Valley Modules 9 and 10: Cardiovascular, Valvular Heart Disease, and Hemostasis
What is the dose range for SNP and max dose?
0.3-10 mcg/kg/min, to max rate of 10 mcg/kg/min for 10 minutes.
Myocardial injury and/or ischemia are defined as ST elevation/depression greater than ___ mm.
1 mm
Which clotting factors ARE NOT made in the liver?
1) Factor VIII/vWF 2) Factor III (tissue factor) 3) Factor IV (calcium)
What are 3 methods that produce edema formation?
1) Increase plasma hydrostatic pressure (right or left heart failure) 2) Decreased plasma colloid osmotic pressure (low albumin). 3) Obstruction of lymphatics.
What are strategies to avoid sickling in Sickle Cell Disease patients? When should they be transfused?
1) Keep the patient warm 2) Keep them hydrated 3) Supplement with oxygen 4) Avoid venous stasis (vasconstriction and tourniquets). Transfuse these patients to maintain the Hgb S at less than 40% of total Hemoglobin.
Aside from avoiding drugs that may prolong the QT (droperidol, haldol, ondansetron), what other periop factors may increase it?
1) SNS stimulation (anxiety, pain) 2) Hypokalemia from hyperventilation 3) Beta blockers tend to decrease the incidence of QT related cardiac events.
What are 4 contraindications to SNP use?
1) Severe liver Dz. 2) Severe kidney Dz. 3) Severe Hypothyroidsim 4) Severe Vitamin B-12 Deficiency
What are the 2 most important risk factors for preop cardiac risk?
1) Unstable angina 2) Evidence of heart failure
What is the normal life span of an RBC?
120 days.
How soon should Ticlodipine be dc'd before surgery? What kind of drug is it?
14 days. ADP inhibitor.
What are the first and second line treatments for hTN in patients with HOCM?
1st: Fluids, keep full, full, full 2nd: Pure vasonstrictors that don't increase contractility (Phenylephrine).
Normal Hgb as 2 ___ chains and 2 ___ chains. What determines the viscosity of blood?
2 Alpha and 2 beta chains. Hematocrit determines blood viscosity.
Which clotting factors are dependent on Vitamin K?
2, 7, 9, 10.
What is the pump flow rate during CP bypass? What MAP would indicate hypertension while on CPB?
2-2.5 L/min/meters squared. A MAP of greater than 100 mmHg
What is the normal aortic valve surface area?
2.5-3.5 cm squared
What is normal coronary blood flow in an adult? How much oxygen does the heart generally extract for the blood that is delivered to it?
225 ml/min 75% (75-80%) of the oxygen that is delivered is extracted.
How soon should Dipyrimdamole be dc'd before surgery?
24 hours.
How long should Eptifibatide and Tirobfaban be dc'd before surgery? What kind of drugs are these?
24 hours. Anti GPIIb/IIIa
What is normal bleeding time, PT, aPTT, ACT, and Fibrinogen levels?
3-10 minutes 12-14 seconds 25-35 seconds 80-150 >150 mg/dl
The usual age of onset of AR is __ years old. In general less than ___% regurgitant volume is mild, while greater than __% is severe.
50 years old 50% 50% (Remember the rule of 50's for AR)
How long should Abciximab be dc'd before surgery? What kind of drug is it?
72 hours. Anti GPIIb/IIIa
Platelets have a life span of __ days and __% of them are sequestered in the spleen.
8-12 days. 33%.
What unique pattern may be seen on the ABP wave form in a patient with IHHS? Is regional anesthesia possible in these patients?
A bifid waveform (Bisferiens pulse) may be seen. Peripheral nerve blocks, spinals, and epidurals are contraindicated due to the decrease in preload and afterload.
An decrease in Afterload results in a ____ (increase or decrease) in EDV and a ____ (increase or decrease) in ESV. How does this effect the dimensions of the LV, and SV?
A decrease in Afterload decreases BOTH EDV and ESV and the LV empties more completely, so SV increases. The LV shrinks as it fills with less and empties more out.
A ____ in SVR or a ___ in left atrial pressure will decrease the regurgitate volume in MR.
A decrease in SVR or an increase in left atrial pressure.
What kind of murmur is produced in MVP?
A mid-systolic click and late systolic murmur. MVP is the most common form of valvular heart disease.
Sickle cell disease is due to a mutant ___ strand, with the substitution of ___ for ___ on the ____ chain of hemoglobin. Which chromosome controls this?
A mutant beta-globin chain. Valine for Glutamic acid on the 6th position of the beta chain of the Hemoglobin molecule. Chromosome 11
What does a ventricular function curve show?
A ventricular function curve plots some index of ventricular function (stroke volume, stroke volume index) against some measure of EDV/PCWP.
MS will result in a prominent __ wave on the PCWP tracing.
A wave.
Phase 4 of the nodal AP is also known as ___. What ions move in or out?
AKA diastole. In the node, K efflux and Na influx restore the RMP, but they gradually slow as RMP is approached. Unlike phase 4 of the ventricular AP, in the last 1/3 of of this phase, Ca++ influx occurs. This is the basis of the autorhythminicity that nodal cells exhibit that normal cardiac myocytes cannot.
Phase 4 of the ventricular action potential (AP) is also known as ____. Which ions move in/out?
AKA diastole. Na efflux and K influx via the Na/K ATPase pump.
Which substances promote the vasoconstriction that occurs occurs in early hemostasis?
ANS reflexes and TxA2 and ADP from platelets promote vasoconstriction.
What kind of murmur does AR have?
ARDS Aortic regurge Diastolic Left Sternal border
What kind of murmur does AS have?
ASS Arch Aortic stenosis systolic aortic arch to right sternal border
What are causes of acute and chronic MR?
Acute: MI, chordinae rupture, IE, trauma Chronic: Rheumatic fever (this causes them all), IE, mitral annular dilation.
Why is adeonsine given in the EP lab? Is it safe to give to a patient with WPW?
