Cardiac Physiology Flashcards
What is the Ligamentum Arteriosum?
remnant of ductus arteriosus
closes shortly after birth
Name the 3 vessels that drain into the right atrium.
- SVC
- IVC
- Coronary sinus
Fossa ovalis
where the foramen ovale used to be
chordae tendineae
anchor the AV valves to the ventricular papillary muscles
trabeculae carneae
muscular projections of the ventricles
T or F: Cardiac myocytes can regenerate
false
Effect of volatile anesthetics on cardiac function?
depress cardiac contractility
decreased entry of Ca++ into cells during depolarization
Effect of N20 on cardiac function?
dose-dependent decrease in contractility
reduced availability of intracellular Ca++ during contraction
Effect of local anesthetics on cardiac function?
depress contractility
reduced Ca++ influx and release in dose-dependent fashion
Effect of acidosis on cardiac function?
depress contractility
blocks slow Ca++ channels
Effect of phosphodiesterase inhibitors on cardiac function?
increase contractility
prevent the breakdown of intracellular cAMP, allowing for continued recruitment of open Ca++ channels
ex: Milrinone
Effect of Digitalis on cardiac function?
increases contractility
increases intracellular concentration
Anesthetic-induced cardiac depression is potentiated by
hypocalcemia, BB, and CCB
innervation: primary regulation of HR and BP
Medulla
innervation: secondary regulation: what regulates CV response to changes in temp?
hypothalamus
innervation: what adjusts cardiac rxn to a variety of emotional states?
cerebral cortex
Baroreceptors
carotid sinus- hering nerve
aortic arch- vagus nerve
signals are conveyed to afferent receptive regions of the medulla through the Hering and vagus nerves–> activation of baroreceptors leads to drop in BP
where are the chemoreceptors located?
- ) carotid bodies- sit on carotid sinus ( where CCA bifurcates into ICA and ECA)
- ) aortic bodies- sit on aortic arch
Brainbridge Reflex
an increase in the the CVP and RA volume is noted by stretch receptors (baroreceptors) in the atria–> HR INCREASES
Innervation: which fibers primarily innervate the atria and conducting tissues?
parasympathetic
ACh acts on which receptors to produce negative effects? and what are those effects? (3)
muscarinic receptors (M2)
Depressed chronotropy, inotropy, and dromotropy.
dromotropy
conduction velocity of AV node
lusitropy
relaxation of myocardium
where do sympathetic fibers innervate the heart?
all over
where do cardiac sympathetic fibers originate?
T1-T4
NorEpi release from SNS fibers act primarily on which receptors?
B1 adrenergic
where are B2 receptors located in the heart? what happens when they are activated?
primarily the atria
activation increases HR, and to a lesser extent, contractility
Changes in HR with insp/ exp? Why?
Lung’s vagal fibers are stretched (activated) during inspiration, thus inhibiting the cardioinhibitory center of the medulla–> allows unopposed sympathetic acceleration of HR
expiration–> decrease HR
Baroreceptor Reflex
mediated by baroreceptors in the aortic arch and carotid sinus
increased rate of discharge when stretched (increased BP)
neural impulses travel to the medulla
medulla initiates increase in PNS activity:
1. vasodilation 2. HR decreases
if patient is HYPOtensive, the reflex causes inc. HR and vasoconstriction
Baroreceptor Reflex: more effective for hyper- or hypotension?
more effective at compensating for hypotension
Most important determinant of myocardial blood flow?
myocardial O2 demand
Relative contributions to O2 requirements:
basal requirements- 20%
electrical activity- 1%
volume work- 15%
PRESSURE WORK- 65%
what percentage of O2 does the myocardium extract from arterial blood?
65%
so, myocardium cannot compensate for reductions in blood flow by extracting more O2 from Hgb!
most other tissues only extract about 25% 02 from arterial blood
How must the myocardium meet increased O2 demand??
must increase coronary blood flow
already extracts 65% O2 from arterial blood, cannot just increase extraction percentage
How can the heart increase coronary blood flow?
increase time in diastole by decreasing HR
increase aortic diastolic pressure–> increase coronary filling pressure
Coronary perfusion pressure equation
CPP= aortic DBP- LVEDP
what effect does HR have on CPP?
increases in HR decrease CPP bc of disproportionately greater reductions in diastolic time as HR increases
Oxygen content equation
CaO2= 1.36 mL O2/ gm Hb x SaO2/ 100 + 0.0031 mL O2/ (mmHg) dL x PaO2 (mmHg)
How to AS, MR, and decreased coronary diameter affect CPP and myocardial O2 supply?
all decrease supply by worsening blood flow to coronaries
what effect does increased preload have on myocardial O2 demand? afterload?
