The heart Flashcards

1
Q

Regarding the isovolumetric relaxation phase of the cardiac cycle, which of the following statements is correct?

A It is during isovolumetric ventricular relaxation that the ventricles fill
B It occurs in late ventricular diastole
C It is phase 5 of the cardiac cycle
D Isovolumetric ventricular relaxation ends when the ventricular pressure falls below the atrial pressure

A

D

Explanation
After the ventricular muscle is fully contracted, the already falling ventricular pressure does so more rapidly. This period is protodiastole (0.04s). It ends when the momentum of the ejected blood is overcome and the aortic and pulmonary valves close. After the valves close, pressure continues to drop rapidly during the period of isovolumetric ventricular relaxation (early diastole). Isovolumetric ventricular relaxation ends when the ventricular pressure falls below the atrial pressure and the AV valves open, permitting the ventricles to fill (thus ventricular filling occurs after the isovolumetric relaxation occurs). Filling is rapid at first, and then slows as the next cardiac contraction approaches. It is phase 4 of the cardiac cycle.

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2
Q

Regarding ECGs, which of the following statements is FALSE?

A ST represents ventricular repolarisation
B QT interval represents ventricular depolarisation and ventricular repolarisation
C QRS represents ventricular depolarisation and atrial repolarization
D PR interval represents atrial depolarisation and conduction through the SA node

A

D

Explanation
PR interval represents atrial depolarization and conduction through the AV node

Note: ST interval (QT minus QRS) reflects ventricular repolarisation (during T wave). the actual ST interval is the time at which the entire ventricle is depolarized and roughly corresponds to the plateau phase of the ventricular action potential.

Extra: the answer is directly out of the prescribed text book, however from older editions. The new edition writes: PR interval: atrioventricular conduction, measured from the beginning of the P wave to the beginning of the QRS complex.

Extra:

QRS duration represents ventricular depolarisation. It is also when atrial repolarisation occurs but the wave for atrial repolarisation is masked by the wave for ventricular depolarisation.

Human atrial depolarization is represented by the P wave and it is well observed and recorded by the standard 12-lead ECG in sinus rhythm subjects. As the human Ta wave of atrial repolarization occurs during the PR segment and QRS complex, it is not observed and recorded widely in sinus rhythm subjects by the standard 12-lead ECG. This is generally due to the amplitude being very low, usually in the range of 10-60 pV, and also, ventricular activation normally begins before atrial repolarization ends, and therefore, the QRS complex overlaps with the Ta wave (Source: Unmasking of atrial repolarization waves using a simple modified limb lead system. Anatol J Cardio2016 Aug; 15(8): 605–610.

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3
Q

The R wave on an ECG corresponds to which of the following?

A Na efflux
B Ca efflux
C Ca influx
D Na influx

A

D

Explanation
The R wave is due to the initial depolarization of the cardiac muscle due to the sudden influx of Na+ through the rapidly opening Na+ Channels.

EXTRA: The R wave of the ECG correlates to phase 0 of the cardiac action potential, which is due to rapid depolarization due to Na influx through rapidly opening Na channels.

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4
Q

Fasting energy for the heart comes from?

A Free fatty acids (FFA)
B Glucose
C Amino acids
D Glycerol

A

A

Explanation
Under basal conditions, 35% of the caloric needs of the human heart are supplied by carbohydrates, 5% by ketones and amino acids, and 60% by fats. Following large ingestion of glucose, more pyruvate and lactate is used. During prolonged starvation, more fat is used. Circulating free fatty acids normally account for about 50% of the lipid utilized

Note: the question can be “the caloric needs of the heart are met by?”

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5
Q

In a healthy male who is running, which of the following statements is correct?

A Systolic BP rises and diastolic BP either falls or stays the same
B Cardiac output can increase 1500%
C Maximal heart rate is independent of age
D O2 extraction can increase 600%

A

A

Explanation
Blood flow to the heart is 250ml/min or 84ml/100g/min. A normal beating heart, O2 consumption is 9ml/100g/min. (basal heart rate consumption is 2ml/100g/min). The O2 extraction can increase by 100%. Cardiac output can increase by 700% (rest=cardiac output is 6.4L/min and it can go up to 35L/min) and there is a net fall in total peripheral resistance due to vasodilation in exercising muscles. Consequently, systolic blood pressure rises moderately, whereas diastolic pressure usually remains unchanged or falls.

Eating increases CO 30%, and anxiety by 50-100%

Maximal heart rate achieved during exercise decrease with age.

Extra:

Running is a form of ISOTONIC muscle contration.

The systemic cardiovascular response to exercise that provides for the additional blood flow to contracting muscle depends on whether the muscle contractions are primarily isotonic or isometric with the performance of external work.

Isometric muscle contraction: Heart rate rises (decreased vagal tone), systolic and diastolic blood pressure rises sharply. SV changes relatively little, and blood flow to the steadily contracting muscle is reduced as a result to the compression of the blood vessels.

