1
Q
What are the two major phases of the cardiac cycle?
A
Ventricular diastole (relaxing + filling)
Ventricular systole (contracting + ejecting)
2
Q
What happens during ventricular diastole?
A
The ventricles relax and fill with blood.
3
Q
What are the 3 sub-phases of ventricular diastole?
A
1️⃣ Rapid filling 2️⃣ Slow filling 3️⃣ Atrial contraction (final 20–30% of filling)
4
Q
What happens during ventricular systole?
A
The ventricles contract and eject blood.
5
Q
What are the 2 sub-phases of ventricular systole?
A
1️⃣ Isovolumetric contraction 2️⃣ Ejection phase
6
Q
What is the final phase of the cardiac cycle called?
A
Isovolumetric relaxation
7
Q
During which ECG interval does mid-ventricular diastole occur?
A
During the TP interval (heart fully relaxed)
8
Q
What happens to atrial pressure during mid-ventricular diastole?
A
Atrial pressure slowly rises as blood returns from the veins
9
Q
Why does atrial pressure become slightly higher than ventricular pressure in early diastole?
A
Ventricular pressure is low
10
Q
What causes the AV valves (mitral & tricuspid) to open in early diastole?
A
A pressure difference where atrial pressure is slightly higher than ventricular pressure
11
Q
How does blood flow into the ventricles during mid-ventricular diastole?
A
Diastole = relaxing / filling
Ventricles are relaxed, blood flows passively into ventricles
Passively from the atria (no atrial contraction yet
70-80% of filling happens passively
12
Q
What percentage of ventricular filling occurs during this passive phase?
A
70–80%
13
Q
What event on the ECG indicates late ventricular diastole begins?
A
SA node fires → P wave on ECG
14
Q
What causes the brief increase in atrial pressure during late diastole?
A
Atrial contraction
15
Q
During late ventricular diastole, what is the pressure relationship between atria and ventricles?
A
Atrial pressure stays slightly higher than ventricular pressure
16
Q
Which valves remain open during late ventricular diastole?
A
AV valves remain open
17
Q
What is the “atrial kick”?
A
The final 20–30% of ventricular filling contributed by atrial contraction
18
Q
By the end of late diastole, ventricles reach what volume?
A
End-Diastolic Volume (EDV)
19
Q
What is the state of the semilunar valves during late ventricular diastole?
A
They remain closed
20
Q
When are the ventricles at peak filling?
A
At the final moment of diastole
21
Q
What percentage of ventricular filling is passive?
A
70–80%
22
Q
What percentage of ventricular filling is from atrial contraction (“atrial kick”)?
A
20–30%
23
Q
At the end of ventricular diastole, what volume do the ventricles contain?
A
End-Diastolic Volume (EDV)
24
Q
What is a typical EDV value at rest?
A
≈ 135 mL
25
After EDV is reached, does more blood enter the ventricles this cycle?
No more blood enters the ventricles
26
How does ventricular pressure compare to aortic pressure at the end of diastole?
Ventricular pressure is below aortic pressure → aortic valve stays closed
27
How does ventricular pressure compare to atrial pressure at the end of diastole?
Ventricular pressure is just below atrial pressure → AV valves remain open
28
What causes ventricular excitation to begin?
Electrical signal travels through the AV node and conduction system → QRS complex
29
What does the QRS complex represent?
Ventricles depolarizing → begin to contract
30
What happens to ventricular pressure at the start of systole?
It rises quickly
31
What causes the AV valves to close at the start of systole?
Ventricular pressure becomes greater than atrial pressure
32
What heart sound occurs when the AV valves close?
First heart sound (S1)
33
What marks the transition from diastole to systole?
Ventricular excitation as ventricles reach EDV (~135 mL)
34
When does isovolumetric ventricular contraction occur?
After AV valve closure and before aortic valve opens
35
What is the state of the ventricles during isovolumetric contraction?
Closed chamber → ALL valves closed → no inflow, no outflow
36
How does ventricular volume change during isovolumetric contraction?
Volume stays constant
37
Why does muscle fiber length remain constant during isovolumetric contraction?
Muscle is contracting but valves are closed → no change in chamber size
38
During which phase does ventricular pressure increase rapidly with no change in volume?
Isovolumentric contraction, an early phase of ventricular systole
Isovolumetric contraction = pressure change, no volume change
39
What event marks the end of isovolumetric ventricular contraction?
Ventricular pressure exceeds aortic pressure → aortic valve opens
40
What triggers ventricular ejection?
Ventricular pressure exceeds aortic pressure
41
What happens when ventricular pressure exceeds aortic pressure?
The aortic valve opens → blood flows out of the ventricle
42
On the right side of the heart, when does the pulmonary valve open?
When RV pressure exceeds pulmonary artery pressure
43
How does blood leave the heart during ventricular ejection?
Blood is ejected rapidly into the aorta (or pulmonary artery)
44
What happens to ventricular volume during ejection?
Ventricular volume decreases sharply
45
What is stroke volume (SV)?
The amount of blood pumped out per ventricle per beat
46
What is the typical stroke volume at rest?
~70 mL per beat
47
Stroke volume depends on what three factors?
Preload (EDV)
Afterload (aortic pressure)
Contractility
48
What are the two phases of ventricular systole?
Isovolumetric ventricular contraction and ventricular ejection
49
Describe isovolumetric ventricular contraction
All valves closed, pressure rises
50
Describe ventricular ejection
Semilunar valves open, blood flows out
51
Does the ventricle empty completely during ejection?
No, only about half of the EDV is pumped out.
52
What is end-systolic volume (ESV)?
The blood left in the ventricle at the end of systole.
53
What is the average ESV value?
~65 mL
54
What is the lowest volume in the cardiac cycle?
