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BIO 176 LAB + LEC > The Cardiovascular System 2 > Flashcards

The Cardiovascular System 2 Flashcards

1
Q

define AUTORHYTHMIC RIBERS

A
  • the source of the heart’s ELECTRICAL ACTIVITY
  • known as SPECIALIZED CARDIAC MUSCLE FIBERS
  • they are SELF-EXCITABLE
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2
Q

can the heart be OVERRIDDEN?

A
  • the heart can DEPOLARIZE and CONTRACT
  • **WITHOUT NERVOUS SYSTEM STIMULATION
    can also be overridden by the ANS
    (from the PARASYMPATHETIC or SYMPATHETIC SYSTEMS)
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3
Q

describe the pathway of the INTRINSIC CARDIAC CONDUCTION SYSTEM

A

TOTAL TIME;
around 220 MILLISECONDS

  1. begins with the SINOATRIAL (SA) PACEMAKER with the creation of IMPULSES
    - can DEPOLARIZE FASTER THAN EVERYTHING ELSE with 75 BPM
    - SINUS RHYTHM can increase or decrease depending on EXTRINSIC FACTORS
  2. some delay and impulse enter the ATRIOVENTRICULAR NODE
    (lower rate at 50 BPM)
  3. enters the AV BUNDLE (BUNDLE OF HIS) that is seen on the SUPERIOR INTERVENTRICULAR SEPTUM–this is the ONLY CONNECTION between the ATRIA and VENTRICLES
    (rate at 30 BPM)
  4. enters the BUNDLE BRANCHES–conduction of impulses through the INTERVENTRICULAR SEPTUM
  5. enters lastly the SUBENDOCARDIAL CONDUCTING NETWORK aka as the PURKINJE FIBERS (depolarizes BOTH VENTRICLES)
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4
Q

how does the heart set its BASIC RHYTHM?

A

through the presence of GAP JUNCTIONS
- the INTRINISIC CARDIAC CONDUCTION SYSTEM
- has its own NETWORK of NONCONTRACTILE (AUTORHYTHMIC CELLS)–continues to coordinate and DEPOLARIZE/CONTRACT the HEART

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5
Q

describe the CONDUCTION SYSTEM and PACEMAKER POTENTIALS

A
  • we always have a fluctuation of UNSTABLE MEMBRANE POTENTIALS

PACEMAKER POTENTIALS:

REPOLARIZATION:
- the CLOSING of K CHANNELS and OPENING of SLOW NA+ CHANNELS
- creation of an ION IMBALANCE

DEPOLARIZATION:
- CALCIUM CHANNELS OPEN–the creation of a HUGE INFLUX)

REPOLARIZATION:
- K CHANNELS OPEN (EFFLUX OF K)

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6
Q

what are ARRHYTHMIAS?

A
  • irregular heart RHYTHMS
  • indication of uncoordinated atrial and ventricular contractions
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7
Q

what is FIBRILLATION?

A
  • rapid, irregular CONTRACTIONS
    • the heart becomes USELESS in terms of pumping blood
    • circulation begins to CEASE—resulting in brain death

can be treated with DEFIBRILLATION–the INTERRUPTION of CHAOTIC TWITCHING

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8
Q

what are HEART BLOCKS?

A
  • AV NODE:
    • to reach the ventricles—impulse must pass through the AV NODE
    • what happens if our AV NODE is DEFECTIVE?
      • causation of a HEART BLOCK

TREATMENT:
ARTIFICIAL PACEMAKER

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9
Q

compare the CARDIOACCELEATORY CENTER and the CARDIOINHIBITORY CENTER

A

CARDIOACCELEATORY CENTER
- affects the SA NODE, AV NODES, HEART MUSCLES, and CORONARY ARTERIES
- has SYMPATHETIC NEURONS that release NOREPINEPHRINE

*CHRONOTROPIC–increases heart rate

CARDIOINHIBITORY CENTER:
- INHIBITION of the SA and AV NODES through the VAGUS NERVES
- has PARASYMPATHETIC NEURONS that release ACETYCHOLINE

*NEGATIVE CHRONOTROPIC–decreases heart rate

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10
Q

describe the AP within VENTRICULAR MUSCLE FIBERS (4 PHASES)

A

ACTION POTENTIAL:
- a VENTRICULAR CONTRACTILE FIBER

PHASES:
1. RESTING
2. RAPID DEPOLARIZATION
- POSITIVE FEEDBACK INFLUX—entering of sodium channels
- goes to +30 mV

  1. PLATEAU PHASE
    - CALCIUM INFLUX—slow calcium channels
    - the cell becomes DEPOLARIZED; a PLATEAU of AP (cont. contraction)
    - MUSCLE TENSION OCCURS HERE
  2. REPOLARIZATION
    - this is around after 200 ms—INACTIVATION OF CALCIUM CHANNELS (-90 mV)
    - opening of POTASSIUM GATES—restores the RMP (resting membrane potential)
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11
Q

how is energy made within the cardiac muscle?

