Cardiovascular Flashcards
Define the terms: chronotropy inotropy dromotropy lusitropy
- chronotropy: heart rate
- inotropy: contractility
- dromotropy: conduction velocity (how fast action potential travels per time)
- lusitropy: rate of myocardial relaxation (during diastole)
Describe the function of the Sodium-Potassium pump
- it maintains the cells resting membrane potential
- keeps the inside of the cell negative relative to the outside (outside is positive)
- it removes the Na that entered the cell during depolarization and replaces the K that left the cell during repolarization
- takes out 3 Na ions and puts back 2 K ions
List the 5 phases of the ventricular action potential
- Phase 0: Depolarization - Na influx
- Phase 1: Initial repolarization: K efflux and Cl influx
- Phase 2: Plateau phase: Ca influx (slow)
- Phase 3: Repolarization: K efflux
- Phase 4: Na/K Pump restores RMP
List the 3 phases of the SA node action potential
- Phase 4: Spontaneous depolarization- leaky to Na (Ca influx at the very end of phase 4)
- Phase 0: Depolarization - Ca influx
- Phase 3: Repolarization- K efflux
What process determines the intrinsic heart rate?
What physiologic factors alter it?
- rate of spontaneous phase 4 depolarization of the SA node
- can increase heart rate by manipulating 3 variables:
- rate of phase 4 increases (reaches TP sooner)
- TP becomes more negative (shorter distance to RMP)
- RMP becomes more positive (shorter distance to TP)
- when RMP and TP are close it is easier for the cell to depolarize
- when RMP and TP are further apart it is harder for the cell to depolarize
Equation for MAP
SBP + 2(DBP) / 3
[(CO x SVR) / 80] + CVP
Equation for SVR
[(MAP - CVP) / CO] x 80
norm: 800-1500 dynes/sec/cm
Equation for PVR
[(PMAP - PAOP) / CO] x 80
norm: 150-250 dynes/sec/cm
Describe Frank-Starling
- relationship between ventricular volume (preload) and ventricular output (cardiac output)
- increased preload = increased myocyte stretch = increased cardiac output
- decreased preload = decreased myocyte stretch= decreased cardiac output
- increased preload causes an increased CO to a certain point. After that additional volume overstretches the sarcomeres, decreases number of crossbridges and reduces cardiac output. Leads to pulmonary congestion and increases PAOP
What factors cause increased myocardial contractility?
- SNS stimulation
- catecholamines
- calcium
- digitalis
- phosphodiesterase inhibitor
What factors cause decreased myocardial contractility? (labs, drugs, ect.)
- myocardial ischemia
- severe hypoxia
- hypercarbia
- hyperkalemia
- hypocalcemia
- volatile anesthetics
- propofol
- beta blockers
- calcium channel blockers
Excitation-contraction coupling in the cardiac myocyte
- action potential causes cell to depolarize
- During plateau phase (2), Ca+ enters the myocyte through the L-type Ca+ channels in the t-tubules
- Ca+ influx turns on ryanodine receptor which then causes calcium release from the SR (Ca-induced Ca-released)
- Ca+ binds to troponin C (contraction)
- Ca+ unbinds from troponin C (relaxation)
- Ca+ goes back to SR via SERCA2 pump
- Ca+ that is in the SR binds to storage protein calsequestrin
What is afterload and how do you measure it in the clinical setting?
- the force the ventricle must overcome to eject its stoke volume
- measured by SVR
What law can be used to describe ventricular afterload?
wall stress = (intraventricular pr. x radius)/ ventricular thickness
- intraventricular pressure is the force that pushes the heart apart
- wall stress is the force that holds the heart together
How is wall stress reduced?