End-systolic volume (ESV)
55
Stroke volume (SV) formula?
SV = EDV − ESV
56
If EDV = 135 mL and ESV = 65 mL, what is SV?
~70 mL
57
What ECG wave marks ventricular repolarization?
T wave
58
What happens to ventricular pressure at the start of diastole?
It falls below aortic pressure.
59
When ventricular pressure falls below aortic pressure, which valve closes?
Aortic valve
60
What causes the dicrotic notch on the aortic pressure curve?
Brief rise in aortic pressure when the aortic valve closes.
61
Once the aortic valve closes at the start of diastole, how much more blood leaves the ventricle during this cycle?
None
62
What does the closing of semilunar valves indicate?
The end of ventricular systole and beginning of diastole.
63
When does ventricular filling occur?
When AV valves open
64
What is the first phase of ventricular filling?
Rapid filling (blood rushes from atrium to ventricle)
65
What is the second phase of ventricular filling?
Reduced filling (slower, continuous filling from veins)
66
What is the final phase of ventricular filling?
Atrial contraction — the “atrial kick”
67
What does the atrial kick do?
Pushes the last blood into the ventricles at the end of filling
68
How is ventricular filling impacted at fast heart rates?
Atrial contraction contributes more to filling because reduced filling time is shortened
69
What is the first heart sound called?
“Lub” (S₁)
70
What causes S₁ ("lub")?
AV valves (mitral & tricuspid) close
71
When does S₁ occur in the cardiac cycle?
Start of ventricular contraction (systole)
72
What type of pitch is the first heart sound?
Low-pitched and soft
73
What causes the actual sound of S₁?
Vibrations in the heart and big vessels (not valve flaps “slamming”)
74
What is the second heart sound called?
“Dup” (S₂)
75
What causes S₂ ("dup")?
Semilunar valves (aortic & pulmonary) close
76
When does S₂ occur in the cardiac cycle?
Start of ventricular relaxation (diastole)
77
What type of pitch is the second heart sound?
Higher-pitched “dup”
78
What causes the actual sound of S₂?
Vibrations, not the valve flaps themselves
79
What does the statement “Lub = closing of the AV valves” actually mean and NOT mean?
Means: The first heart sound (S₁) occurs when the AV valves (mitral & tricuspid) close, marking the start of ventricular systole.
Does NOT mean: The sound is caused by the valve flaps closing — the sound actually comes from vibrations in the heart and big vessels.
80
What is the most common cause of stenosis and insufficiency?
Rheumatic fever (autoimmune reaction after streptococcal throat infection)
81
In what age group does rheumatic fever often occur, and when might valve problems appear?
Occurs in children/teens; valve problems may appear years later in adulthood
82
How does rheumatic fever damage heart valves? (3 bullet points)
• Antibodies attack valve tissue → inflammation, thickening, stiffness, scarring
• Fibrous lesions may form
• Valve leaflets may stick together
83
What is stenosis?
Valve does not fully open
84
What is valve insufficiency (regurgitation)?
Valve does not fully close, causing backward flow
85
What is a heart murmur?
An extra or unusual sound heard with a stethoscope.
86
What causes most heart murmurs?
Turbulent blood flow (messy/swirl) instead of smooth flow.
87
How does turbulent flow create a murmur sound?
It creates vibrations in the heart and nearby vessels.
88
Are murmurs always a sign of cardiac disease?
No — usually (but not always).
89
What are murmurs in young, healthy people called?
Functional murmurs — harmless.
90
How to identify a murmur
- each valve is heart best at a specific spot on the chest
- determines which valve is affected
91
What does the timing of a murmur indicate?
When the abnormal blood flow occurs in the cardiac cycle.
92
What heart sound marks the start of ventricular systole?
S₁ (“lub”).
93
What heart sound marks the start of ventricular diastole?
S₂ (“dup”).
94
When does a systolic murmur occur? (by timing)
Between S₁ and S₂ (lub – murmur – dup).
95
When does a diastolic murmur occur? (by timing)
Between S₂ and the next S₁ (dup – murmur – lub).
96
What type of murmur produces a whistling sound?
A stenotic valve murmur. (by sound)
97
What type of murmur produces a swishing/gurgling sound?
An insufficient (leaky) valve murmur. (by sound)
98
What is a stenotic valve?
A narrowed valve that does not open fully.
99
What sound does a stenotic valve cause? Why?
blood forces through a tight opening, flow causes turbulence, A whistling sound due to fast, turbulent flow through a tight opening.
100
Give an example of a stenotic valve condition.
Aortic stenosis.
101
What is an insufficient (incompetent/leaky) valve?
A valve that does not close properly, allowing blood to flow backward.
102
Backward flow due to an insufficient valve is called what?
Regurgitation.
103
What sound does an insufficient valve cause? Why?
Swishing/gurgling sound due to backward flow colliding with forward flow.
104
Example of a condition with insufficient valve closure?
Mitral or Aortic regurgitation.
105
What dies a Lub-Whistle-Dup murmur indicate?
Stenotic semilunar valve — systolic murmur.
- a whistling systolic murmur signifies that a valve should be open during systole (a semilunar valve) does not open completely
106
During which phase does a Stenotic semilunar valve murmur phase occur?
Systole (valve should be open but doesn’t fully).
107
What does a Lub-Dup-Whistle murmur indicate?
Stenotic AV valve — diastolic murmur.
- a whistling diastolic murmur signifies that a valve that should be open during diastole (AV Valve) does not open completely
108
During which phase does a Stenotic AV valve murmur occur?
Diastole (valve should be open but doesn’t fully).
109
What does a Lub-Swish-Dup murmur indicate?
Insufficient AV valve — systolic murmur.