A

through the OXIDATION of FATTY ACIDS (60%) and GLUCOSE (40%)

  • AEROBIC CELLULAR RESPIRATION
  • CREATINE PHOSPHATE
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12
Q

what is an ELECTROCARDIOGRAPHY?

A

a graphic recording of the ELECTRICAL ACTIVITY (POTENTIALS) that are produced by the heart’s CONDUCTION SYSTEM and the MYOCARDIUM —through the DEPOLARIZATION AND REPOLARIZATION CYCLE

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13
Q

describe each part of the PQRST complex

A
    • P WAVE (.008s)
      • the FIRST DEFLECTION from the baseline
      • the DEPOLARIZATION of the SA node and ATRIA (atrial contraction)
    • PR SEGMENT (0.12s)
      • the RETURN to BASELINE
      • the AFTER-ATRIA L CONTRACTION
    • PR INTERVAL (.016s)
      • the beginning of ATRIAL EXCITATION
        • leads all the way to BEGINNING OF VENTRICULAR EXCITATION
    • QRS COMPLEX (.008s)
      • VENTRICULAR DEPOLARIZATION
      • ATRIAL REPOLARIZATION
        • (ventricles contraction + atrial relaxation)
    • ST SEGMENT (.04s)
      • the ENTIRE VENTRICULAR MYOCARDIUM is DEPOLARIZED
    • T WAVE (.016s)
      • VENTRICULAR REPOLARIZATION
    • QT INTERVAL (.038s)
      • the BEGINNING OF VENTRICULAR DEPOLARIZATION
        • through VENTRICULAR REPOLARIZATION
        (ventricular relaxation)
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14
Q

define DEPOLARIZATION and REPOLARIZATION

A
  • DEPOLARIZATION:
    • the CONTRACTION PHASE;
      • the electrical system of the heart STIMULATES THE MYOCARDIUM
  • REPOLARIZATION:
    • the RESTING STATE/PHASE;
      • myocardium returns to RESTING STATE before it can be ELECTRICALLY STIMULATED AGAIN
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15
Q

what happens if we have EKG changes?

A

any changes in terms of EKG pattern or timing can reveal a DISEASED or DAMAGED HEART–issues with the heart’s CONDUCTION SYSTEM

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16
Q

what are the SINUS RHYTHMS?

A

NORMAL SINUS RHYTHM:
- around 60-100 BPM (avg. 75 BPM)

SINUS BRADY CARDIA:
anything lower than 60 BPM

SINUS TACHYCARDIA
anything higher than 100 BPM

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17
Q

describe the HEART SOUNDS and their CORRELATION to the CONDUCTION SYS

A

has TWO SOUNDS (LUB-DUB)
- asso. with the CLOSING OF THE HEART VALVES
1. AV VALVES CLOSE—the beginning of SYSTOLE - “LUB”
2. SL VALVES CLOSE—the beginning of VENTRICULAR DIASTOLE - “DUB”
3. PAUSE—the indication of HEART RELAXATION

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18
Q

where can we hear the heart sounds in order?

A

“all physicians take money”

  • aortic
  • pulmonary
  • mitral
  • tricuspid
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19
Q

what are HEART MURMURS?

A
  • abnormal heart sounds
    • indication of INCOMPETENT or STENOTIC VALVES
20
Q

what does one cardiac cycle equal?