Adenosine slows conduction through the AV node, as such it is useful for terminating SVT's, and can be used in WPW (avoid Digoxin and Verapamil in WPW). Adenosine interrupts re-entry pathways within the AV node, and this is why its given in the EP lab to aid in ablation.
Which of the following (adhesion, activation, aggregation) needs: vWF, thrombin, ADP and TxA2?
Adhesion: vWF/Factor 8 Activation: Thrombin/Factor 2a Aggregation: ADP and Thromboxane A2
Which point on the PV loop corresponds to afterload? What else occurs at this point?
Afterload is represented when the Aortic valve opens.
What is the term for the tension/force that pushes against the wall of the LV when the aortic valve opens? Does increasing this increase or decrease CO?
Afterload. Increasing afterload decreases CO.
Which hormone most controls intravascular volume?
Aldosterone.
Fibrin production involves ____ (all, some, or none) of the clotting factors?
All of them
What condition arises if there is a defect in the production of 1 or more of the subunits on Hemoglobin?
Alpha (if its the alpha chain) and Beta (if its the beta chin) Thalassemia will develop. This condition is more prevalent in Southeast Asian and Mediterranean individuals.
Alpha-2 adrenergic receptor agonists antagonize the sympathetic nervous system peripherally. How?
Alpha-2 receptors are found peripherally in the surface membranes of norepinephrine-containing presynaptic nerve terminals of sympathetic postganglionic neurons. Stimulation of these receptors decreases the release of norepinephrine from the presynaptic nerve terminal. This decreased release of norepinephrine contributes modestly to the clonidine-induced decrease in blood pressure
An increase in Afterload results in a ____ (increase or decrease) in EDV and a ____ (increase or decrease) in ESV. How does this effect the dimensions of the LV, and SV?
An increase in Afterload increases BOTH EDV and ESV (unlike preload which only increased EDV), so SV decreases, and the LV dilates to accommodate the increased volume (think of giving Phenylephrine).
Briefly describe the Bainbridge reflex.
An increase in atrial stretch receptors stimulates the SNS to increase heart rate, increase CO, and therein decrease the stretching of the atria.
Sinus arrhythmia is defined as an _____ (increase or decrease) in heart rate during _____ (inspiration or expiration) due to ____ tone.
An increase in heart rate during inspiration from an increase in vagal tone.
What is the medical management for MS?
Anticoagulation, diuretics, and heart rate control.
The aortic stretch receptors transmit afferently via the ___ nerve, while stretch receptors in the carotid bodies transmit afferently via the ____ nerve. ____ are the more important of the 2.
Aortic bodies via the Vagus nerve (think A goes with V just like the AV node). Carotid bodies via Herring's Nerve which a branch of the Glossopharyngeal nerve (CN9). The carotid baroreceptors are physiologically more important.
Which valvular disease causes the LARGEST increase in EDV?
Aortic regurge.
The _____ under the arterial pressure curve divided by ___ yields mean arterial pressure.
Area divided by time.
Action potentials with plateau phases are found in ___ and ___ muscle cells.
Atrial and ventricular muscle cells have a plateau phase. Those in the SA and AV node do not.
Which EKG wave represents: atrial depolarization, atrial systole, ventricular depolarization, ventricular systole?
Atrial depolarization: P wave Atrial systole: PR interval Ventricular Depolarization: QRS Ventricular Systole: QT interval Remember the electrical event proceeds the mechanical
90% of patients with MS present with ___ and ___. Why might they also present with hoarseness?
Atrial fibrillation and pulmonary edema. Left atrial enlargement can compress the left RLN and cause hoarseness.
If a patient has intraop MI evidence with an increased BP and increased PCWP, what is the cause and what is treatment?
BP is increased causing an increased in afterload, leading to increased myocardial oxygen consumption. Treatment: increase anesthetic depth, NTG or SNP to dilate veins, decrease venous return, decrease myocardial oxygen consumption.
What does does Anti-thrombin bind to? Where is it made? What drug potentiates it?
Binds factors IIa and Xa (greatly) and factors IX, XI, and XII (less so). It is made in the liver and Heparin potentiates it 1,000-10,000 fold.
Volatile agents depress the amount of ___ that enters into cardiac cells and therein cause _____.
Block the entry of calcium into cardiac cells. This causes a decrease in contractility.
Aplastic anemia is due to a lack of functioning ____. Megaloblastic anemia is due to a lack of ____ or ____, and causes RBC's that are large and ____.
Bone marrow Lack of B12 or Folic acid. Large and immature.
____ (SNP or NTG) has Nitric oxide in its chemical configuration. Which has a more complex metabolic pathway for generating NO, and which works mainly on venous vessels?
Both SNP and NTG are Nitric oxide donors (as are Dinatrates). SNP has NO in its chemical configuration. NTG has a more complex metabolic pathway for generating NO, that is lacking in arterial vessels. SNP has NO in its chemical configuration and effects both arterial and venous vessels.
WPW syndrome involves conduction of atrial impulses via an accessory pathway, through the bundle of ____. What are 2 drugs that must be avoided in any WPW patient?
Bundle of Kent Verapamil and Digoxin will both increase conduction through the accessory pathway leading to V-Tach/V-fib.
Which 2 factors comprise MAP?
CO x SVR
What comprises CO and SVR respectively?
CO=SV x HR SVR= MAP-CVP/CO x 80
1st messengers/ligands such as ACh and Bradykinin bind to receptors on endothelial cells and activate ___, which increases the amount of ____, which ultimately catalyzes the conversion of L-arginine to NO.
Ca++ regulates the synthesis of Nitric oxide synthetase. This enzyme then catalyzes the conversion of L-arginine into NO. NO is a lipid soluble gaseous substances that then diffuses into vascular smooth muscle and causes vasodilation.
What ECG changes will be seen in a patient who exhibits Chvostek's sign?
Chvostek's=Hypocalcemia. 1) Prolonged QT 2) Prolonged ST 3) Flat or inverted T waves
Besides prolonged QT and hypomagnesemia, what other drugs can cause Torsades de Point?