Isotonic contracting muscle: Prompt increase in HR, but different to isometric contraction in that there is a marked increase in SV. In addition, there is a net fall in total peripheral resistance due to vasodilation in exercising muscle. Consequently, systolic blood pressure rises only moderately , whereas diastolic pressure usually remains unchanged or falls.

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6
Q

In a man with congestive heart failure, which of the following occurs?

A Increased atrial pressure
B Prolonged decrease in sodium reabsorption in the proximal convoluted tubule
C Increased albumin
D Increased renin secretion

A

A

Explanation
Congestive cardiac failure results in an increase in ventricular and atrial pressures. This causes atrial stretch which stimulates the release of ANP (atrial natriuretic peptide). Renal effects caused by ANP include increased GFR (dilatation of the afferent arteriole and constriction of the efferent arteriole), decreased Na reabsorption (in the DCT and collecting tubules), and an inhibition of renin secretion, thereby inhibiting the renin-angiotensin-aldosterone system. Once the cardiac output drops the RAAS system regains the ascendency and increases sodium resorption.

Note: not a great question, but it has been seen before.

Extra: Both B-type natriuretic peptide and A-type natriuretic peptide have beneficial haemodynamic effects during heart failure and represent another natural mechanism to relieve symptoms. They are released primarily in the atrium as the elevated cardiac pressures stretch the atrial myocytes. (www.haelio.com)

Extra:

Atrial natriuretic peptide (ANP) is a 28-amino acid peptide that is synthesized, stored, and released by atrial myocytes in response to atrial distension, angiotensin II, stimulation, endothelin and sympathetic stimulation (beta adrenoceptor mediated). Therefore, elevated levels of ANP are found during hypervolemic states (elevated blood volume), such as occurs in heart failure. ANP is first synthesized and stored in cardiac myocytes as prepro-ANP, which is then cleaved to pro-ANP and finally to ANP. ANP is the biologically active peptide.

Cardiovascular and Renal Effects

Natriuretic peptides (NPs) are involved in the long-term regulation of sodium and water balance, blood volume and arterial pressure. There are two major pathways of natriuretic peptide actions: 1) vasodilator effects, and 2) renal effects that leads to natriuresis and diuresis.

NPs directly dilate veins (increase venous compliance and thereby decrease central venous pressure, which reduces cardiac output by decreasing ventricular preload. NPs also dilate arteries, which decreases systemic vascular resistance and systemic arterial pressure. Chronic elevations of NPs appear to decrease arterial blood pressure primarily by decreasing systemic vascular resistance. The mechanism of systemic vasodilation involves NP receptor-mediated elevations in vascular smooth muscle cGMP as well as attenuation of sympathetic vascular tone. This latter mechanism may involve NPs acting on sites within the central nervous system as well as through inhibition of norepinephrine release by sympathetic nerve terminals.

NPs affect the kidneys by increasing glomerular filtration rate (GFR) and filtration fraction, which produces natriuresis (increased sodium excretion) and diuresis (increased fluid excretion). These renal effects of NPs are potassium sparing unlike most diuretic drugs that are used to induce natriuresis and diuresis in patients.

A second renal action of NPs is that they decrease renin release, thereby decreasing circulating levels of angiotensin II and aldosterone. This leads to further natriuresis and diuresis. Decreased angiotensin II also contributes to systemic vasodilation and decreased systemic vascular resistance.

Taken together, these actions of NPs decrease blood volume, arterial pressure, central venous pressure, pulmonary capillary wedge pressure and cardiac output. To summarize, natriuretic peptides serve as a counter regulatory system for the renin-angiotensin-aldosterone system (RAAS).

Source

CVSphysiology.com

The question is still producing grief.

Another feedback explanation:

“Heart failure occurs when the heart is unable to put out an amount of blood that is adequate for the needs of the tissues. It can be acute and associated with sudden death, or chronic. The failure may involve primarily the right ventricle (cor pulmo- nale), but much more commonly it involves the larger, thicker left ventricle or both ventricles. Heart failure may also be sys- tolic or diastolic. In systolic failure, stroke volume is reduced because ventricular contraction is weak. This causes an increase in the end-systolic ventricular volume, so that the ejection fraction falls from 65% to as low as 20%. The initial response to failure is activation of the genes that cause cardiac myocytes to hypertrophy, and thickening of the ventricular wall (cardiac remodeling). The incomplete filling of the arterial system leads to increased discharge of the sympathetic nervous system and INCREASED SECRETION OF RENIN and aldosterone, so Na+ and water are retained. These responses are initially compensatory, but eventually the failure worsens and the ventricles dilate.”

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7
Q

Regarding the cardiac action potential of a typical ventricular cell, which of the following statements is correct?

