Heart Physiology (Exam 1) Flashcards

1
Q

Pericardium: Tissues (2) and Functions

A
  • Fibrous
    • Inelastic, dense irregular tissue
    • Prevents overstretching, protects and anchors
  • Serous (made of epithelial tissue)
    • Parietal layer - fused to fibrous (attached to surrounding structures)
    • Visceral layer - on heart surface - AKA epicardium
    • Pericardial cavity with fluid between layers - reduces friction
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2
Q

Right and Left Atria: Flow direction and location

A
  • Blood in
  • Top
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3
Q

RIght and Left Ventricle: Flow direction, location, pressure (high or low)

A
  • Blood out
  • Bottom
  • High Pressure
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4
Q

Interventricular Septum: Functions and components/location

A
  • separates sides of heart in adults
    • Tricuspid - “Tri to get it right.”
    • Bicuspid - Left side
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5
Q

Flow of blood through the heart

A

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  1. Superior and inferior vena cavae and the coronary sinus
  2. Rt. atrium
  3. Tricuspid valve (also called the rt. atrioventricular valve)
  4. Rt. ventricle
  5. Pulmonary semilunar valve
  6. Pulmonary trunk
  7. Right and left pulmonary arteries
  8. Lungs
  9. Pulmonary veins
  10. Lt. atrium
  11. Bicuspid valve (also called the lt. atrioventricular valve or mitral vale )
  12. Lt. ventricle
  13. Aortic semilunar valve
  14. Ascending aorta
  15. Coronary arteries
  16. Arch of aorta
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6
Q

Right and Left Ventricle: Density and reasoning

A
  • Right Ventricle - Thinner since it only pumps to lungs which are very close in proximity
  • Left Ventricle - Thicker due to having to pump against gravity
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7
Q

Heart Valves: Names (2), location, mechanism, purpose

A
  • Atrioventricular valves
    • Connected to papillary muscles by chordae tendinae
    • Ventricles relax, chordae are slack, valve opens due to pressure from atria
    • Chordae prevent backflow
  • Semilunar valves
    • Opened by ventricular pressure
    • Backflow fills cusps and closes valves
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8
Q

Coronary Circulation: Origin and endpoint

A
  • Nutrients cannot diffuse easily to myocardium from chambers
  • Coronary arteries branch from aorta
  • Coronary veins empty into sinus and then to right atrium
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9
Q

Histology of Cardiac Muscle: Overview and Structures (3)/Functions

A
  • Striated like skeletal muscle
  • Involuntary
  • Branched; shorter than skeletal muscle

Desmosomes - protein linker that keeps things intact

Intercalated discs - Junction point between fibers

Gap Junctions - Act as pores, allow for things to travel quickly from one place to another

SIB DIG

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10
Q

Action Potential in Cardiac Muscle: Stages (3) and description (ions)

A
  • Depolarization - Voltage-gated fast Na+ channels open - rapid depolarization
  • Plateau - sustained depolarization due to Ca2+ inflow balancing K+ outflow
  • Repolarization - Ca2+ channels close, K+ channels open
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11
Q

ATP Production: Cause and feedback

A
  • Aerobic respiration
    • Breakdown of sugar in presence of Oxygen; allows production of ATP
  • Oxygen diffuses from coronary circulation and released from myoglobin
  • At rest, mostly from oxidation of fatty acids and glucose
  • During exercise, lactic acid use rises
    • Lactic acid - byproduct of anaerobic activity
  • Creatine phosphate also used (presence of creatine kinase in blood is sign of injured/dying muscle fibers)
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12
Q

(Intrinsic) Conduction System: Origin, function, flow of current

A
  • Autorhythmic fibers repeatedly and rhythmically generate action potentials
  • SA node spontaneously depolarizes (pacemaker potential) - potential spreads to both atria
  • SA node > AV node > AV bundle > Bundle branches > Purkinje fibers

** SA = Sinoatrial

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13
Q

Electrocardiogram: Wave names/cause, description

A
  • P wave = atrial depolarization
    • blip
  • QRS complex = rapid ventricular depolarization
    • spike
    • disguises atrial repolarization
  • T wave = ventricular repolarization
    • bump
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14
Q

Cardiac Cycle: 3 Major steps and corresponding feedback per step

A
  • Atrial Systole (systole = period of contraction)
    • SA node depolarizes
    • Atria depolarize
    • Blood moves through AV valves
    • Coincides w/ ventricular diastole
    • End-diastolic volume (EDV) in ventricles
      • EDV - preferably high pressure
    • P wave and part of QRS
  • Ventricular systole
    • Ventricles depolarize
    • Pressure forces AV valves shut
    • Isovolumetric contraction (AV and SL valves closed, fibers contracting but not shortening)
    • SL valves open = ventricular ejection
    • End-systolic volume (ESV) - volume in vents. at end of systole
      • ESV - preferably low pressure
    • Stroke volume = EDV - ESV
  • Relaxation period
    • Ventricular diastole (diastole - period of relaxation)
    • Lowered ventricular pressure causes backflow of blood and closing of SL valves
    • All four valves closed briefly - isovolumetric relaxation
    • Atrial pressure > Vent pressure = AV valves open (Ventricular filling)
    • New P wave
      • beginning of new cycle
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15
Q

Heart Sounds: Observation method, cause, stroke count/sound/sound origin (if audible), defects

