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CPC > Myocardial Protection > Flashcards

Myocardial Protection Flashcards

1
Q

Myocardial basal oxygen consumption rate

A

8-10 mL O2/min/100 g tissue

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2
Q

Myocardial basal oxygen extraction rate

A

10-13 mL O2/100 mL blood or 70% CaO2

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3
Q

Basal coronary blood flow

A

1 mL/min/100 g, or 5% total CO

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4
Q

Coronary artery autoregulation (BP and flow)

A

60-140 mmHg, flow matches demand to 5x basal rate (25% CO), or 50-150 mmhg

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5
Q

Adult Myocardial energy substrates

A

70% is free fatty acids when fasting, after eating can be 100% glucose and other carbohydrates

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6
Q

MvO2 rate reduction

A

1/3 reduction in MvO2 when heart is not doing mechanical work (Gravlee says decompression by venting and CPB decreases work by 30%)
90% reduction with electromechanical arrest (1.1 mL O2/min/100 mg tissue compared to 8-10)
Further reduction with cooling, with 50% reduction for each 10C (Q10). 97% reduction at 4C

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7
Q

3 principal metabolic cardiomyocyte reactions requiring ATP

A
  1. Myosin ATPase for contraction
  2. Ca/Mg ATPase for removal of Ca
  3. Na/K/ATPase for removal of Na

Contraction accounts for 85% of MvO2, resting cell pumps account for 15%

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8
Q

Mechanism of Myocardial Ischemic Damage

A
  1. Loss of contractile function due to pumps not working from no ATP, accumulating intracellular Na and Ca
  2. Anerobic metabolism producing lactic acidosis
  3. Increased mitochondrial membrane permeability
  4. Incrased complement activation and inflammatory mediators
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9
Q

Molecular mechanisms of ischemia-reperfusion injury

A
  1. Reactive oxygen species generated by neutrophils and electron transport chain malfunction
  2. Intracellular calcium accumulation within the cytoplasm and mitochondria, which activate Ca-dependent phospholipases and proteases and the mPTP
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10
Q

Techniques to limit myocardial ischemia prior to x-clamp

A
  1. Avoidance of ischemia preoperatively with adequate anesthesia
  2. Ischemic preconditioning with volatile anesthesia
  3. Systemic cooling using Q10 principle (10 degrees=50% reduction in MvO2)
  4. Quick initiation of CPB to unload the heart
  5. Avoid distension
  6. Myocardial preconditioning
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11
Q

Mechanism of depolarizing cardiac arrest

A

Requires K of 10 mmol/L (Mike’s note is 20-30 initial arrest, Gravlee says 12-30 )
This (10) raises TMP to -65 (usual resting TMP is -90 mV)
Inactivates voltage-dependent fast Na channel (phase 0)

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12
Q

General forms of depolarizing crystalloid cardioplegia

A

Extracellular depolarizing: High amounts of Na/Ca/Mg with high amounts of K (St Thomas Solution)

Intracellular depolarizing cardioplegia: Low or no Na/Ca. (HTK/Bretschneider/Custodiol). These theoretically reduce intracellular edema and reperfusion injury and prolongs arrest due to hypocalcemia. Still use K

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13
Q

Theoretical benefits of blood cardioplegia

A
  1. Oxygen carrying capacity
  2. Viscosity/rheologic properties for improved microcirculatory perfusion
  3. Metabolic substrates
  4. Acid buffering capacity
  5. Has antioxidants
  6. Has oncotic force decreasing edema
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14
Q

Del Nido Cardioplegia

A

Depolarizing crystalloid cardioplegia
4 crystalloid: 1 blood
Bicarb, Mg, 24Na with Mannitol, Lidocaine
1L single shot achieves safe arrest of 90 minutes
Low calcium, mannitol for scavenging

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15
Q

Non-Depolarizing Cardioplegia Mechanisms

A

Lidocaine: Blocks fast Na channels to prevent depolarization
Adenosine: opens K channels which increases hyper polarization with adenosine receptor
Esmolol: short acting beta blockade and also blocks the Ca and Na channels

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16
Q

Problems associated with K cardioplegia

A

Hyperkalemia causes:

  1. Intracellular Na and Ca accumulation with ATP use to run the pumps to reverse this
  2. Endothelial injury
  3. local inflammation
  4. cardiac arrhythmia
  5. coronary vasoconstriction
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17
Q

Adequate cooling of myocardium

A

Traditional: 15 C

Adequate cooling: 4-10

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18
Q

Benefits of warm blood cardioplegia

A

For induction dose: maximizes oxygen uptake during delivery period and therefore minimizes ATP depletion

Warm blood prevents the leftward shift of dissociation curve which then promotes the uptake of oxygen

Can be used as a hot shot to replenish ATP stores

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19
Q

Antegrade cardioplegia delivery

A

200-300 ml/min to achieve aortic root pressure of 70-100.

