You are on page 1of 26

Arteriosclerosis: Artery thicker, harder, less elastic

Atherosclerosis: Hardening from plaque (athromatous plaque in endometrium) in large artery


Arteriolosclerosis: hardeining of arteriole (caused by HTN, DM)

Arteriosclerosis:

Anotther Arteriosclerosis : Monckeberg (medial Calcific) sclerosis


- Formation ca crytsal at muscle layer cause hardening
- But, diamter not affected so blood flow not affected
- Often detecte d incidentally ( mammogram)

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

2. Hypreplastic Arteriolosclerosis (malignant hypertension


- Smooth muscle growth – stronger but make lumen smaller
- Microscope : like onion
- Can then cause ischaemia
- Typically Affect arteriole wall in kidney
- Renal ischaemia
- ** diff: kidney looks like insect bite everywhere ( high blood pressure cause bv rupture cause haemorrhage)

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

Artheroslerosis plaque: will cause ??


Downstream ischemic injury ( descd order)
1. Aorta (abdomen> thoracic)
2. Coronary arteries - angina +MI
3. Popliteal arteries –peripheral ischaemia (gangrene/leg cramp)
4. Internal carotid & middle cerebral – stroke + cerebral atrophy
5. Superior Messenteric arteries –small intestine
6. Renal arteries
*Weakened wall – aneurysm (abdominal Aortic)

**Artherosclerosis plaque vs fatty streak


- Fatty streak: lipid-filled foam cell

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)

Risk (same as Artherosclerosis)


1. Male
2. Smoke
3. >60
4. Hypertension

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

1. First part of aorta


- Thick wall, suppiled by vasa vasorum
- Hypertension, hyaline arteriolosclerosis
- Narrow lumen , ischaemia, tunica media smooth muscle atrophy, weaken aorta wall

2. Abdominal Aortic Aneurysm


o Plaque built up in tunica intima, oxygen cant pass

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

Sign & Symptoms


Abdominal Aortic Aneurysm
1. Severe Left Frank Pain : abdomen, chest, lower back, grain
2. Pulsating mass with hearbeat
3. Hypotension

Thoracic Aortic Aneurysm Sign


1. Usually no symptoms
2. Severe back and abdominal pain

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

Ischaemic Heart Disease (IHD)


Risk
1. Age
2. Sex: men, women protected during reproductive year
3. Postmenopause: low oestrogen level
4. Hypertension
5. Diabets melllitus
6. Genetic hypercholesterolemia
7. Hyperlipoproteinemia
Pathogenesis
1. plaque accumulation (angina)
2. Plaque aggrgate cause mural thrombosis /emboli (unstable angina/MI/sudden death)
3. Or heal -> severe coronary obstruction (chronic IHD)
Prevention
1. Dont smoke,
2. Diet
3. Treat obesity
4. Exercise
5. Control blood glucose
Treat
1. Use cholesterol lowering agent
2. Thrombolysis
3. Angioplasty
4. Endovascular stent
5. Coronary artery bypass graft surgery

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

MYOCARDIAL INFARCTION (MI)


Definition
- Death of cardiac muscle
- Due to prolonged severe ischameia, decreased oxygenation
- Decreased blood floe
- Artherosclerosis plaque
Risk
1. Male
2. Postmenopause
3. Age
4. Obesity
5. Hypertension
6. Arrythmia
7. Smoking
8. Hyperlipidemia
9. Diabetes Mellitus
10. Type A personality
11. Family history
12. Diet
Etiology
1. CAD
2. Coronary spasm
3. Coronary artery occlusion by embolism or thrombus
4. Haemorrghage or shock that decrease perfusion
Symptoms :
1. Chest pain : tightness, pressure, squeezing (elephant)- substernal
o Radiate to left arm, lower jaw, neck, epigastrium
o Greater than 30 mins
o Especially menaupause lady, levine’s Sign
o Cant relieved by GTN
2. Palpitations
3. SOB- Dyspnea
4. Arrthymias
5. Nause and vomitting
6. Headcahe
7. Diaphoresis
8. S3 and dysrythmnas
*Symptoms induced by catecholamine from sympathetic nervous system
* Damage to heart cause less blood flow to left ventricle, cause Left ventricular failure and then, pulmonary edema
Pathogenesis
1. Vasospasm (coronary artheroscleorissis)-> Accumulation of plaque and platelet
2. Occlusive thrombus due to transmural acute Myocardial Infarction
3. Coronary blood flow decreased due to ischaemia -> MI
4. Anaerobic myocardial metabolism for few hours
5. Myocardial death
6. Depreseed cardiac function and then trigger autonomic nerbois system response
7. Further imbalance of myocardial O2 demand and supply
Type
1. Stemi
o Whole
o Coronary thrombus occlude artery
2. Non- stemi
o Inner third
o ST segment depession
o 1/3 or 1.2 left ventricular walll
Test Procedure
1. Patient with chest pain (Acute coronary syndrome)
2. ECG
3. IF got ST elevation , confirm MI- sometimes tall positive T (hyperacute)
4. If no ST elevation, do blood test - cardiac markers
5. Cardiac marker +ve : MI
6. Cardiac marker –ve : unstable angina
7. Now, lets see types of MI
8. Stemi: ST elevation
9. Non-stemi: no ST elevation
Lab Findings :
1. ECG- ST segment elevated, T inversion , presence Q wave
2. Myocardial enzyme (elevated)
o CKMB (Creatine Kinase)
o Specific, but por marker
o LDH
o Troponin I (elevated long time) and T
3. CBC: elevated WBC
4. Test after the acute stage - Exercise tolerance test, thallium scans, cardiac catheterization
Diagnosis:
1. ECG
2. Cardiac marker (3-6 hours later)
o Troponin T and I
o Myoglobin
3. CKMB

