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Cardio Pulmonary > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

aerobic requirements of the heart

A
  1. cardiac tissue is metabolically very active
  2. cardiac energy needs can increase 9x from rest to heavy exercise
  3. O2 extraction from the blood remains fairly constant regardless of work load
  4. Blood flow increases from 80 ml to 400 ml/min/100g tissue
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2
Q

describe cardiac myocyte structure

A
  1. y-shaped cells
  2. striated
  3. contain a single nuclei
  4. limited ability to replicate
  5. linked together by intercalated disks
  6. lack of distinct fiber types
  7. do not fatigue
  8. all fibers contract with each beat
  9. provide graded muscle contractions
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3
Q

describe cardiac myocyte force production

A
  1. all cardiac muscle cells contract regardless of HR and contractility
  2. cardiac muscle cells regulate their force production by regulating availability of calcium to their sarcomeric proteins
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4
Q

Describe the steps in a cardiac action potential

A
  1. resting membrane at -90mV, all channels but K+ are closed
  2. rapid Na influx through open fast Na channels results in rapid increase to >0
  3. transient K+ channels open and K+ efflux returns TMP to 0mV
  4. Influx of Ca through L-type Ca channels is electrically balanced by K+ efflux, through delayed rectifier K+ channels
  5. Ca channels close by delayed rectifier K+ channels remain open and return TMP to -90mV
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5
Q

compare the time of a skeletal muscle AP to a cardiac muscle AP

A
  1. skeletal → 4-8 ms
  2. cardiac → 100-300 ms
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6
Q

what are refractory periods?

A

periods of time in which cardiac muscles allow complete emptying of the ventricles prior to next contraction

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7
Q

list the refractory periods

A
  1. ARP (absolute refractory period)
  2. ERP (effective refractory period)
  3. RRP (relative refractory period)
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8
Q

how is SV calculated?

A

LVEDV - LVESV

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9
Q

how is EF calculated?

A

(LVEDV - LVESV)/LVEDV * 100

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10
Q

define the relative norm values for various cardiac values like EDV, ESV, SV, and EF

A
  1. EDV → 110-120 mls
  2. ESV → 40-50 mls
  3. SV → ~70 mls
  4. EF → 60% is WNL
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11
Q

T/F: changing EDV or ESV does not impact SV

A

FALSE

changing either will result in a change to SV

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12
Q

T/F: Atrial failure is often unnoticed

A

TRUE

but with A-Fib on the other hand, the atria contract to frequently which reduces the amount of blood flowing to the ventricles

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13
Q

describe the process of filling the ventricles

A
  1. substantial filling of the ventricles occurs during the first 1/3 of ventricular diastole
  2. middle 1/3 of ventricle diastole there is a modest amount of blood entering the ventricles
  3. during the last 1/3 the “tank is topped off” via the atrial contraction
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14
Q

T/F: there is a substantial change in volume during a isovolumetric ventricular contraction?

A

FALSE

short (0.02 - 0.03 seconds)

all valves are shut and pressure is building but no volume loss/change

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15
Q

when does ventricular contraction shift from isovolumetric to an ejection contraction?

A

once the LV SP >80 mmHg (in a normatensive pt)

rapid ejection → 70% occurs in first 1/3 of systole

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16
Q

what is isovolumetric diastolic or relaxation of the LV?

A

this is when ventricular pressure < aortic pressure and thus the aortic valve closes and remains closed resulting in no net blood flow

  • early part of ventricular relaxation
  • LV pressure is decreasing
  • both aortic and AV valves are closed
  • AV valves open when atrial pressure is greater than that of the ventricles
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17
Q

what does an elevated RV pressure suggest?

A
  1. pulmonary HTN
  2. RV failure
  3. CHF
  4. increased blood volume
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18
Q

list the pulmonary pressures

A
  1. systolic → 20-30 mmHg
  2. diastolic → 8-12 mmHg
  3. mean pulmonary pressure → 25 mmHg
19
Q

what allows the pulmonary ciruculation to function as a low pressure system?

A
  1. RV pumps through a shorter length of pipe
  2. pulmonary vasculature is more compliant
    • lower resistance to bloow flow
    • vessels walls are thinner and contain less muscle
  3. expansion of lungs result in vascular dilation
  4. much lower impact of gravity
  5. benefit-reduced risk of pulmonary edema
20
Q

List clinical markers of cardiac function and how to determine them

A
  1. Cardiac output
    • CO = HR * SV
    • ~4-8 L/min
  2. EF (LVEF)
    • norm ~55-70%
  3. Cardiac Index
    • ratio of CO to body surface area
    • CO/BSA
    • units = L/min/m2
    • norm → 2.5-4
21
Q

what EF is indicative of heart failure?