- decreased intraventricular pressure
- decreased radius
- increased wall thickness
Three conditions that set afterload proximal to the systemic circulation
- aortic stenosis
- hypertrophic cardiomyopathy
- coarctation of the aorta
Use the Wiggers diagram to explain the cardiac cycle
- starts with both atrial and ventricular pressures close to zero
- atrium is getting filled from pulmonary circulation
- atrial pressure is slightly higher so blood enters ventricle through MV and increases ventricular volume
- aortic pressure is high at the top but falling
- atria depolarizes and contracts
- blood enters ventricle through MV and increases ventricular volume and pressure
- ventricle depolarizes and contracts = shuts MV valve
- MV and AV are closed = isovolumetric contraction
- ventricular pressure rises but volume stays the same
- increased ventricular pressure causes a tug on MV valve when it closes = quick jump in atrial pressure
- ventricular pressure rises fast and opens AV
- increase in aortic pressure (blood flows in) and ventricular pressure still increased (being actively stretched)
- tug on MV valve is released = drop in atrial pressure
- atrial pressure starts to rise as it gets blood back from the lungs
- aortic and ventricular pressure fall = ventricular relaxation
- ventricular pressure falls faster and AV slams shut
- causes back flow of blood = dicrotic notch
- both valves closed = isovolumetric relaxation
- ventricular and aortic pressure continue to fall and blood flows to systemic circulation
- atrial pressure exceeds ventricular as it is filled with blood from the lungs and the MV valve will open again
Relate the 6 stages of the cardiac cycle to the LV pressure-volume loop
- rapid filling = diastole
- reduced filling = diastole
- atrial kick = diastole
- isovolumetric contraction = systole
- ejection = systole
- isovolumetric relaxation = diastole
Ejection Fraction Calculation
EF = EDV - ESV / EDV x 100
- EF is mesure of systolic function (contractility)
- is the percentage of the blood that is ejected during systole
- normal EF = 60-70%
- LV dysfunction when EF < 40%
Best TEE view for diagnosing MI
mid papillary muscle level in short axis
Equation for coronary perfusion pressure
CPP = AoDBP - LVEDP
LVEDP = PAOP = Diastolic PA pressure
- CPP can be improved by increasing AoDBP or decreasing LVEDP
What region of the heart is most susceptible to ischemia?
- LV subendocardium
- as aortic pressure increases, the LV tissue compresses the subendocardium and reduces blood flow
- the high compressive pressure and decreased coronary blood supply during systole increases coronary vascular resistance and can lead to ischemia
What factors cause decreased myocardial oxygen delivery?
DECREASED CORONARY FLOW - tachycardia - decreased aortic pressure - decreased vessel diameter - increased end diastolic pressure DECREASED CaO2 - hypoxemia - anemia DECREASED OXYGEN EXTRACTION - left shift of Hgb dissociation curve (decrease P50) - decreased capillary density
What factors cause increased myocardial oxygen demand?
- tachycardia
- HTN
- SNS stimulation
- increased wall tension
- increased EDV
- increased afterload
- increased contractility
Nitric oxide pathway of vasodilation
- nitric oxide synthase converts L-arginine to nitric oxide
- NO diffuses from endothelium into smooth muscle
- NO activates guanylate cyclase
- guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate (cGMP)
- cGMP reduces intracellular Ca, causing smooth muscle relaxation
- phosphodiesterase deactivates cGMP
Where are the heart sounds on the LE pressure-volume loop?
S1: at closure of MV (and tricuspid) = onset of systole
S2: at closure of AV (and pulmonic) = onset of diastole
S3: could be heard during early ventricular filling = may be systolic dysfunction
S4: could be heard at late filling just before MV closes = may be diastolic dysfunction
What are the two primary ways a heart valve can fail?
- stenosis
- fixed obstruction to froward flow; must generate higher pressures
- regurgitation
- valve is leaky and some blood flows forward and backward
Heart’s pressure compensation
- concentric hypertrophy results from pressure overload
- sarcomeres are added in parallel
Heart’s volume overload compensation
- eccentric hypertrophy results from volume overload
- sarcomeres are added in series
Hemodynamic goals for aortic stenosis
slow, skinny, normal
- increase preload
- maintain or increase SVR (CO depends on BP since SV is fixed at the stenotic valve)
Hemodynamic goals for aortic regurgitation
fast, full, forward
- increase preload
- decrease SVR
Hemodynamic goals for mitral stenosis
slow, full, constricted
- maintain normal preload, SVR and contractility
- avoid increases in PVR
Hemodynamic goals for mitral regurgitation
fast, full, forward
- increase preload
- decrease afterload
- avoid increase in PVR
Most common dysrhythmia associates with mitral stenosis?