A The plateau phase is 100 x longer than depolarisation
B The relative refractory period prevents tetanus
C The plateau phase is based on K+ efflux
D Unlike nerve action potential, there is no overshoot

A

A

Explanation
In mammalian cardiac muscle cells, depolarization proceeds rapidly, and an overshoot of the zero potential is present, as in skeletal and nerve, but this is followed by a plateau before the membrane potential returns to the base line. There is an overshoot in cardiac action potential and there is a plateau phase (unlike in nerve action potential) before a return to the baseline. The plateau phase is due to calcium influx (slow but prolonged opening of the voltage gated calcium channels. Cardiac depolarization lasts about 2ms, but the plateau phase and repolarization lasts 200ms or more. The plateau phase coincides with the absolute refractory period and repolarisation coincides with the relative refractory period. Repolarisation is not complete until the contraction is half over. The absolute refractory period (phases 0-2 and half of three) prevents tetanus. No matter the type of stimulus, the muscle cannot be excited again

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8
Q

The slowest conducting cardiac tissue is?

A Atrioventricular (AV) node
B Atrial Pathways
C Ventricular muscle
D Bundle of His

A

A

Explanation
- AV node= 0.05m/s (meters per second)

  • SA node=0.05m/s
  • Purkinje System=4m/s
  • Atrial pathways=1m/s
  • Ventricular muscles= 1m/s
  • Bundle of His=1m/s

The conduction system within the heart is very important because it permits a rapid and organized depolarization of ventricular myocytes that is necessary for the efficient generation of pressure during systole. The time (in seconds) to activate the different regions of the heart are shown in the figure to the right. Atrial activation is complete within about 0.09 sec (90 milisec) following SA nodal firing. After a delay at the AV node, the septum becomes activated (0.16 sec). All the ventricular mass is activated by about 0.23 sec.

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9
Q

During strenuous exercise, a fit 20 yr male can increase his stroke volume by?

A 400%
B 500%
C 300%
D < 200%

A

D

Explanation
Normal stroke volume (SV) is 70-90mls. A fit person can increase his SV to a max of 126ml, which is, less than a 200% increase. Any further increases in exercise will result in a decrease in SV due to a rising heart rate and thus a shortening of diastole

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10
Q

Question 10
Regarding cardiac muscle, which of the following statements is correct?

A It can display tetanus
B Time of contraction is less than action potential
C The relative refractory period (RRP) is longer than the absolute refractory period (ARP)
D Calcium release from sarcoplasmic reticulum initiates contraction

A

D

Explanation
The role of calcium in the excitation-contraction coupling is similar to its role is skeletal muscle. However, it is the influx of extracellular calcium that is triggered by activation of the dihydropyroidine channels in the T system, rather than depolarization per se, that triggers release of stored calcium from the sarcoplasmic reticulum. The absolute refractory period (ARP) is longer than the relative refractory period (RRP). The time of contraction is about 1.5 times longer. The cardiac muscle can never display tetanus

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11
Q

In the fasting state, which of the following meets most of the hearts basic caloric requirements?

A Protein
B Lactate
C Glucose
D Free fatty acids

A

D

Explanation
Under basal conditions, 35% of the caloric needs of the human heart are supplied by carbohydrates, 5% by ketones and amino acids, and 60% by fats. Following large ingestion of glucose, more pyruvate and lactate is used. During prolonged starvation, more fat is used

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12
Q

The cardiac output during exercise can increase by?

A 600%
B 700%
C 500%
D 200%

A

B

Explanation
Further, eating increases CO 30% and anxiety by 50-100%

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13
Q

Cardiac output is changed as listed in all of the following circumstances except?

A Decreases when moving from a lying to a sitting position
B Decreased by sleep
C Increased on eating
D Increased during exercise

A

B

Explanation
There is no change to cardiac output during sleep or moderate changes in environmental temperature.

Decrease in cardiac output occurs during rapid arrhythmias, heart disease and when sitting or standing from a lying position.

Increase in cardiac output occurs during anxiety and excitement, eating, exercise, high environmental temperatures, pregnancy and adrenaline

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14
Q

During exercise in a fit, healthy young male, which of the following options is correct?

A Stroke volume increases more than 700%
B Stroke volume increases more than 400%
C Stroke volume increases more than 300%
D Stroke volume increases less than 200%

A

D

Explanation
Normal stroke volume (SV) is 70-90mls. A fit person can increase his SV to a max of 126ml, which is, less than a 200% increase. Any further increases in exercise will result in a decrease in SV due to a rising heart rate and thus a shortening of diastole

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15
Q

Under basal conditions the percentage of the heart’s caloric needs which is met by fat is?

A 40%
B 50%
C 60%
D 70%

A

C

Explanation
Under basal conditions, 35% of the caloric needs of the human heart are supplied by carbohydrates, 5% by ketones and amino acids, and 60% by fats.

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16
Q

Myocardial contractility is decreased by all of the following except?

