Cardiovascular System Flashcards

1
Q

heart anatomy

A

location:
-in the mediastinum btwn second rib and fifth intercostal space

  • on the superior surface of diaphragm
  • to the left of the midsternal line
  • anterior to the vertebral column, posterior to the sternum

-enclosed in pericardium, a double-walled sac

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2
Q

pericardium

A
  • superficial fibrous pericardium
  • protects, anchors, and prevents overfilling
  • Deep two-layered serous pericardium
  • Parietal layer lines the internal surface of the fibrous pericardium
  • Visceral layer (epicardium) on external surface of the heart
  • Separated by fluid-filled pericardial cavity (decreases friction)
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3
Q

layers of the heart wall

A
  1. epicardium
    * visceral layer of pericardium
  2. myocardium
    * cardiac muscle, layer that contracts
    * connective tissue of heart (anchors cardiac muscle fibers, supports great vessels and valves, limits the spread of action potentials to specific paths
  3. endocardium
    * lines chambers, is continuous with vessels
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4
Q

chambers

A

4 chamber
-> 2 atria (receiving chambers; partition called interatrial septum

-> 2 ventricles (pumping chambers, separated by the interventricular septum)

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5
Q

atria: the receiving chambers (entranceway)

A
  • > 3 veins entering right atrium
  • superior vena cava
  • inferior vena cava
  • coronary sinus (from heart)
  • > 2 veins entering left atrium
  • right and left pulmonary veins
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6
Q

ventricles: the discharging chambers

A
  • > vessel leaving the right ventricle
  • pulmonary trunk (artery) to lung has limited oxygen
  • > vessel leaving the left ventricle
  • aorta to body- has oxygen
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7
Q

pathway of blood through the heart

A
  • The heart is two side-by-side pumps
  • Equal volumes of blood are pumped to the pulmonary and systemic circuits

-Pulmonary circuit (right)
is a short, low-pressure circulation

-Systemic circuit (left)
blood encounters much resistance in the long pathways

-Size of the ventricles reflects these differences

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8
Q

the pathway of blood flow through the heart

A

slide 16

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9
Q

coronary circulation

A
  • Blood supply to the heart muscle itself
  • Collateral routes provide additional routes for blood delivery
  • O2 utilization – 70 to 80% extracted from blood supply
  • If vigorous exercise must increase blood flow by dilating coronary vessels
  • Practically one capillary per muscle fiber
  • Impairment in flow = angina
  • Partial/complete blockage of coronary = myocardial infarction (heart attack)
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10
Q

coronary artery disease

A

treatment:

  • CABG- great saphenous vein
  • ballon angioplasty
  • cardiac stents-metal mesh tubes
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11
Q

heart valves

A

atrioventricular (av) valves:

  • close when ventricles contract, prevents backflow
  • tricuspid valve (right)
  • mitral (bicuspid) valve (left)

semilunar (sl) valves:

  • aortic semilunar valve(left)
  • pulmonary semilunar valve (right)

-chordae tendineae (collagen strings) anchor AV valve cusps to papillary muscles (prevent valves from turning inside out)

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12
Q

valve disease

A

Faulty valves makes heart work harder, Either blood leaks backward or flow is restricted through valves. (murmurs, mitral valve prolapse, aortic valve stenosis)

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13
Q

cardiac muscle

A

gap junctions, striated, short

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14
Q

skeletal vs cardiac MM

A
  1. stimulation:
    - skeletal MM is stimulated by nerve ending;
    - cardiac MM are self excitable; intrinsic conduction system
  2. contraction:
    - skeletal MM contract from motor unit
    - cardiac MM contracts as a unit or not at all (gap junctions)
  3. absolute refractory:
    - cardiac MM has longer period, prevents tetanic contractions (stop pumping action)
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15
Q

cardiac MM contraction

A
  1. depolarization: Na channels open and Na rushes in. Membrane potential rises from -90mV to +30mV
  2. Transmission of depolarization wave Opens special calcium channels in membrane to release 20% of calcium. Then T tubules cause SR to release the remaining calcium needed for contraction.
  3. Excitation-Coupling Ca provides signal for cross bridge activation (calcium channel blockers – HTN)
  4. Repolarization – Ca channels close and K channels open & returns to resting voltage
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16
Q

energy requirments

A
  • heart is exclusively aerobic
  • has more mitochondria than skeletal MM
  • cardiac MM able to use whatever nutrient available, including lactic acid
  • danger of inadequate blood supply to heart is not lack of nutrients but lack of O2
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17
Q

sequence of excitation:

A

Cardiac pacemaker cells are found:
1. Sino-atrial node
2. Atrioventricular node (delay for atria to finish contracting)
3. Atrioventricular bundle (bundle of HIS) (only electrical connection btwn atria and ventricle)
4. Right and Left bundle branches (intraventricular septum)
5. Subendocardial conducting network (Purkinje fibers)
SLIDE 31

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18
Q

Arrhythmias

A
  • Irregular heart rhythms due to defects in intrinsic conduction system
  • Atrial-fibrillation (a-fib) & ventricular fibrillation (v-fib), can be life threatening if not treated within minutes
19
Q

extrinsic innervation of the heart

A
  • heartbeat is modified by the ANS
  • cardiac centers are located in the medulla oblongata
  • Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons

Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves (note no heart muscle)

20
Q

the vagus nerve (parasympathetic) decreases heart rate

A

true

21
Q

sympathetic cardiac nerves increase heart rate and force of contraction

A

true

22
Q

electrocardiography

A
  • ECG or EKG
  • a composite of all the action potentials generated by nodal and contractile cells at a given time

3 waves:
1. P WAVE: DEPOLARIZATION OF SA NODE (ATRIA)

  1. QRS COMPLEX: VENTRICULAR DEPOLARIZATION
  2. T WAVE: VENTRICULAR REPOLARIZATION

slide 36

23
Q

depolarization, repolarization steps

A
  1. Atrial depolarization, initiated by the SA node, causes the P wave.
  2. with atrial depolarization complete, the impulse is delayed at the AV node
  3. ventricular depolarization begins at apex, causing the QRS complex. atrial repolarization occurs
  4. ventricular depolarization is complete
  5. ventricular repolarization begins at apex, causing the T wave
  6. ventricular repolarization is complete
24
Q

Heart sounds

A

2 sounds (lub-dub) associated with closing of heart valves

  • > first sound occurs as AV valves close and signifies beginning of ventricular systole (contraction)
  • > second sound occurs when SL valves close at the beginning of ventricular diastole (relaxation)
25
Q

heart murmurs

A

abnormal heart sounds most often indicative of valve problems
-swishing sound since valves are incompetent

26
Q

Phases of the cardiac cycle:

1. ventricular filling

A
  • takes place in mid-to-late diastole (relaxation)
  • > AV valves are open, SL valves are closed
  • > 80% of blood passively flows into ventricles
  • > atrial systole occurs, delivering the remaining 20%
  • > end diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole, maximum amount of blood
27
Q

Phases of the cardiac cycle:

2. ventricular systole (contraction)

A
  • atria relax and ventricles begin to contract
  • rising ventricular pressure results in closing of AV valves
  • Isovolumetric contraction phase (all valves are closed)
  • in ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open
  • end systolic volume (ESV): volume of blood remaining in each ventricle
28
Q

Phases of the cardiac cycle:

3. Isovolumetric relaxation

A
  • occurs in early diastole
  • ventricles relax
  • backflow of blood in aorta and pulmonary trunk closes SL valves
  • ventricles again are closed chambers because all valves are closed
29
Q

This valve is found between the right atrium and the right ventricle

A

tricuspid valve

30
Q

Which of the following structures is an exception to the general principle surrounding blood vessel oxygenation levels?

A

pulmonary artery and pulmonary veins

31
Q

Atrial repolarization occurs during this period of time, seen on an ECG

A

QRS complex

32
Q

Cardiac output (CO)

A
  • volume of blood pumped by each ventricle in 1 minute
  • CO=heart rate (HR) x stroke volume (SV)

HR = number of beats per minute

SV = volume of blood pumped out by a ventricle with each beat

Cardiac output is main indicator if the supply (circulation) is meeting demand (O2 at tissues)

33
Q

cardiac output

A

with endurance training, the SA node comes under greater influence of acetylcholine (PNS) which has slowing effect on HR

34
Q

regulation of stroke volume

A

SV= EDV- ESV ((amt of blood in ventricle during diastole vs and the volume of blood remaining after contraction)

Three main factors affect SV:
Preload
Contractility
Afterload

35
Q

regulation of stroke volume

A

Preload: degree of stretch of cardiac muscle cells before they contract (frank-starling law of the heart). ENhanced cardiac filling
-> at rest, cardiac muscle cells are shorter than optimal length

  • > slow heartbeat and exercise increase venous return
  • > increased venous return distends (stretches) the ventricles and increases contraction force
36
Q

regulation of stroke volume

A

contractility: contractile strength at a given muscle length

  • positive inotropic agents increase contractility:
  • increased calcium influx due to sympathetic stimulation
  • hormones (thyroxine, glucagon, and epinephrine)
  • drug digitalis
  • negative inotropic agents DECREASE contractility:
  • acidosis
  • increased extracellular potassium
  • calcium channel blockers
37
Q

regulation of stroke volume

A

afterload: pressure that must be overcome for ventricles to eject blood
- hypertension increases afterload, resulting in increased ESV and reduced SV

38
Q

regulation of heart rate

A

Sympathetic stimulation of pacemaker cells:
*norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility)

Parasympathetic NS- inhibits pacemaker

  • the heart at rest exhibits vagal tone
  • parasympathetic activity has little or no effect on cardiac contractility
  • hormones
  • ions
  • age, gender, exercise, and temp
39
Q

chemical regulation of heart rate

A
  1. hormones
    * Epinephrine from adrenal medulla enhances heart rate and contractility
    * Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine
  2. intra- and extracellular ion concentrations (e.g., Ca and K) must be maintained for normal heart function
40
Q

other factors that influence heart rate

A

Age – fastest in fetus, declines with age

Gender – females faster than males

Exercise – increases HR, training decreases overall

Body temperature – heat increases HR

41
Q

The “lub-dup” heart sounds are produced by _______.

A

the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”).

42
Q

Atrial systole occurs _______ the firing of the sinoatrial node.

A

after

43
Q

Predict what would happen to the end systolic volume (ESV) if contraction force were to increase

A

it would decrease