1 L induction dose is typical followed by maintenance doses every 20 min

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20
Q

Retrograde cardioplegia delivery

A

Coronary sinus pressure must be less than 40 mmHg to produce a flow usually of 150-200 mL/min

It is not adequate to protect the right heart because the RV’s drainage is primarily through the Thebesian system which do not anastomose with the coronary sinus

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21
Q

Controlled reperfusion

A

Allowing systemic MAP to be 40 for 2 minutes following x-clamp removal. The goal is to prevent the poorly contracting heart from distending.

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22
Q

Cross-clamp fibrillation technique

A

Deliberate application of fibrillation followed by cross clamp. A side biting clamp was then used for the proximal CABG anastomoses.
Traditionally done with mild hypothermia 28-30 with RSPV Vent
1-6 Volts is used to create current

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23
Q

Formula to calculate K administered

A

(concentration of solution x #parts) + (concentration blood x #parts)/ total sum of parts

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24
Q

Temperature classification of cardioplegia

A

Warm=34-35
Tepid= 29
Cold=4
Moderate hypothermia=24-28

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25
Q

Definition of myocardial stunning

A

Postischemic myocardial contractile dysfunction in the absence of morphologic injury or necrosis

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26
Q

Local control mechanism of coronary blood flow

A

Increased workload decreases O2, increases CO2, lowers pH, increases lactate and adenosine. These all cause a decrease in CVR. The opposite is true for Increased CVR
Alpha 1= constriction
ALpha 2 are involved with NO and caused dilation
B cause dilation
Under most circumstances local control overrides SNS

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27
Q

Hormonal influence of coronary blood flow

A

ADH/Vasopressin and Angiotensin are the most potent coronary vasoconstrictors
Thromboxane vasoconstricts during ischemic events
Prostaglandin causes dilation

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28
Q

Coronary perfusion Pressure calculation.

A

Aortic (systemic) diastolic pressure-LVEDP

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29
Q

LV and RV Coronary Artery Flow proportions

A

85% diastolic, 15% systolic in LV

constant in low pressure RV system

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30
Q

Determinants of myocardial oxygen demand

A
  1. HR (Increases in HR does not linearly increase MVO2 because of stepwise increase in contractility)
  2. Contractility, especially in the endocardium because they contract more than the epicardium
  3. Wall stress (afterload.) Stress is PR/2thickness. Volume is proportional to cubed radius. Increasing size (with increasing preload) increases radius and stress. Thickness decreases stress but also increases the amount of tissue.
31
Q

EKG monitoring of ischemia

A

90% of events seen with only leads II and V5

32
Q

Propofol and cardiac ischemia

A

Decreases SVR and contractility, reflex increase in HR

33
Q

Ketamine and cardiac ischemia

A

Increases SNS which increases SVR, pressures, contractility and HR, and should never be used in ACS

34
Q

Etomidate and cardiac ischemia

A

Ideal induction drug because it does not alter HR or cardiac output.
(Allosteric GABA agonist at high concentrations.)

35
Q

Alpha2 adrenergic agonists (precedex, dexmetetomidine) and cardiac ischemia

A

Reduce central SNS stimulation and therefore decrease HR and BP

36
Q

Volatile Anesthesia and cardiac ischemia

A

Variable effects on HR depending on substance. All decrease contractility and impair LV function in already impaired hearts. Decrease in afterload from SVR.
Therefore, cause a low CPP but lower demand.
Can cause coronary steal from vessels that are already dilated from ischemia

37
Q

General time points for ischemic-reperfusion injury

A
  1. Before CPB due to ACS, hypotension, coronary artery spasm and collateral flow
  2. At initiation of CPB due to sudden establishment of high oxygen flow
  3. during cardioplegia protected time: between intermittent doses, due to maldistribution or unprotected right side during retrograde
  4. upon cross clamp release
38
Q

Determinants of surgical myocardial ischemia

A
  • duration and severity of antecedent and unprotected ischemia
  • elimination of mechanical activity during cross clamp
  • myocardial Q10
  • nutrition and stress status (catechol stimulation)
  • comorbidities like hyperlipidemia
39
Q

Myocardial stunning phenomenon

A

Temporary contractile dysfunction likely due to reperfusion injury which has the absence of morphologic injury or necrosis.

