Mean arterial pressure is determined by what 2 factors:
Cardiac Output and SVR
Cardiac Output is determined by what 2 factors?
heart rate and stroke volume
Stroke volume is determined by the interplay of what 3 factors?
preload, after load, and contractility
End Diastolic Volume (Preload) is determined by what 3 factors?
intravascular volume venous tone (Filling pressures) ventricular compliance
The major determinant of intravascular volume is?
The amount of sodium in the body
What hormone is the most important for controlling vascular volume?
Aldosterone
End Systolic Volume is influenced by
Afterload
Contractility
Cardiac output is influenced by
SV and HR
SV is influenced by
End Diastolic Volume (Preload)
End systolic Volume
Oxygen delivery is influenced by
Tissue blood Flow and Oxygen Carrying Capacity: CaO2 (How much O2 is carried in arterial blood)
Tissue blood flow is influenced by
MAP and Local vascular resistance
Effects of Beta 1 stimulation
G-Protein: Gs => increase Adenylate Cyclase => increase cyclic adenosine monophosphate (cAMP)
cAMP increases production of phosphokinase A leading to:
1. Activation of more L-type Ca2 channels
2. Stimulation of RyR2 to release more Ca2
3. Stimulation of SERCA2 pump to increase Ca2 uptake
The net effect is a more forceful contraction over a shorter period of time.
Factors that increased contractility?
Chemicals affect Contractility - particularly Calcium SNS Stimulation Catecholamines Calcium Phosphodiesterase inhibitors Digitalis
Factors that decreased contractility?
Myocardial Ischemia Severe Hypoxia Acidosis Hypercapnia Hyperkalemia Hypocalcemia Volatile Anesthetics Propofol Beta Blocker CCB
ANS causes of coronary artery constriction?
Alpha (epicardial): Alpha 1 is greater than alpha 2 on coronary artery constriction:
Phospholipase C => increase IP3 => increase intracellular Ca+2
Histamine 1: Gq protien => Phospholipase C => increase IP3 => increase intracellular Ca+2
ANS causes of coronary artery dilation?
Beta 2 (endocardial) => increase cAMP => decrease intracellular Ca2+ Histamine 2 => increase cAMP => decrease intracellular Ca2+ Muscarinic => Nitric Oxide (NO)
cAMP Pathway for beta 1
G-Protein: Gs => increase Adenylate Cyclase => increase cyclic adenosine monophosphate (cAMP)
cAMP increases production of phosphokinase A leading to:
1. Activation of more L-type Ca2 channels
2. Stimulation of RyR2 to release more Ca2
3. Stimulation of SERCA2 pump to increase Ca2 uptake
The net effect is a more forceful contraction over a shorter period of time.
cAMP Pathway for beta 2 on vascular tone
NE => B2 => Gs Protein => Adenyl Cyclase => cAMP=> PKA Protein Kinase A => decrease Ca => vasodilation
PKA manipulates excitation- contraction coupling pathway by:
Inhibition of Ca channel in the sarcolemma
Inhibition of Ca release from the SR
Decrease sensitivity of myofilaments to Ca
Facilitation of Ca reuptake into the SR via SERCA2 pump
For regulation of vascular smooth muscle tone, what are the 3 important pathways that affect intracellular Ca2+ concentrations?
- G protein cAMP pathway => decrease Ca2+=> vasodilation.
- Nitric Oxide cGMP pathway => decrease Ca2+ => vasodilation.
- Phospholipase C pathway => increase Ca2+ => vasoconstriction.
Phospholipase C Pathway on vascular tone
angiotensin II => AT II receptor => Gq protein => Phospholipase C => Inositol Trisphosphate IP3 & Diacylglycerol DAG => Ca2+ => vasoconstriction
The activation of phospholipase C increases the production of?
IP3 and DAG
IP3 Augments Ca2+ release from the SR
DAG activates protein Kinase C => opens Ca2+ channels in the sarcolemma and increases Ca2+ influx
Activators of Phospholipase C Pathway are?
PANE
Phenylephrine
Angiotensin II
Norepinephrine
Endothelin-1
Nitric Oxide (NO) / cGMP Pathway
- NO synthetase converts L arginine to NO
- NO diffuses from endothelium into smooth muscle
- NO activates guanylate cyclase
- Guanylate cyclase converts Guanosine Triphosphate (GTP) to cyclic guanosine monophosphate (cGMP)
- Increased cyclic guanosine monophosphate (cGMP) decrease Ca2+ => relaxation and vasodilation
- Phosphodiesterase deactivated cyclic guanosine monophosphate (cGMP) to GMP guanosine monophosphate
Nitric Oxide production is increase by?
B VAST
Bradykinin Vasoactive intestinal peptide Ach Substance P Serotonin Shear Stress Thrombin
G coupled protein for cCAMP and cGMP
cAMP => Gs protein
cGMP => Gq protein
Pathologic Murmurs can be heard where? Aortic Stenosis: ASSS Aortic Regurgitation or Insufficiency: ARDS Mitral Stenosis: MSDA Mitral Regurgitation: MRSA
Aortic Stenosis => Systole.
ASSS = Aortic stenosis is systolic murmur heard over the right sternal border.
Aortic Regurgitation or Insufficiency => Diastole.
ARDS = Aortic regurgitation is a diastolic murmur heard over right sternal border.
Mitral Stenosis => Diastole.
MSDA = Mitral Stenosis is a diastolic murmur heard at the apex and left axilla.
Mitral Regurgitation => Systole.
MRSA = Mitral regurgitation is a systolic murmur heard at the apex and left axilla.
Describe the sound of pathologic murmurs?
Aortic Stenosis: ASSS
Aortic Regurgitation or Insufficiency: ARDS
Mitral Stenosis: MSDA
Mitral Regurgitation: MRSA
Aortic Stenosis: ASSS– Crescendo/ Decrescendo murmur. High velocity through a narrow opening= nozzle effect. Sound transmits through the upper aorta & carotid arteries may be confused with a carotid bruit.
Aortic Regurgitation or Insufficiency: ARDS – High pitch blowing murmur
Mitral Stenosis: MSDA – low intensity rumbling
Mitral Regurgitation: MRSA – Holosystolic murmur characterized by a loud swishing sound.
The best lead to monitor for intraoperative ST changes?
V3 > V4 > V5 > III > aVF
In patients with CAD, Nagelhout suggests the following lead combinations provide the best assessment of the intraoperative ST changes?
5 lead EKG: V3, aVF, & MCL 5 or III
3 lead EKG: aVF and MCL5
Best lead for monitoring for dysryhthmias with a narrow QRS where P wave analysis is critical for diagnosis (Junctional, aflutter or fib)
Lead II
List the 3 cardiac markers:
There elevation times?
Return to baseline time?
Creatine Kinase- MB (CK-MB)
Initial elevation: 3-12 hrs
Peak: 24 hrs
Return to Baseline: 2-3 days
Troponin I
Initial elevation: 3-12 hrs
Peak: 24 hrs
Return to Baseline: 5-10 days
Troponin T:
Initial elevation: 3-12 hrs
Peak: 12- 48 hrs
Return to Baseline: 5-14 days