Atrial fibrillation
Six risk factors for preoperative cardiac morbidity and mortality for non-cardiac surgery
- high risk surgery
- Hx of ischemic heart disease
- Hx of CHF
- Hx of cerebrovascular disease
- DM
- creatinine > 2 mg/dL
Risk of preoperative MI in the pt with a previous MI
- general population = 0.3%
- if MI > 6 mo = 6%
- if MI 3-6 mo = 15%
- IF MI < 3 mo = 30%
When is the highest risk of reinfarction after an acute MI?
within 30 days
*recommended to wait minimum of 4-6 weeks before elective surgery in patient with a recent MI
High cardiac risk surgical procedures
- emergency surgery (esp. elderly)
- open aortic surgery
- peripheral vascular surgery
- long surgeries with lots of blood loss
Intermediate risk cardiac surgical procedures
- carotid
- head and neck surgery
- intrathoracic or intraperitoneal surgery
- orthopedic surgery
- prostate surgery
Low cardiac risk procedures
- endoscopic
- cataracts
- superficial procedures
- breast surgery
- ambulatory procedures
Modified New York Association Functional Classification of Heart Failure
- class I: asymptomatic
- class II: symptomatic with moderate activity
- class III: symptomatic with mild activity
- class IV: symptomatic at rest
Biomarkers released by infarcted myocardium
- creatine kinase- MB
- troponin I
- troponin II
- troponins are more sensitive
Creatine Kinase- MB: initial elevation, peak, return to baseline
- initial: 3-12 hrs
- peak: 24 hrs
- baseline: 2-3 days
Troponin I: initial elevation, peak, return to baseline
- initial: 3-12 hrs
- peak: 24 hrs
- baseline: 5-10 days
Troponin II: initial elevation, peak, return to baseline
- initial: 3-12 hrs
- peak: 12-48 hrs
- baseline: 5-14 days
Treatment of intra-op MI
- caused by increased O2 demand or decreased O2 supply
- increased demand (high HR, BP, PAOP): give beta blocker, increase gas, vasodilator, Nitroglycerine
- decreased supply (low HR and BP, hight PAOP): give anticholinergic, pace, decrease gas, vasoconstrictor, nitro, inotrope
- nitroglycerine decreases PAOP
What factors reduce ventricular compliance?
- age > 60
- ischemia
- pressure overload hypertrophy (AS or HTN)
- hypertrophic obstructive cardiomyopathy
- pericardial pressure
Systolic Heart Failure and hallmark symptoms
- ventricle can’t empty/squeeze well
- hallmark: decreased EF with increased EDV
- caused by volume overload
Diastolic Heart Failure
- ventricle can’t fill properly because it is unable to relax (decreased vent compliance)
- hallmark: symptomatic heart failure with normal EF
Hemodynamic goals for systolic heart failure
- preload: already high (give diuretics if too high)
- afterload: decrease to reduce workload
- contractility: use inotropes as needed (dobutamine)
- heart rate: usually high d/t increased SNS tone; if EF is low then a higher HR is needed to preserve CO
Hemodynamic goals for diastolic heart failure
- preload: maintain/increase (volume needed to stretch noncompliant ventricle
- afterload: elevated to perfuse thick myocardium
- contractility: usually normal
- heart rate: slow/normal to increase filling time
Six complications of HTN
- left ventricular hypertrophy
- ischemic heart disease
- CHF
- arterial aneurysm (aorta, cerebral circus)
- stroke
- end-stage renal disease
How does HTN cause CHF
- HTN increases myocardial wall tension
- increased wall tension causes increased MVO2 and left ventricular hypertrophy
- LVH leads to diastolic CHF
- increased MVO2 causes coronary insufficiency leading directly to CHF and/or infarction dysrhythmias which go on to cause CHF
How does HTN affect cerebral autoregulation?