A Barbituates
B Hypercarbia
C Bradycardia
D Glucagon

A

D

Explanation
Glucagon, which increases the formation of cyclic adenosine monophosphate (cAMP), is positively inotropic, and is recommended in the treatment of some heart diseases. Theophylline and digitalis also have an inotropic effect. Hypercapnia, hypoxia,acidosis and drugs such as quinidine, procainamide and barbiturates depress myocardial contractility. Contractility is also reduced in heart failure. An increase in heart rate will also increase contractility, although the effect is relatively small.

Note: the question is referring to intrinsic myocardial contractility and not myocardial fibre shortening (which is a product of the 3 factors-afterload, contractility and preload)

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17
Q

Cardiac output is decreased by which of the following?

A Sleep
B Exercise
C Pregnancy in the first trimester
D Sitting from a lying position

A

D

Explanation
Cardiac output

Decreased by: sitting or standing form a lying position, rapid arrhythmias and heart disease.

Increased by: anxiety and excitement, eating, exercise, high environmental temperatures, pregnancy and adrenaline.

No change: sleep, moderate changes in environmental temperature

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18
Q

With regard to the cardiac cycle, which of the following options is correct?

A The c wave is due to tricuspid valve opening
B The T wave of the ECG occurs during phase 4
C The aortic valve opens at the beginning of phase 2
D Phase 1 represents atrial systole

A

D

Explanation
The aortic valve opens at the end of stage 2. The T wave of the ECG occurs during phase 3 (ventricular ejection). The c wave is the transmitted manifestation of the rise in atrial pressure produced by the bulging of the tricuspid wave into the atria during isovolumetric ventricular contraction. This isovolumetric ventricular contraction follows atrial systole and lasts about 0.05s until the pressures in the left and right ventricles exceed the pressures in the aorta and pulmonary artery and the aortic and pulmonary valves open

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19
Q

Which of the following statements is correct with regard to the 12 lead ECG?

A The standard limb leads record the potential difference between 2 limbs
B Lead II is at 90 degrees for vector analysis
C +130 degrees is within the normal range for the axis
D V2 is placed in the 3rd left intercostal space

A

A

Explanation
Regarding the 12 lead ECG; V2 is placed in the 4th intercostal space. -30 to 110 degrees is considered a normal axis. Lead II lies at 60 degrees for vector analysis. The unipolar limb leads form the points of an equilateral triangle and heart lies in the centre

Issue:

The current textbook writes that the normal direction of the mean QRS vector is generally said to be -30 to 110 degrees. LAD or RAD is said to be present if the calculated axis falls to the left of -30 degrees or to the right of 110 degrees.

A web search states: A normal heart axis is between -30 and +90 degrees.

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20
Q

With regard to cardiac action potentials, which of the following options is correct?

A The action potential in the AV node is largely due to calcium fluxes
B Phase 0 and phase 1 are steepest in the AV node
C The resting membrane potential decreases by vagal stimulation
D Cholinergic stimulation increases the slope of the pre-potential

A

A

Explanation
Cholinergic and vagal stimulation both decrease the peripotentials as the nodal tissue membranes become hyperpolarized or more negative. There are no phases to the cardiac pacemaker’s action potential (unlike the ventricular muscle). The action potentials in the SA and the AV nodes are largely due to Ca with no contribution of Na influx.

The opening and closing of ion channels can induce a departure from the resting potential. This is called a depolarisation if the interior voltage becomes more positive (say from –70 mV to –60 mV), or hyperpolarisation if the interior voltage becomes more negative (say from –70 mV to –80 mV).

Therefore vagal stimulation causes the cell RMP to become hyperpolarised- greater MV. The value goes form -90MV to say -130MV. The negative reflects the inside of the cell. (The negative voltage inside the cell once measured)

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21
Q

The most rapid conduction of electrical impulses occur in which of the following?

A Purkinje system
B Bundle of His
C Atrial pathways
D Atrioventricular (AV) node

A

A

Explanation
- AV node= 0.05m/s (metres/second)

  • SA node=0.05m/s
  • Purkinje System=4m/s
  • Atrial pathways=1m/s
  • Ventricular muscles= 1m/s
  • Bundle of His=1m/s

The conduction system within the heart is very important because it permits a rapid and organized depolarization of ventricular myocytes that is necessary for the efficient generation of pressure during systole. The time (in seconds) to activate the different regions of the heart are shown in the figure to the right. Atrial activation is complete within about 0.09 sec (90 msec) following SA nodal firing. After a delay at the AV node, the septum becomes activated (0.16 sec). All the ventricular mass is activated by about 0.23 sec.

NOTE: the question can be asked: “whoich is the slowest conduction”

22
Q

Regarding the T wave of the ECG, which is correct?

