Cardiac - Surgery, Physiology, Pathology Flashcards
Describe the anatomy of the right ventricle
The body of the RV receives blood from the RA, while the outflow tract delivers blood to the pulmonary artery. The RA and PA are seperated by crista supraventricularis. The RV is the most anterior chamber of the normal heart - residing immediately behind the sternum. It is crescent shaped in cross section and triangular in side profile.
Describe the anatomy of the right ventricle
The body of the RV receives blood from the RA, while the outflow tract delivers blood to the pulmonary artery. The RA and PA are seperated by crista supraventricularis. The RV is the most anterior chamber of the normal heart - residing immediately behind the sternum. It is crescent shaped in cross section and triangular in side profile.
Discuss the managment of cardiac arrest following cardiac surgery
Discuss common causes of deterioration following cardiac surgery
Hypovolaemia and Bleeding
- multifactorial - preop anticogaultion, inherited/acquired bleeding disorders, emergency surgery, prolonged bypass times, residual heparin, surgical beleding. (sternal wires, anastomotic or side brach leak from graft sites)
Low Output Cardiac State (LOCS)
Ventricular function normally decreases 24-72hrs post op
metabolic dysfunction, reperfusion injusty, ischaemia, hypocalcaemia
GRAFT and VALVE failure
can be masked by temporary epicardial pacing
hallmark features include new ECG changes and persistant LCOS
TOE can identify new RWMD
TAMPONADE
rapid compression of the heart by acculumlation of blood in the pericardiu,
Arrthymias
AF is the most common post op arrthymia and should be managed via conventional management.
VASODILATIOn
Common finding. likely due to active warming causing a decrease in SVR
also possible: sepsis, anaphylaxis, adrenal insufficiency, vasoplegic syndrome, and unopposed inodilators.
Describe the RV blood supply
Dependant on the dominance of the coronary system for each individual. 80% supplied by RCA, Unlike the LV - it is supplied in systole and diastole. This only occurs in normal hearts - eg Pulm HTN - increased RV pressure. becomes more like LV
Discuss RV Cardiodynamics
RV performance is affected by preload, afterload and ventricular interdependence. Preload - affected by atrial contractility, ventricular compliance, venous return, wall tension and heart rate. “Preload tolerant” Afterload - intolerant of preload , influenced by PVR Ventricular Interdependence - phenomenon whereby the vol/Pressure of one ventricle can directly influence that of the other (shared septum, in pericardial sac) Right heart haemodynamics affected by resp effort - spont breathing increasing RV preload, and decreased RV afterload (expansion of pulm vascularture) COMPARED TO MECHANICAL VENTILATION Increase in intrathoracic pressure ( less preload) and extra alveolar capillaries are compress ( higher afterload) marked systolic pressure/ stroke volume variation with patients with RV dysfunction. CAUTION - not always hypovolaemia
Describe the RV blood supply
Dependant on the dominance of the coronary system for each individual. 80% supplied by RCA, Unlike the LV - it is supplied in systole and diastole. This only occurs in normal hearts - eg Pulm HTN - increased RV pressure. becomes more like LV
Discuss RV Cardiodynamics
RV performance is affected by preload, afterload and ventricular interdependence. Preload - affected by atrial contractility, ventricular compliance, venous return, wall tension and heart rate. “Preload tolerant” Afterload - intolerant of preload , influenced by PVR Ventricular Interdependence - phenomenon whereby the vol/Pressure of one ventricle can directly influence that of the other (shared septum, in pericardial sac) Right heart haemodynamics affected by resp effort - spont breathing increasing RV preload, and decreased RV afterload (expansion of pulm vascularture) COMPARED TO MECHANICAL VENTILATION Increase in intrathoracic pressure ( less preload) and extra alveolar capillaries are compress ( higher afterload) marked systolic pressure/ stroke volume variation with patients with RV dysfunction. CAUTION - not always hypovolaemia
Define cardiomyopathy Classify cardiomyopathies
myocardial disorder in which the heart muslce is structurally and functionally abnormal in the absence of CAD, HTN, and congenital heart diease Dilated Hypertrophic Restrictive cardiomyopathy Arrhythmogenic Right Ventricle Unclassified (familial non familial)
Dicuss Dilated Cardiomyopathy. Pathogenesis Aetiology Clinical Features Anaesthesia Management
