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AVD Prin III > Cardiac > Flashcards

Flashcards in Cardiac Deck (31)
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1
Q

Mean arterial pressure is determined by what 2 factors:

A

Cardiac Output and SVR

2
Q

Cardiac Output is determined by what 2 factors?

A

heart rate and stroke volume

3
Q

Stroke volume is determined by the interplay of what 3 factors?

A

preload, after load, and contractility

4
Q

End Diastolic Volume (Preload) is determined by what 3 factors?

A
intravascular volume
 venous tone (Filling pressures)
 ventricular compliance
5
Q

The major determinant of intravascular volume is?

A

The amount of sodium in the body

6
Q

What hormone is the most important for controlling vascular volume?

A

Aldosterone

7
Q

End Systolic Volume is influenced by

A

Afterload

Contractility

8
Q

Cardiac output is influenced by

A

SV and HR

9
Q

SV is influenced by

A

End Diastolic Volume (Preload)

End systolic Volume

10
Q

Oxygen delivery is influenced by

A

Tissue blood Flow and Oxygen Carrying Capacity: CaO2 (How much O2 is carried in arterial blood)

11
Q

Tissue blood flow is influenced by

A

MAP and Local vascular resistance

12
Q

Effects of Beta 1 stimulation

A

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.

13
Q

Factors that increased contractility?

A
Chemicals affect Contractility - particularly Calcium
SNS Stimulation
Catecholamines
Calcium
Phosphodiesterase inhibitors
Digitalis
14
Q

Factors that decreased contractility?

A
Myocardial Ischemia
Severe Hypoxia
Acidosis
Hypercapnia
Hyperkalemia
Hypocalcemia
Volatile  Anesthetics
Propofol 
Beta Blocker 
CCB
15
Q

ANS causes of coronary artery constriction?

A

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

16
Q

ANS causes of coronary artery dilation?

A
Beta 2 (endocardial) => increase cAMP => decrease intracellular Ca2+
Histamine 2 => increase cAMP =>  decrease intracellular Ca2+
Muscarinic => Nitric Oxide (NO)
17
Q

cAMP Pathway for beta 1

A

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.

18
Q

cAMP Pathway for beta 2 on vascular tone

A

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

19
Q

For regulation of vascular smooth muscle tone, what are the 3 important pathways that affect intracellular Ca2+ concentrations?

A
  1. G protein cAMP pathway => decrease Ca2+=> vasodilation.
  2. Nitric Oxide cGMP pathway => decrease Ca2+ => vasodilation.
  3. Phospholipase C pathway => increase Ca2+ => vasoconstriction.
20
Q

Phospholipase C Pathway on vascular tone

A

angiotensin II => AT II receptor => Gq protein => Phospholipase C => Inositol Trisphosphate IP3 & Diacylglycerol DAG => Ca2+ => vasoconstriction

21
Q

The activation of phospholipase C increases the production of?

A

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

22
Q

Activators of Phospholipase C Pathway are?

PANE

A

Phenylephrine
Angiotensin II
Norepinephrine
Endothelin-1

23
Q

Nitric Oxide (NO) / cGMP Pathway

A
  1. NO synthetase converts L arginine to NO
  2. NO diffuses from endothelium into smooth muscle
  3. NO activates guanylate cyclase
  4. Guanylate cyclase converts Guanosine Triphosphate (GTP) to cyclic guanosine monophosphate (cGMP)
  5. Increased cyclic guanosine monophosphate (cGMP) decrease Ca2+ => relaxation and vasodilation
  6. Phosphodiesterase deactivated cyclic guanosine monophosphate (cGMP) to GMP guanosine monophosphate
24
Q

Nitric Oxide production is increase by?

B VAST

A
Bradykinin
Vasoactive intestinal peptide
Ach
Substance P
Serotonin
Shear Stress
Thrombin
25
Q

G coupled protein for cCAMP and cGMP

A

cAMP => Gs protein

cGMP => Gq protein

26
Q
Pathologic Murmurs can be heard where?
Aortic Stenosis: ASSS
Aortic Regurgitation  or Insufficiency: ARDS
Mitral Stenosis: MSDA
Mitral Regurgitation: MRSA
A

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.

27
Q

Describe the sound of pathologic murmurs?
Aortic Stenosis: ASSS
Aortic Regurgitation or Insufficiency: ARDS
Mitral Stenosis: MSDA
Mitral Regurgitation: MRSA

A

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.

28
Q

The best lead to monitor for intraoperative ST changes?

A

V3 > V4 > V5 > III > aVF

29
Q

In patients with CAD, Nagelhout suggests the following lead combinations provide the best assessment of the intraoperative ST changes?

A

5 lead EKG: V3, aVF, & MCL 5 or III

3 lead EKG: aVF and MCL5

30
Q

Best lead for monitoring for dysryhthmias with a narrow QRS where P wave analysis is critical for diagnosis (Junctional, aflutter or fib)

A

Lead II

31
Q

List the 3 cardiac markers:
There elevation times?
Return to baseline time?

A

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