Cardiovascular Flashcards
Discuss the conduction pathway of the heart and the related mechanical and electrical events as represented on an EKG
Conduction:
SA node -> AV node -> Bundles of His -> Bundle branches -> Purkinje fibers -> Ventricular muscle
P-wave: Atrial depolarization
PR-interval: Atrial systole and AV delay (normal .12-.20)
QRS-complex: Ventricular depolarization and atrial repolarization (normal < .12). Phase 0 of cardiac cycle Na+ channels open and Na+ influx into cell
QT-interval: Ventricular systole. Phase 2 of cardiac cycle, Na+ channels in inactivated state, and Ca+ channels open with Ca+ influx into cell. When enough Ca+ accumulates in the cell the Ca+ channels close and K+ channels open. Hypercalcemia will shorten the QT while hypocalcemia will prolong it.
T-wave: Ventricular repolarization. K+ channels open, and Na+ return to activated state when cell is repolarized. T-wave will be peeked in the presence of hyperkalemia
U-wave: Not always present may be seen with Hypokalemia
Discuss QRS nomenclature, what would a qrs, rsr, qr, rs, qs, and rr waveform look like?
Q is the 1st negative deflection
R is the 1st positive deflection
S is a negative deflection following an R
QRS: negative positive negative
RSR: positive negative positive
QR: negative positive to baseline
RS: positive negative to baseline
QS: negative V shaped wave with no positive deflections
RR: Two positive deflections attached to each other saw-tooth
Describe normal ventricular depolarization
Depolarization precedes from left septal wall to right septal wall, the the ventricles depolarize but the overall spread of depolarization of to the left representing left ventricular electrical dominance
V1 lead: RS complex r-wave (septal depolarization) s-wave (ventricular depolarization)
V6 lead: QR complex q-wave (septal depolarization) r-wave (ventricular depolarization)
Describe what a RBBB would look like one EKG
V1 will show an rSR’ wave with a broad R’ wave
V6 will show a qRS type wave with a broad S wave
V1-V3 may show inverted T-waves
Describe what a LBBB would look like on an EKG
When LBBB is present the ventricular septum depolarizes from right to left (opposite normal)
There will be a loss of the normal septal R-wave in V1 and the normal septal Q-wave in V6. In addition left ventricular depolarization will be prolonged resulting in an abnormally wide QRS-complex. V6 will show an entirely positive R-wave with a notch
On what phase of the nodal AP does digitalis work?
Digitalis slows the HR by slowing phase 4 depolarization
Describe what EKG leads can be used to monitor the following anatomical sites, and list the coronary artery responsible for blood supply to that site:
Posterior, inferior walls
Septum, anterior wall
Lateral wall
Posterior, inferior walls: Leads II, III, aVF, right coronary artery (RCA)
Septum, anterior wall: Leads V2-V5, left anterior descending artery (LAD)
Lateral wall: Leads I, aVL, V4-V6, left circumflex (LCX)
On what phase of the nodal AP do Ca+ channels blockers work to slow HR?
Ca+ channel blockers (verapamil, diltiazem, and nifedipine) slow HR by slowing phase 4 depolarization
On what phase of the AP does lidocaine work to control ventricular disrhytmias?
Lidocaine or phenytoin suppress spontaneous phase 4 ventricular depolarization, which is responsible for premature ventricular contractions, as might occur in ischemic ventricles
Name the determinants of intravasuclar volume, preload, stroke volume,cardiac output and mean arterial pressure
MAP: determined by CO and SVR
CO: determined by HR x SV
SV: determined by preload, contractility, and afterload
Preload: determined by intravasuclar volume and venous tone
Intravasuclar volume: determined by Na+ in the body (aldosterone)
On what phase of the cardiac ventricle AP do Ca+ channel blockers work?