40
Q

Determinants of surgical reperfusion injury

A
  • Duration and severity of antecedent ischemia
  • oxygen radical generation by neutrophils, myocytes and vascular endothelium
  • Na and Ca influx and homeostasis disruption
  • mitochondrial dysfunction and opening of membrane pore
  • generalized inflammatory response
41
Q

Sources of oxygen radicals

A
  • Neutrophils: stimulated by C3a and C5a, TNF alpha, platelet activating factor, causing ‘respiratory bust’ and release of ROS causing membrane lipid peroxidation.
  • Cardiomyocyte: through action of xanthine oxidase
  • Mitochondria: electron transfer chain creates ROS, in the mitochondrial matrix superoxide dysmutase creates hydrogen peroxide. This stimulates Ca release from mitochondria
  • Vascular endothelium: XO as above. Inhibits control of local anti inflammatory/dilators causing constriction and inflammation
42
Q

Mechanism of ischemic-reperfusion calcium influx

A
  • diffusion from overt membrane disruption
  • reversal of Na/Ca antiporter by accumulation of Na (H+ from ischemia stimulates Na/H antiporter+ Na pump stops)
  • Decreased Ca uptake to sarcolemma
  • alpha adrenoreceptor stimulation/cAMP stimulation causes Ca accumulation
43
Q

Avoidance of calcium injury in reperfusion

A

If pH normalization occurs before calcium handling mechanisms, then Na, Ca can accumulate and not be handled and can activate oxygenation. Therefore consider permissive acidemia and low oxygen during reperfusion

44
Q

Neutrophil physiology during reperfusion injury

A

C3a deposited on circuit stimulates neutrophils
Neutrophils bind to vascular endothelium, including in coronary arteries via selecting and integrin proteins causing loss of contraction.
Hypothermia delays this effect but has no net benefit

45
Q

Reperfusion Dysrythmias

A

Caused by Na/Ca imbalance, as well as K during cardioplegia.
Most often causes atrial fibrillation

46
Q

Proposed mechanism of Myocardial stunning

A

Post ischemic reperfusion injury, Ca kinetics are dysfunctional which causes changes in excitation-contraction coupling. Also thought to be due to reduced oxygen delivery from hemodilution and low Ca post CPB

47
Q

Proposed mechanism of myocardial edema during ischemia-reperfusion injury

A
  • increased intracellular osmotic pressure due to accumulation of anaerobic metabolites
  • Na/Ca dyshomeostasis
  • microvascular and cellular damage causing interstitial permeability
48
Q

Caridoplegia causes of myocardial edema

A
  • High delivery pressures
  • Hemodilution and hypo osmolarity
  • Na/K pump dysregulation
  • decrease in lymphatic drainage during arrest
49
Q

Pathophysiology of myocardial edema

A

Fluid enters cell, which then causes decreased microvascular perfusion (no reflow phenomenon) as well as increased diffusion distance to myofibrils

50
Q

Ischemic/Reperfusion causes of myocardial ischemia

A

Degree of edema caused by reperfusion by unmodified blood depends primarily on duration of preceding ischemic episode.
Ischemic tissue is hyperosmotic due to Na accumulation from Na/H pump. Inhibiting the pump decreases edema

51
Q

No-Reflow phenomenon

A

Derangement in postischemic blood flow to the at-risk myocardium despite resolution of the coronary obstruction.

52
Q

Etiology of no-reflow phenomenon

A

-postischemic tissue edema and interstitial hemorrhage compressing the vascular space
-active vasoconstriction from loss of endothelial vasodilators (NO, prostacyclin) and release of neutrophil derived vasoconstrictors (platelets make thromboxane, endothelin)
-neutrophil capillary plugging
-embolic debris
Likely associated with reperfusion as the wavefront is similar to reperfusion

53
Q

Endothelial-derived vasoconstrictors

A

Endothelin: stimulated by thrombin, Angiotensin 2, shear stress and epinephrine

54
Q

Endothelial derived vasodilators

A

Prostacycin, NO, endothelial derived hyper polarizing factor EDHF

55
Q

Gravlee usual cardioplegia pressures

A

150-200 which decreased by the resistance of the cardioplegia cannula

56
Q

4 ways cardioplegia delivery avoids ischemic injury

A

All of them work to reduce oxygen demand by over 90%

  1. produce immediate asystole
  2. rapidly induce hypothermia
  3. provide repeat intermittent oxygenation
  4. decreasing/improving anaerobic metabolism
57
Q

4 phases of surgical myocardial protection

A
  1. pretreatment: ischemic and pharmacologic preconditioning via propofol or volatile anesthesia
  2. induction: arrest and hypothermia, including depletion of energy stores with warm plegia
  3. maintenance: restoring of oxygenation and washing out of metabolites
  4. reperfusion and reanimation: warm and increase metabolism, establish ion balance, repolarize if depolarizing agent used
58
Q