A It represents ventricular repolarization
B An inverted T wave is always pathological
C It refers to the absolute refractory period
D It is caused by potassium infflux

A

A

Explanation
The T wave on the ECG refers to ventricular repolarisation. The interval from the beginning of the QRS complex to the apex of the T wave is referred to as the absolute refractory period. The last half of the T wave is referred to as the relative refractory period. An inverted T wave can be normal in a number of leads especially AvR, I, and III. It is due to the efflux of K through multiple type of K channels.

23
Q

Which of the following factors do not cause coronary vasodilation?

A Lactate
B Adenine nucleotides
C Increased concentration of CO2
D Hypokalaemia

A

D

Explanation
The close relationship between coronary blood flow and myocardial O2 consumption indicates that one or more of the products of metabolism cause coronary vasodilation. Factors suspected of playing this role include O2 lack and increased concentrations of CO2, H, K, lactate, PG, adenine nucleotides and adenosine. Asphyxia, hypoxia and intracoronary injections of cyanide all increase coronary blood flow 200-300% in denervated as well as intact hearts.

24
Q

In which phase of the cardiac cycle does the mitral valve close?

A Phase 4
B Phase 3
C Phase 2
D Phase 1

A

C

Explanation
According to the cardiac cycle diagram in the current textbook, the mitral valve closes in phase 2.

Phase 2 is the start of ventricular systole. The AV valves close. The ventricular muscle initially shortens relatively little, but the intraventricular pressure rises sharply as the myocardium presses on the blood in the ventricles. This period of isovolumetric ventricular contraction lasts about 0.05 seconds. During isovolumetric contraction, the AV valves bulge into the atria, causing a small but sharp rise in atrial pressure.

Note: The AV valves refers to the mitral and tricuspid valves- atrio-ventricular valves. The aortic and pulmonary valves are not abbreviated. This is noted in much earlier editions of Ganong Physiology

25
Q

With a heart rate of 75/min, the absolute refractory period of the heart muscle is

A 0.15s
B 0.27s
C 0.25s
D 0.20s

A

Explanation
In seconds

Duration, each cardiac cycle= 0.8s

Duration of systole= 0.27s

Duration of action potential=0.25s

Duration of absolute refractory period=0.2s

Duration of relative refractory period=0.05s

Duration of diastole=0.53s

26
Q

Carotid sinus receptors, which is true?

A The main medullary control of blood pressure occurs in the nucleus ambiguus
B Stretch of the receptor stimulates the tonic discharge of sympathetic nerves
C Transmit afferent fibres via the glossopharyngeal nerve
D Are located in the tunica intima of the vessels

A

C

Explanation
Carotid sinus receptors form part of the baroreceptors that monitor arterial circulation. The carotid sinus is a small dilation of the internal carotid artery just above the bifurcation of the common carotid. The carotid sinus baroreceptor is located here. The receptors are located in the adventitia of the vessel. The afferent fibers from the carotid sinus form a distinct branch of the glossopharyngeal nerve, the carotid sinus nerve. The baroreceptors are stimulated by stretch of the structures in which they are located, and so they discharge at an increased rate when the pressure in these structures rises. The afferent fibers passes to the medulla. Most of them end in the nucleus tractus solitarus (NTS), and the excitatory transmitter is glutamate. Excitatory (glutamate) transmissions extend from the NTS to the caudal venterolateral medualla where they stimulate GABA secreting inhibitory neurons that project to the rostal ventrolateral medulla and the vagal motor neurons in the nucleus ambiguus and the dorsal motor nucleus. Thus, increased baroreceptor discharges INHIBITS the tonic discharge of sympathetic nerves and excites vagal innervation of the heart. These neural changes produce a drop in blood pressure, vasodilation, venodilation, bradycardia and a decrease in cardiac output.

Location of baroreceptors: carotid sinus, aortic arch, right atria, left atria, entrance of the superior and inferior venae cavea, pulmonary veins and pulmonary circulation

Summary: carotid sinus stimulation leads to increased vagal stimulation

27
Q

Myocardial oxygen consumption

A Oxygen consumption in increased by parasympathetic stimulation
B The stroke work of the left ventricle is three time that of the right ventricle
C Increases more with increased preload than afterload
D Is 90ml/kg/min

A

D

Explanation
Basal O2 consumption by the heart is 2ml/100g/min. O2 consumption by beating heart is 9.7ml/100g/min at rest. O2 consumption is determined by intramyocardial tension, the contractile state of the myocardium and the heart rate. Ventricular work per beat correlates with O2 consumption. The work is the product of stroke volume and the mean arterial pressure in the pulmonary and arterial system. Because the pressure aortic pressure is 7 times greater than the pulmonary system, the stroke work of the left ventricle is 7 times that of the right ventricle. An increase in after load causes a greater increase in cardiac O2 consumption than does an increase in preload. I.e. pressure work produces a greater increase in O2 consumption than volume work. (Reason for this is unclear). O2 consumption is increased by sympathetic stimulation. Obviously exercise increase O2 consumption.