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

0-24 hours: arrythmias, cardiogenic shock


1-3 days: pericarditis (inflammation)
3-14 days : myocardial rupture (granulation,macrophage)
2 weeks: heart failure (muscle change shape)

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

There is no wave A wave due to atrial repolarization is


due to depolarization submerged in the QRS complex since the
of SA node ventricular electrical activity is greater than
NW20 14 b
that of the atria

Factors influence ECG Pattern


1. Orientation of Electrode with direction of waves of depolarisationand repolarisation
2. Magnitude of cardiac electrical Activity
3. Transmission Factor (amount and tissue btw heart and body surface)
- Pericardial
- Pleural
- Muscle and bones of chest wall (ribs)
- Skin resistance

Uses of ECG
1) Detect rate and rhythm

2) Diagnose cardiac arrthymias


3) Detect conduction abnormalities (Heart block, accelerated conduction)
4) Diagnose ventricular hypertrophy
ECG helps in the diagnosis of structural changes such as ventricular hypertrophy
Greater muscle mass L.V.
Greater electrical
activity
R.V.

1 3

Negative because depolarization R.V. L.V. Positive because depolarization (arrow 3 )


(arrow 3 ) moving away from this moving towards this electrode is larger
electrode is larger than the one moving than the one moving away (arrow 1)
towards it (arrow 1) Normal)

L.V.

Left Ventricular Hypertrophy – the waves


become taller (R) or deeper (S)
38

5) Diagnose IHD
ST segment
changes

Infarction

Ischaemia

T WAVE FLATTENS OR INVERTS


41

6) Diagnose Acute myocardial infarction


7) Detect electrolyte disturbances (Hyperkalaemia and hypokalemia)

Hexaxial Refrence system


1) To localise part of heart affected
2) To determine wether axis of the ventricle vector i within normal limits / deviated
o Ventricular wall hypertrophy
o Conduction block

Disturbances in ECG
Arrythymia
Application: detect DM – function of autonomic nerve

Sinus Arryhthmia (respiratory Sinus Arrhymia)


MOA
1) Inspiration stimulate lung stretch receptor
2) Vagal nerve (parasympathetic) inhibition
3) Less inhibition SA node (sympathetic)
4) Increase HR

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)

4. Av nodal reentrant tachycardia(150-250) (Woff-Parkinson-white(WPW) synderome):

Ventricular Tachyarrhthmias (QRS broad, bizarre)


1. Ventricular extrasystole ((Ventri. Premature Contractions, VPCs, Ventri. ectopic beats)
2. Ventricular Tachycardia (V-Tach): scarr from heart attack , ( wide and bizarre QRS, no P waves )
- Torse de pounts : QRS varies

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

Arterial Pulse Wave

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

 Cardiac Index : heart performance in relation to body size


17. Increase till age 27 to 30 then decreae CI = SV x HR/BSA
Venous Return Determined By?
1 Blood Volume
2 Venous tone
- Gravity : stand decrease venous return, decrease ventricular preload , decrease CO, decrease SV
3 Respiratory Pump
- Inspiration, diaphragm descent, decrease thoracic pressure, abdominal pressure increase , push blood into heart via
vena cava
4 Muscle Pump- skeletal muscle activity : alternate contraction and relaxation cause compress and decompress, propels
blood forward,one way valve, rhythmic ocntraction and relaxation

