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RUSVM Physiology I > Cardio - Part 2 > Flashcards

Cardio - Part 2 Flashcards

1
Q

What is the 1st sound? What phase is this?

A
  • closing of A-V valves
  • beginning of ventricular systole
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2
Q

What is the 2nd sound? What phase is this?

A
  • closing of semilunar valves
  • end of ventricular systole, beginning of ventricular diastole
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3
Q

What is the 3rd and 4th sound? What species is is heard in?

A
  • 3rd: rash of blood into ventricles
  • 4th: end of diastole during atrial systole
  • large animals, sometimes large dogs
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4
Q

What is a heart murmur?

A
  • abnormal heart sound caused by turbulent flow:
    - exaggerations of cardiac sound
    - extra heart sounds
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5
Q

When can murmurs occur?

A
  • diastole, systole, or continuously
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6
Q

What are systolic murmurs?

A
  • occur during ventricular systole
    • mitral or tricuspid incompetence (regurgitation)
    • aortic or pulmonic stenosis (not open enough)
    • ventricular septal defect (hole in wall)
    • ** continuous murmur: patent ductus arteriosus (aortic pressure is higher than pulmonary artery during entire cycle)
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7
Q

What are diastolic murmurs?

A
  • occurring ventricular diastole
    • tricuspid or mitral stenosis (not open enough)
    • pulmonic or aortic insufficiency (regurgitation)
    • PDA: patent ductus arteriosus (CONTINUOUS)
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8
Q

T/F: diastolic murmurs are more common than systolic murmurs

A
  • False; systolic are more common
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9
Q

What is happening from A-B?

A
  • period of filling
  • mitral valve opens due to decrease in ventricular pressure @ end of systole
  • L ventricular volume increases due to flow of blood fromLA to LV
    • atria contractinthe en increasing volume to 120mL (end diastolic volume) + pressure to ~5-7mmHg
  • at the end of diastole the LV contract and mitral valve closes
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10
Q

What is happening from B-C?

A
  • isovolumetric contraction
  • L ventricular pressure rises without volume changes until the opening of the AV vale
  • pressure inside the ventricle increases to equal the pressure in the aorta (80 mmHg)
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11
Q

What is happening from C-D?

A
  • period of ejection
  • after opening of aortic valve, blood will flow into aorta
  • ventricular contraction increases during ejection
  • volume of LV decreases
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12
Q

What is happening from D-A?

A
  • isovolumetric relaxation
  • at end of ejection the aortic valve closes and LV pressure falls back to diastolic pressure level
  • no change in volume until mitral valve open and a new cycle begins with falling of the ventricle
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13
Q

What are the components of a ECG?

A
  • each component of a ECG tracing is a electrical event occurring in a specific place in the heart
  • ECG evaluation includes determination off HR, heart rhythm, and wave form morphology
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14
Q

What is the first ECG deflection?

A
  • P wave
  • depolarization of atrial muscle
  • discharge of SA node assumed to occur just prior
  • NO depolarization for atrial repolarization
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15
Q

What is a notched P wave?

A
  • presence of left atrial and ventricular enlargement denoted by a wide and notched p wave and wide QRS complex
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16
Q

What is an absent p wave?

A
  • sick sinus syndrome
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17
Q

What is the baseline that follows the p wave?

A
  • return to baseline: P-R segment (between the end of P and beginning of Q)
  • corresponds to A-V node conduction
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18
Q

What is the interval that follows the p-wave?

A
  • P-R interval
  • represents time for the electrical impulse to conduct from the SA node though atria +A-V node + bundle of HIS
  • start of p-wave to first QRS deflection
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19
Q

What factors can increase or decrease the P-R interval?

A
  • sympathetic stimulation: decreases interval, increases conduction velocity
  • parasympathetic stimulation: increase interval, decreases conduction velocity
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20
Q

What produces the QRS complex?

A
  • impulse activating the HIS-purkinje system and ventricular muscle
  • 3 waves together = ventricular depolarization
  • total duration is similar to p-wave
21
Q

What is the Q-T interval?

A
  • the approximate duration of ventricular systole + ventricular refractory period
  • beginning of Q-wave to end of T-wave
22
Q

What does the S-T segment correlate to?

A
  • plateau of ventricular AP
    • end of depolarization and beginning of repolarization
  • ISOELECTRIC because all ventricular muscle is depolarized
23
Q

What is the T-wave?

A
  • ventricular repolarization
  • longer duration than QRS because repolarization does not occur as a synchronized propagated wave
  • high degree of variability in dogs/cats
    • can be +, -, biphasic or very low amplitude
24
Q

What is the R-R interval?

A
  • time between one R-wave and the next = cycle length
  • used to evaluate regularity of the heat beats (rhythm)
  • used to calculate HR when rhythm is regular
25
Q

What is ECG used for in large animals?

A
  • considerable variability in polarity and size of ECG waves
    • variation between individuals of the same species
    • cardiac depol pathways inconsistent
  • ECG only useful for arrhythmia detection
    • less useful for structural abnormalities
26
Q

What are the 3 parameters of ventricle function?

A
  • stroke volume
  • ejection fraction
  • cardiac output
27
Q

What is stroke volume?

A
  • volume of blood (mL) ejected per ventricular contraction
  • stroke volume = EDV - ESV
28
Q

What is ejection fraction?

A
  • % of EDV ejected in one stroke
    • describe effectiveness of ventricles (normally ~60%)
    • indicator of contractility
      • increasing EF reflects an increase in contractility and vice versa
  • ejection fraction = stroke volume / EDV
29
Q

What is cardiac output?