- a swishy systolic murmur signifies that a valve that should be closed during systole (an AV valve) does not close completely
110
Why does an Insufficient AV valve cause of systolic murmur?
Valve should be closed during systole but leaks.
111
What does a Lub-Dup-Swish murmur indicate?
Insufficient semilunar valve — diastolic murmur.
- a swishy diastolic murmur signifies that a valve that should be closed during systole (an AV valve) does not close completely
112
Why does an Insufficient semilunar valve cause a diastolic murmur?
Valve should be closed during diastole but leaks.
113
What is cardiac output the volume of?
Volume of blood ejected by each ventricle each minute (not both ventricles combined)
114
What is the formula for cardiac output (CO)?
heart rate × stroke volume
115
What is the example calculation for cardiac output on the slide?
70 beats/min × 70 ml/beat = 4900 ml/min ~ 5 litres/min
116
Why must CO be equal in right and left ventricle?
Keeps pulmonary and systemic circulation balanced.
117
At rest, how much blood does each ventricle pump every minute?
each ventricle pumps the entire blood volume (5–5.5 L) every minute
118
At rest, how much blood is pumped per year?
≈ 2.5 million liters of blood per year.
119
During exercise, how high can CO increase?
CO can increase to 20–25 L/min; Elite athletes: up to 40 L/min
120
What is Cardiac Reserve?
Cardiac Reserve = Maximum CO – Resting CO
121
How is CO regulated? (two points)
By changing heart rate
By changing stroke volume
122
When do heart rate and stroke volume increase?
Both increase when the body needs more oxygen (exercise, stress)
123
What nerve is responsible for the parasympathetic stimulation on the heart?
Vagus Nerve
124
What does parasympathetic stimulation influence to decrease heart rate?
Influence on the SA node to decrease heart rate
125
How does ACh decrease heart rate at the SA node?
When ACh is released, it increases K⁺ permeability in SA node cells → more K⁺ leaves → SA node slows → HR↓
126
What does parasympathetic stimulation do to the AV node?
Decreases AV node’s excitability
127
What is the effect on atrial and ventricular contraction?
Weakens atrial contraction but little effect on ventricular contraction
128
What does sympathetic stimulation innervate?
Innervates: SA node, AV node, and ventricles
129
What neurotransmitter is released in sympathetic stimulation and where does it bind?
Releases norepinephrine → binds β₁ receptors
130
What happens to pacemaker currents in SA node with sympathetic stimulation?
↑ pacemaker currents in SA node → faster depolarization
131
What causes heart rate to increase?
Reaches threshold sooner → HR increases
132
What happens to conduction through the AV node with sympathetic stimulation?
↑ conduction through AV node → shorter AV nodal delay
133
What happens to the spread of action potential?
Faster spread of action potential through conduction pathway
134
How does sympathetic stimulation affect Ca²⁺?
↑ Ca²⁺ entry in atrial & ventricular muscle
135
What happens to contraction and stroke volume?
Stronger contraction → ↑ stroke volume
136
What is the relationship between parasympathetic and sympathetic effects on heart rate?
The parasympathetic and sympathetic effects on heart rate are antagonistic.
137
What does parasympathetic stimulation do to HR?
Parasympathetic ↓ HR
138
What does sympathetic stimulation do to HR?
Sympathetic ↑ HR
139
What dominates at rest regarding HR control?
Rest: parasympathetic dominates → HR ≈ 70 bpm
140
Without autonomic input, how does the SA node fire?
Without autonomic input → SA node fires at its inherent rate 100 bpm
141
When does HR increase?
HR ↑ when sympathetic ↑ and parasympathetic ↓
142
When does HR decrease?
HR ↓ when parasympathetic ↑ and sympathetic ↓
143
What controls HR regulation?
Controlled by the cardiovascular control center in the brainstem
144
What hormone acts like sympathetic stimulation to increase HR?
Epinephrine (from adrenal medulla): Acts like sympathetic stimulation → Increases HR
145
Parasympathetic effect on SA Node
Decreases the rate of depolarization to threshold; decreases heart rate
146
Sympathetic effect on SA Node
Increases the rate of depolarization to threshold; increases the heart rate
147
Parasympathetic effect on AV Node
Increases nodal delay
148
Sympathetic effect on AV Node
Increases excitability; decreases the AV nodal delay
149
Parasympathetic effect on Ventricular Conduction Pathway
No effect
150
Sympathetic effect on Ventricular Conduction Pathway
Increases excitability; hastens conduction through bundle of His and Purkinje cells
151
Parasympathetic effect on Atrial Muscle
Decreases contractility; weakens contraction
152
Sympathetic effect on Atrial Muscle
Increases contractility; strengthens contraction
153
Parasympathetic effect on Ventricular Muscle
No effect
154
Sympathetic effect on Ventricular Muscle
Increases contractility; strengthens contraction
155
Parasympathetic effect on Adrenal Medulla (Endocrine gland)
No effect
156
Sympathetic effect on Adrenal Medulla (Endocrine gland)
Promotes secretion of epinephrine, a hormone that augments sympathetic nervous system actions on the heart
157
Parasympathetic effect on Veins
No effect
158
Sympathetic effect on Veins
Increases venous return, which is the strength of cardiac contraction through the Frank–Starling mechanism
159
What is the main determinant of cardiac muscle fibre length?
degree of diastolic filling
160
What happens the greater the diastolic filling?
the larger the end-diastolic volume (EDV) and the more heart is stretched
161
What happens the more the heart is stretched?
the longer the length of the fibres.
162
What does longer length result in?
a greater force of contraction and greater stroke volume.
163
More venous return → higher EDV → what happens to cardiac muscle fibres?
cardiac muscle fibres stretch more.
