with myeloperoxidase
3. Churg-Strauss Syndrome- pANCA
- Sinusitis, lund, kidney damage
- High eosinophils
- Symptoms like asthma and allergy
- Granulomatous seen
4. Henoch-Schonlein Purpura (HSP) – no ANCA
- High IgA (from mucosal)
- Directly target endothelial cell
- Skin discolouration (purpura)
- GI tract : Can cause abdominal pain
- Kidney: Hematuria, IgA nephropathy
- Treat : steroids
Treatment:
Corticosteroids + cyclophosphamide
Raynaud’s Phenomenon
- Decreased blood flow to fingers and toes, especially exposed to cold
- Vasoconstriction of digital arteires, precappilary arteries and cutaneous arteriovenous shunt
- Numb, colour change (white -> blie-> red)
Thrombophlebitis
Definition: Inflammation of vein caused by blood clot
Types
1. Deep Vein Thrombosis
- Occurs when thrombus (blood clot) form in one of large vein, usually lower limbs, lead to partially or
completely blocked circulation
- Cause: use of IV line/catheter
- Symptom: Pain, swelll, tender, redness, skin warm
- Exams: Homan’s sign, Mosses sign
- Test: Doppler ultrasound, duplex ultrasound, venography, D dimers
- Treatment: Anticoagulant (warfarin, heparin), Throbolytic Therapy, support stocking
- Complication: Pulmonary embolism, post thrombotic syndrome (PTS), stasis & ulcer
2. Superficial Thrombophlebitis
o Inflammation of vein due to blood clot in vein below skin surface
o Cause: Injury to vein
o Symptom: redness in skin, tender along vein
o Exam: Doppler ultrasound , Duplex ultrasound , blood cultures BP, pulse
o Treatment: support stocking, limb elevation, warm compress, catheter/IV line removal, NSAID
o Complication: cellulitis, gangrene, deep vein thrombosis, septic shock
Factors
1. Stasis of blood-> thrombus formation (platelet & clotting factor adhere and activate clotting cascade)
• Immobility
• Cardiac failure
• Circulatory shock
• Hypotension
2. Damage to blood vessels
• Trauma
• Surgery
3. Hypercoagulability
• Pregnancy
• Malignancy
• Oral contraception
• Coagulation disorders
Pathogenesis
1. Static blood flow
2. Blood clots
3. Composed of fibrin, red cell and platelets
Cause
1. Pancreatic cancer: injury to vein
2. DVT: use IV
3. Factor V Leiden: chemical irritation of the area
4. Thromboangitis obliterans: Pregnancy
Varicose Vein
Definition:
- permanent abnormal dilatation of veins
- due to pooling of blood at lower extremities
- increased pressure towards wall
- loss support of blood vessel
Cause
1. Congenital defective valve
2. Raised intraabdominal pressure
3. Pregnancy
4. Ascites
5. Obesity
6. Constipation
7. Thrombosis of leg vein
8. Spend long time standing (traffic police)
Symptoms
1. Pain: ache, sharp, tingling
2. Cramp, heavy, tires
3. Restless leg at night
4. Itch
5. Hyperpigmentation
6. Ulceration, blood clot
Test :
1. Hand-held Doppler
2. Duplex ultrasound
Treatment:
1. Compression stocking,
2. Elevation
3. Surgery
4. Sclerotherapy
Complications (post thrombotic symptoms)
1. Abnormal vein
2. Abnormal skin: Edema, eczema, corona phlebectatica, lipodermatosclerosis, ulcer
ANGINA PECTORIS
- ST segment depression
Definition
- Paroxysmal
- Recurrent attack of substernal chest discomfort (last few second) usually during exercise
- NO death, reversible injury to cardiomyocytes
Types
1. Stable Angina <20 mins
- central chest pain
- Plaque accumulation
- During physical activity
- ST segment depresssion
2. Unstable ( cresendo) angina
- Plaque dislodge, rupture , thrombossis
- Subendocardium ischaemia
- Chest discomfort not only during exercise but at rest too
- ST segment depression or elevaation
3. Prinzmetal variant Angina (vasospastic)
- Rare, happen any time migt be at rest
- Transmural (all layer)
- Cause by coronary artery spasm (due to ischaemia)
- Smooth muscle contract (vasoconstrictor-Thromboxane A2)
- ST segment depression or elevation
Treat:
1. GTN (nitoglycerin)-vasodilator , put under tongue few minutes , at most 3
2. CCB
3. Beta blocker
4. Bypass surgery
5. Surgery: Baloon
Management
Early Treatment
1. Nitroglycerin (up to 3 doses) – vasodilator but will cause hypotension and headache
2. Aspirin 3oomg chew and swallow
3. GTN sublingually
4. Pain relief with morphine IV- reduce pain and anxiety, relax bronchioe to enhance oxygen
5. Contact doctor , nearest hospital
6. Confirm diagnosis with ECG
Late treatment
7. Analgesic: Morphine – reduce pain and anxiety, relax bronchioe to enhance oxygen
8. ACE inhibitors – prevent formation of angiotensin II, limit area of infarction
9. Thrombolytic therapy : dissolve clot in coronary artery allow blood to flow
10. Nitroglycerin (up to 3 doses)- vasodilator but will cause headache and hypotension
11. Anticoagulant : prevent thrombus formation
Severe : consider Surgery
1.