A
  • total volume ejected per unit time (mL/min)
  • depends on volume ejected in a single beat (stroke volume) and number of beats per min (HR)
  • varies with ACTIVITY
  • cardiac output (mL/min) = stroke volume (mL) x heart rate (beats/min)
30
Q

What are factors that affect cardiac output?

A
  • stroke volume + heart rate
31
Q

What are factors that affect stroke volume?

A
  • pre-load
  • contractility
  • after-load
32
Q

What is pre-load?

A
  • end-diastolic fiber length
    • stretching of cardiac myocytes prior to contraction
    • estimated by end-diastolic volume
    • determined by:
      - diastolic filling and venous return
33
Q

T/F: the less the heart is stretched, the greater the force of contraction

A
  • False;
  • ** increase in cardiac muscle length INCREASES contractile force (length-tension relationship)
34
Q

What is the Frank-Starling mechanism?

A
  • intrinsic relationship between end-diastolic volume and stroke volume
  • “Frank-Starling Law”: volume of blood ejected by the ventricles depends n the volume present in the ventricle at the end of diastole
35
Q

What is contractility (Inotropism)?

A
  • pumping ability of ventricle
  • intrinsic ability of myocardial cells to develop force at a given muscle cell length
  • ** an increase in contractility leads to a more complete emptying of ventricle during systole (decrease in end-diastolic volume)
    • increase in stroke volume without needing to increase end-diastolic volume
36
Q

What are factors that affect contractility/inotropism?

A
  • directly correlated to intracellular calcium concentration
    - larger inward Ca2+ current and intracellular sstores, greater the increase in intracellular Ca2+, greater contractility
  • extrinsic factors increase contractility: positive inotropic effect
    - sympathetic stimulation
    - cathecolamines
  • epinephrine + norepinephrine
    - increase contractile forces and velocity by stimulation of B1 adrenergic receptors
    - increase Ca2+ influx and activation of ryanodine receptors to increase SR Ca2+ release via protein phosphorylation L-type Ca2+ channels
    - speed up Ca2+ accumulation in SR to allow faster cardiomyocyte relaxation
37
Q

What is afterload?

A
  • “impediment”
  • resistance that ventricles must overcome to empty its contents
  • force opposing ejection
  • afterload for the L ventricle is the aortic pressure
    - when aortic blood pressure increases: stroke volume decreases and end diastolic volume/pressure increases
38
Q

What is the Anrep effect?

A
  • allows myocardium to compensate for an increased end-systolic volume and deceased stroke volume that occurs when aortic blood pressure increases
    • increase in after-load will stimulate release of cathecolamines (increase in ventricular contractility)
    • without this, increase in particular blood pressure would create a drop in stroke volume and would compromise circulation
39
Q

What factors influence heart rate?

A
  • autonomic nervous system
    • parasympathetic system (predominant)
    • sympathetic system
40
Q

What sympathetic receptors are dominant in cardiac system?

A
  • primarily B1 adrenergic receptors (in heart)
  • B2 adrenergic receptors (in arterioles of coronaries)
41
Q

What are features of B1 adrenergic receptors in the heart?

A
  • GPCRs that couple to Gs
    • stimulatory G protein: activates cAMP pathway
  • norepinephrine is primary endogenous agonist
    • released from postganglionic neurons
  • found in SA node, AV node, + myocardial cells (atria/ventricle)
  • increases HR, stroke volume, and cardiac output
42
Q

What are features of B2 adrenergic receptors in the arterioles of the coronaries?

A
  • GCPRs that couples to Gs
    • stimulatory G protein: activates cAMP pathway
  • epinephrine is primary endogenous agonist
  • found in vascular smooth muscle
  • cause vasodilation
43
Q

How does sympathetic stimulation increase heart rate?

A
  • B1 receptor activation increases:
    • inward Na current in pacemaker cell (funny sodium channels)
    • inward Ca current in pacemaker cell
  • when HR increases, contractility increases
    • more AP’s per unit time
    • more total Ca entering cell during plateau phase
    • more Ca accumulation by SR
44
Q

What parasympathetic receptors are dominant in cardiac system?

A
  • M2 receptors (in heart)
  • M3 receptors (in arterioles of coronaries)
45
Q

What are features of M2 receptors in the heart?

A
  • GPCRs that couple to Gi
    • inhibitory G-protein: inhibit cAMP pathway
  • acetylcholine is endogenous agonist
    • released from postganglionic neurons
  • found in SA node, AV node, and myocardial cells (mainly atria)
  • slow down discharge rate of SA node, slow or block AV conduction,and decrease atrial/to a small extent ventricular contraction
46
Q

What are features of M3 receptors in the arterioles of the coronaries?

A
  • GPCRs that couple to Gq
    • stimulates phospholipae C > DAG + IP3 > calcium release
    • activates eNOS and production of NO (nitric oxide)
  • acetylcholine is primary endogenous agent
    • released from postganglionic neurons
  • found in vascular smooth muscle
  • cause vasodilation (minor effect)
47
Q

How does parasympathetic activity affect heart?

A
  • decreases HR
  • predominates in heart, but interacts with sympathetic system in reciprocal manner
    • blockade of sympathetic B1 receptors: slight decrease in HR
    • blockade of parasympathetic M2 receptors: substantially increase HR
  • increase in HR usually results from both removal of vagal tone and increase in sympathetic drive
48
Q

What is reciprocal sympathetic vagal activity?

A
  • ACh released from vagal endings reacts with presynaptic muscarinic receptors on sympathetic nerve endings to reduce the amount of norepinephrine released from sympathetic efferent terminals
49
Q

What is accentuated antagonism? FYI

A

RUSVM Physiology I (7 decks)

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