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OS2 - Cardio > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

Ohm’s law in physiology

Ohm’s law applied to arterial pressure

A 
Law for proportionality of pressure and flow:
the flow (Q) between any two points is determined by the pressure difference (∆P) between the points, divided by the resistance (R): Q = ∆P/R.
Applied to arterial pressure: ∆P=Q*R=CO*TPR=arterial pressure
(CO=cardiac output; TPR=total peripheral resistance)
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2
Q

Streamline vs. Turbulent flow and Ohm’s law

A

Streamline flow is when the velocity at the center of the flow is greater than the velocity at the edge.
Turbulent flow doesn’t follow such a pattern and instead has chaotic velocities.
Ohm’s law applies only to streamline flow and fails to apply to turbulent flow.

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3
Q

Formula for flow in terms of resistance

A

R = (8nul)/(pir^4)
Q = (pir^4∆P)/(8nu*l)
Where l = tube length; nu = fluid viscosity; r = tube radius

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4
Q

Effect of hematocrit on viscosity

A

the greater the hematocrit, the greater the viscosity

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5
Q

How does the body regulate blood flow?

A

It alters resistance–so that flow to each organ may be independently regulated. Because resistance is related to r^4, small changes in the radius translate to large changes in resistance.
Does so by:
1. rapid regulation - uses local factors, SNS, and circulating factors
2. slow/long-term regulation - hypertrophy to narrow lumen or increase vascularity

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6
Q

Hyperemia

A

Increased blood flow. It follows either:

  1. increased use: increased tissue activity/metabolism/O2 use (active/functional hyperemia)
  2. decreased delivery: reduction of BF/O2 to specific tissue (reactive hyperemia)
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7
Q

Relationship of BF to:

  • metabolic rate
  • O2 saturation
  • duration of ischemia
A
  • greater metabolic rate, greater BF
  • lower O2 sat, greater BF
  • longer ischemia, greater BF (when vessels reopened)
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8
Q

Feedback for vasodilation (rapid regulation)

A

Proposed hypotheses:
1. low tissue O2 decreases smooth muscle metabolism/contractile force, vessel relax
2. arterioles have some kind of O2-sensor that leads to dilation when O2 is low
+ Tissue metabolism products may be vasodilatory: adenosine, ATP, ADP, AMP, CO2, lactic acid, K+

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9
Q

Dependency of BF on O2, metabolites, and BP

A
  1. depends on O2 because when O2 is low, tissue needs more blood
  2. depends on metabolites because they accumulate and more BF needed to clear them
  3. depends on BP because vessels don’t like having BP change their blood flow
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10
Q

Autoregulation (rapid regulation) and mechanisms

A

When BP increases, vessels will oppose changes in blood flow via these mechanisms:

  1. metabolic - inc. BP/BF means dec metabolites or inc. O2; response is to increase resistance for decreased BF
  2. myogenic - when BP is higher, stretch-activated Ca-channels let in Ca and myocytes contract, decreased radius means decreased BF
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11
Q

SNS control of vessels (rapid regulation)

A

All vessels, except capillaries, are innervated by SNS vasoconstriction fibers who utilize NE as major NT. These fibers have tonic activity. Innervation density varies - heavily innervated are cutaneous, renal, splanchnic, and skeletal muscle; sparsely innervated are cerebral; and coronary arteries.
At lower levels of SNS activity, a relative small increase translates to a large increase in vascular resistance.

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12
Q

Humoral/circulating factors (rapid regulation)

A

Epi and NE - released from adrenal medulla on SNS stimulation. Epi binds both alpha and beta receptors in vessels; NE much prefers alpha. Alpha mainly does vasoconstriction and beta vasodilation.

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13
Q

Effects of Epinephrine on vessel diameter

rapid regulation

A

At low concentrations Epi binds Beta-2 receptors, which causes vasodilation. However, it binds alpha-1 receptors at higher concentrations, which causes vasoconstriction. The vasoconstriction effect is stronger than vasodilation.