- shifts the curve to the right allowing the brain to tolerate higher pressures
- also makes the brain not able to tolerate lower pressures
- BP past the zone of autoregulation is pressure dependent
Primary vs. secondary HTN
- primary (essential) HTN has no identifiable cause (95% of cases)
- secondary HTN is caused by some other pathology (5% of cases)
Seven causes of secondary hypertension
- renal artery stenosis
- coarctation of the aorta
- hyperadrenocorticism (Cushing’s)
- hyperaldosteronism (Conn’s)
- pheochromocytoma
- pregnancy-induced HTN
Classes of calcium channel blockers
DIHYDROPYRIDINES: target vascular smooth muscle
- nicardipine
- nifedipine
- nimodipine
- amlodipine
NON-DIHYDROPYRIDINES: target myocardium
- verapamil
- diltiazem
Pathophysiology of constrictive pericarditis
- fibrosis or any condition that causes the pericardium to become thicker
- ventricles can’t fully relax during diastole which reduces compliance and limits filling
- causes back pressure to peripheral circulation
- ventricles compensate by increasing in mass
- over time systolic function becomes impaired
Anesthetic management of constrictive pericarditis
- avoid bradycardia: CO is dependent on HR
- preserve HR and contractility (ketamine, pancuronium, caution with gas)
- maintain afterload
- aggressive PPV can decrease venous return and CO
Pathophysiology of pericardial tamponade
- fluid accumulation in the pericardium that exerts external pressure on the heart decreasing its ability to fill and pump
- increased CVP with increasing pericardial pressures
- CVP and PAOP equalize as ventricular compliance deteriorates
Kussmal’s sign
- backing up of blood d/t impaired RV filling causing JVD and increased CVP
- is more pronounced during inspiration
Two common conditions associated with Kussmal’s sign
- constrictive pericarditis
- pericardial tamponade
Pulsus Paradoxus
- exaggerated decrease is SBP (more than 10 mmHg) during inspiration
- suggests impaired diastolic filling
- negative intrathoracic pressure on inspiration = increased VR to RV = bowing for ventricular septum towards LV = decreased SV, CO and SBP
2 conditions associated with pulses paradoxus
- constrictive pericarditis
- pericardial tamponade
Beck’s traid and what is it associated with
- JVD
- muffled heart tones
- hypotension
- associated with acute cardiac tamponade
Anesthesia for acute pericardial tamponade undergoing pericardiocentesis?
Drugs to use and drugs to avoid.
- local is preferred
- if general, need to preserve myocardial function
- SV is severely decreased, but increased SNS tone provides compensation
- avoid: gas, propofol, thiopental, high dose opioids, neuraxial
- safe to use: ketamine (best), N2O, Benzes, opioids
- any drug that depresses the myocardium decreases afterload and can cause CV collapse
Six patient factors that warrant abx prophylaxis agains infective endocarditis
- previous endocarditis infection
- unrepaired cyanotic heart disease
- prosthetic heart valve
- congenital heart repair less than six months ago
- repaired congenital heart with residual defects
- heart transplant with valvuloplasty
Three surgical procedures that warrant abx prophylaxis against infective endocarditis
- dental procedures with gingival manipulation
- respiratory procedures that perforate the mucosal lining
- biopsy of the invective lesions on the skin or muscle
Three determinants of LV outflow tract
- systolic LV volume
- force of LV contraction
- transmural pressure gradient
What factors reduce cardiac output in the patient with obstructive hypertrophic cardiomyopathy?
- hypovolemia (decreased systolic volume)
- hypotension (decreased Ao pressure)
- increased contractility
- goal is to distend the LVOT to decrease the obstruction and increase CO (increase systolic volume, decrease contractility, and increase Ao pressure)
What hemodynamic conditions reduce CO in patient with hypertrophic cardiomyopathy?