Ca+ channels blockers (virapamil, diltiazem, nifedipine) work on phase 2 (plateau) of the cardiac ventricular AP
Describe concentric ventricular hypertrophy and it’s causes
Left ventricular wall is thickened but left ventricular chamber size remains normal. Causes include untreated chronic hypertension, chronic AS, and coarctation of aorta
Note IHSS does not apply to this situation
Describe the phases, and ionic flow of the ventricular action potential and the resultant wave form
Wave form with plateau
Phase 0: Rapid Na+ influx depolarization
Phase 1: Brief repolarization Cl- influx and K+ efflux. Na+ channels close in inactivated state
Phase 2: Ca+ influx (plateau) systolie
Phase 3: K+ influx repolarization, Na+ channels returns to activate state
Phase 4: Na-KA-TPase pump restores balance diastole
Describe eccentric ventricular hypertrophy and it’s causes
Dilated left ventricular wall with enormously greater chamber volume. Causes include chronic AI, chronic MR and morbid obesity
Describe the phases, and ionic flow of the nodal action potential and the resultant wave form
Biphasic wave form
Phase 0: Ca+ influx; some Na+ infflux (systolie)
Phase 3: K+ efflux repolarization
Phase 4: k+ efflux progressively slowing while Na+ influx progressively increasing; Ca+ influx starts during last 1/3 of phase 4. Together these ionic movements are the basis for spontaneous depolarization = Autorhythmicity
Describe the pressure-volume loop, what points A,B,C and D represent, where systole begins and ends, where diastole begins and ends, where diastolic filling occurs, where ejection occurs, and where the mitral and aortic valve open and close during each phase of the P-V loop
A: mitral valve opening B: mitral valve closing and end diastolic volume C: aortic valve opening D: aortic valve closing and end systolic volume A-B: diastolic filling B-C: isovolumetric contraction (systole) C-D: ejection, generates SBP D-A: isovolumetric relaxation diastole
Systole begins at B and ends at D
Diastole begins at D a d ends at B
What happens when the rate of phase 4 depolarization is increased or decreased?
When Phase 4 depolarization is slowed (by digitalis for example) it takes longer to reach threshold so there is longer time between AP andHR decreases.
When Phase 4 depolarization is increased (by NE for example) it takes less time to reach threshold so there is less time between AP and HR increases
Discuss changes that might be seen on a P-V loop in the presence of acute preload increases
Ex fluid bonus administration
When preload increases, end-diastolic-volume increases (B). However ventricle will empty to the same point, meaning end-systolic-volume (D) stays the same. The B-C segment is pushed to the right
Therefore, SV increases (SV = B - D) Blood pressure increases, and reflex decreases in HR and SVR
What agents should be avoided in WPW syndrome?
Digoxin and verapamil should be avoided because it decreases AV conduction and increases conduction through the accessory tract (bundle of Kent)
Discuss changes that might be seen on a P-V loop in the presence of acute preload decreases
Ex nitroglycerin administration
When preload is decreased (NTG induced venus pooling) end-diastolic-volume (B) decreases, because ventricle empties to the same point, meaning end-systolic-volume (D) remains the same. P-V loop, B-C segment shifted to the left
Therefore SV is decreased (SV = B - D), which decreases CO, and result in decreased BP. Reflex increase in HR and SVR
How will subendocardial and transmural ischemia and injury present on an EKG?
Subendocardial ischemia and injury will produce ST segment depressions greater than 1mm
Transmural ischemia will produce a symmetrically inverted T-wave
Transmural injury will produce ST segment elevation of greater than 1mm
Discuss changes that might be seen on a P-V loop in the presence of increased after load
When afterload increases, the heart empties less completely (SV decreases), both end-diastolic-volume (preload) and end-systolic-volume increases (ventricular chamber dilates)
P-V loop will shift up and to the right (ie vasopressin given)
Discuss changes that might be seen on a P-V loop in the presence of decreased afterload
When after load decreases the heart empties more completely (SV increases); both end-diastolic-volume (preload) and end-systolic-volume decrease (ventricle shrinks)
P-V loop will show decreased pressure and shifted to the left
Discuss changes that might be seen on a P-V loop in the presence of incread contractility
When contractility increase the ventricle empties more completely (end-systolic-volume decreases); end-diastolic-volume also decreases but not as much, so SV is increased
P-V loop will have higher amplitude and be shifted to the left
Discuss changes that might be seen on a P-V loop in the presence of decreased contractility
When contractility decreases, the ventricle empties less completely (end-systolic-volume increases); end-diastolic-volume also increases (the ventricle dilates) but not as much as so SV decreases
P-V loop will show decreased amplitude and be shifted to the right
Discuss changes that might be seen on a P-V loop in the presence of IHSS