A

ONE CARDIAC CYCLE = ONE CONTRACTION CYCLE AND ONE RELAXATION CYCLE

21
Q

describe the ELECTRICAL EVENTS of the HEART

A

PHASES:
- beginning of ATRIAL SYSTOLE
- then VENTRICULAR SYSTOLE
- RELAXATION PERIOD

  1. ATRIAL DEPOLARIZATION (depolarization of the SA NODE)
  2. VENTRICULAR DEPOLARIZATION (seen within QRS COMPLEX)
  3. VENTRICULAR REPOLARIZATION (seen on T WAVE)
22
Q

describe the HEART SOUNDS

A
  • FIRST HEART SOUND (S1):
    • closing of the AV VALVES
  • SECOND HEART SOUND (S2):
    • closing of the SL VALVES
  • S3 SOUND:
    • benign in youth or in trained athletes/pregnancies
      • can remerge in life—signaling of CARDIAC PROBLEMS or failing of the LEFT VENTRICLE (CHF)
  • S4 SOUND:
    • known as PRE-STYOLIC GALLOP or ATRIAL GALLOP
      • produced due to SOUND OF BLOOD being forced into a STIFF or HYPERTROPHIC VENTRICLE
23
Q

describe the pressure changes of the heart

A
  1. ATRIAL DEPOLARIZATION = ATRIAL SYSTOLE
  2. VENTRICULAR DEPOLARIZATION = VENTRICULAR SYSTOLE

ISO-VOLUME METRIC CONTRACTION:
VENTRICULAR EJECTION:
- increase of LEFT VENTRICULAR PRESSURE > AORTIC PRESSURE
- SL valves OPEN

  • VENTRICULAR REPOLARIZATION - causes VENTRICULAR DIASTOLE
    • backflow is going to CLOSE VALVES (both valves)
  • VENTRICULAR PRESSURE DROPS (below atrial pressure)
    • AV VALVES OPEN
24
Q

describe the VOLUME CHANGES of the HEART (2)

