Cardio - Part 2 Flashcards
(49 cards)
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
What is ECG used for in large animals?
- 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
What are the 3 parameters of ventricle function?
- stroke volume
- ejection fraction
- cardiac output
27
What is stroke volume?
- volume of blood (mL) ejected per ventricular contraction
- stroke volume = EDV - ESV
28
What is ejection fraction?
- % 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
What is cardiac output?
- 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
What are factors that affect cardiac output?
- stroke volume + heart rate
31
What are factors that affect stroke volume?
- pre-load
- contractility
- after-load
32
What is pre-load?
- end-diastolic fiber length
- stretching of cardiac myocytes prior to contraction
- estimated by end-diastolic volume
- determined by:
- diastolic filling and venous return
33
T/F: the less the heart is stretched, the greater the force of contraction
- False;
- ** increase in cardiac muscle length INCREASES contractile force (length-tension relationship)
34
What is the Frank-Starling mechanism?
- 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
What is contractility (Inotropism)?
- 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
What are factors that affect contractility/inotropism?
- 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
What is afterload?
- “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
What is the Anrep effect?
- 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
What factors influence heart rate?
- autonomic nervous system
- parasympathetic system (predominant)
- sympathetic system
40
What sympathetic receptors are dominant in cardiac system?
- primarily B1 adrenergic receptors (in heart)
- B2 adrenergic receptors (in arterioles of coronaries)
41
What are features of B1 adrenergic receptors in the heart?
- 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
What are features of B2 adrenergic receptors in the arterioles of the coronaries?
- GCPRs that couples to Gs
- stimulatory G protein: activates cAMP pathway
- epinephrine is primary endogenous agonist
- found in vascular smooth muscle
- cause vasodilation
43
How does sympathetic stimulation increase heart rate?
- 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
What parasympathetic receptors are dominant in cardiac system?
- M2 receptors (in heart)
- M3 receptors (in arterioles of coronaries)
45
What are features of M2 receptors in the heart?
- 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
What are features of M3 receptors in the arterioles of the coronaries?
- 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
How does parasympathetic activity affect heart?
- 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
What is reciprocal sympathetic vagal activity?
- 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
What is accentuated antagonism? FYI