both will increase oxygen demand by increasing wall tension
Cardiac Output equation
CO= HR x SV
normal cardiac output
5-7 L/ min
cardiac index equation
CI= CO/ BSA
compensates for variations in body size
BSA (m^2)= square root of (wt (kg) x ht (cm)/ 3600)
normal cardiac index
2.5- 4.2 L/ min/ m^2
normal mixed venous oxygen saturation
65-75%
where do you measure mixed venous oxygen saturation? and why do you need it?
pulmonary artery
helpful in assessing the adequacy of CO- are the tissues being perfused?
a decrease in mixed venous O2 saturation in response to increased demand (exercise, sepsis, etc.) usually reflects inadequate tissue perfusion
In the absence of hypoxia or severe anemia, what measurement is the best determination of adequacy of CO?
mixed venous oxygen saturation
T or F: Lactic acid can be used to indirectly assess CO
T
lactic acid is a byproduct of anaerobic metabolism
normal intrinsic rate of the SA node
60-100 bpm
brady for peds- 100
cardiac myocytes are oriented ___________ in the ventricular wall
circumferentially
Law of LaPlace
Tension is proportional to Pressure x radius
T prop. P x r
states the physical relationship between wall tension and internal pressure within a circular structure
The Frank-Starling Law
increased preload–> increased SV
as the heart fills with more blood, the force of the contractions will increase.. to a certain point
stretching of the muscles fibers increases the affinity of troponin C for Ca++
a greater number of cross bridges form within the muscle fibers, thus increasing contractile force
what 3 factors affect stroke volume?
Preload
Afterload
Contractility
preload
muscle length prior to contraction
LVEDP
afterload
tension against which the muscle must contract
T or F: Contractility is independent of preload and afterload
T
increased by nervous, humoral, and chemical influences
Ventricular filling is influenced by:
- venous return
- HR
- heart rhythm
with an increase in HR, does systole or diastole show a greater reduction in time?
diastole
ventricular filling impaired at HR > 120 in adults
how do atrial arrhythmias affect vent. filling?
reduce vent. filling by 20-30% due to loss of atrial kick.
absent (a-fib)
ineffective (a-flutter)
simultaneous atrial and vent. contraction (junctional rhythm)
normal CVP
2-8 mmHg
how to use CVP
useful to monitor TRENDS in CVP as an indicator of preload and volume status
NOT a definitive measure of volume
How can patient positioning affect CVP?
reverse T-berg–> lowers CVP due to venous pooling in BLE
T-berg–> increases CVP
no actual change in volume status
what cardiac pressure does CVP most closely approximate?
RVEDP
what 6 factors affect CVP/ Preload?
- ) blood volume- 2/3 of EBV is in the venous system, so the greater the volume, the greater the pressure
- ) gravity- redistributes about 500mL of blood from intrathoracic vessels into BLE
- ) peripheral venous tone- controlled by SNS
- ) muscle pump- repeated compression of the deep veins of the limbs displaces venous blood centrally to increase CVP
- ) spontaneous respiration- produces negative intrathoracic pressure and positive intra-abdominal pressure, which increases the venous pressure gradient and promotes filling of the central veins
- ) CO- pumping action- decreases CVP by transferring venous blood to arterial system. If uncorrected, the fall in CVP and rise in afterload can lead to heart failure.
what fraction of blood is in the venous system?
2/3
When is the effect of the venous muscle pump lost?
when patient is paralyzed
T or F: the left and right hearts have equal output
true
LVEDP = LVEDV
assumes normal LV compliance
LAP approaches LVEDP
assumes normal mitral valve function
PCWP = LAP
assumes normal airway pressures and PulmVR
How do we estimate LVEDP?
use PA catheter to measure PCWP
equation for SVR
SVR= (80 x (MAP-CVP))/ CO
normal SVR (arterial impedence to ejection)
900-1500 dyn x sec x cm^-5
equation for PVR
PVR= (80 x (PAP-LAP))/ CO
normal PVR (pulmonary)
50-150 dyn x sec x cm^-5
what has the most important effect on contractility?
SNS activity
which cardiac tissues does the SNS innervate?
atria
ventricles
nodes
SNS release of NE in heart does what?
NE release enhances contractility via B1 activation
this also increases HR
what other 2 factors other than SNS activity affect cardiac contractility and HR?
release of EPI from adrenal glands
sympathomimetic drugs
BOTH increase contractility and HR via B1 activation!
which cardiac receptors affect HR and contractility?
B1
what effect does acidosis have on contractility?
decrease
how can we assess systolic function?
LVEF
LVEF equation
LVEF= (LVEDV- LVESV)/ LVEDV
how can we assess diastolic function?
Doppler ECHO
hypokinesis
decreased contraction
akinesis
failure to contract
dyskinesis
paradoxic bulging
how does stenosis of either AV valve affect stroke volume?
decreases ventricular filling/ preload and thus decreases SV
how does stenosis of either semilunar valve (pulmonic or aortic) affect SV?
increases afterload and thus decreases SV
how does regurge affect SV?
AV regurge- part of end diastolic volume flows back toward atria during systole
semilunar regurge- part of EDV flows back into ventricle during systole
