Four chambers:
Left atrium
Right atrium
Left ventricle
Right ventricle
Atria: Receiving chambers.
Ventricles: Discharging chambers (pump blood out).
Right side: Oxygen-poor blood (from systemic circulation to lungs).
Left side: Oxygen-rich blood (from lungs to body).
To right atrium: Superior vena cava and inferior vena cava.
To left atrium: Pulmonary veins.
From right ventricle: Pulmonary trunk (splits into pulmonary arteries to the lungs), carries oxygen-poor blood.
Arteries always carry blood away from the heart.
From left ventricle: Aorta.
Atrioventricular valves: Between atria and ventricles.
Tricuspid: Right side.
Bicuspid (Mitral): Left side.
Prevent backflow with the help of chordae tendineae attached to papillary muscles.
Semilunar valves: Between ventricles and receiving vessels.
Do not require tendinous cords; kept closed by backflow of blood in receiving vessels.
Pulmonary semilunar valve: Between right ventricle and pulmonary trunk.
Aortic semilunar valve: Between left ventricle and aorta.
Systole: Contraction.
Diastole: Relaxation.
Atrial Systole:
SA node signal depolarizes atria.
Atria contract, AV valves are open.
Passive filling of ventricles (70%) before atrial systole.
Atrial contraction pushes remaining blood into ventricles.
Atrial Diastole:
Atria relax and remain in diastole for the rest of the cycle.
Ventricular Systole:
Ventricles depolarize and contract.
AV valves close (isovolumetric contraction).
Pressure builds; semilunar valves open.
Ventricular ejection (blood is pumped out).
Ventricular Diastole:
Ventricles relax; cardiac muscle cannot reach tetany.
Semilunar valves close (isovolumetric relaxation).
Pressure decreases, AV valves open.
Passive filling of ventricles.
Pressure gradients required for blood flow.
Higher pressure in ventricles than atria closes AV valves.
Higher pressure in ventricles than receiving vessels opens semilunar valves.
Unequal pumping can cause:
Systemic edema: Right ventricle not keeping up; backlog in systemic capillaries.
Pulmonary edema: Left ventricle not keeping up; backlog in lungs.
Left atrium pressure increases during atrial contraction.
Left ventricle contracts, AV valve closes, pressure increases (isovolumetric).
Aortic valve opens when left ventricle pressure exceeds aortic pressure.
Ventricular diastole begins, pressure drops; semilunar valve closes.
S1 (Lub): Closing of AV valves.
S2 (Dup): Closing of semilunar valves.
CO = \text{Heart Rate} \times \text{Stroke Volume}
Directly proportional relationship with heart rate and stroke volume.
Measured in milliliters per minute (mL/min).
Heart rate: beats per minute.
Stroke volume: milliliters per beat.
\frac{\text{beats}}{\text{min}} \times \frac{\text{mL}}{\text{beat}} = \frac{\text{mL}}{\text{min}}
Conversion to liters per minute (L/min):
1 \text{ L} = 1000 \text{ mL}
Cardiac output affects blood pressure.
Vital centers for heart rate, vasomotor control, and respiration.
Cardioaccelerator center: Increases heart rate (sympathetic fibers).
Stimulates adrenergic receptors.
Cardioinhibitory center: Slows heart rate (parasympathetic fibers, vagus nerve).
Vagal tone: Parasympathetic influence keeps resting heart rate lower than SA node's intrinsic rate.
Cardiac centers: collections of cardioaccelerator and cardioinhibitory centers.
Pink: cardio accelerator system.
Parasympathetic: via the vagus, targets SA and AV node.
SA node sets the pace; pre-potential or pacemaker potential caused by drifting sodium ions.
Reaches threshold, action potential is sent.
Acetylcholine (ACh) binds to cholinergic receptors, opening potassium channels.
Potassium leaves the cell (hyperpolarization), extending repolarization.
Slower time to reach threshold, decreasing heart rate.
Norepinephrine binds to beta one receptors, opening ion channels.
Sodium gates open faster; shorter time to reach threshold, speeding up action potential.
Normal resting heart rate various with age, general health, and physical conditioning.
Bradycardia: Slower than normal heart rate (less than 60 bpm).
Tachycardia: Faster than normal heart rate (greater than 100 bpm).
P wave: Depolarization of the atria (atrial diastole).
QRS complex: Ventricular systole.
T wave: Ventricular diastole.
Atrio systole: atria start contraction.
QRS complex, start ventricular systole.
\text{Stroke Volume} = \text{End Diastolic Volume} - \text{End Systolic Volume}
End diastolic volume (EDV): Volume of the ventricles at the end of diastole.
End systolic volume (ESV): Volume of ventricles at the end of systole (after contraction).
Manual pump analogy: Volume pumped depends on handle movement.
End Diastolic Volume (EDV): Venous return (affected by blood volume, muscular activity),
Filling time (duration of ventricular diastole), and preload (myocardial stretching; Frank-Starling law).
Increase EDV increases stroke volume.
End Systolic Volume (ESV): Contractility (force of contraction; influenced by sympathetic stimulation, thyroid hormone, glucagon, beta blockers, calcium channel blockers), and afterload (resistance ventricles overcome to eject blood).
Increase afterload increases ESV, decreasing stroke volume.
Blood Volume
Muscular Activity (skeletal muscle pump)
peripheral tissues
Vasoconstriction
Vasodilation
Cardiac output varies depending on needs and demands; brain blood flow remains relatively constant.
Heart failure: Inability of the heart to meet tissue demands.
Left ventricular failure: Pulmonary edema.
Right ventricular failure: Systemic edema.
Cardiac output is affected by factors influencing heart rate and stroke volume.