Explore the key functions of the heart in 'Chapter 17: Function of the Heart'. This quiz assesses understanding of myocardial activities, phases of heart cycles, and the effects of various conditions on heart function. Essential for students and professionals in medical and health-related fields.
Hemotocrit
Total blood volume
Cardiac output
The size of the heart valves
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Bradycardia
Heart block
Fight-or-flight response
Tachycardia
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Increases the force of myocardial contraction
Increases the amount of blood that flows into the heart from the vena cava
Causes tachycardia
Slows the heart rate
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"fight or flight"
Norepinephrine
Parasympathetic
Causes tachycardia
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Stroke volume
Cardiac output
Cardiac cycle
Systole
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In the thorax
In the cerebral cortex
In the cerebellum
In the medulla oblongata
In the hypothalamus
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Hypovolemic
Cardiogenic
Vascular
Obstructive
Neurogenic
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They are all areas where you can not hear Korotkoff sounds
They are all only found on the left side of the body
They are all pulse points
None of them contain baroreceptors
All of the are connected to each other by capillary beds
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The ventricles are filling with blood
All semilunar valves are open
Both AV valves are closed
Blood is pumped to the lungs and systemic circulation
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Stroke volume
Cardiac output
Starling's law of the heart
Inotropic effect
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Hypertension
Bradycardia
Tachycardia
Anemia
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Pericardium
SA node
Myocardium
Mediastinum
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Decreased ventricular filling (with blood)
Failure of the AV valves to open
Failure of the SA node to fire
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Vagolytic drug
Beta1 adrenergic agonist
Sympathomimetic
Beta1 adrenergic blocker
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Sympathetic nerve firing
Vagal discharge
Activation of the beta1 adrenergic receptors
End diastolic volume (EDV)
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A (+) inotrpic drug
A vagolytic drug
A (-) chronotropic drug
A beta1 adrenergic blocker
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Causes a (+) inotropic effect
Decreases cardiac output
Decreases heart rate
Decreases stroke volume
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Stops the heart
Increases the heart rate
Decreases cardiac output
Decreases stroke volume
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Valve damage
Pulmonary edema
Angina pectoris
Bradycardia
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AV valves are closed
Ventricles are relaxed
Ventricles are in systole
Semilunar valves are open
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Activation of the beta1 adrenergic receptors
Discharge of sympathetic nerves
Discharge of the vagal nerve
Binding of norepinephrine to its receptor
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Stroke volume
Cardiac output
Preload
Cardiac reserve
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Increased blood volume
Increased sympathetic stimulation
Increased heart rate
Increased stroke volume
Decreased cardiac output
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Decreased vessel lumen diameter
Increased blood viscosity
Decreased vessel length
Increased vasodilation
Increased blood cell count
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Total blood volume
Blood viscosity
Systemic resistance
Blood vessel length
Size of vessel lumen
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Arteries
Veins
Venules
Capillaries
Arterioles
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Ductus venosus
Umbilicus
Umbilical vein
Foramen ovale
Placenta
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Radial artery
Subclavian artery
Axillary artery
Cephalic artery
Palmar artery
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Left atrium and ventricle
Left atrium only
Right ventricle only
Right atrium and ventricle
Left atrium and right ventricle
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Intermediate discs
Gap junctions
Contractile fibers
Chordae tendinae
Desmosomes
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Bundle of His, SA node, AV node, Purkinje fibers
Sinoatrial (SA), Purkinje fibers, AV node, Bundle of His
Purkinje fibers, AV node, SA node, Bundle of His
SA node, AV node, Bundle of His, Purkinje fibers
Bundle of His, Purkinje fibers, Atrioventricular (AV) node
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Systole
Repolarization
Fibrillation
Filling
Diastole
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Semilunar valves opening
Atrioventricular valves opening
Atrioventricular valves closing
Semilunar valves closing
Valvular stenosis
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Increased sympathetic stimulation
Increased Norepinephrine hormone
Increased Thyroid hormone
Increased calcium levels
Increased potassium levels
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Medulla oblongata
Thalamus
Cerebellum
Midbrain
Cerebrum
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B
D
E
A & C
NONE OF THE ABOVE
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Epicardium.
Fibrous pericardium.
Myocardium.
Endocardium.
Parietal layer of the serous pericardium.
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Activation of beta1 adrenergic receptors
Vagal discharge
Blockade of beta1 adrenergic receptors
Blockade of the muscarinic receptors
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Cardiac output
Blood volume
Hematocrit
Stroke volume
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A (+) inotrpoic effect
Heart rate to slow
Cardiac output to increase
Stroke volume to increase
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Increases myocardial contractile force
Causes a (+) chronotropic effect
Increases cardiac output
Slows heart rate
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The cardiac output
The volume of a ventricle
An average stroke volume
The amount of blood that flows through the pulmonary capillaries in one minute
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Varies with diet
Is set by the hypothalamus
In a resting person is normally 1 minute
Depends on hormones from the liver
Will stop a heart if it is lower than 20 seconds
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Heart rate
Stroke volume
Muscular activity
Blood velocity
Valve opening
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Increased blood pressure
Increased parasympathetic stimulation
Decreased heart rate
Decreased stroke volume
Decreased cardiac output
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Atrial Natriuretic Peptide
Antidiuretic Hormone
Aldosterone
Angiotensin
Increased Norepinephrine
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Increased heart rate
Increased vasoconstriction of blood vessels
Increased blood pressure
Decreased respiratory rate
Decreased heart rate
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Contract more forcefully when stretched
Contract more forcefully when relaxed
Stay in an isotonic state
Less elastic
More elastic
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