Medical
M: Morphine- reduce pain and anxiety, relax bronchioles to enhance oxygenation
O: Oxygen
N: nitrates
A: aspirin
ECG
- Depolarisation wave : positive charge
- P wave: Depolarisation of atrium
- QRS complex: Depolarisation of ventricle
- T waves: Repolarisation ventricle
- U wave : repolarisation of purkinje fibre
12 Leads
- 3 Bipolar (standard ) limb leads : I, II, III
- 3 Unipolar limb leads: aVR, aVL, aVF
- chest / Precordial electrode (V!-V6)
Sequence of Depolarizations
Ventri.
Depol.
Ventricular
Purkinje
Repolarization
Bundle
branches
AV
bundle
AV
Nodal
Atrial
Uses of ECG
1) Detect rate and rhythm
1 3
L.V.
5) Diagnose IHD
ST segment
changes
Infarction
Ischaemia
Disturbances in ECG
Arrythymia
Application: detect DM – function of autonomic nerve
Cardiac Arrhthmias
Cause
1) MI
2) Hyperthyroidism – increase HR
3) Electrolyte & acid- base disturbance (change K & Na)
4) Drugs (catecholamines-noradrnealine, dopamine iincrease HR)
Bradyarrhythmias (<50/min)
Cause
1. Sinus Bradycardia : sleep and atheles, sick sinus syndrome
2. Atrioventricular block (defect in conduction impulse from atria to ventricle)
Types
1. First degree heart block = >0.2s
2. Second Degree Heart Block : atria didnt reach ventricles - dropped beats – no QRS
o Mobitz Type 1 (Wenckebah’s AV Block) : PR interval increase
o Mobitz Type 2: not all atrial impulse conducted to ventricle (2:1 ) (3:1) heart block
3. Third degree heart block: atria dont pass to ventricle (independant pacemaker take over)
- P Waves regular, QRS regular but much slower
- Complete atrio-ventricular dissociation (loss of synchrony)
Tachyarrhythmias : >100/min
Cause
1. Accelerated Automaticity (sinus tachycardia) – reduce threshold, increase prepotential slope (increase sympathetic
noradrenergc-> closure K+ channel)
2. Triggered activity : after depolarisations
3. Re-entry / circus movement
Supraventricular Tachychardia (QRS normal)
1. Sinus Trachyarrythmias ((160-190/min)
2. Atrial Flutter (240-360/min) : AV node block impulse- late (ventricular rate x3 slower)(3:1 heart block) , absence
normal P waves, f waves(saw tooth appearnce)
3. Atrial Fibrillation (>360/min) (most common) : multiple ectopic foci, AV node mostly didnt pass impulse, ventricular
QRS slow to rapid (absence P waves, irregular interval QRS)
3. Ventricullar Fibrillation: multiple weak ectopic site of ventricle, pump little (irrgular from no identify pqrs) the flat
CARDIAC CYCLE
4. Events that occur from the beginning of one heartbeat to beginning of the next
5. Heart Rate = 75 beats/min
6. Duration of each cardiac cycle : 60 sec/75 = 0.8sec
7. When heart rate increase, duraion decrease
8. Heart rate too high Cardiac output drop because cannot filled with blood
Electrical Eveet (ECG)
Haemodynamic (pressure changes)
Mechanical event (systole and Diastole)
1. Atrial Systole :
- Atrial contraction, Atrial pressure increase , force blood into ventricle
- Ventricle pressure increase bit
