Cardiovascular system

The right side of heart receives

Deoxygenated blood and pumps blood to the lungs ( pulmonary circuit)

Left side of the heart receives

Oxygenated blood from the lungs, pumps blood to body tissues ( systemic circuit)

How much does the heart weigh?

less than 1lb

Where is the location of the heart?

The heart is located in the mediastinum between the second rib and the fifth intercostal space, anterior of the vertebral column and posterior to the sternum

Coverings of the heart

Superficial Fibrous Pericardium ( protects and anchors the heart to the area; prevents overfilling)

Parietal layer of the serous pericardium

Pericardial cavity

*Epicardium ( Visceral Layer of the serous pericardium)

*Myocardium

*Endocardium

Heart chamber

*Heart wall

Overall coverings of the heart

Pericardium: double wall sac that surrounds the heart that is made up of two parts ( parietal and Visceral)

Atrioventricular ( AV) Valves

prevent backflow into the atria when the ventricles contract

Tricuspid valve ( right AV valve)

made up of the three cusps and lies between right atria and ventricle

Mitral valve ( left AV valve or bicuspid valve)

Made up of two cusps and lies between the left atrium and ventricle

Chlordane tendineae

Anchors the cusps of the AV valves to the papillary muscles

-Hold valve flaps in a closed position and

prevent flaps from everting back into the atria

Semi lunar Valves

Pulmonary valves and Aortic valves

Prevent backflow from major arteries into ventricles

Open and close in response to pressure changes

3 cusps

incompetent valve

Weakens heart

blood backflows so heart repumps same blood over and over

Valvular stenosis

Stiff flaps that constrict opening

Heart needs to exert more force to pump blood

Pathway of blood ( right side of the heart)

1) Superior/ Inferior vena cava and coronary sinus

2) Right atrium

3) Tricuspid valve

4) Right ventricle

5) Pulmonary valve

6) Pulmonary trunk

7) Pulmonary arteries

8) Lungs

Pathway of blood ( left side of heart)

1) Four pulmonary veins

2)Left atrium

3)Mitral/bicuspid valve

4) Left ventricle

5) Aortic valve

6) Aorta

7) systemic circulation

Pulmonary circuit is

short and low pressure circulation

The systemic circuit is

long, high-friction circulation

Left side of the heart and physiological difference from the right

The left side of the heart is 3x as thick as the right and pumps with greater pressure

The left ventricle is round, while the right ventricle is crescent-shaped and surrounds the left ventricle

Does the heart have its own blood supply?

yes its’s called the coronary circulation,

The shortest circulation in the body

-delivered when the heart is relaxed

**Left ventricle recives most of the coronary blood supply

Coronary arteries

Both the left and right coronary arteries arise from the base of the aorta and supply arterial blood to the heart

encircles heart in coronary sulcus( contains anastomoses joining of blood vessels)

Left coronary artery

Two branches: circumflex artery, anterior interventricular artery

supplies blood to interventricular septum, left ventricle ( anterior/posterior), Left atrium

Right coronary artiery

Two branches: right marginal artery, Posterior interventricular artery

Supplies right atrium and right ventricle with blood

Angina Pectoris

Thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium

Myocardial infarction

Prolonged coronary blockage

Repair with noncontractile scar tissue

Describe cardiac muscle cells

Striated, short, branched , fat, interconnected, large mitochondria

• Has intercalated discs: connecting junctions between cardiac cells

• Desmosomes: hold cells together, prevents seperation during

• Gap junctions: allows ions to pass from cell to cell; electrical impulses

• Has functional syncytium: acts as a unit

Two myocytes

Contractile cells: responsible for contraction

Pacemaker cells: Noncontractile cells that spontaneously depolarize (does not need nervous system stimulation, initiate depolarization of entire heart

Tetanic contraction and the heart

(Continuous contraction does not happen in the heart because the absolute refractory period is almost as long as the contraction itself, allows heart to relax and fill as needed to be an efficent pump