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14
Q

Effects of Norepinephrine on vessel diameter

rapid regulation

A

NE has a greater affinity for alpha receptors than for beta receptors, so it binds them preferentially causing vasoconstriction.

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15
Q

Angiotensin II

rapid regulation

A

Vasoconstrictor:
Oligopeptide that is a direct vasoconstrictor acting on both arteries and veins; also tells kidneys to decrease urine output. Thereby regulates arterial pressure and plasma volume.

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16
Q

Vasopressin

rapid regulation

A

Vasoconstrictor:
Oligopeptide that tells kidneys to decrease urine output. Thereby regulates plasma volume. At high amounts will also constrict arteries and veins (esp. splanchnic)

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17
Q

Bradykinin

rapid regulation

A

Vasodilator:

Polypeptide released by immune cells that vasodilates and increases capillary permeability, contributing to edema.

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18
Q

Histamine

rapid regulation

A

Vasodilator:

Biogenic amine released by immune cells that vasodilates and increases capillary permeability, contributing to edema.

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19
Q

Prostaglandins PGI2 and PGE2

rapid regulation

A 
Vasodilator:
Fatty acid (from ARA)
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20
Q

Thromboxane A2

rapid regulation

A 
Vasoconstrictor:
Fatty acid (from ARA)
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21
Q

Atrial Natriuretic Peptide

rapid regulation

A

Oligopeptide that tells kidneys to decrease urine output. Released from atrial myocytes.

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22
Q

Nitric Oxide

rapid regulation

A

Vasodilator:

Derived from arginine. Decreases IC Ca levels for vasodilation of large vessels upstream of hyperemic tissues.

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23
Q

Long-term regulation of BF - mechanisms

A
  1. change number of blood vessels: angiogenesis/rarefaction

2. reduce radius of vessel lumen: hypertrophic vascular remodeling

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24
Q

Regulation of coronary blood flow

A

Factors involved:

  • NO: dilates epicardial arteries
  • NE: dilates coronary arteries by binding Beta-2 receptors
  • metabolic end products
  • altered O2 levels
25
Q

What’s weird about left ventricular blood flow?

A

It’s out of phase of the other organs because it receives the most flow during diastole. During systole, ventricular contraction compresses the left coronary artery, increasing vascular resistance; therefore perfusion during systole doesn’t happen. This momentary ischemia causes reactive hyperemia when the vessels reopen in diastole. Therefore it’s important for ventricular pressure to remain low during diastole so that the heart can be adequately perfused, and this makes it susceptible to infarction.

26
Q

Regulation of skeletal muscle flow

A
  • during exercise: predominantly local control (such as with local substances: NO, PGs, ARA derivatives, K+, ATP)
  • at rest: SNS - vasoconstriction attenuates hypotension by increasing TPR
27
Q

Two reasons/mechanisms by which BF increases during exercise

A
  1. rhythmic exercises cause rhythmic compression of vessels which increases resistance and causes a miniature ischemic episode; this causes reactive hyperemia
  2. increased metabolic/O2 demand cause an overall active/functional hyperemia
28
Q

Regulation of cerebral blood flow

A
  • Active hyperemia occurs in response to neuronal activity.
  • local control is predominant, although the brain does have both PNS and SNS innervation
  • important local factors include: CO2, Adenosine, NO, PGs, and Non-PG ARA metabolites
  • strong autoregulation with metabolic and myogenic components
29
Q

Splanchnic circulation

A

Splanchnic circulation includes liver, pancreas, spleen, and intestine.
Liver includes portal system (more BF) and arterial system (less BF).
Spleen holds reservoir of RBCs and plasma volume which can be released whenever pressure is low/during exercise.