164
Stretching moves fibres closer to what?
their optimal length (Lo).
165
At a more optimal length, how do fibres contract?
fibres contract more forcefully.
166
Stronger contraction → what?
higher Stroke Volume (SV).
167
What is the Frank–Starling relationship
“The more the heart fills, the more it pumps.”
168
What does the cardiac length-tension relationship equalize?
Equalizing of output between the right and left sides of the heart so that blood pumped out by the heart is equally distributed.
169
What happens if one side pumps more?
If one side pumps more, the other side automatically adjusts.
170
↑ Stroke volume on one side → what effect?
↑ venous return to the other → stronger contraction → balanced output.
171
What does the cardiac length-tension relationship prevent?
Prevents blood from backing up in the circulation.
172
How does it help during exercise?
Helps Increase Cardiac Output During Exercise.
173
When larger cardiac output is needed, what happens?
venous return is increased through sympathetic nervous system and other mechanisms.
- helps increase cardiac output during exercise
174
Stroke Volume (SV)
Amount of blood pumped by each ventricle per beat.
175
the two types of controls that influence Stroke Volume
Intrinsic control (Frank–Starling Mechanism) and Extrinsic Control (Sympathetic Stimulation).
176
Intrinsic control (Frank–Starling Mechanism) depends on what?
Depends on venous return: When ↑ venous return → ↑ stretch of cardiac muscle → stronger contraction → ↑ SV.
177
What does sympathetic stimulation do to Stroke Volume?
Sympathetic nerves → ↑ Ca²⁺ entry into myocardium. Stronger contraction → more blood ejected → ↑ SV.
178
How do both factors increase stroke volume?
Both factors increase stroke volume by increasing strength of heart contraction.
179
Why the heart cannot overstretch?
Cardiac muscle does not stretch past its optimal length like skeletal muscle can because of:
180
What are the three reasons cardiac muscle cannot overstretch?
The pericardium (outer protective sac)
Strong connective tissue in the heart
Limited space for filling inside the chest
181
What is the conclusion about cardiac muscle length on the length-tension curve?
Therefore, cardiac muscle normally stays on the ascending limb of the length-tension curve and never reaches the overstretched descending limb.
182
What primarily determines the length–tension relationship in cardiac muscle?
Changes in lateral spacing between actin and myosin and as a results more or fewer cross-bridges
183
How does stretching cardiac muscle increase contraction strength?
- Stretching reduces the spacing between actin & myosin.
- Filaments come closer → more cross-bridge formation.
- ↑ Calcium sensitivity → stronger contraction.
184
What is afterload?
The pressure the ventricle must overcome to eject blood. (Mostly: aortic pressure for the left ventricle.)
185
What are the effects of increased afterload?
* Higher pressure to overcome — Ventricle must generate more force to open the valve.
* Lower Stroke Volume — Harder to eject blood → more blood left behind (↑ ESV).
186
How does the heart compensate if EDV increases?
Stretch → stronger contraction (Frank–Starling).
187
What happens if EDV does not rise?
Heart relies on sympathetic stimulation →
* NE binds β₁-receptors
* ↑ Ca²⁺ entry + release
* ↑ cross-bridge cycling → stronger contraction helps overcome high pressure.
188
What is the effect of sympathetic stimulation on stroke volume?
SV = EDV - EDS
Stroke Volume = (End-diastolic volume) - (End-systolic volume)
189
A patient has chronic high blood pressure. How does this affect afterload and the long-term workload on the heart?
High blood pressure ↑ aortic pressure → ↑ afterload.
The ventricle must generate more force to open the aortic valve → harder to eject blood → ↑ ESV → ↓ stroke volume.
Over time, the heart must work harder, causing ventricular hypertrophy and ↑ oxygen demand, which can lead to heart failure.
190
What is heart failure? STUDY
Inability of the cardiac output to keep pace with the body’s demands for supplies and removal of wastes.
191
What is the prime defect in heart failure? STUDY
Reduced contractility of the heart muscle (weakened cardiac muscle).
192
What may happen to the ventricles in heart failure? STUDY
One or both ventricles may weaken.
193
What happens when ventricles weaken in heart failure? STUDY
Blood may “back up” → congestion in veins and organs.
194
What is one main cause of heart failure related to cardiac muscle? STUDY
Decreased contractility (weaker cardiac muscle).
195
Decreased contractility often occurs after what event? STUDY
A myocardial infarction.
196
What effect does decreased contractility have on stroke volume? STUDY
Heart pumps a smaller stroke volume.
197
What is one main cause of heart failure related to pressure? STUDY
Increased afterload.
198
Increased afterload can be caused by what? STUDY
Chronic high blood pressure or valve problems.
199
Why does increased afterload weaken the heart over time? STUDY
Ventricle must create very high pressure just to open the valve → over time heart weakens.
200
What happens when contractility is reduced in heart failure? STUDY
The heart ejects a smaller stroke volume.
201
What is the first compensatory mechanism in heart failure? STUDY
Baroreceptor reflex (sympathetic response).
202
What triggers the baroreceptor reflex? STUDY
When cardiac output falls → BP and tissue blood flow drop - Baroreceptors (located in the carotid sinus and aortic arch) activate - sympathetic activity up, norepinephrine released onto the heart - Ca2 up - stronger contraction
203
What do baroreceptors do during heart failure? STUDY
They activate the sympathetic response.
204
What is released onto the heart during the baroreceptor reflex? STUDY
Norepinephrine.
205
What effect does norepinephrine have on the heart? STUDY
↑ Ca²⁺ → stronger contraction.
206
What is the second compensatory mechanism used in heart failure? STUDY
Frank–Starling mechanism (increased EDV).
