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B.V 1 Flashcards

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1
Q

What are the four key characteristics of cardiac muscle?

A

Automaticity, rhythmicity, conductivity, excitability.

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2
Q

Define automaticity.

A

The ability of cardiac muscle to generate spontaneous impulses.

e.g., SA node pacemaker activity.

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3
Q

What structure is the primary pacemaker of the heart?

A

SA node (sinoatrial node).

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4
Q

Where is the SA node located?

A

In the right atrium.

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5
Q

What is the intrinsic firing rate of the SA node?

A

60–100 beats/min.

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6
Q

Which cardiac structure has the second-highest pacemaker rate?

A

AV node (40–60 beats/min).

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7
Q

What is the role of Purkinje fibers?

A

Rapidly conduct impulses to the ventricular myocardium.

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8
Q

What are intercalated discs?

A

Specialized junctions with gap junctions that allow ion movement between cardiac cells.

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9
Q

Why is cardiac muscle called a ‘functional syncytium’?

A

Cells act as a single unit due to gap junctions, despite being anatomically separate.

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10
Q

What separates the atrial and ventricular syncytia?

A

Fibrous atrioventricular (AV) septum.

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11
Q

What is the absolute refractory period (ARP)?

A

Time during which cardiac muscle cannot respond to any stimulus (180–200 ms in ventricles).

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12
Q

Why can’t cardiac muscle be tetanized?

A

Long refractory period ensures relaxation before the next contraction.

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13
Q

What is the ‘all-or-none law’ in cardiac muscle?

A

Cardiac muscle contracts maximally or not at all in response to a threshold stimulus.

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14
Q

Define Starling’s Law (length-tension relationship).

A

Force of contraction is proportional to initial muscle fiber length (preload/EDV).

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15
Q

What is preload?

A

Stretch on cardiac muscle fibers before contraction (determined by EDV).

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16
Q

What is afterload?

A

Resistance the heart must overcome to eject blood (e.g., arterial pressure).

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17
Q

How does increased preload affect contraction?

A

Increases force of contraction (Starling’s Law).

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18
Q

What causes the staircase phenomenon (Treppe)?

A

Increased calcium availability and temperature with successive stimuli.

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19
Q

What is an extrasystole?

A

A premature contraction caused by a stimulus during the relative refractory period.

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20
Q

What follows an extrasystole?

A

A compensatory pause to reset the heart’s rhythm.

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21
Q

What is the mnemonic for the cardiac conduction pathway?

A

SA node → AV node → Bundle of His → Purkinje fibers.

‘SAve A Village, Hurry Promptly’.

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22
Q

Which ion is critical for cardiac muscle contraction?

A

Calcium (Ca²⁺).

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23
Q

What is chronotropism?

A

Rhythmicity; the heart’s ability to beat regularly.

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24
Q

What is dromotropism?

A

Conductivity; the speed of impulse transmission.

