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NUR1112 > Week 7 Bioscience > Flashcards

Week 7 Bioscience Flashcards

1
Q

Size of the heart

A

■ Cone-shaped, muscular organ
■ Typically:
- 12-14 cm long, 9 cm wide
- weights 250-350 grams approx. the size of your fist

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2
Q

Location of the heart

A

The heart sits in the mediastinum – the cavity between the two pleural cavities and rests on the superior surface of the diaphragm.

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3
Q

Coverings of the heart

A

Where the parietal pericardium meets the large blood vessels attached to the base of the heart, the epithelial layer turns to cover the heart itself, forming the epicardium

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4
Q

Components of the heart wall

A

Epicardium (or visceral pericardium) – the outermost layer of epithelial tissue

Myocardium - the middle layer of of cardiac muscle cells

Endocardium - the inner layer of endothelial cells (flattened epithelial cells)

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5
Q

Coronary circulation - arteries

A
  • Right and left coronary arteries arise from base of the aorta and encircle the heart in the coronary sulcus
  • Blood moves into the coronary arteries when the ventricles relax, in between heart beats i.e. the ventricles relax and ventricular pressure drops below arterial pressure - arterial blood flows back towards to the ventricles (down pressure gradient) - as it flows backwards within the aorta it moves into the coronary arteries
  • Left coronary artery gives rise to the anterior interventricular artery and supplies oxygenated blood to the anterior ventricles
  • Right coronary artery supplies the right atrium and gives rise to the posterior interventricular artery which supplies oxygenated blood to the posterior ventricles
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6
Q

Coronary circulation - veins

A
  • Great cardiac vein drains deoxygenated blood from the anterior ventricles
    ■ Middle cardiac vein drains the posterior ventricles
  • All veins all drain into the coronary sinus (thin-walled, expanded vein)à empties into the right atrium
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7
Q

Coronary artery disease (CAD)

A
  • CAD = coronary arteries become narrowed and hardened (less elastic)
  • Most commonly as a result of atherosclerosis (fatty plaques occluding the arteries)
  • Over time, reduced blood flow weakens the myocardium and contributes to heart failure
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8
Q

Innervation of the heart

A
  • The mechanical activity of the heart (i.e. muscle contraction or heart beat) always begins with electrical activity (i.e. an action potential in the myocardial cells)
  • Myocardial activity is controlled by two separate electrical systems:
    1. Intrinsic conduction system (from the inside) - myocardium is able to stimulate its own contractions
    2. Extrinsic innervation (from the outside) = autonomic nervous system - modifies myocardial activity
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9
Q

Intrinsic conduction system

A

The myocardium includes some auto-rhythmic cells called pacemaker cells:
* Unstable resting membrane potential
* Continually depolarise to generate action potentials (AP) * All cardiac muscle cells have electrical connections - an AP in pacemaker cells can be conducted to the adjacent muscle cells and so on - allows coordinated contraction of the entire myocardium
The pacemaker cells form the intrinsic conduction system:
1. Sinoatrial node
2. Atrioventricular node
3. Atrioventricular bundle (bundle of His)
4. Bundle branches
5. Purkinje fibres (subendothelial conducting network)

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10
Q

Sinoatrial node

A
  • Right atrial wall, inferior to entry point of s. vena cava
  • Depolarises 80-100x per minute (fastest component)
  • Acts as pacemaker and determines heart rate (sinus rhythm)
  • Parasympathetic NS reduces this to 75x per minute at rest
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11
Q

Internodal pathway

A
  • SA node myocardial cells depolarize the surrounding myocardial cells until all atrial myocardium is depolarized
  • Depolarisation triggers atrial contraction
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12
Q

Atrioventricular node

A
  • At the junction between the atria and ventricles
  • Depolarises 40-60x per minute (max. 230x per min = upper limit of heart rate)
  • Delays depolarisation for 0.1 s while atria complete contraction
  • Becomes the pacemaker if SA node damaged
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13
Q

Atrioventricular bundle (bundle of His)

A
  • In the upper interventricular septum
  • Only electrical connection between the atria and ventricles
  • Damage - heart block - neither SA or AV node can control heart rate
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14
Q

Bundle branches (right and left)

A

Travels in the interventricular septum to the apex of the heart

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15
Q

Purkinje fibres (subendothelial conducting network)

A
  • Penetrate ventricle walls, depolarise ventricular myocardium
  • Depolarises 30x per minute (this heart rate is too slow for adequate CO)
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16
Q

