cardiac physiology Flashcards
Aerobic requirements of the heart (factors)
- Cardiac tissue metabolically active
- Cardiac energy needs met in real time by changes in energy production
- Cardiac energy needs can increase 9x from rest to heavy exercise
- O2 extraction from blood remains fairly constant regardless of workload
- Blood flow increases from 80 to 500 ml/min/100g tissue
Cardiac Myocytes traits
- Cells are Y shaped
- Striated
- Contain single nuclei
- Limited ability to replicate
- Linked together by intercalated disks
- Lack distinct fiber types
- Do not fatigue
- All fibers contract with each beat
- all cardiac muscle cells contract regardless of HR/contractility
- cardiac muscle cells regulate their force production by regulating availability of CA to sarcomeric proteins
GRADED muscle contractions
Cardiac Excitation Contraction Coupling
- Ca enters myocyte through channels in T tubules
- Triggers release of Ca from SR
- Ca induced Ca release
P wave
depolarization of atria in response to SA node
PR interval
delay of AV node to allow filling of ventricles
QRS complex
Depolarization of ventricles, triggers main pumping contractions
T wave
Ventricular repolarization
ST segment
Beginning of ventricle repolarization, should be flat.
AP of cardiac muscles:
Phase 0
Rapid Na+ influx through open fast Na channels
AP of cardiac muscles:
Phase 1
Transient K channels open and K efflux returns TMP to OmV
AP of cardiac muscles:
Phase 2
Influx of Ca2 through L-type Ca2 channels is electrically balanced by K efflux through delayed K channels
AP of cardiac muscles:
Phase 3
Ca2 channels close but delayed rectifier K channels remain open and return TMP to -90mV
AP of cardiac muscles:
Phase 4
Na, Ca2, channels closed, open K rectifier channels keep TMP stable at -90mB
Absolute refractory period
Stage 0-2
Effective refractory period
Stages 0-2 (slightly further than absolute)
Relative refractory period
Stage 3
SV=
LVEDV-LVESV
EF=
SV/EDV x 100
or
[(EDV-ESV)/EDV] x 100
EDV avg
110-120 ml
ESV avg
40-50 ml
SV avg
70 ml
EF (ejection fraction) avg
60% is wnl
[(EDV-ESV)/EDV] x 100
Atria as a primer
- blood flow into atria is continuous
- 75% blood flows through atria to ventricles during atrial diastole
- 25% ejecting during atrial systole
- Loss of 25% has very limited impact on heart at rest
Which period of ventricular diastole has the most rapid filling of ventricles?
first 1/3
Isovolumetric ventricular contraction phase of systole
- lasts .02-.03 seconds
- No change in volume
ejection following isovolumetric phase
- occurs when LV SP > 80 mmHg
- Period of rapid ejection
- Period of slow ejection (last 30% in last 2/3 of systole)
Ventricular Diastole:
Isovolumetric diastole
- Ventricular pressure < aortic pressure. Aortic valve closes and remains closed; no net blood flow
- Early part of ventricular relaxation
- Ventricular pressure is decreasing, AV valves and aortic valve are closed
When do the AV valves open
Atrial pressure > ventricular pressure
T/F: elastic recoil maintains a high aortic pressure during diastole
True
Incisura
back flow just as aortic valve is closing
Elevated RV pressure suggests:
pulmonary HTN
RV failure
CHF
increased blood volume
Pulmonary artery pressure
Systolic: 20-30 mmHG
Diastolic: 8-12 mmHg
Mean pulm pressure: 25 mmHg
What allows pulmonary circulation to function as a low pressure system
- RV pumps through shorter length
- Pulmonary vasculature more compliant
- expansion of lungs = vascular dilation
- much lower gravity impact
CO
HRxSV
4-8 L/min
EF
- normally 55-70%
- <40% used to suggest Heart failure
Cardiac Index
- Ratio of CO : body surface area
- CO/BSA; units = L/min/m^2
preload
- amount of venous return
- degree of myocardial distention prior to contraction
afterload
- force that ventricles must overcome to eject blood
- largely dependent on arterial BP and vascular tone
- increased afterload like “riding uphill”
effects of sepsis:
- cytokines released during sepsis reduces cardiac contractility
- Usually associated with normal or elevated CO
Which drugs increase cardiac contractility?
positive ionotropic drugs
Regulation of HR:
sympathetic NS
- sympathetic nerves course through atria and ventricles
2. beta blockers trx
Regulation of HR:
assessment of SNS
- resting HR
- HR recovery
- HR response to standing
- HR response to valsalva maneuver
- BP response to standing
Venous Return:
amount of venous blood entering R atria
Factors controlling venous return/EDV
- total blood volume
- venous BP
muscle pump - respiration
- gravity/posture
- Intrapericardial pressure
- R atrial pressure
- increased thoracic pressure
Pulse Pressure
PP = SP - DP - normal is 120-80=40 - PP considered abnormally low if it is < 25% of SP or < 30 mmHg - PP abnormally high if >100 mmHg PP = SV / arterial compliance
Mean Arterial Pressure
MAP= DP + 1/3 (SP-DP) MAP= CO x SVR (systemic vascular resistance)
Normal MAP
65-110 mmHg
Prolonged decreased MAP leads to
ischemia
Maintenance of MAP
- Local control
- increased NO leads to vasodilation and diminished MAP
- endothelin released in response to decreased MAP leading to smooth muscle constriction - ANS
- altered sympathetic and parasympathetic input to vascular smooth muscle - renal regulation of blood volume
Law of LaPlace
T (LV wall stress) = Pressure x Radius
T=PR
T/F:
For a given blood pressure, increasing the radius of the cylinder leads to a linear increase in tension.
True
T/F: For a given blood pressure, increasing the radius of the cylinder leads to a linear decrease in tension.
False (decreasing)
Atrial Natriuretic Peptide
synthesized and store/released by atrial myocytes in response to:
- atrial distension (hypervolemia)
- angiotensin II stim
- sympathetic stim
Atrial Natriuretic Peptide
actions
- involved in long term Na and water balance, blood volume, and arterial pressure
- dilates veins reducing central venous pressure, preload, and CO
- Increases diuresis and sodium loss ( decreases blood volume)
- Decreases renin release, leading to further diuresis