207
How does the Frank–Starling mechanism help in heart failure? STUDY
More filling (higher EDV) → heart muscle stretches → contracts more strongly.
208
What is the purpose of these compensatory mechanisms? STUDY
They temporarily help the heart pump more forcefully despite reduced contractility.
209
What is decompensated heart failure? STUIDY
The point at which the heart can no longer pump out a normal stroke volume despite compensatory measures.
210
What type of heart failure results when the heart can no longer compensate? STUDY
Congestive heart failure.
211
What happens to blood flow in congestive heart failure? STUDY
Blood cannot enter and be pumped out of the heart, and the venous system dams up.
212
What is cor pulmonale? STUDY
Right-side heart failure.
213
What causes cor pulmonale? STUDY
Diseased lungs force the right side of the heart to pump harder.
214
What happens to the right ventricle in cor pulmonale? STUDY
The heart muscle undergoes hypertrophy.
215
Where does blood back up in left-sided heart failure? STUDY
In the lungs.
216
What condition is caused by lung blood backup in left-sided heart failure? STUDY
Pulmonary edema.
217
How does left-sided heart failure affect breathing? STUDY
Fluid in lungs reduces oxygen exchange.
218
How fast does acute heart failure develop? STUDY
Develops rapidly (hours – days)
219
Why can the heart not use long-term compensation in acute heart failure? STUDY
Heart cannot use long-term compensation (e.g., hypertrophy)
220
What are common sudden causes of acute heart failure? STUDY
* Myocardial infarction → sudden loss of contractility
* Pulmonary embolism → acute right ventricular failure
221
What happens when the left heart fails in acute heart failure? STUDY
Left heart fails → pulmonary edema
222
What happens when the right heart fails in acute heart failure? STUDY
Right heart fails → systemic venous congestion (swelling)
223
What is systolic failure? STUDY
Systolic failure = decreased contractility
stretched and thin chambers
- heart can't pump
224
What is diastolic failure? STUDY
Diastolic failure = poor filling (heart stiff, cannot expand well)
stiff and thick chambers
Heart can't fill
225
How is muscle supplied with oxygen and nutrients?
From blood delivered by coronary circulation, not from blood within the heart chambers.
226
What percent of cardiac muscle cell volume is mitochondria?
~40% of cell volume
227
Why does cardiac muscle have a heavy reliance on aerobic metabolism?
Cardiac muscle cells contain many mitochondria.
228
What does myoglobin do in cardiac muscle?
Stores small amounts of O₂ for immediate use.
229
Why can’t the heart use the blood inside its chambers for oxygen?
The heart cannot use the blood inside its chambers.
230
How is oxygen delivered to the heart?
Through the coronary circulation.
231
Where do the coronary arteries branch from?
The aorta.
232
Where do the coronary veins drain into?
The right atrium.
233
When does the heart receive most of its own blood supply?
During diastole (relaxation)
234
What happens to coronary vessels during systole?
Coronary vessels are compressed by contracting heart muscle.
235
How much oxygen does the heart extract at rest?
~65% of oxygen at rest
236
Why must the heart increase coronary blood flow when oxygen demand rises?
The heart has almost no reserve.
237
What primarily adjusts coronary blood flow?
Changes in the heart’s oxygen requirements.
238
During exercise, how much can the rate of coronary blood flow increase?
Up to five times its resting rate.
239
What happens when the heart works harder?
It uses more ATP.
240
What is produced when ATP breaks down?
Adenosine.
241
How does adenosine act?
As a paracrine signal.
242
What effect does adenosine have on coronary arteries?
Causes vasodilation of coronary arteries.
243
What is the result of vasodilation in coronary arteries?
More coronary blood flow → more O₂ delivery.
244
When does this mechanism help meet oxygen demand?
During exercise or stress.
245
What does increased coronary blood flow achieve?
This matches oxygen delivery to oxygen demand.
246
How does the heart increase its own blood flow? (Adenosine – steps in order)
1. When the heart works harder →
2. uses more ATP →
3. produces more adenosine →
4. adenosine diffuses to nearby coronary vessels →
5. causes vasodilation →
6. more oxygen-rich blood flows to heart muscle.
247
How is coronary blood flow matched to the oxygen need of cardiac muscle cells?
* ↑ Metabolic activity of cardiac muscle cells (↑ oxygen need) →
* ↑ Adenosine →
* Vasodilation of coronary vessels →
* ↑ Blood flow to cardiac muscle cells →
* ↑ Oxygen available to meet ↑ oxygen need
248
What is Atherosclerotic Coronary Artery Disease (CAD)?
Pathological changes within coronary artery walls that diminish blood flow through the vessels.
249
How common/severe is CAD in Canada?
Leading cause of death in Canada (≈ 32% of all deaths).
250
What can CAD cause?
Myocardial ischemia (reduced blood flow/oxygen to heart muscle) and possibly lead to acute myocardial infarction (heart attack due to death of heart muscle cells).
251
CAD can lead to myocardial ischemia and myocardial infarction through which 3 major mechanisms?
1️⃣ Vascular Spasm 2️⃣ Atherosclerosis (Main Mechanism) 3️⃣ Thromboembolism
252
What is a vascular spasm?
An abnormal spastic constriction that narrows the coronary vessels.
253
Why does vascular spasm happen in early CAD?
Coronary arteries are overly sensitive.
254
What triggers vascular spasm?
Triggers (cold, stress, exertion) reduce oxygen briefly.
255
What does low-oxygen endothelium release during vascular spasm?
A chemical (PAF = Platelet-Activating Factor).
256
What does PAF cause?
PAF causes the artery’s smooth muscle to tighten → spasm.
257
Is vascular spasm reversible?
Yes, the condition is reversible.