Extrinsic innervation

A
  • Autonomic nervous system modifies the activity of the heart (otherwise heart rate is always 100 bpm – set by the SA node)
  • Cardiac centres in the medulla oblongata:
    1. Cardioacceleratory (cardiostimulatory) centre increases BOTH heart rate and force of contraction. Sympathetic input via thoracic spinal cord (T1-T3) to the SA and AV nodes, ventricular myocardium, coronary arteries (causes dilation)
    2. Cardioinhibitory centre decreases heart rate ONLY Parasympathetic input via vagus nerve (CN X) to the SA and AV nodes slows SA node to ~75 depolarisations per minute at rest
17
Q

The cardiac cycle

A
  • The pumping action of the heart involves alternating periods of contraction and relaxation that produce a series of pressure and blood volume changes in the heart chambers
  • Systole = period of contraction - increased pressure forces blood out of chambers
  • Diastole = period of relaxation - decreased pressure allows chambers to refill
  • Systole and diastole are coordinated mechanical events that are triggered by electrical events (action potentials in the myocardium)
18
Q

Cardiac cycle events

A
  • The cardiac cycle = one complete heartbeat
    • Atrial diastole and systole
    • Ventricular diastole and systole
      The sequence of events during a single heartbeat:
      1. Relaxation- atria and ventricles relaxed
      2. Atria contract- ventricles relaxed
      3. Ventricles contract- atria relaxed
      4. Relaxation- atria and ventricles relaxed
19
Q

Phase 1: Ventricular filling:

A
  1. All 4 chambers are relaxed; mid-late ventricular diastole (passive filling)
    • AV valves are open, SL valves closed blood returning to atria moves directly into ventricles (passive filling) à fills ventricles to ~ 70-80% capacity
  2. Atrial systole
    • both atria contract simultaneously, completely filling the relaxed ventricles with blood (this volume = EDV)
  3. Atrial systole ends and atrial diastole begins and continues until the next cycle
20
Q

Phase 2a: Ventricular systole – isovolumetric contraction

A
  1. Ventricular systole
    • both ventricles contract - beginning at the apex, pushing blood upwards and increasing ventricular pressure
    • upward movement of blood and increased pressure (greater than atrial pressure) closes the AV valves (produces heart sound, S1)
    • ventricular pressure not yet great enough to open SL valves so blood cannot yet exit the ventricles = isovolumetric contraction (“iso” = “the same”) - no change in ventricular blood volume
    • atria in diastole, AV valves closed
21
Q

Phase 2b: Ventricular systole – ventricular ejection

A
  1. Ventricular systole
    • increasing force of ventricular contraction - ventricular pressure increases above arterial pressure - SL valves open
    • blood ejected into aorta and pulmonary trunk = ventricular ejection (volume ejected = SV, volume remaining = ESV)
    • AV valves closed as ventricular pressure is greater than atrial pressure, thus blood cannot move backwards
    • atria in diastole
22
Q

Phase 3: Ventricular diastole (early)– isovolumetric relaxation

A
  1. Ventricular diastole (early)
    • ventricles relax - ventricular pressure drops below arterial pressure - arterial blood flows backwards (blood flows down a pressure gradient) - closes the SL valves (produces heart sound, S2)
  2. Isovolumetric relaxation
    • as ventricular pressure is still greater than atrial pressure the AV valves are still closed, thus blood cannot move from atria into ventricles - no change in ventricular blood volume
  3. Ventricular diastole (mid-late)
    • ventricles continue to relax - ventricular pressure drops below atrial pressure (atria have been filling with blood returning to the heart) - AV valves open - return to passive ventricular filling (Phase 1)
23
Q

Heart sounds

A
  • Four heart sounds (S1-S4)
  • Heartbeat = S1 and S2 = “lubb-dubb”
  • “Lubb” (S1) = closure of the AV valves
  • “Dubb” (S2) = closure of the SL valves
  • Heart murmur = swishing sound as blood backflows though an incompetent valve
24
Q

Cardiac output

A
  • The goal of cardiovascular function is the maintenance of adequate blood flow (i.e. oxygen) to (vital) tissues/organs
    • Oxygen demands vary (i.e. depending on whether we are at rest or active) thus blood flow must vary
    • A measure of peripheral blood flow is cardiac output
    • Cardiac output is the volume of blood pumped by the left (or right) ventricle in one minute

Cardiac output = stroke volume x heart rate CO = SV x HR

* Heart rate (HR) = number of beats per minute (bpm) 
* Stroke volume (SV) = volume of blood ejected from the left (or right) ventricle per beat (mL Cardiac output (CO) = volume blood pumped into the systemic (or pulmonary) circuit per minute (L/min)
25
Q