A
  • END DIASTOLIC VOLUME (EDV) (3):
    • the end of atrial systole is also the end of ventricular diastole (130 mL)
  • END SYSTOLIC VOLUME (ESV) (7):
    • the volume remaining in each ventricle at the end of systole (60 mL)
25
describe STROKE VOLUME
- volume of blood ejected per beat from each ventricle = end-diastolic volume - end systolic volume - SV = EDV - ESV - AT REST: - SV (130 mL - 60 mL = 70 mL)
26
describe MECHANICAL EVENTS
1. VENTRICULAR FILLING (within MID-TO-LATE DIASTOLE) - AV VALVES OPEN (LOW PRESSURE) - ATRIAL CONTRACTION 2. VENTRICULAR SYSTOLE (ATRIAL DIASTOLE) - ISOVOLUMETRIC CONTRACTION (VALVES CLOSE) - VENTRICULAR EJECTION (enters into the PULMONARY TRUNK + AORTA) 3. ISOVOLUMENTRIC RELAXATION - VENTRICLES RELAX and ATRIA RELAX - SL VALVES CLOSE
27
what is CARDIAC OUTPUT?
- the volume of blood pumped by EACH VENTRICLE in one MINUTE - *average: 5.25 L/min* - speed of blood flow LEAVING the HEART CO - HR x STROKE VOLUME **meaning if either SV or HR is INCREASED--so does CO
28
what is HEART RATE?
- HR: - number of BEATS PER MIN - *average = 75 BPM*
29
what is stroke volume (definition and avg.)?
- SV: - the volume of blood pumped out by ONE VENTRICLE WITH EACH BEAT - average = 70 mL/min
30
what is CARDIAC RESERVE?
- the difference between RESTING AND MAXIMAL CO - NONATHLETES: - CR = 4-5 times resting CO (20-25 L/min) - ATHLETES: - CR = 7 times resting CO (35 L/min)
31
how do we REGULATE STROKE VOLUME?
- STROKE VOLUME (SV): - SV = EDV - ESV EDV: - affected by the LENGTH OF VENTRICULAR DIASTOLE - affected by VENOUS PRESSURE (~120 mL/beat) ESV: - affected by ARTERIAL BP - affected by FORCE OF VENTRICULAR CONTRACTION (~50 mL/beat) NORMAL SV: - 120 mL - 50 mL = 70 mL/beat
32
what are the THREE MAIN FACTORS that affect SV?
1. PRELOAD 2. INOTROPY (CONTRACTILITY) 3. AFTERLOAD
33
what is PRELOAD? what happens if there are any changes with PRELOAD?
PRELOAD: - the degree of STRETCH OF THE HEART MUSCLE - the degree to which CARDIAC MUSCLE CELLS are STRETCHED just before they CONTRACT **any changes with EDV--this affects the SV known as the FRANK-STARLING LAW OF THE HEART
34
what is the most important factor in terms of PRELOAD?
- VENOUS RETURN: - the most important factor in PRELOAD STRETCHING OF CARDIAC MUSCLE - increases contraction force with exercise or slow return of blood - the amount of BLOOD RETURNING TO THE HEART
35
what is CONTRACTILITY/INOTROPY?
CONTRACTILITY: - the contractile strength at given muscle length - independent of MUSCLE STRETCH + EDV **if we have an INCREASED CONTRACTILITY--this LOWERS THE ESV - have a SYMPATHETIC RELEASE OF EPINEPHRINE which also INCREASES CALCIUM - more BLOOD EJECTION + CROSS-BRIDGE FORMATIONS
36
what is AFTERLOAD?
the backup pressure exerted by ARTERIAL BLOOD - the pressure that VENTRICLES must OVERCOME TO EJECT BLOOD - back pressure from ARTERIAL BLOOD—begins to PUSH ON SL VALVES; creating a MAJOR PRESSURE
37
describe SV, EDV, and ESV connections
PRELOAD INCREASE = SV INCREASE + EDV INCREASE AFTERLOAD INCREASE = SV DECREASE + ESV INCREASE INOTROPHY INCREASE = SV INCREASE + ESV DECREASE
38
what is CONGESTIVE HEART FAILURE?
PROGRESSIVE CONDITION; - **CO is extremely LOW—blood circulation becomes INADEQUATE to meet the tissue needs** - heart cannot work as a proper PUMP - reflection of a WEAKENED MYOCARDIUM
39
what is PULMONARY EDEMA?
- PULMONARY CONGESTION: - the LEFT SIDE FAILS—blood begins to BACK UP into the LUNGS - PERIPHERAL CONGESTION: - the RIGHT SIDE FAILS—blood begins to pool in BODY ORGANS and causes EDEMA - failing of either side ultimately weakens the other - TREATMENT: - removing of fluid - reducing afterload - increasing contractility
40
describe HYPERTENSION--what is SYSTOLIC and DIASTOLIC BP?
a sustained and increased SYSTEMIC ARTERIAL PRESSURE - SYSTOLIC BLOOD PRESSURE: - greater than or equal to **140 mmHg** - DIASTOLIC BLOOD PRESSURE: - greater than or equal to **90 mmHg**
41
how can we regulate the heart rate?
can be due to the DECREASE of the SV (due to DECREASED BV or a WEAKENED HEART) - POSITIVE CHRONOTROPIC FACTORS: - INCREASES HEART RATE - NEGATIVE CHRONOTROPIC FACTORS: - DECREASES HEART RATE
42
how does the NERVOUS SYSTEM regulate the heart ?
- NERVOUS SYSTEM REGULATION: - originated in the cardiovascular center within the MEDULLA OBLONGATA - receives input from higher brain centers (the LIMBIC SYSTEM + CEREBRAL CORTEX) - also have other sensory receptors that PROVIDE INPUT—CHEMORECEPTORS + BARORECEPTORS
43
how does the ANS regulate the heart?
the ANS IS PART OF THE SNS - activated by EMOTIONAL and PHYSICAL STRESSORS NOREPINEPHRINE: - allows the PACEMAKER TO FIRE MORE RAPIDLY—INCREASES HR - EDV decreased (*decreased fill time)* - INCREASED CONTRACTILITY - ESV decreased *(increased volume of ejected blood)*
44
what hormones help regulate heart rate?
EPINEPHRINE (from adrenal medulla)— - INCREASES HEART RATE + CONTRACTILITY NE (released from sympathetic nerves)— - INCREASES HEART RATE + CONTRACTILITY THYROXINE: - INCREASES HEART RATE - enhances the effects of NOREPINEPHRINE + EPINEPHRINE
45
describe homeostatic imbalances of either CALCIUM and POTASSIUM
HYPOCALCEMIA: - depresses the heart HYPERCALCEMIA: - increases HR and contractility HYPERKALEMIA: - alters ELECTRICAL ACTIVITY - can lead to heart blocks and cardiac arrest HYPOKALEMIA: - results in FEEBLE HEARTBEAT—arrhythmias
46
where does the heart develop from?
mesoderm - begins as TWO ENDOTHELIAL CHAMBERS--forms into SINGLE ACTIVE PUMPING CHAMBER
47
describe CONGENITAL HEART DEFECTS
- CONGENITAL HEART DEFECTS: - the most common birth defects- often treated with SURGERY TWO TYPES: 1. the mixing or O2-poor and O2-rich blood - seen in septal defects, patent ductus arteriosus 2. narrowed valves or vessels—this INCREASES WORKLOAD on the HEART - seen in coarctation of aorta **TETRALOGY OF FALLOT--both types of disorders are present

BIO 176 LAB + LEC (20 decks)

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