Oxygen delivery potential of cold crystalloid cardioplegia

A

4 mL o2/100 mL crystalloid at 10 C

59
Q

Negative effects of blood cardioplegia

A

Contains inflammatory cells such as neutrophils and pro inflammatory cytokines

60
Q

Benefits of all-blood or microplegia

A
  • Eliminates need for buffers like THAM
  • Maintains aerobic metabolism through delivery of oxygen which then allows for the maintenance of ATP-requiring Na,Ca, Cl pumps and prevents Na/Ca accumulation
  • Incrased delivery of blood antioxidants
  • Deceased volume to reduce dilution
  • Cost effectiveness
61
Q

Maximum K concentration

A

Gravlee recommends max is 40-50 mEq/L should be avoided because of vascular and tissue endothelial damage

62
Q

Max ischemic time at 4C

A

45 min per Gravlee

63
Q

Tolerance of regional heterogeneity in myocardial temperature

A

Differences between 22 and 4C are small do to exponential effect of Q10. Therefore if work and calcium are limited then regions between 22-4 do not significantly change the arrested heart MVO2. Benefits may be only seen with going cold in cases of prolonged ischemia.
Emphasize cooling via grafts if distribution of carioplegia impaired

64
Q

Negative effects of myocardial hypothermia

A

Impaired oxygen delivery and HgB dissociation

  • decreases contractility
  • VF
  • Intravascular Na accumulation and edema
  • Impaired auto regulation
  • Decreases RBC deformation ability, membrane fluidity
  • Inhibits Ca uptake into SR
  • Decreases membrane receptor activity
65
Q

Use of topical slush

A

Use; prevents rewarming via convection
Problem: phrenic nerve damage and diaphragmatic paralysis, epicardial freezing.
No benefit shown over cold blood cardioplegia

66
Q

Warm-Cold Cardioplegic Induction

A

Warm arrest reduces energy demand but theoretically repays oxygen debt.
Demonstrated superiority in high risk procedures or long clamp times and in children

67
Q

Hot shot benefits

A
  • Washes out metabolites and may improve post ischemic myocardial derangements
  • can act as delivery for drugs targeting reperfusion injury
  • decrease instability if temperature is gradually increased
  • re establish K gradient/temperature and acidosis
68
Q

Calcium Paradox

A

Sudden influx of Ca from reperfusates after prolonged hypocalcemia. This causes increased risk for I-R injury.
Difficult to manage due to interaction with other electrolytes and Ca intake is stimulated by catecholamines

69
Q

Strategies to limit Ca influx from cardioplegia

A
  • Mg is a Ca antagonist
  • citrate in CPD chelates, but also inhibits glycolysis
  • adenosine limits K-induced Ca by maybe opening K channels
  • ischemic preconditioning
70
Q

Disadvantages of hyperkalemic polarizing arrest

A

Note: at 30 mEq/L K the L type Ca channel opens causing calcium influx.
At high K (16-20) there is inactivation of the Na channel but there is persistent Na influx “window current” down the electrochemical gradient causing intracellular Na accumulation, which leads to H, which leads to intracellular acidosis , Na/Ca exchanger and Ca accumulation

71
Q

Magnesium in caridoplegia

A
  • Blocks L type Ca channels by displacing calcium, decreasing calcium accumulation during ischemia
  • improves high energy phosphate availability
  • can be used as the arresting agent
72
Q

Alternative cardioplegia pharmacologic additives other than hyperkalemia

A
  • Low Na, Low Ca
  • Na blockers like procaine, Ach, tetrodotoxin
  • adenosine hyper polarizes
  • hyperpolarizing K channel openers like nicorandil
  • Magnesium
  • Esmolol beta blockade
73
Q

Molecular mechanism for ischemic preconditioning

A

Triggers of conditioning like autocoid (adenosine,) bradykinin activate G proteins. Mediator pathways occur and then cause the opening of the K ATP channel causing hyperpolarization and prevent opening of the mitochondrial mPTP

74
Q

Role of the mPTP in cell death

A

mitochondrial membrane permeability transition pore: in the membrane of the mitochondria.

  • transition point from reversible to irreversible injury
  • voltage gated, requires Ca. Opens with ROS,Ca. Stays closed in ischemia because of low pH, Mag and ADP
  • Reperfusion injury opens the mPTP from Ca, normalizing pH and ROS.
  • Open MTP causes water and solutes to enter mitochondria, stopping ETC and stimulating apoptosis factors

CPC (8 decks)

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