Extra: The reason why pressure work produces a greater increase in MVo2 than volume work- Cardiac O2 consumption is closely related to wall tension, assuming contractility remains the same. For a given pressure, according to LaPlace’s law: T is proportional to P x r Assuming the ventricle is a sphere: Volume, V = 4/3 x π x r^3 , therefore r is proportional to cub√ V Therefore, T is proportional to P x cub√ V

28
Q

Which is FALSE regarding coronary blood flow?

A There is blood perfusion to the right ventricle muscle and the two atria during systole
B The heart compresses its coronary vessels during contraction
C Systole and diastole shorten when the heart rate increases
D The subendocardial portion of the heart is perfused only during systole

A

D

Explanation
The heart (like skeletal muscle) compresses its vessels when it contracts. This is why flow only occurs in the arteries supplying the subendocardial portion of the left ventricle during diastole. Both systole and diastole shorten as the heart rate increases, however, the duration of systole is much more fixed that of diastole, and when the heart rate is increased, diastole shortens to a much greater degree, resulting in a reduction in LV coronary blood flow. Because the pressure difference between the aorta and right ventricle and aorta and the two atria, there is flow to these regions during systole.

29
Q

Regarding the oxygen consumption of the heart. Which of the following is TRUE?

A Stroke work of the left ventricle is seven times that of the right ventricle
B An increase in pre-load cause the same increase in O2 consumption as an increase in after-load
C The 02 usage of the heart at a pulse rate of 100/min is 1430ml/min
D The beating heart O2 consumption is 2ml/100g/min

A

A

Explanation
O2 basal consumption of cardiac muscle is about 2ml/100g/min (non beating), much higher than resting skeletal muscle. O2 consumption of a beating heart is 9ml/100g/min. O2 consumption by the heart is determined primarily by the intramyocardial tension, the contractile state of the myocardium and the heart rate. Ventricular work per beat correlates with O2 consumption. The work is a product of SV (stroke vol) and the mean arterial pressure in the pulmonary artery (PA) or the aorta. Since the pressure in the aorta is seven times that of the PA, the stroke work of the left ventricle is approximately seven times that of the right ventricle. Of note an increase in after-load cause a greater increase in cardiac consumption of O2 than does an increase in preload (reasons not completely understood), therefore angina is more likely in aortic stenosis than in aortic insufficiency. The 02 usage of the heart at a pulse rate of 100/min is 910ml/m (directly form the table)

30
Q

Which substance (metabolite) is vasodilatory on the heart, but not on skeletal muscle?

A Histamine
B Adenosine
C Lactate
D Potassium

A

B

Explanation
Adenosine plays a role in cardiac muscle but not in skeletal muscle

Additional substances which are vasodilatory metabolites:

Increased osmolality, hyperkalaemia, lactate, histamine (from injured/inflammed tissues)

Other factors which lead to vasodilation: hypoxia, decreased oxygen tension, increased CO2 tension and an increase in tempreture

31
Q

Which is correct regarding the ECG?

A Bipolar leads can be placed at the tips of catheters and inserted into the oesophagus and the heart.
B QT represents ventricular repolarisation
C U waves are thought to represent repolarization of the papillary muscles or Purkinje fibres
D The standard unipolar limb leads I, II, III each record the difference in potential between two limbs

A

C

Explanation
The standard bipolar limb leads I, II, III each record the difference in potential between two limbs. 9 unipolar leads record the potential difference between an exploring electrode and an indifferent electrode. V1-V6= are the unipolar chest leads. VR, VL, VF= unipolar limb leads. Augmented limb leads, designated by the letter a, aVR, aVL, aVF are generally used. The augmented leads are recordings between one limb and the other two limbs. This increases the size of the potentials by 50%without any change in configuration from the non-augmented leads. Unipolar leads can be placed at the tips of catheters and inserted into the oesophagus and the heart.

U waves are thought to represent repolarization of the papillary muscles or Purkinje fibres.

QT represents ventricular depolarisation and ventricular repolarisation.

ST interval (QT minus QRS) represents ventricular repolarisation.

Note: in older editions of the prescribed TB-it reads: ST interval (QT-QRS)-ventricular repolarisation (during T wave). In the current edition it reads: Plateau portion of the ventricular action potential

ST interval is the plateau portion of the ventricular action potential. Table 29-2 p 526 Ganong 24th Edition.

32
Q

Which is the main risk factor for diastolic dysfunction?

A Hypertension
B Bilateral renal artery stenosis
C Coronary heart disease
D Diabetic heart disease

A

A

Explanation
Diastolic failure occurs predominantly in patients over 65yrs. Women >men. Hypertension and age are the most common risk factors.