Class IA (Procainamide) and III (Amiodorone, Ibutilide) anti-arrhthmics.
State and rank the conduction velocities (not intrinsic firing rates) of cardiac tissues. What is the "tropy" term for conduction velocity?
Conduction velocities of cardiac tissues, from fastest to slowest are: Purkinje fibers (4 m/s) >ventricular myocytes (1m/s)= atrial myocytes (1m/s) = bundle ofHis (I m/s) >SA & AV nodes (0.02-0.l m/s). The specific cardiac term for conduction velocity is dromotropy.
What is the most common congenital and acquired cause of AS?
Congenital: Bicuspid aortic valve Acquired: Rheumatic heart disease
Which point of the PV loop corresponds to contractility? What else occurs at this point? Where on the PV loop is the second heart sound heard?
Contractility is represented by size and slope of the ejection portion, which occurs from opening of the Aortic valve and ends at closing of the Aortic valve. This sound causes the second heart sound, S2.
What is the term for the ability of the LV to generate force for a given preload and afterload? Aside from preload and afterload, what determines this?
Contractility. This is determined by the chemical state of the cardiac myocytes.
Aside from NSAID's, what other drug inhibits the formation of TxA2?
Corticosteroids
The enzyme ____ is acetylated by apsirin, rendering the platelet ineffective for how long?
Cyclooxygnease. For the life of the platelet: 8-12 days.
How is Von Willebrand's disease treated?
DDAVP 0.3 mcg/kg over 20-30 minutes will cause release of endogenous vWF within 30 minutes and last 4-6 hours. If this not effective then purified Factor 8 or Cryo (contains factors 1, 8, 13) can be given.
What is DIC in 1 sentence?
DIC is an excessive form of fibrin breakdown/fibrinolysis that occurs in response to increased clot formation.
What are the 3 classic symptoms of AS? What age do these S/S usually present?
DOE, Angina, Syncope 30-60 years old
Which factors enhance ventricular emptying and which retard it? How does this look on a ventricular function curve?
Decreased Afterload and increased contractility enhance ventricular emptying (dec EDV/PCWP and inc SV). This shifts the curve up and to the left. Increased Afterlaod and decreased contractility retard ventricular emptying (inc EDV/PCWP and dec SV). This shifts the curve down and to the right.
Decreasing contractility ____ (increases or decreases) EDV and ____ (increases or decreases) ESV. How does it effect SV, HR, PCWP, and systemic BP?
Decreasing contractility causes both EDV and ESV to increase, the LV does not empty as well, so SV decreases. PCWP increases (increased EDV), systemic BP decreases (decreased SV), and HR reflexively increases.
A decrease in polarity occurs in ____. This means that there is a ____ (increased or decreased) number of positive charges on the outside of the cell and a ___ (increased or decreased) number of negative charges on the inside of the cell.
Depolarization. An decrease in both the number of positive charges on the outside of the cell and the number of negative charges on the inside of the cell. Remember that normally the inside of the cell is slightly negative and the outside is slightly positive.
When in the cardiac cycle does AR occur? Is it a volume or pressure overload, and what kind of hypertrophy occurs?
Diastole Volume Eccentric
Where are systole and diastole on the PV loop?
Diastsole begins with closing of the Aortic valve and ends with closure of the mitral valve. Systole begins with closure of the mitral valve and ends with closure the Aortic valve.
Aside from surgery, what is medical treatment for AR?
Digitalis, diuretics, and afterload reduction (ACE inhibitors).
On what phase of the nodal AP does digitalis/digoxin work?
Digitalis/digoxin works on Phase 4/Spontaneous Depolarization of the SA and AV nodes.
How should life-threatening hypertension associated with clonidine withdrawal be treated? What should be avoided?
Direct acting vasodilators such as NTG and SNP. Avoid beta blockers unless concurrent alpha blockade is established. Blocking the beta receptors alone will result in unopposed alpha stimulation and create heart failure (similar to what happens with Pheo).
Arterial pulse pressure is ____ related to arterial compliance and ____ related to stroke volume.
Directly related to stroke volume but inversely related to arterial compliance.
Pulse pressure is greatest in ____ (proximal or distal) arteries? What principle explains this?
Distal. A blood pressure obtained from the Dorsalis Pedis artery will have a much wider pulse pressure than the radial artery. The Superimposition Principle.
What is the characteristic ECG change with digitalis ("digitalis effect")?
Down sloping of the ST segment.
Why is fibrinolysis accelerated in liver disease? What lab test would this elevate?
Due to poor clearance of tPA, plasminogen keeps getting activated into plamsin and breaking down Fibrin into Fibrin split products, which would be increased if tested.
An increase in EDV of the LV corresponds to which hemodynamic measurement? When EDV increases, ESV remains the same, so SV increases. How does all of this effect: systemic BP, HR, and SVR?
EDV is PCWP. Systemic BP increases, HR and SVR reflexively decrease via the Baroreceptor reflex. The opposite occurs with decreased EDV.
What happens to Preload/PCWP and Stroke volume on a ventricular function curve if Preload is increased with no change to afterload or contractility?
EDV/PCWP will increase. Stroke volume will increase.
What is the formula for ejection fraction?
EF=EDV-ESV/ EDV
When preload increases, EDV volume increases, ESV _____ (increases, decreases, or remains the same) and SV increases.
ESV remains the same. This is why increasing or decreasing preload will increase/decrease SV (think of giving IVF).
Which kind of hypertrophy occurs in AR? Which concurrent valve problem will eventually also occur? Is regional okay?
Eccentric hypertrophy from chronic volume overload. MR will eventually develop. Regional is okay as long as preload is maintained (regional will decrease afterload and reflexively increase HR which are good things).
The best EKG answer is always the one that is ______.
Electrical.
What is the vasopressor and muscle relaxant of choice for regurgitant valves?
Ephedrine Pancuronium
List which factors are involved in each coagulation pathway.
Extrinsic: 3, 7 Intrinsic: 12, 11, 9, 8 Common Final: 5, 10, 1, 2, 13
Which 2 Factors is transfused blood deficient in?