- a wave (due to atrial contraction, backpressure go back to jugular vein )
2. Isovolumetric Ventricular Contraction- ventricular systole
- Ventricle pressure increase rapidly
- Ventricle Pressure > atrial pressure, AV valve close – S1
3. Ventricular Ejection
- When ventricle pressure> aortuc pressure , aortic valve (semilunar) open
- Atrial pressure rise because blood flow into atrium
4. Isovolumetric Ventricular Relaxation
- Ventricle pressure falls, aortic valve close- S2
- Ventricle volume constant becuase all valve closed
- Atrial pressure increase bit because of venous return
5. Rapid Filling
- Ventricle pressure fall , Atrial Pressure> ventricle pressure , AV valve open
- Ventricle filling start , Atrial Pressure fall
- Ventricle filling normally silent, if S3 heard --> tensing of chordae tendinae and AV ring
6. Slow filling
- Ventricle continue to be filled
- Ventricle pressure increase
- Reduce pressure gradient, so slow
Cardiac Output
9. Amount of blood pumped per minute
CO = HR x SV
10. Average HR : 70, Average SV:80
11. Average CO: 5.6 L/min
*Transplant Heart rate usually higher, around 100
Heart Rate
How to increase HR/co
1. Sympathetic Activation- NE --> B2&B1 (while parasym(vagus) : Ach -->M2)
2. Parasympathetic Inhibition (vagus nerve)
3. Low K +ion
4. Circulating catecholamine
5. Xanthine (caffeine, theophylline )
6. Thyroid hormone
7. Age
8. Exercise : epinephrine increase HR
9. Temperature (Fever)
10. pregnancy
*Definition
- Chronotrophy : Heart raet ( parasympathetic & symp effect almost same)
- Inotrophy : force of contraction almost same
- Dromotrophy : conduction speed at AV node
- Lusitrophy : how quiclkheart muscle contract
Stroke Volume
12. Definition: Amount of blood pumped by each ventricle per contraction
13. EDV-ESV= 120-40 = 80
How to increase SV ? Determined by ?
1. Preload (venous return ) (end diastolic pressure ) – Frank-Starling Law of Heart : increase
14. Increase in hypervolemia, regurgitation of cardiac values, aortic insufficiency
2. Afterload (aortic pressure during systole) : decrease
15. Resistance to left ventricle
16. Increase in hypertension, vasoconstriction, aortic stenosis
3. Contractability
4. Regular Exercise
PRESSURE-VOLUME LOOP
Problems....
1. Systolic dysfunction (Inotrophy decrease )- ventricular failure
o increase end –systolic volume
o bit increae end-diastolic volume because there some ESV left
o stroke volume decrease
o Shift to right
2. Diastolic Dysfunction ( compliance decrease) – vetricular hypertrophy
o more muscle, heart ventrcle area decrease, blood filled decrease
o End diastolic volume decrease
o Stroke volume decrease
o ventricular presssure at EDV increase
① explain why SA node is the normal pacemaker of the heart: fastest rate of impulse generation
② explain why there is rapid cell to cell conduction between the myocardial cells
Define excitation contraction coupling and outline the process of excitation –contraction coupling in cardiac muscle.
