PSIO 241 CH 9 cont..

pathway to lungs

superior vena cava to right atrium through tricuspid valve to right ventricle through pulmonary valve to pulmonary artery to lungs

pathway to rest of body

pulmonary vein to left atrium through mitral valve through left ventricle through aortic valve to aorta to rest of the body

conduction pathway

Excitation of one cell to threshold leads to spread of action potential throughout the heart

contraction pathway

Myocytes contain proteins needed to contract and receive signal to do so from the conduction system

atria; ventricles

delay at AV nose allows for blood from the *_* to be pushed to the _

Arrhythmia

any variation from the normal rhythm and sequence of excitation.

Hyperkalemia

increased rate of repolarization, **sharp spiked T waves**

pacemakers

multiple different kinds (double lead, single lead, wireless)

– Function in sensing normal cardiac rhythm and produce shock if rate falls below appropriate range

– Commonly placed due to arrythmias, post myocardial infraction sustained damage

systole

cardiac muscle contraction (empties)

diastole

cardiac muscle relaxation (fills)

End-diastolic volume

Volume of blood in ventricle **before contraction (120 ml)**

End-systolic volume

Volume of blood in the ventricle **after contraction (50 ml)**

Stroke volume

Volume of blood ejected by the ventricle per beat

– SV = EDV – ESV **(70 ml)**

Ejection fraction

EF = SV/EDV

– Normal > 50%

Ventricular diastole

ventricles relaxed and fill with blood

Isovolumetric ventricular contraction

ventricles contract, all 4 valves are closed, **pressurization**

Ventricular ejection

pressure forces blood past the semilunar valves, **ejection**

Isovolumetric ventricular relaxation

**pressure falls,** return to ventricular diastole

ventricular diastole (filling)

• Pressure is low in ventricles.

• Blood is entering the atria, AV valves forced open, and blood **passively flows** into ventricles (80% of blood enters ventricles passively).

• **SA node fires, leads to P wave**; then atria contracts (**atrial systole)** and push remaining 20% of blood into ventricles.

• Ventricles now filled with blood (EDV)

isovolumetric ventricular contraction (empties)

• **AV node fires, leads to QRS**, ventricle contracts.

• Ventricle pressure rises, **AV-valves close, S1 heart sound.**

• **Seminlunar valves remain closed.**

• At this point in time, all 4 valves are closed.

• Volume of blood in the ventricle is not changing

• __**Ventricular pressure is rising**__.

• When it reaches a critical level, semilunar valves are forced open to begin next phase.

ventricular ejection

• Ventricular pressure rises to a point that exceeds the pressure in the pulmonary trunk and aorta.

• **Semilunar valves are forced open**

• Blood is ejected from ventricle and flows through the **pulmonary artery and aorta**

• During ventricular systole, the atria are in diastole, are filling with blood, pressure is rising in atria.

isovolumetric ventricular relaxation

• **depolarization**

• **T wave**

• **Semilunar valves close, S2 heart sound.**

• Ventricles relax, pressure falls; **isovolumetric relaxation.**

• When pressure in atria exceed ventricular pressure, AV valves forced open and filling begins again.

**Cardiac output**

the volume of blood ejected by each ventricle each minute **CO= heart rate x stroke volume**

• 70 beats/min x 80 ml/beat = 5,600 ml/min

**Heart rate**

decreased by parasympathetic stimulation and increased by sympathetic stimulation

**Stroke volume**

determined by venous return and by sympathetic activity**.**

cardiac ouput- autonomic control

• Increased sympathetic stimulation results in increased strength of contraction and increased stroke volume

• Norepinephrine (NE) acts directly on cardiac muscle, increases **contractility; also causes veins to constrict, increasing venous return**

preload

• Increased venous return increases ventricular filling (EDV)

• Increased preload  results in a larger stroke volume

• due to length–tension relationship described by the **Frank–Starling law**

increased preload

end diastolic volume 175 ml; end systolic volume 35 ml

stroke volume: 140 ml

normal cardiac output

end diastolic volume 135 ml; end systolic volume 65 ml

stroke volume: 70 ml

increased contractility

end diastolic volume 135 ml; end systolic volume 35 ml

stroke volume: 100 ml

coronary artery diseases (CAD)

refers to pathological changes within the coronary artery walls that diminish blood flow.

diastole

• Heart give most of its own blood supply through the coronary circulation **during _**

• Coronary blood flow normally varies to keep pace with cardiac oxygen needs.

ischemia

hypoxia

not enough oxygen in blood flow