Factor 5/Proaccelerin Factor VIII (both Factor VIII/vWF and VIII:C)
Which factor is considered the physiologic initiator of the coagulation cascade?
Factor III/Tissue Factor/Thromboblastin
What combines with both activated Factor VIIa and Factor VIII:Ca to activate Factor X and initiate the final common pathway?
Factor IV/Calcium
What is the difference between Factor VIII:vWF and Factor VIII:C/Antihemophilliac Factor?
Factor VIII:vWF regulates the production or release of Factor VIII:C. It also serves as a carrier in the blood for coagulation factor VIII:C. Factor VIII:C is made in the liver.
What is Fibrin broken down into by tPA?
Fibrin degradation products, aka Fibrin split products.
What's another name for the GPIIa/IIIb receptor?
Fibrinogen receptor.
____ aggregates platelets.
Fibrinogen/Factor 1
What is the treatment for intraop evidence of an MI with no hemodynamic changes?
Give NTG to dilate veins, or a CCB.
CP bypass decreases the number of _____ receptors on platelets and contributes to increased bleeding.
Glycoprotein receptors, such as the GP IIb/IIIa receptor, aka Fibrinogen/Factor 1 receptor. If Fibrinogen cannot bind to platelets, then hemostasis cannot occur.
What are anesthetic goals for MR?
HR: Increase Rhythm: NSR Preload: Maintain (excessive IVF will dilate the LV and worsen regurge) Afterload: Decrease Contracitlity: Maintain
What are anesthetic goals for AR?
HR: Increased Rhythm: NSR Preload: Increase Afterload: Decrease Contractility: Maintain
What are the anesthetic goals for a patient with HOCM (HR, rhythm, Preload, Afterload, Contractility)?
HR: Normal Rhythm: NSR but A-fib common Pre-Load: Increase Afterload: Increase Contractility: Decrease
What are anesthetic goals for AS?
HR: decreased (60-90 bpm) Rhythm: NSR is crucial as atrial kick contributes up to 40% of CO. Prelaod: Maintain Afterload: Increase/Maintain Contractility: Maintain
What are anesthetic goals for MS?
HR: slow Rhythm: NSR, control rate if in A-Fib Preload: Maintain (excess will promote pulmonary edema) Afterload: Maintain Contractility: Maintain
How much will 1 unit of PRBC's increase H/H? 1 ml/kg of RBC will increase Hct by __%. One unit of platelets will increase platelet count by _____.
Hct 3-4% and Hgb 1 g/dL 1% 5,000-10,000 mm3.
Sickle cell disease and G6PD deficiency cause what kind of anemia?
Hemolytic anemia.
What is the second most common inherited coagulation disorder and how is it treated?
Hemophillia A or Factor VIII:C deficiency. Treatment is purified factor VIII. You could also give blood products that contain factor VIII, such as FFP (contains all) and Cryo (I, 8, 13, vWF).
Your patient has an ECG tracing with a wide QRS and short QT, and a large upward deflection after the QRS (Osborn Wave). What electrolyte abnormality is present?
Hypercalcemia. Hypothermia also causes Osborne Waves.
An increase in polarity is called ____. This means that there is a ____ (increased or decreased) number of positive charges on the outside of the cell and a ___ (increased or decreased) number of negative charges on the inside of the cell.
Hyperpolarization. An increase in both the number of positive charges on the outside of the cell and the number of negative charges on the inside of the cell.
Hypocalcemia ____ (increases or decreases) the QT interval while hypercalcemia ___ (increases or decreases the QT interval?
Hypo: increases/prolongs Hyper: decreases/shortens
How does hypo and hyper calcemia effect Phase 2 of the ventricular AP?
Hypo: less Ca diffuses into the cell during Phase 2 and it takes longer to open the voltage gated K channels, so Phase 2 is prolonged. Hyper: more Ca diffuses into the cell during Phase 2 and it takes less time to open voltage gated K channels, so phase 2 is shortened.
Which clotting factor is known as: Fibriniogen, Prothrombin, Fibrin-stabilizing factor, Christmas factor, Stuart-Prower factor, Anti-hemophilliac factor?
I II XIII IX X VIII:C
What is the only kind of condition that results in smaller volumes and higher pressures on a PV loop?
IHHS.
What happens to Preload/PCWP and Stroke volume on a ventricular function curve if Afterload is increased or decreased?
If Afterload is increased EDV/PCWP increases, while SV decreases. This shifts the curve down and to the right. If Afterload is decreased EDV/PCWP decreases but SV increases. This shifts the curve up an to the left.
What happens to Preload/PCWP and Stroke volume on a ventricular function curve if Contractility is increased or decreased?
If Contractility is increased then EDV/PCWP decreases but SV increases. This shifts the curve up and to the left. If Contractility is decreased then EDV/PCWP increases but SV decreases. This shifts the curve down and to the right.
In homozygous sickle cell disease there is__% HgbS, in heterozygous sickle cell disease there is __% HgbS?
In heterozygous aka Sickle Cell Trait only 40% of Hgb is the S type. In homozygous aka Sickle Cell Disease 60% of Hgb is the S type.
Where is normal Hemoglobin broken down and what is it broken down into?
In the liver it is broken down into Iron and Porphyrin. The Porphyrin is later converted into bilirubin.
The AV node is located in the ___ wall of the ____.
In the septal wall of the right atrium.
Which directions does increasing afterload move the PV loop? Which directions does decreasing afterload move the PV loop?
Increased Afterload= Higher pressures (up) and higher volumes (to the right) Decreased Afterload=Lower pressures (down) and lower volumes (to the left).
In what directions do increases/decreases in contractility move PV loop?
Increased Contractility: higher pressures (taller) and smaller volumes (to the left). Decreased Contractility: lower pressures (shorter) and higher volumes (to the right).
In MR, the LV compensates by increasing ___ via eccentric hypertrophy. As such the LV can maintain the ESV within normal.
Increases EDV/LVEDP. According to Frank-Starling this will increase SV.