What type of respiration does the heart have and why

Aerobic respiration due its dependency of oxygen, has larger mitochondria

Electrical events of the Heart

The heart depolarizes and contracts without nervous stimulation, though the autonomic nervous system can change the rhythm

Intrinsic cardiac conduction system

Pacemaker cells initiate and distribute impulses to coordinate depolarization and contraction of the heart

What sets the basic rhythm of the heart

Pacemaker cells initiating action potential

Steps of action potential in pacemaker cells

Pacemaker potential: K+ channels are closed, and slow Na+ channels are open; the interior is more positive, the threshold(-40mV) must be met before depolarization happens, and depolarization happens slowly because of slow Na+ channels

Depolarization: Ca2+ channels open (around -40mV), allowing huge influx of Ca2+, leading to rising phase of action potential

Repolarization: Ca2+ channels close and K+ channels open, allowing and efflux of k+ions and the cell becomes more negative

Sequence of Excitation

1. Sinoatrial node

2. Atrioventricular node

3. Atrioventricular bundle

4. Right and left branches

5. Subendocardial conducting network ( Purkinje fibers)

Sinoatrial node

Pacemaker of the heart and is located in the Right atrial wall

Depolarizes faster than the rest of the myocardium

Generates impulses about 75x/min

inherent rate (100x/min) due to extrinsic factors

Impulse spread across atria into AV node

Atrioventricular AV node

In the inferior atrial septum

Delays impulses by approx 0.1sec

Rate is 50x/ in the absence of SA node input

why is the Atrioventricular node delayed?

The fibers are smaller and have fewer gap junctions

Allows atrial contraction prior to ventricular contraction

Atrioventricular bundle

In the superior interventricular septum

only electrical connection between atrial and ventricles ( not connected by gap junctions)

Right and Left branches

two pathways in inter ventricular septum

carries impulses towards apex of the heart

Subendocardial conducting network (Purkinje fibers)

Complete pathway through septum into apex and into ventricular walls, after it contract this follows from the apex towards atria

in absence of the AV node, AV bundle and subendocardial conducting network depolarizes 30x/min

How long does the electrical event of the heart take ( sa node- purkinje fibers)

0.22 seconds

Arrhythmias

irregular heart rhythyms

Fibrillation

Rapid, irregular contractions, the heart becomes useless for pumping, circulation ceases, brain death

If Sa node is defective what can happpen

Ectopic focus, where an abnormal pacemaker takes over pacing, If AV node takes over it set junctional rhythm ( 40-60 beats/ min)

Always remeber

Contraction follows excitation

What happens if Av node is defective

May cause Heart block; ventricles will beat at their own intrinsic rate ( 30x beat/ min)

Treatment: Artificial pacemaker

Where does the ANS modify the heartbeat?

Medulla oblongata

Contractile muscle fibers function

Responsible for pumping action

Steps of Action Potential of Contractile Cardiac muscle cells

1) Depolarization: due to Na+ influx through fast voltage-gated Na+ channels, a positive feedback cycle opens many Na+ channels, reversing the membrane potential. Depolarization sky rockets

2) Plateau phase: Due to Ca2+ influx through slow Ca2+ channels, this keeps the cell depolarized with K+ channels still closed

3) Repolarization Ca2+ channels inactivated an K= channels opening K+ efflux, membrane potential back to resting voltage

P wave

Depolarization of Sa node and atria

QRS complex

ventricular depolarization and atrial repolarization

T wave

ventricular repolarization begins at Apex

P-R interval

Beginning of Atrial excitation to beginning of ventricular excitation

S-T segment:

Entire ventricular myocardium depolarized

Q-T interval

Beginning of ventricular depolarization through ventricular repolarization

What is happening between the end of the P wave and before the QRS complex

With Atrial depolarization complete, the atrioventricular bundle delays contraction by 0.1 sec

What happens after the T-wave and before the next cycle ( p-wave)

Ventricular repolarization is complete

What can an enlarged R wave mean

Enlarged ventricles

Elevated or depressed S-T segment

indicates cardiac ischemia

Cardiac ischemia

happens when reduced blood flow limits the oxygen reaching your heart

Prolonged Q-T interval

reveals a repolarization abnormality that increases the risk of ventricular Arrhythmias

