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Cardiovascular and Respiratory > Cardiac Output 1 & 2 > Flashcards

Cardiac Output 1 & 2 Flashcards

1
Q

what is the cardiac output?

A

output of each ventricle per minute (5-7 liters per minute at rest)

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2
Q

what is the cardiac index?

A

output of ventricles per minute per msquared

3-5 L/min/m^2 at rest

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3
Q

To which muscle/organ does the most cardiac output go to?

A

To the liver (28% of CO)

next is the kidney at (23.3%) and

brain (13.9%)

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4
Q

when does cardiac output increase?

A

it increases to meet metabolic demand i.e) physiologically in exercise, anxiety, eating, pregnancy

increases pathologically i.e) due to hyperthyroidism

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5
Q

when does cardiac output decrease?

A

when you go from standing to lying position

pathologically due to myocardial damage ex) heart failure

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6
Q

what are the determinants of cardiac output?

A

Heart rate and stroke volume

CO= HR X SV

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7
Q

what components determine the stroke volume?

A

preload/venous return

contractility/change in force

afterload/resistance to outflow

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8
Q

which roots of the SNS supply the heart?

A

T1-4 via the cervical and stellate ganglia

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9
Q

what neurotransmitters are released in the SNS to the heart?

A

NA and adrenaline - bind to adrenergic receptors (mostly beta1 in the heart)

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10
Q

describe the PNS that extends to the heart?

A

The supply to the heart arises from the medulla from the dorsal motor nucleus of vagus and nucleus ambiguus routed via ganglia on surface or within heart

acetylcholin acts on the cholinergic receptors (mainly muscarinic M2)

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11
Q

how do the SNS and PNS balace in the SA node?

A

SA node has intrinsic automaticity

Also innervated by SNS and PNS

  • at rest, the SA node is primarily influenced by the PNS “vagal tone” - with inhibition of the SNS
  • during sympathetic response, increased dominance of SNS on SA node, with PNS inhibition
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12
Q

how does the PNS decrease the pacemaker rate?

A

acetylcholine increases outward gated K+ channels and decreases the slow inward gatec Ca++ and gated Na+ channels

it therefore decreases the slope of stage 4 and therefore increases the time required to reach threshold potential yet again

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13
Q

how does the SNS increase the rate of the SA node?

A

Noradrenaline increases the rate by increasing all three ion currents

  • increases outward gated K+ channel
  • increases slow inward gated Ca++ and gated Na+ channels

therefore it increases the slope of phase 4 allowing it to reach threshold potential much sooner

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14
Q

How do beta blockers work?

A

they block the beta 1 adrenergic receptors - decreasing heart rate and contractility

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15
Q

what can we take that would increase the heart rate?

A

Atropine = blocks muscarinic M2 Ach receptors (PNS) therefore the heart rate increases

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16
Q

what factors determine preload?

A

blood volume (RAAS, ADH, and Atrial natriuretic peptide)

and venous return

17
Q

what factors influence heart contractility?

A

Sarcomere length : overstretching of the cardiac muscle fibers make them less contractible

sympathetic NS : increases contractility or inotropic effect

parasympathetic NS : minimal negative effect on contractility

hormones : insulin has positive effect on contractility

18
Q

describe the contraction/relaxation of the cardiac muscle process

A
  1. in relaxed state, binding of actin to myosin is blocked and the myosin binding sites on actin are covered by tropomyosin
  2. when action potential leads to increased calcium, the calcium binds to toponin causing tropomyosin to move and uncover the myosin binding sites
  3. myosin binds to acting binding site and a ratcheting action of myosin occurs which shortens the sarcomere as actin/myosin slide past eachotehr
  4. ADP and Pi are released
  5. binding of ATP to myosin head group causes detachment of actin/myosin
19
Q

What is Starling’s law of the heart?

A

when the rate at which blood flows into the heart changes, the heart automatically adjusts its outflow to match inflow

  • unlike skeletal muscless, cardiac sarcomeres have an optimum length that is greater than their resting length so increasing the volume increases contactility force
20
Q

stretching cardiac muscle leads to what?

A

increase in contractility force

increase Ca++ sensitivity of contration

21
Q

what effect do beta1agonists have on the ion levels of the heart?

A

they act on beta1adrenoceptors coupled to increased cyclic AMP formation - this activates protein kinases and increases all of the following

  • Ca++ flux
  • release of Ca+ from SR
  • Affinity of myofilaments for Ca++
  • reuptake of Ca++ into SR

therefore the myocytes contract faster and with more force

22
Q

What is the MOA of digitalis?

A

inhibits Na/K/ATPase - raises intracellular Na+ decreasing Na+/Ca++

results in rise of intracellular Ca++ which increases contractility

23
Q

what sort of drugs have negative inotropic effects on the myocardium?

A

hypoxia, hypercapnoea, acidosis

beta blockers

calcium channel blockers

24
Q

what is the afterload?

A

it is the force opposing cardiac muscle shortening and ejection of blood during ventricular contraction

25
Q

what factors effect the afterload?

A

tension in ventricular wall

arterial impedance

26
Q

What is the Fick’s Principle?

A

the quantity of O2 delivered to the pulmonary capillaries via the pulmonary artery plus the quantity of O2 that enters the pulmonary capillaries from the alveoli must equal the quantity of O2 that is carried away by the pulmonary veins

essentially: the only O2 in the blood comes from the lungs and already oxygenated blood

27
Q

How does the echocardiogram measure CO?

A

via ultrasonic waves - detects movement /velocity of volume flow through the valves -

28
Q

Larger than normal ventricular end diastolic volume (“enlarged” hearts) seen in patients with cardiomyopathy can compensate somewhat in the early stages for the reduced contractility that occurs in this condition because stretching of the ventricular muscle cells..

  • A. Decreases influx of calcium during ventricular repolarisation
  • B. Enhances reuptake of calcium by sarcoplasmic reticulum
  • C. Decreases influx of calcium during ventricular depolarisation
  • D. Changes the overlap of thick and thin filaments
  • E. Improves conduction among muscle cells
A

• D. Changes the overlap of thick and thin filaments

29
Q

Discuss the Frank Starling relationship in terms of venous pressure and cardiac output?

A

When the rate at which blood flows into the heart from the veins changes, the

heart automatically adjusts its outflow to match inflow

  • increase in VEDV results in increase in SV & CO
  • decrease in VEDV results in decrease in SV & CO

Cardiovascular and Respiratory (39 decks)

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