Increasing contractility ____ (increases or decreases) EDV and ____ (increases or decreases) ESV. How does it effect SV, HR, PCWP, and systemic BP?
Increasing contractility causes BOTH EDV and ESV to decrease, but ESV much more than EDV, so SV increases (think of giving an inotrope). PCWP decreases (decreased EDV). Systemic BP rises (due to an increase in SV) and this causes heart rate to reflexively decrease.
What is the most common acquired blood clotting defect?
Inhibition of COX by aspirin or other NSAIDS's.
What 3 factors comprise Preload?
Intravascular volume, venous tone, and ventricular compliance.
When using the thermodilution method, cardiac output is ____ (directly or inversely) proportional to the area under the curve?
Inversely. This means that a smaller curve represents a higher CO.
Which parts of the coagulation cascade does Anti-thrombin work on?
It inhibits Factors IIa and Xa. Both are part of the final common pathway. It also inhibits Factors IX, XI, and XII, which are part of the intrinsic pathway.
Where does erythropoetin come from? What does it do?
Kidneys 90% and liver 10%. Stimulates the release of RBC's from bone marrow.
In both chronic Aortic and Mitral regurgitation the PV loops are ___ (small or large).
Large
What might the EKG of a patient with AS show?
Large R waves representing LVH.
What is the lifespan of RBC's that have Hgb S? What is the P50 of these cells? At what PaO2 do they begin to sickle?
Lifespan is much lower, 10-15 days, resulting in a lower Hct. The P50 is 31 mmHg (lower affinity for O2, curve shifted to right). Sickling begins at a PaO2 of 50 mmHg.
What are S/S of worsening IHHS? What other valve problem has similar reprecussions if afterload is suddenly decreased?
Like AS, the S/S of worsening IHHS are syncope, angina, and DOE. Similar to AS, if Afterload is suddenly decreased, the coronary arteries will not be perfused (as they arise just after the aortic valve).
What is the most common cause of an isolated high PT?
Liver disease.
What kind of murmur does MR have?
MRSA Mitral regurge systolic apex to axilla
What kind of murmur does MS have?
MSDA Mitral stenosis diastolic apex to axilla
What aortic valve area, peak transvalvular gradient, and mean transvalvular gradient corresponds to severe AS?
MTG: 20-50 mmHg PTG: greater than 50 mmHg Valve area: 0.8-1
What aortic valve area, peak transvalvular gradient, and mean transvalvular gradient corresponds to critical AS?
MTG: greater than 50 mmHg PTG: greater than 80 mmHg Valve area less than 0.8
What aortic valve area, peak transvalvular gradient, and mean transvalvular gradient corresponds to mild/moderate AS?
MTG: less than 20 mmHg PTG: less than 36 mmHg Valve area: 1-1.5
What is medical treatment for MR? Are regional techniques acceptable?
Medical treatment is the same as AR: digoxin, diuretics, and vasodilators. Regional is okay as long as bradycardia is avoided and preload maintained.
What is the best indicator of CO if the patient has a normal PaO2 and H/H?
Mixed venous oxygen saturation
What is the most common cause of MS? What gender does it effect more and how long do S/S take to develop? What is the normal MV area?
More common in women (2:1) MS occurs as a complication of Rheumatic Fever. The normal valve area is 4-6 cm squared, and S/S take 20-30 years to develop.
NO diffuses into vascular smooth muscle cells (1st messenger) and activates the enzyme _____, which catatlyzes the conversion of ___ to ___ (2nd messenger). The end result is vasodilation and ____.
NO diffuses into cells (1st messenger) and activates soluble guanylyl cyclase, which catalyzes the conversion of GTP to cGMP (2nd messenger). Vasodilation and platelet inhibition.
After depolarization the Na channels snap into what kind of state that created what kind of period? When they snap shut there is a small __ influx and __ efflux that create Phase ___ aka the ___.
Na channels snap into the closed, inactivated state and create the absolute refractory period. After Phase 0, Phase 1 (aka Transient/Brief) repolarization occurs from Cl- influx and K+ efflux.
Which of the following CCB's cause increased heart rate: Verapimil, Diltiazem, Nifedpine?
Nifedipine (a dihydropyridine) is an arterial dilator that causes a reflex increase in heart rate. Verapamil and Diltiazem (both non-dihydropyridines) cause arterial dilation and decreased heart rate.
The enzyme ___ converts the amino acid ____ to NO.
Nitrous oxide synthetase Arginine
Which 2 phases are absent in the nodal AP compared to the ventricular AP?
No Phase 1 Transient/Brief repolarization. No Phase 2/Plateau
What changes coronary vascular resistance tone the most: PaO2, SNS, or metabolic demands?
Normally coronary blood flow is completely and directly related to metabolic demand.
What are the normal PR and QRS values? What is the value of each mm on EKG paper?
PR: 0.12-0.20 seconds QRS: less than 0.12 seconds. Each small square/1mm is 0.04 seconds.
The QRS complex results from phase __ of the ventricular AP, while the T wave results from phase __. Which phase creates the QT interval?
Phase 0/Rapid Depolarization Phase 3/Repolarization Phase 2/Plateau
At threshold, or Phase __, fast gated Na channels open and the membrane potential changes from -90 mV to ___ mV.
Phase 0/Rapid Depolarization +30 mV
Acetylcholine and NE alter the slope of phase ___, which is set by Na/Ca entry in nodal tissues. This is what actually causes the increase/decreases in HR that are associated with them.
Phase 4/Spontaneous depolarization aka Diastole
What phase of depolarization sets the heart rate? Which tissues in the cardiac conduction system have the fastest phase 4 depolarization?
Phase 4/Spontaneous depolarization aka Diastole Fastest in the SA node, slower in the AV node, and slowest in the Purkinje fibers.
As clots are formed, ____ is incorporated into them as well. When exposed to tPA or uPA it will be converted to _____, its active form, and break down Fibrin.
Plasminogen Plasmin
What is the name for phase 2 of the ventricular AP and what ion moves in and what ion moves out?
