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Cardiac output
The volume of blood pumped each minute by each ventricle (CO = stroke volume × heart rate)
Stroke volume
Amount of blood pumped per beat by one ventricle
Heart rate
Number of heartbeats per minute
Average cardiac output
~5,500 mL/min in a healthy adult
SA node
Primary pacemaker of the heart that initiates spontaneous depolarization
HCN channels
Channels in SA node that allow Na+ influx during pacemaker potential
Positive chronotropic effect
Increase in heart rate
Negative chronotropic effect
Decrease in heart rate
Sympathetic stimulation (heart)
Increases heart rate via norepinephrine/epinephrine
Parasympathetic stimulation (heart)
Decreases heart rate via acetylcholine
Medulla oblongata cardiac center
Brain region that regulates heart rate via autonomic input
End diastolic volume (EDV)
Volume of blood in ventricles at end of diastole (preload)
Afterload
Resistance the heart must overcome to eject blood (total peripheral resistance)
Contractility
Strength of ventricular contraction
Ejection fraction
Percentage of EDV ejected (~60%)
Frank-Starling law
More EDV → stronger contraction → increased stroke volume
Myocardial stretch
Increases contraction strength due to increased fiber length
Anrep effect
Increased contractility due to sustained increased afterload
Venous return
Volume of blood returning to the heart
Veins
High compliance vessels that store most blood volume
Capacitance vessels
Veins that hold ~2/3 of blood volume
Total blood volume
Total amount of blood in circulation
Interstitial fluid
Fluid between cells in tissues
Plasma
Fluid portion of blood
Net filtration pressure
Force driving fluid out of capillaries
Oncotic pressure
Osmotic pressure due to plasma proteins pulling fluid into capillaries
Starling forces
Balance of hydrostatic and oncotic pressures controlling fluid movement
Edema
Excess fluid accumulation in interstitial spaces
Filariasis
Parasitic infection causing lymphatic blockage and elephantiasis
Glomeruli
Kidney capillaries where filtration begins
ADH (vasopressin)
Hormone that increases water reabsorption in kidneys
Osmoreceptors
Sense plasma osmolarity and regulate ADH release
Aldosterone
Hormone that increases Na+ and water reabsorption
Renin
Enzyme released by kidneys to activate RAAS
Angiotensin II
Vasoconstrictor that increases blood pressure and stimulates aldosterone
ACE
Enzyme that converts angiotensin I to angiotensin II
ANP
Hormone that increases salt and water excretion to reduce blood volume
Hypertension
High blood pressure above normal range
Primary hypertension
High blood pressure with no identifiable cause
Secondary hypertension
High blood pressure due to another disease
Essential hypertension
Common form caused by multiple interacting factors
Atherosclerosis
Buildup of plaque in arteries
Stroke
Brain damage caused by interrupted blood flow
Beta blockers
Drugs that reduce heart rate and cardiac output
ACE inhibitors
Drugs that block formation of angiotensin II
ARBs
Drugs that block angiotensin II receptors
Preeclampsia
Pregnancy disorder involving hypertension and organ damage
Proteinuria
Excess protein in urine
Circulatory shock
Inadequate blood flow/oxygen delivery to tissues
Hypovolemic shock
Shock caused by low blood volume
Septic shock
Shock caused by infection-induced vasodilation
Anaphylactic shock
Severe allergic reaction causing vasodilation
Neurogenic shock
Shock caused by loss of sympathetic control
Cardiogenic shock
Shock caused by heart failure
Congestive heart failure (CHF)
Inability of heart to maintain adequate cardiac output
Left-sided heart failure
Causes pulmonary congestion and shortness of breath
Right-sided heart failure
Causes systemic edema and congestion
Digitalis
Drug that increases cardiac contractility
Diuretics
Increase urine output to reduce blood volume
Baroreceptors
Sense blood pressure changes and trigger reflexes
Baroreceptor reflex
Homeostatic response to stabilize blood pressure
Skeletal muscle pump
Assists venous return during movement
Respiratory pump
Pressure changes during breathing that aid venous return
Hypertrophy
Enlargement of heart muscle due to increased workload