Stroke volume

A
  • SV = volume of blood pumped out of a ventricle with each beat
  • SV = EDV - ESV
  • End diastolic volume = the volume of blood in a ventricle at the end its relaxation period, i.e. diastole (just before it contracts) (~ 120 ml at rest)
  • End systolic volume = the volume of blood remaining in a ventricle after it has contracted (~ 50 ml or 40% of EDV)
  • Factors which affect EDV and/or ESV will determine SV and thus CO
26
Q

Factors effecting EDV

A
  • EDV is determined by:
    1. Venous return = amount of blood returning to the heart from systemic or pulmonary circuits – depends on:
    • Total blood volume
    • Patterns of blood flow determined by muscle/organ activity, sympathetic activity and body position
      1. Passive filling time = time both the atria and ventricles are in diastole (i.e. Phase 1)
    • decreases as HR increases (i.e. during physical activity but increasing filling time compensated for by ­ decreasing venous return)
  • If HR > 200 bpm à big ¯ in passive filling time à ¯ EDV à ¯ SV and CO
27
Q

EDV determines preload

A
  • The EDV determines the preload
  • Preload = degree the myocardium is stretched before it contracts - determines the force of ventricular myocardial contraction - determines SV
  • A greater EDV - increased preload (myocardial stretch) - more efficient myocardial contraction - greater the SV =Frank-Starling law of the heart, OR
  • MORE BLOOD IN = MORE BLOOD OUT
28
Q

Factors affecting ESV

A
  • Contractility
    • Amount of force produced by myocardial contraction
    • contractility - higher SV (thus lower ESV) - higher CO
    • Contractility is increased by:
    • Sympathetic stimulation of ventricular myocardium
    • Hormones: adrenalin, noradrenalin, thyroxine (T4)
    • High levels of extracellular Ca2+
    • Exercise (increases size of the myocardium)
    • Contractility is decreased by:
    • Acidosis (low ECF pH)
      • Increased extracellular K+ levels
29
Q

Factors affecting ESV

A
  • Afterload
  • The pressure that the ventricles must overcome to open the SL valves to eject blood into the arteries (i.e. how hard the ventricles must work to eject blood)
  • Not a major factor in determining SV in healthy people
  • Increased by factors that restrict flow into arteries, e.g. atherosclerosis in the aorta - narrows vessel and decreases compliance (i.e. stretchability)
  • The longer it takes for the ventricles to generate enough pressure to open the SL valves, the less time there is for blood ejection, thus increasing­ afterload and decreasing SV (and ­ ESV)
30
Q

Heart rate

A
  • Altering HR is an important shortterm control of CO and blood pressure
  • HR is rapidly altered to: ¡ Meet the needs of our tissues/organs, e.g. increased physical activity
  • Compensate for changes in SV, i.e. if myocardium is damaged or blood volume reduced due to dehydration
  • Each individual has a characteristic resting heart rate that varies with age, gender, general health, physical fitness
  • Normal range = 60 – 100 beats per minute (bpm)
  • Average rate = 75 bpm (80 bpm)
31
Q

Factors affecting HR – The ANS

A
  • Cardiovascular centres in the medulla oblongata
  • Receives input from: ¡ Proprioceptors – monitor movement
  • Chemoreceptors – monitor CO2, O2 and H+ levels
  • Baroreceptors – monitor blood pressure
  • Autonomic output:
  • Sympathetic from cardioacceleratory centre
  • NA binding β1 receptors which
  • Speeds up depolarisation of SA and AV nodes -­ HR
  • Parasympathetic from cardioinhibitory centre
  • ACh binding muscarinic receptors which
  • Slows depolarisation of SA and AV nodes - decreases HR
  • Slows depolarisation of SA node (pacemaker) from ~ 100/min to ~ 75/min at rest
32
Q

Hormones and temperature affect HR

A
  • Adrenalin and noradrenalin
  • Released from the adrenal medulla à­ HR
  • Thyroxine (T4) ¡ Thyroid hormones (­ cellular metabolism) à ­ HR
  • Body temperature
  • Increased temperature ­ HR and vice versa
  • Plasma electrolytes
  • Increased extracellular Na+ or K+ à ¯ HR
  • Increased extracellular Ca2+ à ­ HR and vice versa
  • Age/gender/general health/physical fitness
  • Exercise - hypertrophy (enlargement) of the myocardium - ­ SV - HR can decrease at rest and still maintain CO

NUR1112 (24 decks)

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