Plateau. Ca+ Influx K+ Efflux
All procoagulant factors are present in FFP except? What is the most common cause of coagulalopathy in patients receiving massive transfusions? What defines a "Massive" transfusion?
Platelets Lack of functioning platelets (they are non-functional after 1-2 days in stored blood). Massive Transfusion: defined as 1 complete blood volume infused within 24 hours.
What 2 things are deficient in platelets in patients with renal disease? What is the treatment for uremic coagulopathy?
Platelets have impaired adherence and are deficient in: ADP and TxA2. Treatment is DDAVP, Cryo, and dialysis. Transfused platelets rapidly become abnormal.
Leads II, III, aVF monitor the ___ walls and the ____ coronary artery. Leads I, aVL, V4-V6 monitor the ___ walls and the ___ coronary artery. Leads V1-V4 monitor the ___ walls and the ___ coronary artery.
Posterior and inferior walls/RCA Lateral wall and Left Cx Intraventricular septim and anterior walls/LAD
Where is Preload visually depicted on a pressure volume (PV) loop? Where on the loop is the first heart sound heard?
Preload occurs at end diastole, or when the mitral valve closes on the PV loop. This also corresponds to the closure of the mitral and tricupsid valves, which creates S1.
What 3 factors comprise SV?
Preload, afterload, and contractility
What is the term for tension placed on the wall of the LV at end diastole, what determines it, and what part of the cardiac cycle does it occur in?
Preload. Preload is determined by the volume of blood that enters the LV during diastole, but the term specifically refers to the tension placed on the wall of the LV by the increased volume.
1% of the population has G6PD deficiency. What 2 drugs must be avoided in this group?
Prilocaine and Nitroprusside, due to risk of cyanide toxicity.
What are 3 characteristic ECG changes with hypokalemia?
Prolongation of PR interval, prolongation of QT interval, and appearance of prominent U waves.
What are three characteristic ECG changes with hyperkalemia?
Prolongation of PR interval, widening of QRS complex, and peaked, or tented, T waves.
Arachidonic acid is converted into ____ by COX-1, which is then metabolized into ___, and eventually TxA2.
Prostoglandin G2 (PGG2) Prostoglandin H2 (PGH2) This is what becomes Thromboxane A2
Where is Protein C made and what does it do?
Protein C is a vitamin K dependent anticoagulant made in the liver. It promotes fibrinolysis by stimulating the release of tPA, inhibiting plasminogen activator inhibitor, and cleaving factors Va and VIIa.
Which is more prevalent or more ominous: RBBB or LBBB?
RBBB is common in the general healthy population without clinical evidence of structural heart disease and has no prognostic significance in that group. RBBB occurs in about 1% of hospitalized patients and is much more common than LBBB. LBBB is more ominous and DOES NOT occur in healthy individuals. LBBB is often associated with ischemic heart disease, HTN, and valvular heart disease. LBBB obscures or stimulates other EKG patterns, making diagnosis of LVH, MI difficult.
What is the name for phase 0 of the ventricular AP and what ions move in and out?
Rapid depolarization. Na efflux
What is the name for phase 0 in the nodal cardiac cell and what ions move in/out?
Rapid depolarization. Na+ influx AND Ca+ influx.
What is the name for phase 3 of the ventricular AP and what ions move in and out?
Re polarization/Delayed re polarization. K efflux.
What happens first: activation, aggregation, or adhesion?
Remember DCG: aDhesion, aCtviation, aGgreation.
With HOCM, things that increase LV emptying will worsen the obstruction. How can you remember what preload, afterload, and contractility will do to the obstruction?
Remember the acronym: Old Cats Pee A lot. Make a table from where O=Outflow tract obstruction, C=Contractility, P=Preload, A=Afterload. (Add pic here)
What is the name for phase 3 in the nodal cardiac cell and what ions move in/out?
Repolarization/Delayed re polarization. K efflux.
The goal in treating intraoperative MI is to return the heart to a ___, ____, perfused state.
Return the heart to a slow, small, perfused state.
What are some causes of AR?
Rheumatic heart disease can cause every valve problem. Others include: infective endocarditis, SLE, syphillus, aortic root dilation, ankylosing spondylitis, and Marfans Dz.
Which direct acting vasodilators can cause angina?
SNP causes coronary steal syndrome and decreases DBP and therein CPP. NTG decreases DBP which decreases CPP. Hydralazine causes a reflex increase in HR and contractility.
If a patient has intraop MI evidence with a decreased BP and a normal PCWP, what is the cause and what is treatment?
SVR is decreased and this is decreasing CPP leading to the begining of LV failure. Treatment: Decrease anesthetic depth, give a vasoconstrictor like Phenylephrine to increase BP and CPP.
In both acute Aortic and Mitral regurgitation the PV loops are ____ (small or large).
Small
What is the best test of primary hemostasis or platelet function?
Standard skin bleeding time (3-10 minutes normal).
The alpha-2 adrenergic receptor agonist, clonidine, acts where centrally to produce what therapeutic effect?
Stimulation of alpha-2A receptors of inhibitory neurons in the vasomotor center of the medulla in the brain stem inhibits sympathetic nervous system outflow. This action decreases blood pressure.
What is the primary treatment for SNP cyanide toxicity. What are 2 other treatments if this is ineffective?
Stop the SNP infusion, give 100% oxygen. Give sodium thiosulfate (150 mg/kg IV) over 15 minutes. Thiosulfate acts as a sulfur donor and converts cyanide to thiocyanate. If cyanide toxicity is severe after thiosulfate administration, with deteriorating hemodynamics and metabolic acidosis, the treatment is slow administration of sodium nitrate (5 mg/kg IV). Sodium nitrate converts hemoglobin to methemoglobin, which acts as an antidote by converting cyanide to cyanomethemoglobin. Alternatively, hydroxocobalamin (vitamin B12), which binds cyanide to form cyanocobalamin (vitamin B12) can be administered (25 mg per hour IV to a maximum of 100 mg) to treat cyanide toxicity.