Other risk factors include diabetes, coronary heart disease, obesity and bilateral renal artery stenosis. The reduction in the ability of the left ventricle to relax and fill may stem from myocardial fibrosis (cardiomyopathies and IHD), infiltrative disorders associated with restrictive cardiomyopathies (amyloidosis) and restrictive pericarditis. Diastolic failure may also appear in elderly patients without any known predisposing factors. This may be due to an exaggeration of the normal stiffening of the heart with age.

33
Q

How long does it take troponis levels to return to normal after an AMI?

A 5-7 days
B 3-5 days
C 72hrs
D 48hrs

A

A

Explanation
Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.

Source: medscape

34
Q

What is the normal ejection fraction of the heart?

A 70%
B 65%
C 55%
D 40%

A

B

Explanation
The amount of blood ejected by each ventricle per stroke at rest is 70-90ml. The end-diastolic ventricular volume is about 130ml. Thus, about 50ml of blood remains in each ventricle at the end of systole (end systolic ventricular volume), and the ejection fraction, the percentage of the end-diastolic ventricular volume that is ejected with each stroke, is about 65%

Extra:

Based on stroke volume of 70-90ml and EDV 130ml, the answer could be 54-70%.

But based on the Textbook: “the ejection fraction, the percentage of the end diastolic ventricular volume that is ejected with each stroke is about 65%”

It appears that the required answer is based on this wording.

35
Q

What is the normal stroke volume of the heart?

A 130ml
B 110ml
C 80ml
D 40ml

A

C

Explanation
The amount of blood ejected by each ventricle per stroke at rest is 70-90ml. The end-diastolic ventricular volume is about 130ml. Thus, about 50ml of blood remains in each ventricle at the end of systole (end systolic ventricular volume), and the ejection fraction, the percentage of the end-diastolic ventricular volume hat is ejected with each stroke, is about 65%

36
Q

What is end-diastolic ventricular volume of the heart?

A 130ml
B 120ml
C 110ml
D 100ml

A

A

Explanation
The amount of blood ejected by each ventricle per stroke at rest is 70-90ml. The end-diastolic ventricular volume is about 130ml. Thus, about 50ml of blood remains in each ventricle at the end of systole (end systolic ventricular volume), and the ejection fraction, the percentage of the end-diastolic ventricular volume hat is ejected with each stroke, is about 65%

37
Q

The third heart sound correpsonds to?

A Closure of the Pulmonary valve
B Vibrations through a stiff ventricle
C Closure of the atria ventricular valve
D In rushing of blood with the period of rapid ventricular filling

A

D

Explanation
Two sounds are normally heard through a stethoscope during each cardiac cycle. The first is a low, slightly prolonged “lub” (first sound), caused by vibrations set up by the sudden closure of the AV valves at the start of ventricular systole.

The second is a shorter, high pitched “dup” (second sound), caused by vibrations associated with closure of the aortic and pulmonary valves just after the end of ventricular systole.

A soft, low pitched third sound is heard about one third of the way through diastole in many normal young individuals. It coincides with the period of rapid ventricular filling and is probably due to vibrations set up by the inrush of blood.

A fourth sound can sometimes be heard immediately before the first heart sound when atrial pressure is high or the ventricle is stiff in conditions such as ventricular hypertrophy. It is due to ventricular filling and is rarely heard in normal adults

38
Q

The first heart sound correpsonds to?

A Closure of the Pulmonary valve
B Vibrations through a stiff ventricle
C Closure of the atria ventricular valve
D In rushing of blood with the period of rapid ventricular filling

A

C

Explanation
Two sounds are normally heard through a stethoscope during each cardiac cycle. The first is a low, slightly prolonged “lub” (first sound), caused by vibrations set up by the sudden closure of the AV valves at the start of ventricular systole.

The second is a shorter, high pitched “dup” (second sound), caused by vibrations associated with closure of the aortic and pulmonary valves just after the end of ventricular systole.

A soft, low pitched third sound is heard about one third of the way through diastole in many normal young individuals. It coincides with the period of rapid ventricular filling and is probably due to vibrations set up by the inrush of blood.

A fourth sound can sometimes be heard immediately before the first heart sound when atrial pressure is high or the ventricle is stiff in conditions such as ventricular hypertrophy. It is due to ventricular filling and is rarely hear din normal adults

39
Q

In which part of the heart is conduction slowest?

A AV node
B Atrial pathways
C Purkinje fibres
D Ventricular muscle

A

A

Explanation
Conduction speeds:
SA node 0.05m/s
Atrial pathways 1m/s
AV node 0.05m/s
Bundle of His 1m/s
Purkinje system 4m/s
Ventricular muscle 1m/s

40
Q

60-year-old woman has a routine ECG and is found to have a rhythm with gradual prolongation of the PR interval followed by an absent QRS complex. Which of the following describes her rhythm?

A Type II Mobitz
B Type I Mobitz
C 3rd degree heart block
D 1st degree heart block

A

B

Explanation
Mobitz type I (Wenckebach AV block): progressive prolongation of the PR interval culminating in a non-conducted P wave.