258
What type of disease is atherosclerosis?
Progressive, degenerative arterial disease that leads to occlusion of vessels.
259
What does atherosclerotic plaque consist of?
A lipid-rich core covered by abnormal overgrowth of smooth muscle cells, topped with connective tissue.
260
How does atherosclerosis start?
Starts with injury to the blood vessel, which triggers an inflammatory response that sets the stage for plaque buildup.
261
What is the first step in the development of atherosclerosis?
Damage to the artery lining occurs (from high BP, smoking, oxidized LDL, etc.).
262
What happens after damage to the artery lining?
LDL (“bad cholesterol”) enters the injured area and becomes oxidized.
263
What does oxidized LDL attract?
Immune cells (monocytes).
264
What do monocytes turn into, and what do they become?
Monocytes turn into macrophages and fill with fat → become foam cells → form a fatty streak.
265
What do smooth muscle cells do to contribute to plaque growth?
Smooth muscle cells move over the fatty streak and multiply, making the plaque grow.
266
How does plaque affect the vessel opening?
The plaque bulges into the vessel and narrows the opening for blood flow.
267
How does oxidized LDL affect nitric oxide (NO) production?
Oxidized LDL damages the endothelium, so it produces less nitric oxide (NO). With less NO, the artery cannot relax and widen properly.
268
What role does calcium play in plaque development?
Calcium deposits harden the plaque and stiffen the artery.
269
What happens as plaque enlarges?
Blood flow becomes limited → ischemia during stress or exercise.
270
What happens if the fibrous cap of an atherosclerotic plaque ruptures?
Collagen underneath is suddenly exposed to the blood.
271
What do platelets do when collagen is exposed?
Platelets assume the vessel is injured and immediately stick to the collagen and activate to form a blood clot (thrombus).
272
What are the two dangerous outcomes of thromboembolism?
1️⃣ Thrombus enlarges → fully blocks the artery 2️⃣ Piece breaks off → becomes an embolus → blocks a smaller downstream artery
273
What vessels are most serious consequences of atherosclerosis associated with?
Damage to the vessels of the brain and heart.
274
What is the prime cause of stroke in the brain and myocardial ischemia in the heart?
Atherosclerosis.
275
What are the potential complications of coronary atherosclerosis?
• Angina pectoris
• Thromboembolism
• Heart attack
276
What is myocardial infarction?
Heart attack.
277
What happens if the coronary artery becomes completely blocked?
Heart muscle supplied by that artery dies.
278
What determines the area of damage in a heart attack?
Larger artery = larger area of damage.
279
Which coronary artery blockage is worst and why?
Left coronary artery blockage is worst (supplies ~85% of myocardium).
280
What are the two categories in the table “Possible Outcomes of Acute Myocardial Infarction (Heart Attack)”
Immediate Death and Delayed Death from Complications.
281
What causes acute cardiac failure leading to immediate death? STUDY
The heart is too weak to pump effectively to support the body tissues.
282
What is a fatal ventricular fibrillation caused by in immediate death?
Damage to the specialized conducting tissue occurring because the weakened heart is deprived of oxygen.
283
What is one delayed fatal outcome of a heart attack?
Fatal rupture of the dead, degenerating area of the heart wall.
284
What is another delayed death outcome from complications of a heart attack? STUDY
Slowly progressing congestive heart failure where the heart becomes unable to pump out all the blood returned to it.
285
What are the two major phases of the cardiac cycle? STUDY
Ventricular Diastole (Relax & Fill)
Ventricular Systole (Contract & Eject)
286
What are the three components of Ventricular Diastole? (Relax & Fill)? STUDY
Rapid filling
Reduced (slow) filling
Atrial contraction (“atrial kick”)
287
What are the two components of Ventricular Systole (Contract & Eject)? STUDY
1. Isovolumetric contraction
2. Ventricular ejection
Followed by isovolumetric ejection
288
What follows ventricular ejection? STUDY
Isovolumetric relaxation
289
When does Mid-Ventricular Diastole (Early Filling) occur? STUDY
Occurs during TP interval
290
During Mid-Ventricular Diastole, how does atrial pressure compare to ventricular pressure? STUDY
Atrial Pressure (P) > Ventricular Pressure (P)
291
Which valves open during Mid-Ventricular Diastole (Early Filling)? STUDY
AV valves open (mitral, tricuspid)
292
Passive filling accounts for what percentage of total filling in Mid-Ventricular Diastole? STUDY
Passive filling → 70–80% of total
293
What happens when the SA node fires during Late Ventricular Diastole (Atrial Contraction)? STUDY
SA node fires → P wave
294
What effect does atrial contraction have on atrial pressure during late ventricular diastole? STUDY
Atria contract → slight ↑ atrial pressure
295
What does atrial contraction add to ventricular filling during late ventricular diastole? STUDY
Adds final 20–30% (atrial kick)
296
During Late Ventricular Diastole (atrial contraction), what happens to the semilunar valves? STUDY
semilunar valves remain closed
297
What is End-Diastolic Volume (EDV) defined as? STUDY
Maximum ventricular filling
298
What is the approximate End-Diastolic Volume (EDV) at rest? STUDY
≈135 mL at rest
299
During Onset of Systole, what does ventricular depolarization lead to? STUDY
Ventricular depolarization --> QRS complex
300
During Onset of Systole, what happens when ventricular P > atrial P? STUDY
Ventricular P > atrial P --> AV valves close --> S₁ (“lub”).
301
During Isovolumetric Contraction, what is the status of the valves? STUDY
All valves closed
302
During Isovolumetric Contraction, what happens to blood movement? STUDY
No blood movement
303
During Isovolumetric Contraction, what happens to ventricular pressure? STUDY
Sharp ↑ ventricular pressure.