What are the 4 determinants of myocardial oxygen supply and demand?
Supply: Heart rate, H/H and SpO2, DBP, Coronary vascular resistance. Demand: Heart rate, Preload, Afterload, Contractility
Where is vWF/Factor 8 made, what is it released from? What layer of tissue does it attach to that anchors platelets? What specific receptor on platelets does it bind to?
Synthesized and released from endothelial cells. Attaches to the subendothelial collagen layer. The GP1b receptor on platelets.
How does a decrease in Afterload effect systemic BP, HR, PCWP, and SVR?
Systemic BP decreases, HR increases reflexively, PCWP decreases (decreased EDV), and SVR decreases.
How does an increase in Afterload effect systemic BP, HR, PCWP, and SVR?
Systemic BP is increased, HR decreases reflexively, PCWP increases (increased EDV), and SVR increases.
What nasty side effects occurs in 10-20% of patients that chronically take hydralazine?
Systemic Lupus Erythmetous
When in the cardiac cycle does AS occur? Is it a volume or pressure overload, and what kind of hypertrophy occurs?
Systole Pressure Concentric
When in the cardiac cycle does MR occur? Is it a volume or pressure overload, and what kind of hypertrophy occurs?
Systole Volume Eccentric
In general when interpreting PV loops, taller or shorter loops are a ____ (pressure or volume) issue, while fatter or thinner loops are ____ (pressure or volume) issues.
Taller and shorter=Pressure Fatter and thinner loops=Volume Remember which axis on the PV loop is volume and pressure.
What will be unique about the BP of patients with AR? What about the PA tracing?
The BP will have a widened pulse pressure due to backflow during diastole decreasing their DBP. Large V waves on the PA tracing suggest MR (which eventually will occur with AR).
What is the J point on an EKG?
The J point is where the QRS ends and the ST segment begins. ST elevation/depression is measured by comparing the lead voltage at 60 or 80 milliseconds after the J point to the isoelectric value.
Calcium channel blockers bind to the ___ but not the ___ type of calcium channels.
The L-type, or slow type, of calcium channels. They do not bind to the T-type calcium channels.
In the ventricular cell, what restores RMP?
The Na/K pump extrudes the Na ions that entered the cell and recaptures the K ions that were lost from the cell.
If a patient has intraop MI evidence with a decreased BP and increased PCWP, what is the cause and what is treatment?
The cause is LV failure (inc PCWP, dec SV, dec CO). Treatment: Phenylephrine to inc BP/CPP, NTG to dilate veins and increase venous return, and an Inotrope to increase contractility.
There are 3 forms of the enzyme Nitrous oxide synthetase: the constitutive, the inducible, and the neuronal. Which of significance to anethesia?
The constitutive form is present in endothelial cells and is regulated by calcium. It produces NO and causes vasodilation. The inducible is produced in response to immunological stimuli, and the neuronal form is confined to neural tissues.
Recite the Valley formula for remembering the intrinsic, extrinsic, and final common pathways.
The extrinsic pathway can be purchased for 37 cents. If you cannot buy the instrinsic pathway for $12, you can buy it for $11.98. The final common pathway can be purchased at the five and dime, on the 1st or second day of the month, for $13.
When the ventricular cell is in the resting state, or Phase 4/RMP which ion gates are normally closed? Which are open/working?
The gated Na, K, and Ca channels are closed. The leaky K channel and Na/K pump are open/working.
What is an easy way to figure out whether a PV loop showing regurgitation is mitral or aortic?
The left side of the PV loop represents Isovolumetric relaxation from when the Aortic valve closes, to when the mitral valve opens. If this side of the PV loop is wonky, its an aortic valve issue. You can also draw an A with the slanted line created. The right side of the PV loop represents Isovolumetric contraction from when the mitral valve closes to when the Aortic Valve opens. If this side of the PV loop is wonky, then its a mitral valve issue. You can also draw M from the slanted line created.
How can you remember what amount of MR causes mild, moderate, and severe symptoms?
The rule of 3's. less than 30%=mild S/S 30-60%=Moderate S/S greater than 60%=Severe S/S
In what direction does depolarization spread from the intraventricular septim? What is the overall spread of depolarization in the ventricles?
The septim depolarizes from the left towards the right. Somewhat counter-intuitively, the overall spread of depolarization in the ventricles is from right to left.
What layer of the cardiac tissue is most sensitive to ischemia?
The sub endocardium of the left ventricle.
What specific nerves and actions comprise the efferent part of the baroreceptor reflex?
The vagus nerve innervates the SA node, AV node, and the atria. Vagus firing is INCREASED. The sympathetic nerves (T1-T4) firing is DECREASED. The situation could be reversed if BP suddenly dropped.
How does chronic Mitral Stenosis shift the PV loop (think pressure and volume)?
There is a decrease in preoload to the LV, this results in smaller pressures (shorter). LV emptying remains about the same (not thinner or fatter). This PV looks a lot like that for deceased preload because this is basically the same situation but its created by a valve.
How does chronic Aortic Stenosis shift the PV loop (think pressure and volume)?
There is an increase in afterload, so there are higher pressures (taller). The LV compensates via concentric hypertrophy and maintains a relatively normal SV, so volume is unchanged (not thinner or fatter).
The patient is hypokalemic. What change in heart rate may be seen?
There is increased automaticity of both atria and ventricles, reflecting more rapid rate of spontaneous phase 4 depolarization. Thus heart rate increases.
Which factor is missing from the coagulation factors?
There is no factor VI.
Is there any pathognomic tests for DIC? Which counts or time are down or up?
There is none. DIC is a diagnosis of exclusion and treatment is to treat the cause (infection, trauma, shock, ischemia, etc). All counts are down: Firbinogen < 150 mg/dl, Platelets < 50,000. All times are, and Fibrin Degradation Products, are up: PT, INR, aPTT.
Where and what is thickened in IHHS aka HOCM aka ASH? What other valve problem occurs due to this?