Mobitz type II (Hay AV block): intermittent non-conducted P waves without progressive prolongation of PR interval.

41
Q

Which part of the ECG represents the entire ventricular action potential?t

A R-R interval
B QT interval
C ST interval
D QRS complex

A

B

Explanation
The QT interval represents ventricular depolarization plus ventricular repolarization, and has an average duration of 0.40 seconds.

The ST interval represents ventricular repolarization (during T wave), and has an average duration of 0.32 seconds. It is equal to the QT interval minus the QRS.

The QRS complex has an average duration of 0.08 seconds, and represents ventricular depolarization and atrial repolarization.

42
Q

Carotid sinus massage can sometimes revert SVT due to release of acetylcholine at atrial musculature and the AV node. The afferent pathway of this reflex is conveyed by which nerve?

A CN XI
B CN X
C CN IX
D Sympathetic trunks

A

C

Explanation
Baroreceptors in the carotid sinus respond to stretch by stimulating afferent fibres that travel via the glossopharyngeal nerve to the NTS, releasing glutamate and increasing vagal stimulation of the heart as well as causing peripheral vasodilation.

43
Q

What is the mechanism of oedema in congestive cardiac failure?

A Decreased osmotic pressure
B Increased osmotic pressure
C Increased venous pressure
D Decreased venous pressure

A

C

Explanation
Other mechanisms include RAA system activation leading to salt and water retention.

Salt and water retention is a factor in oedema seen in heart failure, nephrosis and cirrhosis. In heart failure in venous pressure is usually elevated, with a consequent elevation in capillary pressure. In cirrhosis of the liver, oncotic pressure is low because hepatic synthesis of plasma proteins is depressed. In nephrosis, oncotic pressure is low because large amounts of protein are lost in the urine.

44
Q

What is the approximate % of blood volume located in the venous system at rest?

A 60-70%
B 50-60%
C 40-50%
D 30-40%

A

B

Explanation
Veins, venules and vena cava contain 54% of blood volume. The aorta, arteries and arterioles contain 11%. Capillaries contain 5%. There is an additional 12% in the heart and 18% in pulmonary circulation.

45
Q

During inspiration, what occurs to heart rate in a young healthy male?

A Increases 30-60%
B Increases <30%
C Decreases 30-60%
D Decreases < 30%

A

A

Explanation
Heart rate increases during inspiration and decreases during post-inspiration/expiration. This sinus arrythmia is primarily due to fluctuations in parasympathetic output to the heart. During inspiration, impulses in the vagi from the stretch receptors in lungs inhibit the cardioinhibitory area in the medulla oblongata. The tonic vagal discharge that keeps the heart rate slow decreases, and HR Increases. Figure 29-10 in Ganong Physiology demonstrates HR increasing from approximately 45 to 65bpm, meaning 30-60% would be the correct answer in this case.

46
Q

What is the normal ejection fraction of the heart?

A 80%
B 65%
C 50%
D 30%

A

B

47
Q

What is the normal stroke volume?

A 130ml
B 80ml
C 65ml
D 30ml

A

B

48
Q

ECG changes of hypocalcaemia include:

A Deep Q waves
B Prolongation of PR
C Prolongation of QRS
D QT abnormalities

A

D

Explanation
Hypocalcaemia causes QTc prolongation primarily by prolonging the ST segment. Dysrhythmias are uncommon. The T wave is typically left unchanged.

Torsade de pointes may occur, but is much less common with hypocalcaemia than with hypokalaemia or hypomagnesaemia.

49
Q

Which features are consistent with a patient with diastolic heart failure?

A Increased diastolic filling, increased stroke volume
B Decreased diastolic filling, decreased stroke volume
C Decreased diastolic filling, increased stroke volume
D Increased diastolic filling, decreased stroke volume

A

B

Explanation
Patients with diastolic heart failure have impaired filling capacity, and thus decreased diastolic filling and decreased stroke volume.

50
Q

What is the affect of histamine on heart rate and contractility?

A Decreased heart rate, increased contractility
B Decreased heart rate, decreased contractility
C Increased heart rate, increased contractility
D Increased heart rate, decreased contractility

A

C

Explanation
Histamine is known to act as a direct stimulator. In the heart, two types of histamine receptors are present: H1- and H2-receptors. H2-receptors cause an increase in heart rate and contractility as well as coronary vasodilatation, whereas H1-receptors mediate chronotropic effects and coronary vasoconstriction. During anaphylactic states, histamine is released from cardiac tissue where it is stored in large amounts.

51
Q

Which of these would be considered a normal PR interval?

A 150ms
B 100ms
C 75ms
D 25ms

A

A

Explanation
PR interval (representing atrioventricular conduction) has a normal range of 0.12 – 0.20 seconds, average 0.18 seconds