CardioAnesthesia Flashcards
Miocardial perfusion
Dominance : coronary supply to POSTERIOR DESCENDING ARTERY
RIGHT 65% left 15% ( circumflex)
Anterior wall: Left anterior descending artery
Lateral wall: left circumflex artery
Posterior wall: RCA
*posteromedial papillary muscle rupture > anterolateral because of double blood supply
Coronary perfusion pressure
CPP= aortic dyastolic pressure- LVEDP
Intra aortic ballon pump
Fill with hellium laminar flow pass through
Indication: cardiogenic shock
Failure to wean from CPB
SEVERE MITRAL REGURGITATION
bridge to transplantation
Right ventricular disfunction
Contraindications: aortic insufficiency
Aortic dissection
Arterial injury
Ischemia - plaque
Thromboembolism
Hemolysis
Infection
The ballon is inflated to augment aortic diastolic pressure CPP
In early diastole to late diastole
CPB goals
Pump blood flow 1-3 ml/min/m2
MAP 50-90 mmhg
SatvO2 65%
Fick method to measure CO
Oxygen consumption is equal to CO+ difference in oxygen content A-V
CO = Vo2 /(CaO2-CvO2)
A-V difference:1.34 mlO2/g Hb x[hb] X( diferencia saturacion A-V)
Limitaciones : Pneumonia High output states Shunt Narrow differences A-V
Brugada
Channelopathy Na
EKG PSEUDO RIGHT BBB
Wide QRSwith R’ V1 exaggerated S wave in V5V6
ST elevations in V1-V3
Cardiodesfibrilador
Anesthesia : not propofol infusion or bupivacaine
No BB
Avoid sodium channel blocker’s
Benzold jarish
Response to noxious stimulus to ventricule
Aferent : vagus
Increased parasympathetic response
Response bradycardia
Hypotension
Coronary vasodilation
Brainbridge
Stretch Receptor between atria an vena cava
Afferent through vagus nerve to CV center in medulla
Increased in stretch (pressure) cause inhibition of PNS= increased in heart rate
Decreased in stretch : decreased in HR ( neuroaxial)
La place law
Wall stress = pressure x radius/2x wall tickness
Sistemic vascular resistance
SVR= CVP-MAP/CO x80 dynes/sec/cm5
Normal 700-1500 dynes/sec/cm5
Normal oxigen delivery
Normal 900-1000 ml/min
Critical ( not supply demand( <700 ml/min
Stroke volume/ ejection fraction
SV= EDV-ESV EF= SV /EDV x 100 =%
HOCM
The goals of anesthetic management of HOCM include: (1) reduced myocardial contractility, (2) maintenance of (or increase in) of SVR, and (3) increased preload and cardiac output. Etomidate is a good choice for intravenous induction in patients with HOCM given its ability to maintain or increase SVR
Stents and surgery
The minimum time after placement of a drug-eluting stent is six months for elective procedures.
everolimus in newer stents and paclitaxel in older stents.
If the patient had received a bare-metal stent, a 30-day interval could be considered.
early invasive strategy:
ACC/AHA guidelines, qualify for early invasive strategy:
- Recurrent angina or ischemia at rest with low-level activities despite intensive medical therapy
- Elevated cardiac biomarkers
- New ST-segment depression
- Signs or symptoms of heart failure or new or worsening mitral regurgitation
- Hemodynamic instability
- Sustained ventricular tachycardia
- PCI within 6 months
- Prior coronary artery bypass
- High-risk TIMI score (> 2 points)
- Reduced left ventricular function (LVEF < 40%)
TAVR
AVRs are currently only indicated for symptomatic aortic stenosis.
TAVR is most beneficial for patients who are considered high surgical risk, and conversely, low-risk patients with severe AS should be considered for surgical repair.
In patients who are extremely high risk such as those whose survival is expected to be less than 12 months, TAVR may provide a small benefit over standard medical therapy.
Torsades de pointes
Tto
includes recognizing TDP from normal VT and removal or correction of the offending agent. Correcting electrolytes with the early use of magnesium is recommended. Magnesium can be given as an initial 1-2 gram IV bolus over 30-60 seconds, which can then be repeated in 5-15 minutes. Alternatively, a continuous infusion can be started at a rate of 3-10 mg/min. Magnesium is effective even in patients with normal magnesium levels.
Torsades can be induced by many antiarrhythmic drugs including class Ia (sodium channel blockade) and class III (inhibit potassium channels) by prolonging the QT interval.
Hypokalemia and hypomagnesemia are also known to be associated with TDP
Mitral regurgitation
Mitral regurgitation patients should be kept “fast, full, forward” by avoiding bradycardia, ensuring adequate preload, and avoiding high afterload
There are several goals for anesthetic management of patients with severe mitral regurgitation.
1) Bradycardia should be avoided as this increases the regurgitant volumes accumulating during systole. In addition, a slower heart rate increases ventricular diastolic filling time which will increase the regurgitant volume during the next systole.
2) Normovolemia should be maintained in order to avoid left ventricular and mitral annular distension and the subsequent increase in regurgitant volume. Hypovolemia is not helpful either.
3) Afterload, measured in terms of systemic vascular resistance (SVR), should be kept relatively low to help with aortic flow of the generated cardiac output. This can be accomplished via vasodilators, inodilators, and/or an intra-aortic balloon pump.
4) Avoid pulmonary vasoconstriction. Patients with severe MR have varying degrees of pulmonary hypertension. Factors that cause pulmonary vasoconstriction (e.g. acidosis, hypoxia, and hypercapnia) should therefore be avoided.
Hypertrophied cardiomyopathy
Factors that promote LVOT obstruction in HCM include: tachycardia, hypovolemia, vasodilation, and a high chronotopic/inotropic state. In this scenario, options for the treatment of hypotension are phenylephrine, fluid boluses, and beta-blockade.
the anesthetic goals are: Maintenance of sinus rhythm Reduction in sympathetic stimulation Maintenance of left ventricular filling Maintenance of systemic vascular resistance
Septal myectomy is the treatment of choice in a patient with hypertrophic cardio