30
Q

Regulation of splanchnic circulation

A
  • Active hyperemia: local metabolites > hormones (released during digestion)
  • Extrinsic control: SNS
  • Autoregulation
  • During eating: SNS active, increased resistance. After eating: active hyperemia due to increased tissue demand.
31
Q

Regulation of skin circulation

A
  • almost entirely controlled by CNS/ANS: activity of AV anastomoses are controlled by SNS; hypothalamus senses skin temps and will decrease SNS activity to AVAs, meaning vasodilation/decreased resistance and opening of the anastomoses, thus increased BF at skin
  • increases when ambient temp rises (so the heat in blood can be lost to environment)
  • when skin is cooled that info is sent to hypothalamus by cutaneous sensory nerves, and the SNS activity increased to close up the anastomoses
32
Q

Regulation of renal circulation

A
  • high degree of autoregulation for both BF and GFR

- highly innervated with SNS fibers, so SNS can override autoregulation and increase renal vascular resistance

33
Q

Describe CNS innervation of the heart in terms of PNS/SNS pathways and targets.

A

Both cardioinhibitory and cardiostimulatory centers are in medulla oblongata.
PNS: cardioinhibitory center stimulates DMN of vagus (also in medulla); vagus nerve travels down to innervate SA node and AV node.
SNS: nerve from cardiostimulatory center travels down to thoracic spinal cord and synapses to pre-ganglionic nerve which then synapses in sympathetic chain ganglion to post-ganglionic sympathetic cardiac nerve which innervates the SA node, AV node, and ventricular cells.

34
Q

Describe the phases of ventricular action potential.

A

Phase 4 = resting, -85mV set primarily by K+ channels
Phase 0 = rapid rise in potential to +20mV due to Na influx through fast Na channel, plus inactivation of K channels
Phase 1 = small repolarization, achieved by transient outward K channel (I-to)
Phase 2 = polarization plateau caused by balance of inward Ca current and 3 outward K currents (I-kur, I-kr, I-ks)
End Phase 2 = repolarization occurs due to reactivation of K-1, I-KATP, and I-KACh

35
Q

Which potassium channels are active in hyperpolarized ventricular cells, and which in depolarized ventricular cells?

A

Active in hyperpolarized cells: I-K1, I-kATP, I-KACh

Active in depolarized cells: I-kur, I-kr, and I-ks

36
Q

Describe the opening/closing action of the fast sodium channel in the ventricular cell.

A

There are 2 gates, activated at different voltages: V gate is closed at rest and opens at voltage more positive than -40mV; inactivation gate is open at rest and closes at voltages more positive than -65mV. So when the cell is depolarizing the voltage is becoming more positive, and while the V gate goes from closed to open first (@ -40mV), the inactivation gate takes a while to catch up and close. But when repolarizing the V gate closes at -40mV and the inactivation gate stays closed until -65mV is reached.

37
Q

What is the funny current?

A

This is an inward sodium current in SA node cells that is activated by negative membrane potential (so at SA node resting potential, which is -65mV). This accounts for the unstable resting membrane potential.

38
Q

Describe the Ca+ flux into and out of pacemaker cells throughout the pacemaker and action potentials.

A

During the pacemaker potential: Ca channels start out closed and then open. T-type channels open and close rapidly. This helps voltage approach action potential threshold. At the threshold, L-type channels open.
During action potential: Ca is flowing into the cell, continuing to depolarize it. Ca channels are slower than Na channels in conducting current, therefore the AP slope is less steep than in ventricular cells. At the AP peak, Ca channels close and voltage-gated K channels open; cell repolarizes.

39
Q

Describe the refractory periods.

A
  1. Absolute refractory period (ARP) = no stimulus can induce AP, period. Dependent on refractory fast Na channels. Occurs down to ~-40mV.
  2. Effective refractory period (ERP) = no stimulus by surrounding cells can induce AP. Occurs down to ~-65mV.
  3. Relative refractory period (RRP) = normal stimulus can’t induce AP, but a supramaximal (large) stimulus can induce a weak AP. Occurs between ~-35mV to ~-80mV.
  4. Supranormal period (SNP) = a weaker than normal stimulus can elicit a regular AP. Dependent on refractory K channels that are unable to clamp the resting voltage because they have not fully activated. Occurs from ~-80 to -85mV.
40
Q

What sets the heartbeat and why?