The P-V loop will be shifted to smaller volumes and higher pressures, meaning increased amplitude and shifted to the left
Discuss changes that might be seen on a P-V loop in the presence of chronic aortic stenosis
With chronic aortic stenosis, concentric hypertrophy permits the LV to generate great pressures so LV volumes remain about the same as normal
P-V loop will be shifted upward
Discuss changes that might be seen on a P-V loop in the presence of mitral stenosis
With mitral stenosis, left ventricular filling is diminished. There is reduced filling (preload) but emptying (end-systolic-volume) is about the same as normal
P-v loop reflects a decrease in preload; the B-C segment is shifted to the left
What are the formulas and normal values for:
MAP, CO, CI, SV, SI, SVR, PVR
MAP = DBP + DBP + SBP / 3 CO = HR x SV CI = CO/BSA SV = CO/HR (60-90ml) SI = SV / BSA (40-60ml/m2) SVR = (MAP-CVP)/CO x 80 (900-1500 dynes) PVR = (PAP-PCWP)/CO x 80 ( 50-150 dynes)
How would you Tx ischemia in the presence of Increased BP and increased PCWP
BP has increased because SVR has increased; work of the heart has increased and O2 consumption has increased due to increased afterload
Tx with increased depth of anesthesia (to dilate vasculature) and give NTG or NTP
How would you Tx ischemia in the presence of increased HR
Tachycardia has increased myocardial O2 consumption and decreased diastolic myocardial perfusion
Tx with beta antagonist or Ca+ channel blocker
How would you Tx ischemia in the presence of decreased blood pressure and decreased or normal PCWP
BP is decreased because SVR is decreased; coronary perfusion pressure and blood flow are decreased as a result
Decrease anesthetic depth and give vasoconstrictor such as phenylephrine to improve coronary perfusion
How would you Tx ischemia in the presence of decreased BP and increased PCWP
Suggests heart failure
Tx with phenylephrine to increase coronary perfusion pressure, NTG to dilate veins and decrease venous return (preload) and give a positive isotopic agent to increase contractility
How would you Tx ischemia in the presence of normal hemodynamics
Give NTG or Ca+ channel blocker
Describe the control of blood pressure via the baroreceptor reflex
Increased BP -> increased stretch of carotid sinus and aortic arch baroreceptors -> increased AP from afferent vagus nerve in aortic arch and Herrings nerve (glosopharangeal IX) from the carotid sinus to the medulla -> increased efferent vagus nerve discharge to SA node decreasing HR and CO; decreased efferent Sympathetic out flow decreased HR, CO, venodilation and decreased preload, arteriodilation and decreased SVR
Discuss management of IHSS
Maintain normal HR and sinus rhythm as these patients need atrial kick. Maintain preload and give volume as 1st Tx for hypotension, maintain afterload and give pure alpha vasoconstrictor to tx hypotension
AOFT obstruction made worst by: Increased contractility; avoid beta agonist Decreased preload and afterload AOFT obstruction improves by: Decreased contractility Increased preload and afterload
MR may be present, dysrthmias result from disorganized cellular architecture, most common cause of sudden death in people 30 and younger
Discuss the anesthetic management and pathophysiology of aortic regurgitation
Management: maintain increased HR 80-100 this decreases regurgitant fraction, maintain preload and decrease afterload to maximize forward cardiac output
Pathophysiology: can be congenial or due to rheumatic fever.
Acute AI: Most commonly follows infective endocarditis, trauma, or aortic dissection. Will present as sudden onset pulmonary edema, severe dyspnea, hypotension and weakness
Chronic AI: Will lead to LV pressure overload and eccentric hypertrophy. Presents as diastolic murmur, wide pulse pressure, decreased DBP, and bounding peripheral pulses
Discuss the anesthetic management and pathophysiology of mitral regurgitation
Management: Maintain elevated HR normal preload, and decreased afterload to reduce regurgitant fraction, avoid sudden increases in SVR
Pathophysiology: Chronic MR usually due to rheumatic fever, acute MR usually due to ischemia, infarction, infective endocarditis, or chest trauma. Eccentric LV hypertrophy will eventually ensue
Symptomatic progression:
Mild symptoms < 30% regurgitant
Moderate symptoms 30-60% regurgitant
Severe > 60% regurgitant
Discuss the anesthetic management and pathophysiology of aortic stenosis
Management: Avoid bradycardia or tachycardia, maintain NSR (loss of atrial kick may lead yo 40% decrease in CO) maintain preload and afterload
Pathophysiology: Most common cause of LV outflow obstruction. Obstruction develops gradually, development of concentric hypertrophy will maintain SV, but will eventually deteriorate. May have angina at rest and in the absence of CAD
AVA Normal (2.5-3) Mild (1.0-1.5) Mod (0.8-1.0) Severe (< 0.8)
Discuss the anesthetic management and pathophysiology of mitral stenosis
Management: keep HR slow to allow for diastolic filling, maintain NSR and preload, and afterload. Avoid decreases in afterload, and increases in PVR
Pathophysiology: delayed complication of acute rheumatic fever, stenosis begins 2 years following. RV failure develops from acute or chronic elevations in RV afterload