- increased HR (treat with B-blockers or CCBs)
- increased contractility (treat with B-blockers or CCBs)
- decreased preload (treat with volume)
- decreased afterload (treat with Neo)
How long should elective surgery be delayed in pt with bare metal stent?
Drug eluting stent?
Post CABG?
- bare metal stent: 30 days
- drug eluting stent
- stable ischemic heart disease = 12 mo for first gen and 6 mo for current gen
- acute coronary syndrome = 12 mo minimum
- s/p CABG: 6 weeks (3 mo preferred)
Alpha-stat vs pH-stat blood gas measurement during CPB
- alpha-stat: doesn’t account for pt temp when measuring blood gas/pH (better outcomes in adults)
- pH stat: corrects for the pt temp (better outcome in peds)
- decreased temp allows for more CO2 to dissolve in the blood
Why is a left ventricular vent used during CABG surgery?
removes blood from the LV (blood that comes from the thebesian veins and bronchial circulation)
How does intra-aortic balloon pump function throughout the cardiac cycle
DIASTOLE
- inflates during diastole to augment coronary perfusion
- inflation correlates with dicrotic notch
SYSTOLE
- deflates during systole to reduce afterload and improve CO
- deflation correlates with R wave on EKG
- IAoBP improves O2 supply and decreases O2 demand
Four contraindications to the intra-aortic balloon pump
- severe aortic insufficiency
- descending aortic disease
- severe PVD
- sepsis
Crawford classification of aortic aneurysms
Describes thoracoabdominal aneurysms
- type 1: all or most of descending thoracic and only upper of abdominal aorta
- type 2: all or most of descending thoracic and most of abdominal aorta
- type 3: lower only descending thoracic and most of abdominal aorta
- type 4: none of descending thoracic and most of abdominal aorta
Stanford classification of aortic dissection
- Type A: involves ascending aorta
- Type B: does not involve ascending aorta
DeBakey classification of aortic dissection
- Type 1: tear in ascending aorta and dissection along entire aorta
- Type 2: tear in ascending aorta and dissection only in ascending aorta
- Type 3: tear in proximal descending aorta
- 3a- dissection only in thoracic aorta
- 3b- dissection along thoracic and abdominal aorta
When is surgical correction for a AAA recommended?
- when the aneurysm exceeds 5.5 cm or if it grows more than 0.6-0.8 cm/year
How does aortic cross clamp contribute to the risk of anterior spinal artery syndrome?
- AoX clamp placed above artery of Adamkiewicz may cause ischemia to lower portion of spinal cord
- can result in anterior spinal syndrome (aka Beck’s syndrome)
How does anterior spinal syndrome present?
- flaccid lower extremities
- bowel and bladder dysfunction
- loss of temp and pain
- preserved touch and proprioception
What is amaurosis fugax?
- blindness in one eye that is a sign of impending stroke
- clot travels from internal carotid to ophthalmic artery
What information does EEG monitoring provide during a carotid endarterectomy?
- cortical electrical function (no subcortical)
- risk of cerebral hypo perfusion with loss of amplitude, decreased beta wave, and/or slow wave activity
Causes of false-negatives with EEG monitoring
Increased frequency
- mild hypercarbia
- early hypoxia
- seizure activity
- ketamine
- N2O
- Light anesthesia
Decreased frequency
- extreme hypercarbia
- hypoxia
- cerebral ischemia
- hypothermia
- anesthetic overdose
- opioids
Regional technique that is used for a carotid and what levels must be blocked
- cervical plexus block (superficial or deep)
- local infiltration
- C2-C4 must be blocked
What reflex can be activated during a carotid endarterectomy?
baroreceptor reflex
what needs to be done if post-op carotid develops hematoma that causes airway compromise?
- emergency decompression of surgical site
- cricothyroidotomy if surgeon isn’t immediately available