Frank Starling Law :


18. Ability heart to change its force of contraction therefore stroke volume in respond to changes in venous return
19. Otto Frank : contraction increased when streched
20. Ernest Starling : increase end diastoic volume (preload) will increase SV provided other factors constant
21. Increase vol stretch ventricle wall, cause cardiac muscle contract more forcefully hence decrease Afterload
Factors affeecting Preload & end Diastolc Volume
1. Ventricular Filling Volume (venous return)
- Gravity
- Respiratory or thoracic pump
- Skeletal muscle pup

2. Ventricular filling time


3. Ventricular filling capacity (ventricular compliance )
22. Pericardial limitation : pericardial effusion, cardiac temponade
23. Change thoracic pressure (breathing)
24. Decreased myocardial compliance (myocardial, hypertrophy, infarction)
Blood Pressure
BP= CO x TPR

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

Ejection Fraction (EF)


25. Fraction of blood ejected from ventricle with each contraction
26. Calculated by Echocardiography
27. EF= SV / EDV

SPREAD AND EXCITATION


Cardiac Excitation
4 properties of cardiac muscle
1. Conductivity : conduct impulse (chronotropic effect)
2. Excitability: respond stimulus
3. Contractility :( inotropic effect)
4. ??

2 Functioning populations of caridac cell


1. Conducting Tissue (modifird non-contractile cardiac cell) = generate nerve impulae
2. Working Myocardial cell : contract and cause pumping

sinus rhythm : hierarrchy


1. SA nose (pacemaker) : fastest rate of impulse generation
2. AV nose
3. Atrioventricular Branches ( Bundle Of His)
4. Puekinje Fibre The origin and the sequence of
spread of cardiac excitation

The origin and spread


Apex of cardiac excitation
Ape
x
SA Node
AV nodal delay 0.1 sec 1 RA LA
Atrial
Atrial Muscle
Muscle AV Node
2 Cardiac
6 AV Bundle fibrous
skeleton
Right Left Non-conducting
3 4 4a
RV Bundle Branch Bundle Branch
6 LV
4 4 Purkinje Fiber Purkinje Fiber
5
5
Ventricular Muscle Ventricular Muscle
12 = Cell to cell conduction 11

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

28. Pass left to right: activator of interventricular septum


29. Left Bundle Branch thicker, hence reach midseptum, left then right
③ state the significance of AV Nodal dely.

30. ensure atrial systole is followed by ventricular systole


④ state the significance of AV bundle

31. electrical link between the atria to ventricle


32. Fibrous skeleton of heart between the atria and ventricles)
• identify the 4 numerical phases of cardiac action potentials
1. Firing Level (threshold) : unstable AP
2. Spontaneous Depolarisation : Pacemaler potential (-70 to -50mV)
3. Rapid repolarisation
4. Late repolarisation
5. Resting Membrane Potential (RMP) = -70mV
Permeability -> Conductance -> Flux -> Current
• describe the ionic basis of action potentials of
– SA node and AV node
1. `Prepotential initial : K+ (P) , efflux, (I) decline; Na(P),influx(I) increase
2. Prepotential Final : Ca2+ channel open transcient , (P), influx, (I) increase
3. Depolarisation AP: Ca2+channel open long lasting , (P) , influx (I) increase
4. Repoarisation AP: K+channel open, (P), efflux (I) increase
*Sympathetic Stimulation: Prepotential steeper, increase HR
*Parasympathetic : prepotential less, decreasee HR
Action Potentials of Atrial and Ventricular Myocytes: Ionic basis

Phase 1. initial rapid repolarization;


