AP II midterm (physio)

pulmonary circulation

pump blood from heart to lungs only (right side)

systematic circulation

pump blood from heart to body (left side)

size of the heart

250-350gram

location of the heart

within mediastinum

Base of the heart

in line with 2nd rib

Apex of the heart

in line with 5th intercostal space

Interatrial septum

separate L&R atrium

Interventricular septum

separate L&R ventricle

heart valves’ function

ensure unidirectional blood flow

Atrio-Ventricular (AV) valves contain […]

• Bicuspid valve (left)

• Tricuspid valve (right)

→ prevent backflow into atria

Semilunar valves contain […]

• aortic valve

• pulmonary valve

→ prevent backflow into ventricles

Chordae tendineae’s function

prevent AV valves opening backwards during ventricular contraction

Papillary muscles’ function

prevent AV valves from prolapsing during ventricular contraction

Coronary arteries

carry blood away from the heart

Collateral blood vessels’ function

stimulate angiogenesis (blood vessels formation)

Veins’ function

carry blood toward the heart

Fibrous pericardium

protect the heart

Parietal layer of Serous pericardium

form the outer lining

Pericardial cavity

Reduces friction as the heart beats by allowing it to move smoothly

Visceral layer of Serous pericardium

attach directly to the heart’s surface

Myocardium

contain contractile cells to form pumping function

Endocardium

• release substances to prevent blood clots

• creat blood clots if damaged

AV valves opening

atrial pressure > ventricular pressure
→ blood flows into ventricles.

AV valves closing

ventricular pressure > atrial pressure
→ prevents blood flowing back into the atria

Semilunar valves opening

ventricular pressure > artery pressure
→ blood leaves the ventricles

Semilunar valves closing

artery pressure > ventricular pressure
→ prevents blood flowing back into ventricles

Pericarditis

problem with heart filling
→ can reduce cardiac output

Pericarditis’ symptoms

chest pain, friction pain, cough, fever

Pericarditis’ causes

• viral/ bacterial infection

• idiopathic (occurs on its own)

• myocardial infarction (heart attack)

Pericarditis’ treatment for infections

antibiotics, non-steroidal, anti-inflammatory

Pericarditis’ treatment for cardiac tamponade

drain fluid from cavity via syringe

Myocarditis

problem with heart’s pumping ability (contraction)

Myocarditis’ symptoms

chest pain, heart failure, arrhythmias

Myocarditis’ causes

• viral/ bacterial infections

• autoimmune reaction

Myocarditis’ treatment

antibiotics, positive inotropes, diuretics

Endocarditis

problem with valves
→ blood flow backward, reduce the heart’s efficiency

Endocarditis’ symptoms

leaky valves, heart failure, blood clot on valves’ leaflets

Endocarditis’ causes

infective and non-infective cause

Endocarditis’ treatment

antibiotics, valve replacement surgery

Angia Pectoris

temporary chest pain caused by reduced blood flow/oxygen to the heart muscle

Myocardial Infarction (heart failure)

heart muscle death due to artery occlusion and prolonged oxygen deprivation

Mitochondria

produce ATP (energy) for heart muscle contraction

Intercalated disc (in heart muscle cells)

connect cardiomyocytes
→ help them contract together

Intercalated disc contains:

• desmosomes

• gap junction

Desmosomes’ function

hold cardiomyocytes together during heart contractions

Gap junction’ function

allow ions (electrical signals) to pass between cells

The heart’s functional syncytium

all fibers contract together as a single, coordinated unit

How is skeletal muscle contraction initiated?

Motor neurons trigger contraction

How is cardiac muscle contraction initiated?

AV nodes generate AP that triggers contraction

How does skeletal muscle increase contraction force?

Recruit more muscle fibres

How does cardiac muscle increase contraction force?