- Excitation-Contraction Coupling: spread of AP along muscle membrane
Summary
1. Electrical excitation (AP) cause musscle contraction (excitation Contraction coupling )
2. Spread impulse in atria, electrical excitation of atria, contraction , systole then diastole
3. Spread impulse in ventricle, electrical excitation of ventricle , contraction, sytole then diastole
4. One heart beat
7. Renin : vasoconstriction
8. Aldosterone: increase tubular Na rebsorption + H2O, affect blood dvolume
9. Cortisol (stress hormone) : in fat increase sympathetic synthesis of blood vessel (vascular tone more constricted)
Chemoreceptor reflex
1. Peripheral Chemoreceptors – carotid and aortic bodies
a. Respond to Decrease PO2 and increae PCo2 or H+
2. Central Chemoreceptors
b. Respond: increase H +
Effect: hyperventilation, sympathetic vasoconstriciton, mainly in skeletal muscle
# Hormonal
1) Epinephrne: increase HR & vasoconstriction
2) ADH: increase water retention and vasoconstriction
3) Cortisol: increase sensitivity to epinephrine and norepineprine
4) Aldosterone : increase Na H2) retention
5) Thyroid Hormone: increase HR
Antihypertensive drug
Alpha 1 Blocker
SHOCK
CARDIOGENIC SHOCK
Causes
1) Cardiomyopathy
2) MI
3) Septal Defects
4) Aortic stenosis
5) Arrythmia : bradyarryhtmias
6) Obstructive disorder :PE, tension penumothorax, pericardial tamponaede , constrictive pericarditis
Risk
1) Age > 65
2) Femake
3) DM
4) HTN
Symptoms
1) COLD SHOCK: low blood flow, low heat, cold and clammy
2) Acute pulmonary oedema
3) Oliguria
Classic Criteria
4) Systemic Hypotension: Sysytolic arterial pressure <90mmHg
5) Persistant Hypotension: at least 30 mins
6) Reduce systolic cardiac function
7) Tissue hypoperfusion: oliguria
8) Increased left ventricular filling
Pathophysiology& Complication
1) Stenosis, decrease in aortic pressure, coronary hypoperfusion
2) Decrease Left ventricle End-Diastolic Pressure (LVEDP)
3) Decrease CO
4) Pericardial Temponade
Critical stenosis + Hypotension + LVEDP = MI
Heart ischamia due to heart attack, muscle die, Hypoperfusion -> LV dysfunction (CO decrease) -> systemic lactic
acidosis -> impairment myocardium -> worsen hypotension
Obstruction (pericardial sac – fluid), constrict heart muscle to expand, decrease stroke volume, low bp
Diagnosis
1) Angiography
2) Hemodynamics (PA Catheter): decrease CO,
3) Echocardiography
4) PE (stethoscope) : increase JVP (right heart ) + s3, Rale- palpitation
5) Microscopy: Pale area – nut-make liver (bcos of congestion )
6) Urine test: Oliguria
7) Acute pulmonary oedema
Hypovolemic Shock
Cause
1) Rapid fluid loss( burns, gatroenteritis) – lead to organ failure
2) Rapid blood loss
Symptoms
1) Dull pupils dilated
2) Breathing shallow
3) Skin pale to bluish
4) Pulse weak
5) Nausea and vomit
6) Thirst
7) COLD SHOCK ( low blood flow, low heat )
Pathogenesis
1) Low Blood volume
2) Low O2
3) Low left over
4) Low MvO2 (mmixed veous Oxygen saturarion)
Stages
1) Initial (non-progresive) : reduction in intravascular volume (15%)
2) Progresssive: 30-40% fluid loss, low BP, tachychrdia, vital organ like kidney, brai, liver, lungs
3) Refractory : Irreversible, lead to cell necrosis&MODS (>40%- >20000ml)
Compensatory Mechanism
1) Low Cardiac output
2) Hamatology : cathecholamine (epinephrine, norepinephrine)
3) Neuroendocrine: ADH
4) Renal : Angiotensin II
5) Vasoconstriction, increase resistance to blood flow
6) Increase blood pressure
7) Increase CO
8) Increase HR
Summary
Shock: Failure in tissue perfusion
Hypovolemic Shock: dehydraiton/haemorrhage reduce blood volume
Cardiogenic Shock: Injury/Onstruction prevent heart from pumping efficiently
Distributive Shock: allergic reaction/damage to nervous sytem cause blood to vasodilate and become leaky -> reduce resistance
& reduce BP
SHOCK Treatment
1) Fluid replacemnt
2) Medications- to increase heart cinreactility , vasoconstriction, increase retainfluid
3) Supplemental O2
CARDIOVASCULAR RISK FACTOR AND PREVENTION
Types of CVS
1. Coronary Heart Disease (CHD)
2. Hypertension
3. Cerebrovascular disease
4. Rheumatoid heart disease
20)
5. Peripheral Artery Disease
6. Congenital Heart Disease
21) Eg :
Incidence of Cardiovascular System Malformation
Ventricular septal defect
Atrial Septal Defect
Pulmonary stenosis
Complete Transpositions
Truncus Arteriosus
22) Cause
Maternal Rubella (German Measles)
Maternal Alcoho abuse- septal defect
Genetic abnormalities- down synderome, septal defect, motral and tricuspid defects
23) Prevention
Genetic counselling
Mumps rubella and measles (MMR) vaccine