A

The SA node because it has the highest rate of spontaneous discharge, at 100-120bpm.
If the SA node breaks down, the AV node can carry on at 80-100bpm, and if that breaks then the bundle of His or purkinje cells can run the show at 30-50bpm, but not long term because they don’t beat fast enough.

41
Q

Effect of Sympathetic and Parasympathetic activity in the heart

A

PSA: decreases HR, decreases conduction velocity (particularly in AV node), decreases excitability of latent pacemakers
SA: increases HR, increases conduction velocity (particularly in AV node), decreases threshold of Ca channels and thereby increases excitability of latent pacemakers/other cells

42
Q

What factors influence the time to reach the threshold potential for activating Ca channels to generate an action potential?

A

Increasing the time to AP:
- decreasing the funny current
- decreasing (that is, more negative) the maximal diastolic potential (MDP)
- increased K channel activity, mediated by increased
^This is how parasympathetic activity slows HR.
Increasing the threshold (more positive) for generating AP:
- decreased cAMP levels

43
Q

Dromotropy

A

increased speed of conduction of electrical activity in the heart

44
Q

Describe the opposing effects of autonomic tone on HR.

A

resting tone comes predominantly from PNS which sets normal at 60bpm
Experiment:
- block PNS, get SNS only which makes 120bpm
- block SNS, get PNS only which is 50bpm
- block everything get intrinsic SA node activity which is 100bpm

45
Q

Temporal relationship of AP, [Ca], and cardiac myocyte contraction

A
  1. AP
  2. intracellular [Ca] increases and peaks about 100ms after AP
  3. muscle contraction occurs and peaks about 300ms after AP
46
Q

Factors regulating strength of cardiac myocyte contraction

A
  • IC Ca levels during AP: the amount of Ca that enters through channels is not enough to contract fibers; requires supplemental release of Ca from SR. The faster and larger the Ca influx through channels the more is released from SR.
  • initial length of cardiac fibers: this is related to pre-load volume (the end diastolic pressure in ventricles) which stretches fibers
47
Q

Life and regulation of IC Calcium

A

Binding of NE/Epi to beta receptor activates AC–>cAMP which activates PKA to phosphorylate Ca channel to open it. When ACh binds the M2 receptor, it inhibits AC, so no cAMP, no phosphorylation of anything, no IC Ca increase.

  1. influx - voltage-gated Ca channels open upon membrane depolarization, Ca enters cells
  2. release from SR - Ca binds ryanodine receptor (RyR) and induces Ca release
  3. Ca does its job by binding the myofilaments; released upon phosphorylation of troponin I
  4. return to SR - uptaken by ATP-PLB (phospholamban) transporter when PLB is phosphorylated by PKA
  5. efflux from the cell - membrane pumps
    * some Ca stored in mitochondria, not significant in IC Ca concentration but may play long-term role as reservoir
48
Q

Frank-Starling mechanism

A

States that the stroke volume of the heart will increase when the end diastolic volume increases (when all else stays constant).
The increased cardiac force is generated by a fast (inc. Ca sensitivity of myofilaments) or slow (activation of Ca channels) response to stretch.
Also expressed in terms of the longer the sarcomere length the greater the active and resting tension, up to the physiological limit, because they are more sensitive to Ca.

49
Q

Describe the P, QRS, and T waves of an ECG.

A

P = atrial depolarization
QRS = ventricular depolarization (happens quickly)
T = ventricular repolarization (happens more slowly)
*Atrial repolarization also has a wave but it’s buried under the QRS complex.
**Intensity of the wave corresponds with the mass of tissue being depolarized.

50
Q

Describe the waves of atrial and ventricular pressure/contraction.