A

<40%

22
Q

List determinants of cardiac performance as defined by CO

A
  1. HR
  2. Contractility
  3. Preload
  4. Afterload
23
Q

what is contractility and how does it impact cardiac performance?

A

strength of contraction/force production

  • if increased → increase in CO
  • if decreased → decrease in CO
24
Q

how is preload a determinant of cardiac performance?

A

it reflects the amount of venous return which impacts how much myocardial distension occurs prior to contraction

Frank-Starling mechanism

25
Q

how is afterload a determinant of cardiac performance?

A

this is the force that the ventricles must overcome in order to eject blood and it is largely dependent on arterial BP and vascular tone

if increased its makes the heart work harder (like riding uphill you slow down)

26
Q

list determinants of energy cost of cardiac performance

A
  1. HR
  2. contractility
  3. wall tension
    • systolic force or work per surface unit
  4. Double Product
    • SBP * HR
27
Q

how does sepsis impact cardiac performance?

A
  1. cytokines released during sepsis reduces cardiac contracility
    • impaired Ca handling
  2. sepsis is usually associated with normal or elevated CO
28
Q

how do positive iontrophic drugs impact cardiac contractility?

A

they act to increase it

typically used in heart failure pts to preserve CO

examples:

  1. Digoxin
  2. Dopamine
  3. Dobutamine
  4. adrenaline
  5. noradrenaline
29
Q

how is the SNS assessed in its ability to regulate HR?

A
  1. resting HR (HR at rest)
  2. HR recovery
  3. HR response to standing
  4. HR response to valsalva
  5. BP response to standing
30
Q

list factors that control venous return

A
  1. total blood volume
  2. venous blood pressure (driving force for blood return)
  3. muscle pump
  4. respiration
  5. gravity/posture
  6. intrapericardial pressure
  7. right atrial pressure/increased thoracic pressure
31
Q

T/F: the frank-starling mechanism is ideally suited for matching CO to venous return

A

TRUE

a sudden excessive output by one ventricle very soon increases venous return to the other ventricle

the stimulus to increase output in the 2nd ventricle is an increase in diastolic length with an accompanying increase in force of contraction

32
Q

what is Pulse Pressure?

A

SBP - DBP

  • normal = 40
  • considered abnormally low if it is <25% of SP (~30)
  • considered abnormally high if >100
  • PP = SV/arterial compliance
33
Q

what can decrease PP?

A
  1. directly proportional to volume changes (SV)
  2. inversely proportional to arterial compliance
  3. in trauma, a low or narrow PP suggests sig blood loss
  4. aortic valve stenosis
  5. cardiac tamponade
34
Q

is it better to focus on PP or SBP?

A

while PP may be a better predictor of heart health than SP or DP independently it should not be taken out of context and doesn’t provide unique info in most cases

current recommendations are to focus on SBP in determining need for therapy

35
Q

what is mean arterial pressure (MAP)?

A

describes the average arterial pressure across a cardiac cycle

  • considered to be the perfusion pressure seen by organs in the body
  • MAP = CO * SVR
    • SVR = systemic vascular resistance
  • MAP = DP + 1/3(SP - DP)
36
Q

MAP norms

A
  • norm → 65-110
  • MAP > 60 → is enough to adequately perfuse organs of the average person
  • MAP <60 → signals decreased organ perfusion
  • long term depressed MAP results in ischemia and injury
37
Q

decreased MAP can lead to ____, _______, and ______

A

poor perfusion of brain, LOC, and death

38
Q

other than the radius of the vessel what else impacts systemic vascular resisance?

A
  1. Local control
    • NO release → results in vasodilation and diminished MAP
    • endothelin released in presence of decreased MAP leads to smooth muscle contraction
  2. ANS
    • altered sympathetic and parasympathetic input to vascular smooth muscle
  3. renal regulation of blood volume
39
Q

what is the Law of LaPlace?

A

T(LV wall stress) = Pressure * radius

T= PR

the tension (T) in the wall of a hallow cylinder is directly proportional to the cylinder’s radius (r) and the pressure (p) across the wall caused by the flow inside

40
Q

for a given blood pressure ________ the radius of the cylinder leads to a _____________ in tension

A

increasing

linear increase

41
Q

what is atrial natriuretic peptide?

A
  • 28-amino acid peptide
  • synthesized, stored and relased by atrial myoctyes in response to:
    • atrial distension (hypervolemia)
    • angiotension II stimulation
    • sympathetic stimulation
42
Q

what are the action of the ANP?

A
  1. involved in long term Na and water balance, blood volume and arterial pressure
    • increases diuresis and sodium loss → reduces blod volume
    • decreases renin release which further leads to diuresis and Na loss
  2. dilates veins reducing central venous pressure, preload and CO
    3.
43
Q
A

Cardio Pulmonary (21 decks)

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