Systole

Period of heart contraction

Diastole:

Period of Heart relaxation

Cardiac cycle

blood flow during a complete heartbeat ( Atrial systole and diastole then ventricular systole and diastole)

First step of the cardiac cycle

Ventricular filling: mid to late diastole

80% of blood moves passively in low-pressure form from atria through open AV valves into ventricles from Atria ( SL vales are closed)

Atrial depolarization ( SA node initiated) triggers atrial systole (P wave) atria contract, pushing the remaining 20% of blood into the ventricles

Left with EDV= End Diastolic Volume: volume of blood at the end of ventricular diastole ( average 120ml)

Isovolumeteric contraction

Atria relax; ventricles begin to depolarize ( QRS wave) and contract; rising ventricular pressure causes AV valves to close

** Split-second period when ventricles are completely closed; volumes remain constant, and ventricles continue to contract

It is only when the ventricular pressure exceeds the pressure in the large arteries that semilunar valves are forced open

Isovolumetric Relaxation : early diastole

Following ventricular repolarization (T-wave), ventricular relaxation

ESV (end-systolic volume: volume of blood remaining in each ventricle after systole

Ventricular pressure drops, causing backflow of blood into large arteries causing closing of SL valves

Dicrotic notch

Closure of the aortic valve raises aortic pressure as backflow rebounds off closed valve cusps

What happens after ventricular systole

Atria continue to fill with blood, and when the atrial pressure exceeds ventricular pressre av vales open, and the cardiac cycle happens again

cardiac cycle last

0.8 seconds

Atrial systole lasts

0.1 seconds

Ventricular systole lasts

about 0.3 seconds

Quiescent period

heart relaxation 0.4 seconds

How are heart sound smade

as valves close the resulting turbulent blood flow creates a sound

When can you hear a systole

between the first and second heart sounds

When can you hear the diastole

occurs between second sound and the first heart sound of the next cycle

Stroke volume

amount of Blood ejected from ventricle

First sound is when

Av valves close at the beginning of ventricular systole

second sound

closing of SL valves at the beginning of ventricular diastole

Cardiac output

Amount of blood pumped out by each ventricle in 1 minute

Cardiac output formula

Hr x SV= CO

What is the normal resting CO?

75/beats/min x 70 ml/beat= 5.25L/min

Maximal CO in non-athletic people

20-25L/min

Maximal CO reach in athletes

35L/min

Cardiac reserve

resting- maximal CO

Stroke volume ( SV) formula

EDV(120ml/beat)- ESV(50ml)= 70ml/beat

EDV End diastolic volume

ventricular diastole/venous pressure

ESV End Systolic volume

Arterial BP

Ventricular contraction

Normal SV

70ml/beat

Stroke volume regulated by

preload, contractility, afterload

Preload

Degree of stretch of the heart muscle before contraction

An increase in preload increases SV ( more specifically EDV increases)

Frank sterling law of the heart

SV+ Preload

Contractility

Increased contractility lowers ESV, aka increases SV

Caused by sympathetic epinephrine releases stimulus increasing Ca+ influx

What is the relationship with heart contractility?

Norepinephrine increases Heart contractility( HR) via Cyclic AMP second messenger system

What is Afterload and how does it affect SV?

Pressure that ventricles must overcome to eject blood.

Aortic pressure is around 80mmHg

Pulmonary pressure is around 10mmHg

An increase in afterload due to hypertension increases ESV and lowers SV

If SV decreases as a result of

Decreased BV or weakened heart, CO can be maintained HR and contractility

Chemical regulated by HR

Epinephrine and Thyroxine both increase HR

Ions - Ca2+, k+ and Na+ must be in homeostasis

Hypocalcemia

Depresses HR

Hypercalcemia

Increases HR and contractility

Hyperkalemia

Alters electrical activity, lead to heart block and cardiac arrest

Hypokalemia

results in feeble heartbeat, Arrthymias