EXPH 2115 Key Terms -- Lecture 8 The Cardiovascular System

vascular networks in series

when blood flows in order from point A to B to C (e.g. R ventricle to lungs to L ventricle to body)

vascular networks in parallel

when blood flows from point A to either B or C before D (e.g. L ventricle to brain or kidney to R ventricle)

vasculature

blood vessels

coronary arteries

systemic blood vessels off the proximal aorta that supply the myocardium with oxygenated blood

intercalated discs

connecting structures with gap junctions for electrical conduction between two adjacent cardiomyocytes

calcium-induced calcium release

myocardial t-tubule voltage changes open Ca2+ channels that prolong action potentials and SR Ca2+ release

conduction system of the heart

specialized tissue circuit that sequentially depolarizes regions of the heart for a coordinated contraction

Sinoatrial (SA) Node

myocardial conduction tissue of the upper right atrial wall that acts as the heart pacemaker

Atrioventricular (AV) Node

myocardial conduction tissue in the inferior right atrial septum, only A-V electrical connection

resting membrane potential delay

conduction system cell inability to maintain a constant RMP due to inward leak of Na+, results in AP

intrinsic heart rate

frequency of spontaneous SA node depolarization without neuroendocrine influences (~100 bpm)

SA node cholinergic receptors

membrane receptor that when engaged by PSNS acetylcholine slows down RMP decay to decrease HR

vagal tone

degree of parasympathetic activity on the heart via the vagus nerve (CN X)

anticholinergic agent

pharmacologic antagonist of cholinergic receptors and thus the acetylcholine (e.g. atropine)

SA node beta-adrenergic receptors

membrane receptor that when engaged by SNS catecholamines speeds up RMP decay to increase HR

beta-blocker

pharmacologic antagonist of beta-adrenergic receptors and thus the catecholamines epi/norepi (e.g. atenolol)

bradycardia

HR below 60 bpm, more common at rest following endurance training, can be pathological

tachycardia

HR above 100 bpm, cause for concern when at rest as it could be due to an arrhythmia

electrocardiogram (ECG or EKG)

record of the electrical currents generated by the depolarization and repolarization of the myocardium

P wave

ECG representation of atrial depolarization

QRS complex

ECG representation of ventricular depolarization

T wave

ECG representation of ventricular repolarization

ST segment

ECG representation of when all ventricular cells are in the plateau phase of the AP, should be isoelectric

ECG isoelectric line

neutral ECG baseline from which deflections are noted

cardiac cycle

heart activity composed of two stages: systole and diastole

systole

contraction (pressurizing) phase of the cardiac cycle, includes isovolumetric and ejection phases

diastole

relaxation phase of the cardiac cycle, involves isovolumetric and filling phases

1st heart sound

caused by the closure of the AV valves, occurs at the beginning of ventricular systole

2nd heart sound

caused by the closure of the semilunar valves, occurs at the beginning of ventricular diastole

isovolumetric contraction phase

1st systolic period when pressure rises but yields no ejection as ventricular pressure is below arterial BP

ejection phase

2nd systole period when the ventricle ejects the stroke volume into the aorta (and lungs from right side)

isovolumetric relaxation phase

1st diastolic period when pressure falls but yields no filling as ventricular pressure is above atrial pressure

filling phase

2nd diastolic period when the ventricles receive the venous return to fill up to the end diastolic volume

stroke volume (SV)

amount of blood ejected by the ventricles per beat, difference between EDV and ESV, expressed in mL/bt

end-diastolic volume (EDV)

amount of blood in the ventricle just prior to contraction (i.e. following filling)

end-systolic volume (ESV)

amount of blood in the ventricle just following contraction (i.e. prior to filling)

ejection fraction

% of the EDV that is ejected during systole

arterioles (resistance vessels)

microscopic blood vessels connecting arteries with capillaries, main site of blood flow resistance

vascular tone

relative degree of blood vessel smooth muscle activity

vasoconstriction

contraction of arteriolar wall smooth muscle such that the lumen diameter decreases

vasodilation

relaxation of arteriolar wall smooth muscle such that the lumen diameter increases

venoconstriction

contraction of venous wall smooth muscle such that the lumen diameter decreases

venodilation

relaxation of venous wall smooth muscle such that the lumen diameter increases

venous return

flow of blood back to the heart

skeletal muscle pump

venous compression by surrounding skeletal muscle contraction that aids venous return

respiratory (intrathoracic) pump

lower atrial pressure due to negative inspiratory pleural pressure causing increased venous return

Mean Arterial Pressure (MAP)

average force exerted by blood on artery walls, product of cardiac output and vascular resistance

systolic blood pressure

maximal pressure exerted by blood on arterial walls due to left ventricular ejection during systole

diastolic blood pressure

lowest pressure exerted by blood on arterial walls due to left ventricular relaxation in diastole

basic flow law (Poiseuille’s Law)

law describing laminar flow in a tube, states that flow = pressure difference across tube / resistance

cardiac output (Q)

rate at which blood is pumped out of the left ventricle into systemic circulation, expressed in L/min

total peripheral resistance (TPR)

sum total of systemic blood flow resistance in the vasculature

alpha-adrenergic receptor

arteriolar (and venous) smooth muscle receptor activated by norepinephrine, causes vasoconstriction

metabolite-induced vasodilation

arteriolar smooth muscle relaxation due to direct contact with metabolites (such as K+, H+, CO2, adenosine)