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
2
Q
What is the 2nd sound? What phase is this?
A
- closing of semilunar valves
- end of ventricular systole, beginning of ventricular diastole
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
4
Q
What is a heart murmur?
A
- abnormal heart sound caused by turbulent flow:
- exaggerations of cardiac sound
- extra heart sounds
5
Q
When can murmurs occur?
A
- diastole, systole, or continuously
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)
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)
8
Q
T/F: diastolic murmurs are more common than systolic murmurs
A
- False; systolic are more common
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
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)
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
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
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
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
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
16
Q
What is an absent p wave?
A
- sick sinus syndrome
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
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
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
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