A
  • Auscultation
  • Blood turbulence caused by valves closing
  • S1 (“lubb”) = AV valves closing
  • S2 (“dupp”) = SL valves closing
  • S3 = turbulence during vent filling (not heard)
  • S4 = turbulence during atrial systole (not heard)
  • Murmur - abnormal heart sounds, usually indicating valve disorders (such as stenosis or valve incompetence)
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16
Q

Cardiac output: defined, CO and Cardiac Reserve equations, CO and SV equalities

A
  • Blood volume (mL) ejected by left ventricle per minute
    • left ventricle - heavy pusher
  • CO = SV x HR (mL/min = mL/beat x beats/min)
  • Cardiac reserve = Max CO - Resting CO
  • CO should equal venous return (output = input, what goes out must come back in)
  • SV of left vent. = SV of right vent.
17
Q

Stroke Volume (Cardiac Output Factor 1): Regulators (3) and rules/variants

A
  • Regulated by:
    • Preload (stretch before contraction)
      • Frank-Starling Law: Preload proportional to EDV (Why?)
        • EDV = End Diastolic Volume
      • EDV determined by venous return and duration of vent filling (diastole)
      • Keeps both sides proportional - Why?
    • Contractility (strength of contraction)
      • Positive inotropic agents - increased Ca2+, epinephrine/norepinephrine, sympathetic stimulation
        • increases strength of contraction
      • Negative inotropic agents - anoxia, anesthetics, increased K+
        • decreases strength of contraction
    • Afterload (pressure needed to open SL valve)
      • Arterial pressure
      • Negative correlation w/ SV
      • Hypertension, artherosclerosis
        • Higher BP =
          • Higher Afterload
          • Higher Stroke Volume
18
Q

Heart Rate (Cardiac Output Factor 2): Regulation center and messengers, Sympathetic and Parasympathetic response nerve flow and triggers/effects

A
  • Autonomic regulation:
    • Cardiovascular center in medulla oblongata receives input from:
      • Cortex, limbic system and hypothalamus
        • hypothalamus = involuntary
      • Proprioreceptors, chemoreceptors, baroreceptors
    • Sympathetic response (Speed up HR):
      • Cardiac accelerator nerves to SA and AV nodes, myocardium
      • NE (norepinephrine) increases depolarization of pacemakers
      • Increased Ca2+ to fibers
    • Parasympathetic response (slow down HR):
      • Vagus nerves to SA and AV nodes, atrial myocardium
      • ACh slows depolarization of autorhythmic fibers
19
Q

Heart Rate: Regulators

A
  • Chemical regulation
    • Hypoxia, acidosis, alkalosis all decrease HR
    • Hormones
      • Epinephrine and NE increase HR
      • Thyroid hormones increase HR
    • Cations
      • Excess Na+ in blood blocks Ca2+ inflow (lower contractility) (depolarization)
      • Excess K+ in blood blocks action potentials (repolarization)
      • Excess Ca2+ in intracellular fluid speeds HR (muscle contraction)
  • Other factors that increase HR
    • Age (infants and seniors)
    • Low fitness
    • Female
    • Increased body temp.
20
Q

Arrhythmias: definition, common conditions (3)

A
  • Abnormal rhythm due to defect in conduction system
  • Bradycardia - HR < 50 bpm*
  • Tachycardia - HR > 100 bpm*
  • Fibrillation - rapid and uncoordinated
21
Q

Specific Arrhythmias: Heart Block (3 degrees), 5 others

A
  • Heart block - pathway between atria and ventricles blocked (usually AV node)
    • 1st degree block - P-Q interval prolonged due to slow AV node conduction
    • 2nd degree block - fewer QRS complexes than P due to lost potentials between SA and AV (“dropped beats”)
    • 3rd degree block - no potentials through AV - chambers paced separately
  • Atrial flutter - rapid atrial contractions coupled w/ 2nd degree block
  • Atrial fibrillation - atria at 300-600 bpm (no defined P waves) - irregular heart beat, reduced efficiency, stroke
    • not performing full stroke
  • Ventricular tachycardia - heart disease or recent infarct - low BP and heart failure
  • Ventricular fibrillation - ventricles “quiver” and stop pumping - no defined waves on ECG
    • flatline
  • Premature ventricular contraction - due to ectopic focus - can be benign (stress, stimulatants, etc)
    • slightly offbeat
22
Q

Heart Block definition

A

pathway between atria and ventricles is blocked (usually the AV node)

23
Q

What is 1st degree heart block?

A
  • an arrhythmia characterized by a prolonged P-Q interval due to slow AV node conduction
24
Q

What is second degree heart block?

A
  • an arrhythmia characterized by fewer QRS complexes than P due to lost potentials between SA and AV
    • “dropped beats”
25
Q

What is 3rd degree heart block?

A
  • an arrhythmia characterized by no potentials through the AV
    • chambers are paced separately
26
Q

What is an atrial flutter?

A
  • an arrhythmia characterized rapid atrial contractions coupled with 2nd degree heart block
27
Q

What is atrial fibrillation?

A
  • arrhythmia characterized by atria at 300-600 bpm (no defined P wave)
  • irregular heart beat
    • reduced efficiency/stroke
    • not performing full stroke
28
Q

What is ventricular tachycardia?

A
  • arrhythmia
  • heart disease or recent infarct
    • characterized by low BP and Heart failure
29
Q

What is ventricular fibrillation?

A
  • arrhythmia
  • ventricles quiver and stop pumping
    • no defined waves on ECG
    • flatline
30
Q

What is premature ventricular contraction?

A
  • arrhythmia
  • due to ectopic focus - can be benign (stress, stimulants, etc)
    • slightly offbeat