A
  1. Atrial contraction - depolarization of atrium (P wave), increased atrial pressure, mitral valve is open, filling of ventricle (preload)
  2. Isovolumetric contraction - when VP>AP the mitral valve shuts, the ventricle contracts (QRS complex) with both valves shut, volume is constant while pressure increases (afterload), atria begin refilling
  3. Rapid ejection - when VP>Aortic Pressure, the aortic valve busts open and ventricle is still contracting while the rapid ejection of blood happens, both ventricular and aortic pressures peak
  4. Reduced ejection - ventricles relax (start repolarizing) but are still ejecting, aortic pressure begins to fall as blood flows off into branches
  5. Isovolumetric relaxation - when VP<AP the mitral valve opens and blood fills the ventricle from the atrium, ventricle pressure starts to increase (preload)
  6. Reduced Ventricular Filling - ventricles still relaxed and now being filled more, this is before the atria contract so you end up with the EDV, this phase gets shortened when the HR increases
51
Q

Describe the heart sounds.

A 
S1 = the sound of the mitral and tricuspid valves closing (during ventricular systole)
S2 = the sound of the aortic and pulmonic valves closing (during ventricular diastole); can be split during inspiration because of delayed pulmonic valve closing because the decreased intrathoracic pressure pulls in more blood to right heart
S3 = the sound of the ventricle being overfilled by the atrium (in ventricular diastole, the reduced filling phase) because there's already high ESV and the new blood is mixing with the old
S4 = the sound of the blood on atrial contraction hitting the stiff/hypertrophied wall of the ventricle, instead of the ventricle being compliant
52
Q

Describe: preload change, with constant afterload and contractility

A 
INCREASED preload (EDV) means same afterload, increased PSP and SV, same ESV
DECREASED preload (EDV) means same afterload, lower PSP and SV, same ESV
53
Q

Describe: afterload change, with constant preload and contractility

A

INCREASED afterload means increased PSP but lower SV, increased ESV and same EDV (preload)
DECREASED afterload means decreased PSP but increased SV, decreased ESV and same EDV (preload)
*When afterload is higher less is pumped out because it’s harder to pump and therefore does it more slowly

54
Q

Describe: contractility change, with constant and preload and afterload

A

INCREASED contractility means increased PSP and SV, decreased ESV, same EDV (preload) and afterload
DECREASED contractility means decreased PSP and SV, and higher ESV, same EDV (preload) and afterload

55
Q

Describe the compensation when afterload is changed but contractility is constant.

A

INCREASED afterload means increased PSP but decreased SV, increased ESV and increased EDV/preload, feeding back into increased afterload
DECREASED afterload means decreased PSP but increased SV, decreased ESV and decreased EDV/preload feeding back into decreased afterload

56
Q

Describe the compensation when preload is changed but contractility is constant.

A

INCREASED preload means increased afterload, increased PSP and SV, but with increased afterload there’s slightly increased ESV which feeds back into increased EDV
DECREASED preload means decreased afterload, decreased PSP and SV, decreased ESV which feeds into decreased EDV

57
Q

Describe compensation when contractility is changed.

A

INCREASED contractility means increased afterload, increased PSP and SV, decreased ESV and also EDV/preload
DECREASED contractility means decreased afterload, decreased PSP and SV, and increased ESV and also EDV/preload

58
Q

Effect of aortic and mitral valve stenosis on cardiac events

A
  • smaller openings mean increased resistance (requires larger ∆P), slower flow, and audible turbulence–>murmur
  • aortic stenosis increases afterload, thus ESV and EDV; associated with decreased stroke volume and ventricular systolic murmur
  • mitral stenosis means increased L atrial pressure; creates diastolic murmur
59
Q

Effect of regurgitation on cardiac events

A
  • leaky valves means retrograde flow, turbulence–>murmur
  • aortic regurgitation occurs when the ventricular pressure falls rapidly after relaxation and the valve insufficiently closes or lets blood fall back down into the ventricle; results in ineffective cardiac output and a diastolic murmur
  • mitral regurgitation occurs when the mitral valve lets blood into atrium during ventricular systole, causes systolic murmur; also seen in venous pulsation which can be visible in V wave and neck

OS2 - Cardio (6 decks)

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