Disease myocardium characterised by IMPAIRED systolic function and dilation of the left and right ventricles’ 2/3 cases idiopathic Rest either familial, post-viral, part of IHD, HTN, Diabetes, ETOH DCM is a leading cause for heart transplantation in children and young adults. Characterized predominantly by systolic dysfunction. Progressive enlargement of one or both ventricles to the stage where the interaction between actin and myosin filaments becomes inefficient, leading to a reduction in stroke volume and systolic impairment The severely dilated ventricles have a low wall thickeness to diametre ratio -> leading to significant increase in ventricular wall stress and O2 demand which further impairs systolic function (LaPlaces Law) Clinical features depend on degree of systolic dysfunction May be asymptomatic initially Progressing to heart failure Emobolic events and sudden death may occur in later stages Diagnosis TTE - EF < 45%, fractional shorterning <25% LVEDD >117% predicted Increased sphericity of LV (length/diameter ratio) Diastolic dysfunction (poor prognosis) Tricuspid annular prox systolic excursion <14mm, -> RV dysfucntion and poor prognosis MR if frequntly seen - cause or consequnce. Managment Control Symptoms , prevent progression Perioperative High Post Op Mortality Risk of arrhythmias , CCF, embolic events 1. continue all meds, and heart failure symtoms optimised. 2. arrhythmias should be treated before operation via drug therpay or implantation device - rate/rhythm 3. TTE - severity and valvular. Anaesthesia 1. Avoid myocardial depression 2. Maintain preload, prevent increases in afterload 3.Avoid Tachycardia 4.Prevent sudden hypotension Regional Peripheral nerve blocks - minimal haemdynamic changes CNB - reduces afterload and improves CO but resulting myocardial hypotension must be prevented. GA Gentle induction - increased circulation time Avoid ketamine as causes increase in SVR Propofol negative ionotrope but does drop SVR Opioids minimal cardiovascular effects and reduce requirement of induction agents. All volatiles cause myocardial depression in high doses. Monitoring - IAL , consider TOE Cardiovascular Support Can use norad for hypotension but care with increasing afterload. Biventricular pacing and IABP Post OP HDU/ICU - optimise haemodynamics and fluid therapy Adequate analgesia reduces deletrious effects of increased svr Poor predictors EF <20% elevated LVEDP LV hypokinesis Non sustrained VT
What are the indications for Deep Hypothermic Cardiac Arrest
Cardiac: Aortic Surgery (complex arch work), pulmonary thromboendarterectomy, complex congenital surgery
Neurological: Cerebral aneurysms, AVMs
Other: RCC with caval invasion, other tumours with caval invasion
Adverse effects with DHCA
DHCA - method of cerebral protection
Safe time 30mins
CVS: arrthymias second to K+ loss, increased plasma viscosity , vasoconstriction impairing microcirculation,
Coag: impaired coagulation, reduced platelet count
Renal and Metabolic: reduced GFR, metabolic acidosis
hyperglycaemia due to impaired glucose metabolism,
effects on PD and PK of drugs (variable)
Cerebral: Vasoconstriction during cooling
Brain injury from hyperthermia during rewarming.
Why do we use DHCA
What are the other options for cerebral protection
Excellent operating conditions
reduce the consequences of organ ischaemia - particularly cerebral.
Safe period is 30mins at 18-20 degrees
Other options for cerbral protections
Pharmacological
Glucose control
Acid-Base management
Haemodilution
Discuss alpha stat vs ph stat.
Solubility of gases changes with temperature. AS temperature decreases solubility INCREASES.
ABG during hypothermia reveals alkalosis, reduced Pa02, PaCO2
Alpha stat (uncorrected temp 37*) - maintain “normal “ PaCo2
pH stat (temp corrected) - maintain a normal pH no matter the CO2 ( usually done by adding CO2 to CPB sweep gas)
alpha stat @ mild - mod hypothermia maintains CBF /CMRO2 coupling where as pH stat progressively obtunds cerebral autoregulation and cerebral blodd becomes pressure passive.
THe Ph stat leads to increased cerebral oxygen deliery to the brain and is thought to give more even cerebral cooling at the expense of more microemboli delivered to the brain.
No evidence of superiority of one technique over another.
Some animal models so ph stat better histologically during COOLING>
Discuss Cerebral Protection DHCA
Haemodilution - as temp decreases - increased plasma viscosity erthyrocyte rigidity and vasoconstruction - impairs mircocirculation - to counter this haemodilute to Hct 20% thought to improve flow (<10% not enough 02 delivery)
Pharmacological
STP /Propofol decrease CMRO2 - no evidence that either drug improves neurological outcome.
Glycaemic Control
evidence that hyperglycaemia during hypothermia worsens impact of ischaemia through increased glycolysis and intracellular acidosis.
Surgical Techniques
Retrograde Cerebral Perfusion and Selective antegrade cerebral protection.
Post Op Care
Avoid hyperthermia
avoid hypotension / hypoxiaemia