rapid decrease in PNa+ and incr. PK+
Ionic basis of
Depolarization phase of action potential: due to activation è incr. K+ efflux è outward K+
of long-lasting Ca 2 + channels è increased Pca 2 + è Ca
SA node 2 + influx è I Ca2 +L
Phase 0 . INa+ IK+ current
Action Potential Phase 2 . Plateau phase;
Depolarization;
incr. PNa+ IK . ICa2+
+ [incr. P K+ è incr. K+ efflux
Repolarization phase of è outward K+ current ] vs.
action potential: due to è incr. Na+ influx
[incr. PCa2+ è incr. Ca2+
activation of K+ channels
è Inward Na+ current . ICa2+
è increase in PK+ influxè inward Ca2+ current]
èincrease in K+ efflux è
INa+
I K+ Phase 3 , late rapid
IK+ repolarization; incr. PK+
Final phase of prepotential: due to activation of è incr. K+ efflux è
transiently opening Ca 2 + channels è 4 outward K+ current
increase in Pca 2 + èCa 2 + influx è I Ca2 +T Phase 4 . Baseline Ca2+
(RMP): stable(until
Initial phase of prepotential: due to (1) decline in PK+ è depolarized by arriving
declines in K+ efflux and K+ current (IK+); (2 ) increase in impulse )
PNa+ è increase in Na+ influx, the 'funny' ( I (f )) current K+
(funny because Na channels are activated during Myocardial cell
hyperpolarization). 20

– Atrial and ventricular myocytes 25

1. Phase 0 (Depolarisation) – Na+ (P), influx, (I) increase


2. Phase 1 (Initial rapid repolarisation) : Na(P) rapid decrease, K(P),efflux,outward (I) increase
3. Phase 2 (playeu) – K (P),efflux , outward (I) increase, Ca influx increase
4. Phase 3 ( Late Rapid Repolarisation) – K (P) increase,Efflux outward o increae
5. Baseline (RMP)

Define excitation contraction coupling and outline the process of excitation –contraction coupling in cardiac muscle.
- Excitation-Contraction Coupling: spread of AP along muscle membrane

The Sliding myofilaments (contraction)


1. AP spread along sarcolemma and transverse tubules (excitation)
2. Ca Voltage gated channel open , Ca enter from ECF to sarcoplasm
3. Influx of Ca cause opening Ca channel(ryanodine receptor) , Ca release from sarcoplasmic reticulum into sarcoplasm
4. Ca diffuse into myofilaments
5. Trigger sliding of myofilaments
6. Muscle contraction
7. Sytole
8. Release of Ca stimuater Pump in sarcoplasmic reticulum membrane
9. Ca pump back into sarcoplasmic reticulum

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

BLOOD PRESSURE : VARIATION AND HOMEOSTASIS


33. Blood pressure to blood flow and tissue perfusion
34. Factors affecting systolic and diastolic BP
35. Determinants of arterial BP and effect on BP
36. Factors cause variation in arterial BP
37. BP regulating mechanism (neural, hormonal, renal) role and significance in BP homeostasis

Normal systolic pressure: 120mmHg


Normal Diastolic pressure: 70-80mmHg
Mean Arterial Pressure= diastolic pressure + pulse pressure/3 (ssytolic-diastolic)
Blood pressure= Blood flow (C)) x PR

Factors Affecting Arterial Pressure:


1. CO
- Blood volume increases as aortic pressure increase ( provided arterial compliance is constant )
- Complance= vol/ pressure
2. Total Peripheral Resistance
- Higher when arterial lumen is small and total cross sectional area is small
- Cappilary smallest lumen size but largest csa
3. Age
- Age increase, Systolic BP increases ( bcos pressure increase, so Arteriol compliance reduce)
- Diastolic BP not much change
4. Gender
- Before 60, systolic and diastolic pressure: male> female
- After 60, systolic and diastolic pressure: male < female ( low oestrogen, arterial compliance reduce)
- Low oestrogen, higher LDL,lowe HDL , increase risk artherosclerosis
- Less Prostacylcin and thromboxane produced bcos lack of oestrogen, no vasodilation
5. Gravity
- Hydrostatic pressure at bottom highest (P=hpg)
6. Circadian Rhythm
- Blood pressure highest mid-morning, lowest 3am

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)

Regulation of BP (Homeostatic Mechanism)


# Neural :
Baroreceptor Reflex
1) Low CO and Low peripheral vascular resistance
2) Low Arterial Blood Pressure
3) Detected by baroreceptors (btw carotid bodies and carotid sinus)
4) Controlled by medulla (thalamus-sympathetic, hypothalamus-temp, cerebral cortes-behavior)
5) Effect :
- inhibit Parasympathetic nervous system and activate sympathetic nervous system
- HEART: Activate B1 receptor: Increase HR , increase force contraction, CO, then BP
- BLOOD VESSEL: Activate A1 – increase vascular resistance (vasoconstriction),
- Kidney (Adrenal medulla): increase cathecholamine
*Cerebral Cortex
Blushing & Rage
6) Loss sympathetic activity
7) Cutabeous vessel
8) Increase HR, contractility
Fainting (extreme stress)
9) Low cerebral blood flow due to sudden loss of arteroal BP
10) Loss smpathetic tone, low HR