304
During Ventricular Ejection, what happens when ventricular P > aortic P? STUDY
Ventricular P > aortic P --> aortic valve opens
305
During Ventricular Ejection, what happens when blood is ejected? STUDY
Blood ejected --> ventricular volume decreases quickly
306
During Ventricular Ejection, what three factors determine stroke volume (SV)? STUDY
* Preload (EDV);
* Afterload (aortic pressure); and
* Contractility
307
At the End of Ventricular Systole, does the ventricle empty completely? STUDY
Ventricle never empties completely
308
What is the End-Systolic Volume (ESV) at the End of Ventricular Systole? STUDY
End-Systolic Volume (ESV) ≈ 65 mL
309
How is stroke volume (SV) calculated at the End of Ventricular Systole? STUDY
SV = EDV – ESV ≈ 70 mL
310
What electrical event marks Ventricular Repolarization (Start of Diastole)? STUDY
T wave
311
During Ventricular Repolarization (Start of Diastole), how does ventricular P compare to aortic P?STUDY
Ventricular P < aortic P
312
During Ventricular Repolarization (Start of Diastole), what happens to the aortic valve? STUDY
Aortic valve closes --> S₂ (“dup”), seen as dicrotic notch.
313
In Heart Sounds, what is S₁ (“Lub”)? STUDY
When AV valves close; and
* Start of systole.
314
In Heart Sounds, what are the heart sounds from? STUDY
Sounds are from vibrations, not valves physically hitting shut.
315
In Heart Sounds, what is S₂ (“Dup”)? STUDY
When semilunar valves close; and
* Start of diastole.
316
In Heart Murmur, what causes the sound? STUDY
Turbulent blood flow;
317
In Heart Murmur, what can murmurs be? STUDY
Can be functional or pathological
318
In Valve Disorders, what is stenosis? STUDY
Stenosis (narrowing)
- whistling sounds
319
In Valve Disorders, what is an example of stenosis? STUDY
Aortic stenosis
320
In Valve Disorders, what is insufficiency/regurgitation? STUDY
Insufficiency / Regurgitation (leak)
321
In Valve Disorders, what sound is associated with insufficiency/regurgitation? STUDY
Swishing/gurgling sound.
322
In Valve Disorders, what is an example of regurgitation? STUDY
Ex: Mitral regurgitation.
323
In Rheumatic Fever, what is the reaction described? STUDY
Autoimmune reaction post-strep
324
In Rheumatic Fever, what does it cause? STUDY
Causes valve thickening, scarring --> later stenosis or regurgitation.
325
In Cardiac Output (CO), what is the formula for CO? STUDY
CO = HR × SV
326
In Cardiac Output (CO), what is the CO at rest? STUDY
Rest:
* 70 bpm × 70 mL = ~5 L/min;
327
In Cardiac Output (CO), what is CO during exercise? STUDY
Exercise: 20–25 L/min;
328
In Cardiac Output (CO), what is CO for elite athletes? STUDY
Elite athletes: up to 40 L/min.
329
In Cardiac Reserve, how is cardiac reserve defined? STUDY
Maximum CO – Resting CO
330
In Autonomic Control of the Heart, what does the parasympathetic system do to heart rate? STUDY
↓ Heart rate
331
In Autonomic Control of the Heart, what does the parasympathetic system do to AV node conduction? STUDY
↓ AV node conduction
332
In Autonomic Control of the Heart, what does the parasympathetic system do to atrial contraction? STUDY
Weakens atrial contraction
333
In Autonomic Control of the Heart, what does the sympathetic system do to HR? STUDY
↑ HR
334
In Autonomic Control of the Heart, what does the sympathetic system do to conduction speed? STUDY
↑ Conduction speed
335
In Autonomic Control of the Heart, what does the sympathetic system do to contractility and SV? STUDY
↑ Contractility --> ↑ SV
336
In Autonomic Control of the Heart, what system dominates at rest and what HR does it produce? STUDY
At rest: Parasympathetic dominance --> HR ≈ 70 bpm
337
In Autonomic Control of the Heart, what is the intrinsic SA node rate? STUDY
Intrinsic SA node rate: ≈ 100 bpm
338
What is stated in the Frank–Starling Law of the Heart? STUDY
“Increased filling --> increased contraction --> increased SV.”
339
In the Frank–Starling Law of the Heart, what does increased venous return lead to? STUDY
↑ Venous return --> ↑ EDV --> ↑ stretch --> ↑ Ca²⁺ sensitivity --> ↑ SV;
340
In the Frank–Starling Law of the Heart, what does it balance? STUDY
Balances output of left vs. right heart;
341
In the Frank–Starling Law of the Heart, what does it prevent? STUDY
Prevents blood backup; and
342
In the Frank–Starling Law of the Heart, what limits the heart’s ability to stretch? STUDY
* Pericardium; * Connective tissue; and * Chest cavity space
343
In Afterload, what must the ventricle overcome to eject blood? STUDY
Pressure ventricle must overcome to eject blood;
344
In Afterload, what is the main contributor? STUDY
Mainly aortic pressure; and
345
In Afterload, what is the effect of increased afterload? STUDY
↑ Afterload --> ↓ SV --> ↑ ESV
346
In Afterload — Compensation, what increases EDV? STUDY
Frank-Starling (↑ EDV); and
347
In Afterload — Compensation, what increases contractility? STUDY
Sympathetic activity (↑ Ca²⁺ --> ↑ contractility)
348
In Heart Failure, what is the definition? STUDY
Heart cannot meet metabolic demands.