There is septal thickening just below where the Aortic valve is. During late systole the Venturi Effect/Bournoulli's principle will cause the anterior leaflet of the mitral valve to bow backward, creating mitral regurge.
What are Hirudin, Ximelgatran, and Argatroban?
They are direct Thrombin (IIa) inhibitors.
How specifically do ADP and TxA2 cause the activation and aggregation of platelets?
They are ligands that activate GCPR's on platelets. Via signal transduction, they stimulate the production of GPIIb/IIIa receptors on the surface of platelets.
How do Cyanide ions interfere with oxygen utilization? What are 4 S/S of cyanide toxicity and which is the best indicator?
They bind to tissue cytochrome oxidases and uncouple oxidative phopshorylation, preventing the formation of ATP. S/S: Metabolic acidosis, Arrhythmia, Increased Venous O2, and tachyphylaxis. Metabolic acidosis (as measure by base deficit) is the best indicator.
How do Amicar and TXA work?
They both are plasmin antagonists. Both displace plasmin from its binding site, inhibiting the breakdown of fibrin (fibrinolysis).
Patients with acute AR present in fulminant heart failure (dypsnea, hTN, pulmonary edema). Those with chronic AR can be asymptomatic for up to __ years. Which symptoms eventually occur?
They can be symptom free for up to 20 years. DOE, orthopnea, and paroxysmal nocturnal dyspnea are initial symptoms. Life expectancy is 5 years without treatment.
ADP and TxA2 uncover ___ receptors (aka GP IIb/IIIa) on _____, allowing it to link platelets and form a water-soluble platelet plug (aka White thrombus or white clot).
They uncover fibrinogen/Factor 1 receptors (GP IIb/IIIa). This links platelets together.
On what phase of the ventricular AP do phenytoin and lidocaine work to suppress arrhythmias?
They work on Phase 4 (aka RMP/Diastole) of the VENTRICULAR action potential.
What causes the decrease in ABP often seen CPB is initiated?
This is due to large decrease in blood viscosity from dilution of the patients blood within the CPB system. This decreased blood viscosity causes SVR to fall.
When is a clot insoluble to water? Which coagulation factor is required for this to occur, and what is its name?
This occurs when fibrin strands cross link, then it is insoluble to water and is known as a red clot or red thrombus. Factor XIIIa/Fibrin is required.
Which 2 groups of patients are prone to AT3 deficiency? What would treatment be if adequate heparinization was needed?
Those with Cirrhosis (not making proteins) and Nephrotic syndrome (peeing out proteins). Treatment would be FFP to increase AT3 levels.
___ activates platelets by binding to specific receptors on the platelet. This changes the platelet's shape and causes release of ___ and ___ (among other things).
Thrombin aka Factor 2a This changes the shape of the platelet from round to spiky, and causes release of ADP and Thromboxane A2 (TxA2).
When the platelet is activated by ___, the enzyme Phospholipase cleaves off phospholipids from the cell membrane, liberating ____.
Thromib/Factor 2 Arachidonic Acid
What is the name for phase 1 of the ventricular AP and what ions move in and out?
Transient/Brief re polarization. K+ efflux Cl- influx
What do cardiac myocytes actually bind to that causes contraction to occur? What is required for this to occur?
Troponin C Calcium
True or false: blood flow through capillaries is non-pulsatile?
True. Blood flow through large arteries is pulsatile, but by the time blood reaches the capillaries blood flow is non-pulsatile and laminar.
Over 90% of cases of DIC are type __. This type reflects excessive generation of ____, which is known to trigger the activation of plasmin, and therein the breakdown of fibrin to fibrin degradation products.
Type II Factor IIa/Thrombin
The best overall lead for detecting MI is lead ___.
V5
Which is the best lead to detect LV ischemia?
V5
The resting membrane potential (RMP) of cardiac ventricular cells is ___ mV, while in nodal cells its __mV.
Ventricular: -90 Nodal: -70
On what phase of the AP do calcium channel blockers work to slow heart rate? What other AP do they effect?
Verapimil, Diltiazem, and Nifedipine slow heart rate by altering Phase 4 of the NODAL action potential in the SA/AV nodes. They also alter Phase 2 of the VENTRICULAR action potential. This is not generally clinically relevant.
Some calcium that enters during Phase 2 is used for contraction. Another role is to trigger the opening of voltage gated ___ channels that begin Phase __ aka ______.
Voltage gated K channels open from Ca accumulation. This causes Phase 3/Repolarization.
What is the most common inherited coagulation defect that should be suspected in any patient with increased bleeding times despite a normal platelet count?
Von Willebrand's Disease
Which pathway and which coagulation tests are effected by Warfarin and Heparin?
Warfarin: Extrinsic and final common pathways. Measured by PT/INR. Heparin: Intrinsic and final common pathways. Measured by ACT and aPTT.
How is cyanide produced from Sodium Nitroprusside?
With high doses of nitroprusside, the ferrous iron of nitroprusside reacts with sulfhydryl groups in red blood cells and releases cyanide.
Are spinals and epidurals contraindicated in patients with AS?
With severe AS they are contraindicated. Mild/Moderate AS can have spinals and epidurals, although epidurals are preferred and dilute LA's are preferred.
Hemophilia B is also known as ______. What is the treatment?
aka Christmas Disease or Factor 9 Deficiency (Christmas is a associated with the trinity and 9 is divisible by 3). Treatment is purified factor 9.
Review Einthoven's Triangle an which lead positions are I, II, and III.
https://en.wikipedia.org/wiki/Einthoven%27s_triangle
Learn how to differentiate between left and right bundle branch blocks.
https://www.youtube.com/watch?v=qjIoMrMVECc
Which form of plasminogen activator, tPA or uPA, is produced by endothelial cells and is the most active?
tPA is produced by endothelial cells and released in response to venous stasis and thrombin. uPA has little affinity for fibrin, but is exogenously administered via the arterial route to provide anticoagulation.
___% of blood volume is found in veins, while ___% is found in the arterial system.
~ 70% is venous. ~ 30% is arterial.