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25
What is bathmotropism?
Excitability; the ability to respond to stimuli.
26
What is inotropism?
Contractility; the force of contraction.
27
How does sympathetic stimulation affect contractility?
Increases it (positive inotropic effect via norepinephrine).
28
What is the Frank-Starling mechanism?
Increased EDV stretches muscle fibers, leading to stronger contractions.
29
What is the force-velocity relationship?
Velocity of contraction decreases with increased afterload.
30
What is the significance of gap junctions?
Allow rapid electrical coupling between cardiac cells.
31
What is the normal duration of ventricular ARP?
180–200 ms.
32
What happens during the relative refractory period (RRP)?
A stronger-than-normal stimulus can trigger a response.
33
How does decreased distensibility affect the heart?
Reduces ventricular filling (lower EDV).
34
What is the role of the AV bundle (Bundle of His)?
Connects atrial and ventricular syncytia, ensuring coordinated contraction.
35
What is the intrinsic rate of ventricular muscle pacemakers?
15–30 beats/min.
36
What is electromechanical coupling?
Electrical depolarization (action potential) triggers calcium release and mechanical contraction.
37
Why do electrical events precede mechanical events?
Depolarization must occur before calcium release and contraction.
38
What is the significance of the SA node’s automaticity?
Ensures the heart beats independently of nervous input.
39
What is a syncytium?
A group of cells functioning as a single unit.
40
What are the three types of cardiac muscle?
Atrial, ventricular, and specialized excitatory/conduction fibers.
41
What is the function of ventricular syncytium?
Coordinated contraction to pump blood into circulation.
42
What is the 'load-velocity relationship'?
Increased afterload reduces contraction velocity.
43
What is the effect of increased afterload on cardiac work?
Increases workload (e.g., hypertension → left ventricular hypertrophy).
44
What causes beat loss in the force-frequency relationship?
A skipped beat leads to a stronger subsequent contraction due to increased filling time.
45
What is the clinical term for a ventricular extrasystole?
Premature ventricular contraction (PVC).
46
What ion imbalance could reduce cardiac excitability?
Hyperkalemia (high K⁺) depolarizes cells, reducing responsiveness.
47
What is the 'staircase phenomenon' also called?
Treppe.
48
What is the role of the His bundle?
Transmits impulses from the AV node to the Purkinje fibers.
49
What is the normal heart rate range?
60–100 beats/min (set by SA node).
50
What is automaticity in cardiac muscle?
The ability to generate spontaneous impulses without stimuli (But, By SA node pacemaker impulses).
51
Where is the SA node located?
In the right atrium. It is the primary pacemaker of the heart.
52
What is the function of intercalated discs?
They contain gap junctions that allow rapid ion movement, enabling the heart to act as a functional syncytium.
53
What prevents tetanization in cardiac muscle?
The long refractory period (ARP + RRP), ensuring relaxation before the next contraction.
54
Define Starling’s Law.
The force of contraction is directly proportional to the initial length of cardiac muscle fibers (within physiological limits).
55
What is the difference between preload and afterload?
Preload = stretch on the muscle before contraction (EDV). Afterload = resistance the heart must overcome to eject blood (e.g., arterial pressure).
56
Which structure connects the atrial and ventricular syncytia?
The A-V bundle (Bundle of His).
57
What is an extrasystole?
An extra contraction caused by a stimulus during the relative refractory period, often due to an ectopic focus.
58
Why does the SA node set the heart rate?
It has the fastest intrinsic firing rate (60–100 beats/min).
59
What is the significance of the 'all-or-none law'?
Cardiac muscle contracts maximally or not at all in response to a threshold stimulus.
60
Name the two syncytia in the heart.
Atrial syncytium and ventricular syncytium.
61
What is the staircase phenomenon (Treppe)?
Increased force of contraction with successive stimuli due to calcium accumulation and temperature rise.
62
Which ion is critical for electromechanical coupling?
Calcium (Ca²⁺).
63
What happens during the absolute refractory period (ARP)?
The cardiac muscle cannot respond to any stimulus, preventing tetanization.
64
How does increased sympathetic activity affect contractility?
It increases contractility (positive inotropic effect) via norepinephrine.
65
What is the normal rate of the AV node?
40–60 beats/min.
66
What is a compensatory pause?
A prolonged diastolic pause following an extrasystole, allowing the heart to reset.
67
Why do electrical events precede mechanical events?
Electrical depolarization (action potential) triggers calcium release and contraction.
68
What is the role of Purkinje fibers?
Rapidly conduct impulses to the ventricular myocardium to ensure coordinated contraction.
69
How does decreased distensibility affect the heart?
Reduces ventricular filling (lower EDV), decreasing stroke volume (Starling’s Law).
70
What is the mnemonic for the pacemaker hierarchy?
SAve A Village, Hurry Promptly (SA node → AV node → His bundle → Purkinje).
71
What are the two types of atrioventricular (AV) valves?
Mitral (bicuspid) valve (left atrium to left ventricle) and tricuspid valve (right atrium to right ventricle).
72
What is the function of semilunar valves?
Prevent backflow of blood into the ventricles (aortic valve: LV to aorta; pulmonary valve: RV to pulmonary trunk).
73
How do AV valves prevent backflow?
Papillary muscles and chordae tendineae tighten during ventricular contraction, preventing valve flaps from inverting into the atria.
74
What are the three layers of blood vessels (except capillaries)?
Tunica intima (endothelium), tunica media (smooth muscle/elastic tissue), tunica externa (connective tissue).
75
Which vessels hold 64% of blood volume at rest?
Systemic veins and venules (capacitance vessels).
76
What are Windkessel vessels?
Elastic arteries (e.g., aorta) that stretch during ventricular contraction and recoil during relaxation to maintain blood flow.
77
What is the role of muscular (distribution) arteries?
Adjust blood flow via vasoconstriction/vasodilation (e.g., brachial, radial arteries).
78
Which vessels are called 'resistance vessels'?
Arterioles, metarterioles, and precapillary sphincters (regulate blood flow into capillaries).
79
What is the function of precapillary sphincters?
Control blood flow into capillaries based on tissue demand.
80
Why are veins called capacitance vessels?
They hold ~64% of blood volume and can expand to accommodate changes in blood volume.
81
How do venous valves prevent backflow?
Valves close when muscles relax, preventing retrograde blood flow (aided by the muscle pump).
82
What are arteriovenous (AV) shunts?
Vessels connecting metarterioles directly to venules, bypassing capillaries (e.g., for collateral circulation).
83
Which vessels are exchange vessels?
Capillaries (5% of blood volume; single endothelial layer for diffusion/filtration).
84
Name the three types of capillaries.
Continuous (most tissues), fenestrated (kidneys, intestines), sinusoids (liver, bone marrow).
85
What drives transcapillary exchange?
Diffusion (small molecules), transcytosis (vesicles for proteins), and bulk flow (filtration/reabsorption via Starling forces).
86
What factors affect diffusion across capillaries?
Distance, concentration gradient, molecular size, lipid solubility.
87
Define Starling’s hypothesis.
Fluid movement across capillaries depends on hydrostatic pressure (HP) and oncotic pressure (COP) gradients.
88
Calculate net filtration pressure (NFP).
NFP = (Pc – Pif) – (πp – πif), where Pc = capillary HP, Pif = interstitial HP, πp = plasma COP, πif = interstitial COP.
89
What is capillary hydrostatic pressure (Pc)?
Blood pressure pushing fluid out of capillaries (higher at arteriolar end, lower at venous end).
90
What is oncotic pressure?
Osmotic pressure from plasma proteins (e.g., albumin) that pulls fluid back into capillaries.
91
Why does filtration occur at the arteriolar end of capillaries?
HP > COP (e.g., Pc = 37 mmHg, COP = 25 mmHg → net outward pressure).
92
Why does reabsorption occur at the venous end?
COP > HP (e.g., Pc = 15 mmHg, COP = 25 mmHg → net inward pressure).
93
How do lymphatics control interstitial fluid volume?
Lymph vessels collect excess fluid, aided by smooth muscle contractions and external compression (muscle pump).
94
What increases lymph flow (lymphagogues)?
Increased capillary permeability, decreased plasma oncotic pressure, or mechanical compression.
95
Which veins lack valves?
Vena cava, portal veins, and cerebral veins.

B.V 1 (1 decks)

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