349
In Heart Failure, what causes decreased contractility? STUDY
↓ Contractility (MI); and
350
In Heart Failure, what increases afterload? STUDY
↑ Afterload (hypertension, valve disease)
351
In Heart Failure — Compensations, what are the compensation mechanisms? STUDY
1. Sympathetic activation
2. Frank-Starling
352
In Heart Failure — Compensations, what does Frank–Starling increase? STUDY
Frank–Starling (↑ EDV)
353
In Decompensated Failure, what happens when compensation fails? STUDY
Compensation fails --> congestive heart failure (CHF)
354
In Heart Failure — Types, what happens in right-sided failure? ZSTUDY
Right-sided: systemic congestion, edema;
355
In Heart Failure — Types, what happens in left-sided failure? ZSTUDY
Left-sided: pulmonary edema;
356
In Heart Failure — Types, what happens in systolic failure? zsTUDY
Systolic: poor contraction; and
357
In Heart Failure — Types, what happens in diastolic failure? STUDY
Diastolic: poor filling
358
In Coronary Circulation, where does the heart receive O₂ from? STUDY
Heart receives O₂ from coronary arteries, not chamber blood;
359
In Coronary Circulation, how much O₂ does the heart extract at rest? STUDY
Extracts ~65% of O₂ at rest (very high); and
360
In Coronary Circulation, what must increase during exercise? STUDY
Must ↑ coronary blood flow during exercise.
361
In the Adenosine Mechanism, what does increased cardiac metabolism cause? STUDY
↑ Cardiac metabolism --> ↑ adenosine --> vasodilation --> ↑ coronary flow
362
In Coronary Artery Disease (CAD), what is its significance in Canada? STUDY
Leading cause of death in Canada; and
363
In Coronary Artery Disease (CAD), what does decreased coronary flow lead to? STUDY
↓ Coronary flow --> ischemia --> MI.
364
In Coronary Artery Disease (CAD) - What are the 3 mechanisms? STUDY
1. Vascular spasm
2. Atherosclerosis (main)
3. Thromboembolism
365
In Atherosclerosis Development, what is step 1? STUDY
Endothelial injury
366
In Atherosclerosis Development, what is step 2? STUDY
LDL oxidation
367
In Atherosclerosis Development, what is step 3? STUDY
Macrophage --> foam cells
368
In Atherosclerosis Development, what is step 4? STUDY
Fatty streak
369
In Atherosclerosis Development, what is step 5? STUDY
Plaque growth
370
In Atherosclerosis Development, what is step 6? STUDY
↓ Nitric oxide --> ↓ vasodilation
371
In Atherosclerosis Development, what is step 7? STUDY
Calcium deposition
372
In Atherosclerosis Development, what is step 8? STUDY
↓ Flow --> ischemia
373
In Atherosclerosis Development, what can plaque rupture lead to? TSUDY
Plaque rupture --> thrombus --> embolus --> MI or stroke
374
In Atherosclerosis Development, which artery blockage is most lethal and why? STUDY
Left coronary artery blockage is most lethal (supplies ~85% of myocardium)
375
A nurse explains why an isotonic solution is used in a patient with dehydration.
Which explanation is correct? EXAMM
It maintains equilibrium between intracellular and extracellular fluid
376
Which situation best illustrates secondary active transport across a cell membrane? EXAMM
A. Sodium ions being pumped out of the cell using ATP
B. Water moving across a membrane in response to an osmotic gradient
C. A molecule moving down its concentration gradient through a channel
D. A solute entering the cell by coupling its movement to sodium ions
D. A solute entering the cell by coupling its movement to sodium ions
377
A person accidentally touches a very hot surface and pulls their hand away
immediately, before becoming fully aware of the pain. What best explains this
response? EXAM
A. Pain signals travel faster than motor signals
B. The withdrawal reflex is processed at the spinal cord level
C. Pain receptors are inhibited during injury
D. Myelinated fibres block pain transmission
B. The withdrawal reflex is processed at the spinal cord level
378
Which statement best describes the role of cerebrospinal fluid? EXAMM
A. It supplies oxygen directly to neurons
B. It cushions and protects the brain and spinal cord
C. It transmits electrical signals
D. It strengthens connective tissue
B. It cushions and protects the brain and spinal cord
379
5. Which type of synapse uses chemical messengers to transmit signals? EXAMM
A. Electrical synapse
B. Chemical synapse
C. Mechanical synapse
D. Stretch synapse
B. Chemical synapse
380
Why is voluntary movement lost below the level of a severed spinal nerve? EXAMM
A. Muscles lose their ability to contract
B. Action potentials cannot travel past the damaged area
C. Sensory receptors become inactive
D. Synapses release excess neurotransmitter
B. Action potentials cannot travel past the damaged area
381
7. Which statement about action potentials is correct?
EXAMM
A. Stronger stimuli produce larger action potentials
B. Action potentials occur only in dendrites
C. Once threshold is reached, action potentials are all-or-none
D. Action potentials remain localized
C. Once threshold is reached, action potentials are all-or-none
382
A neuron is at rest with a membrane potential of approximately −70 mV. At this resting
state, the membrane is much more permeable to one ion than to others. When the
neuron receives a stimulus, voltage-gated sodium channels open, causing the
membrane potential to move toward zero. This phase is followed by the opening of
voltage-gated potassium channels, which bring the membrane potential back toward
its resting value.
Now consider a patient who develops low blood potassium levels (hypokalemia).
Which statement best describes what happens in this situation? EXAMM
A. The neuron becomes more excitable because the resting membrane potential is
closer to threshold
B. The resting membrane potential becomes more negative, making it harder for the
neuron to fire
C. Depolarization occurs because potassium enters the cell
D. Repolarization is prevented because sodium cannot leave the cell
B. The resting membrane potential becomes more negative, making it harder for the neuron to
fire