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

# Renal Regulation (RAAS)


1) Blood pressure decrease
2) Detected by baaroceptor
3) Kidney release renin : convert angiotensinogen into angiotensin I
4) Lung release Angiotensin converting enzyme (ACE) : convert angiotensin I into Angiotensin II
5)Stimulate
- Adrenal Gland: Cortex- increase aldosterone(Na+H2O retention), medulla-increase cathecholamine
- Vascular smooth muscle : vasoconstriciton
- CNS: increase ADH(h2O reabsorption) , thirst
- Kidney: Na retention, reduce GFR
1) Arterial pressure <50mmHg : Anuria
2) Arterial pressure < 100mmHg : Oliguria
i. Low BP, low GRF, low urine vol
3) Arterial pressure Normal : 100 mmHg
4) Arterial Pressure > > 100mmHg :
ii. pressure diuresis (increase urine formation)
1. Increase arteriol pressure, increase GFR, more water loss into lumen, blood vol reduce,
arterial BP decrease
iii. Pressure natriuresis (increase urinary Na excretion)
1. Due to increased GFR , large vol bcos water follow Na
Summary :

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

DISTRIBUTIVE SHOCK (SEPTIC SHOCK)


11) Leaky blood vessels
12) Excessive vasodilation (widening of peripheral blood vessel ) due to bacteria infection
Symptoms
1) Deep breathing
2) Fever
3) Burns
4) Warm bounding pulse
5) Edema
6) Purpura, DIC
7) ** waterhouse Fredrischen Syndrome
8) WARM SHOCK: high blood flow, high heat
Clinical Criteria (at least 2 out of 4)
1) Temperature >38 or <36
2) HR >90beats/min
3) Respiratory rate >20 breath.min
4) WBC count > 12000/mm3
Progression
1) Sepsis : Raised WBC
2) Severe sepsis: Infection + end organ dysfunction (hypoperfusion)
3) Septic Shock: severe sepsis+ persistant hypotension -> tissue hypoperfusion
Pathogenesis
9) Endotoxins (Liposaccharide-LPS) from pathogen- bacteria
10) Damage endothelial cell
11) Vasodilators (NO) released
12) Acrivate complement system -> macrophage release histamine
13) Activate macrophage and neutrophil to scerete cytokines, and inflammamtory mediators TNF, IL-1, IL-6
14) Stimulate endothelial cell to release vasodilators like NO, prostaglandins, thromboxane A2
15) Vasodilation and endothelial damage
16) Hypoperfusion and cappilary leak
17) Low BP
18) Decrease perfusion to vital organ
13) Vasodialtion
14) Low Resistance
15) Blood moving too fast to unload O2
16) Leftover O2
17) MvO2 normal or increase

DISTRIBUTIVE SHOCK (ANAPHYLACTIC SHOCK)


- Allergic reaction
- Low BP
Types
1) Urticaria (Hives)
2) Angioedema – difficulty in breathing
3) Hypotension: release inflammatory mediators
4) Bronchospasm- inflammatory mediators
5) Allergy: hives, hay fever, asthma
Cause
1) Penicillin
2) Bee stings
3) Peanuts
4) IV contrast materials
Pathogenesis
1. First eposure B cell make LgE
2. LgE attach to mast cell
3. Expose to antigen
4. Degranulation of mast cell , release allergenic mediators like histamine, leukotrienes, prostaglandin
5. Increase mucus secretion, increase bronchial smooth muscle tone, vasodilation(increase cappilary permeability)
6. Histamine: vasodilation, bronchoconstriction, headache, act on neural cel
7. Leukotriene (asthma response): bronchoconstriction, airway obstruction
8. Histamine: excessive mucus, tear, bronchoconstriction, vasodilation, increae peristalsis intestine, diarrheas, vomit
DISTRIBUTIVE SHOCK ( NEUROGENIC SHOCK)
18) Damaged central nervous system
19) Low bP
Clinical Situation
1) Change in body posture
2) Spinal anesthetia
3) Spinal cord injury , brain stem damage
Pathogenesis
1) Injury to spinal cord
2) Loss vascualr tone ( manage venous return)
3) Vasodilation
4) Low blood pressure & reduce BP
Management
1) Shock position
2) Keep warm and comfortable
3) Turn head to one side if no neck injury

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