Increase calcium concentration
→ increase contraction force

Tetanus

continuous muscle contraction from rapid, repeated stimulation

Why skeletal muscle can go into tetanus phase?

short refractory period → can be stimulated again quickly

Why cardia muscle CAN’T go into tetanus phase?

already have long Plateau phase to rest

SA node (sino-atrial)

specialized cells generate APs for heart contraction

AV node (atrioventricular)

electrical relay station
→ pause impulse for 0.1s

AV bundle (atrioventricular)

carry AP from atria (AV node) → ventricles

Bundle branches

bifurcate from AV bundle
→ carry impulses through IV septum

SA node’s initial rate

70-100 bpm

AV node’s initial rate

40-60 bpm

AV bundle’s initial rate

20-40 bpm

Heart block

Impulse from atria to ventricles is delayed/blocked
→ damage to AV node

Bundle branch block

Impulse is delayed/blocked in a bundle branch
→ uncoordinated ventricular contraction

Ectopic foci

another place generates impulses instead of SA node
→ backup nodes take over when primary node is damaged

Ventricular extrasystoles (palpitation)

Extra ventricular heartbeat
→ caffein, nicotine, stress, exercise, etc.

Vagus nerve → heart

From parasympathetic center

• decrease AP generation

• slow HR (innervate SA, AV node)

Sympathetic cardiac nerve → heart

From sympathetic center

• increase AP generation

• increase HR (innervate SA, AV, contractile cells)

Sympathetic stimulation to increase HR

increase Sodium (Na+) and Calcium (Ca2+) permeability

Parasympathetic stimulation to decrease HR

Release ACh
→ increase Potassium (K+) permeability
→ decrease Calcium (Ca2+) permeability

Refractory period

The period when cardiac cell can’t generate another AP
→ prevent tetanus in heart muscles

Plateau phase

when Ca²⁺ enters while K⁺ (potassium) leaves
→ keeping membrane potential elevated

Systole

heart contraction (pumps out blood)
→ depolarization

Diastole

heart relaxes and fills up blood
→ repolarization

ECG function

reflects the electrical changes in the heart over one cardiac cycle

ECG helps to determine:

HR, heart rhythm

Sinus rhythm

normal HR - 75 bpm

Sinus bradycardia

low HR ~35-40 bpm

Sinus tachycardia

high HR >100 bpm

P wave represents:

atrial depolarization (systole)

P-Q interval represents:

atrial depolarization → ventricular depolarization

QRS complex represents:

ventricular depolarization (systole)

S-T segment represents:

ventricular depolarization → repolarization

elevated S-T segment represents:

myocardial infrarction

T wave represents:

ventricular repolarization

Q-T interval represents:

venticular depolarization → repolarization

Heart block (ECG)

Impulse is blocked at AV node
→ slow, irregular heartbeat
→ prolonged P-R interval

Junctional rhythm (ECG)

AV node takes over damaged SA node
→ slower heartbeat
→ no P wave

VF (ventricular fibrillation) - ECG

ventricles can’t pump blood effectively
→ rapid heartbeat

Isovolumetric contraction phase

ventricles start contracting
→ ventricular pressure rising up
→ all valves closed

Isovolumetric ejection phase

ventricular pressure > arterial pressure
→ semilunar valves open
→ blood is pumped out

Isovolumetric relaxation

ventricles relax after the pump
→ pressure falls down
→ all valves shut

Dicrotic notch

small drop in aortic pressure
→ aortic valve closes
→ pressure drops

Dicrotic wave

small rise in aortic pressure after the notch
→ aorta recoils
→ pressure rises slightly

EDV (end-diastolic volume)

blood volume in ventricle before ventricular contraction

ESV (end-systolic volume)

remaining blood volume in ventricles after contraction

SV (stroke volume)

amount of blood pumped out per heartbeat
= EDV-ESV

Increased SV cause:

• increase contraction force

• decrease ESV

Contractility

the heart’s ability to contract properly

Contraction force

actual strength of the heart’s contraction

‘Lub’ heart sound (1st)

AV valves closure