Cardiovascular Flashcards
Define chronotropy, inotropy, dromotropy and lusitropy
Chronotropy: heart rate
Inotropy: strength of contraction
Dromotropy: conduction velocity
Lusitropy: rate of myocardial relaxation (during diastole)
Describe the function of the sodium-potassium pump.
the sodium-potassium pump maintains the cell’s resting potential. Said another way, it separates the charge across the cell membrane keeping the inside of the cell relatively negative and the outside of the cell relatively positive.
How it works:
* it removes the Na+ that enters the cell during depolarization
* it returns K+ that has left the cell during repolarization
* For every 3 Na+ ions it removes, it brings 2 K+ ions into the cell
List the 5 phases of the ventricular action potential, and describe the ionic movement during each phase
Phase 0: Depolarization -> Na+ influx
Phase 1: Initial repolarization -> K+ efflux & Cl- influx
Phase 2: Plateau -> Ca +2 influx
Phase 3: Repolarization -> K+ efflux
Phase 4: Na+/K+ pump restores resting membrane potential
List the 3 phases of the SA node action potential, and describe the ionic movement during each phase.
Phase 4: Spontaneous depolarization -> leaky to Na+ (Ca+2 influx occurs at the very end of phase 4)
Phase 0: Depolarization -> ca +2 influx
Phase 3: Repolarization -> K+ efflux
What process determines the intrinsic heart rate, and what physiologic factors alter it?
The rate of spontaneous phase 4 depolarization in the SA node determines heart rate.
We can increase HR by manipulating 3 variables:
* the rate of spontaneous phase 4 depolarization increases (reaches TP faster)
* TP becomes more negative (shorter distance between RMP and TP)
* RMP becomes less negative (shorter distance between RMP and TP)
When RMP and TP are close, it’s easier for the cell to depolarize
When RMP and TP are far, it’s harder for the cell to depolarize
MAP calculation
MAP = (2x Diastolic) + systolic/3
or ((COxSVR)/80)+CVP
normal 70-107 mmHg
What is the formula for systemic vascular resistance
((MAP-CVP)/CO)X 80
Normal: 800-1500 dynes/sec/cm-5
like all of these calculations, you’ll see the normal values vary from book to book
What is the equation for pulmonary vascular resistance?
((MPAP-PAOP)/CO)x 80
Normal 150-250 dynes/sec/cm-5
Describe the Frank-Starling relationship
describes the relationship between ventricular volume (preload) and ventricular output (cardiac output)
* Increased preload -> increased myocyte stretch -> ventricular output
* decreased preload-> decreased myocyte stretch -> ventricular output
Increasing preload increases ventricular output, but only up to a point. To the right of the plateau, additional volume overstretches the ventricular sarcomeres, decreasing the number of cross-bridges that can be formed and ultimately reducing cardiac output. This contributes to pulmonary congestion and increases PAOP.
What factors affect myocardial contractility
Contractility (inotropy) describes the contractile strength of the heart.
Just remember that Chemicals affect Contractility-particularly Calcium (C’s)
Most examples in the table either alters the amount of Ca+2 available to bind to the myofilaments or impacts the sensitivity of the myofilaments to Ca+2
increased contractility: SNS stimulation, catecholamines, calcium, digitalis, phosphodiesterase inhibitors
Decreased contractility: myocardial ischemia, severe hypoxia, acidosis, hypercapnia, hyperkalemia, hypocalcemia, volatile anesthetics, propofol, beta-blockers, calcium channel blockers
Discuss excitation-contraction coupling in the cardiac myocyte
- an action potential is propagated from an adjacent cell.
- depolarization of the T-tubule opens voltage-gated L-type Ca channels. Ca enters the myocyte. This occurs during phase 2 of the action potential
- The influx of Ca activates the ryanodine-2 receptor (RyR2)
- Ca+ is released from the sarcoplasmic reticulum. This is called calcium-induced calcium- release
- Ca binds to troponin C . This stimulates cross-bridge formation and causes myocardial contraction
- Ca unbinds from troponin C. this causes myocardial relaxation
- Most of the calcium is returned to the sarcoplasmic reticulum via the SERCA 2 pump (ATP dependent). Once inside, Ca binds to a storage protein called calsequestrin (CSQ)
- Some calcium is removed from the myocyte by the sodium/calcium exchange pump (NCX)
- The Na/K-ATPase restores resting membrane potential
*the duration of contraction is determine by the action potential duration
What is afterload, and how do you measure it in the clinical setting?
Afterload is the force the ventricle must overcome to eject its stroke volume.
In the clinical setting, we use the systemic vascular resistance as a surrogate for LV afterload.
What law can be used to describe ventricular afterload?
We can apply the law of Laplace to better understand ventricular afterload
Wall stress + (intraventricular pressure x radius)/ ventricular thickness
* intraventricular pressure is the force that pushes the heart apart
* wall stress is the force that hold the heart together (it counterbalances intraventricular pressure)
Wall stress is reduced by:
* Decreased intraventricular pressure
* decreased radius
* Increased wall thickness
List 2 conditions that set afterload proximal to the systemic circulation
Aortic stenosis, coarctation of the aorta
Use the wiggers diagram to explain the cardiac cycle
Pay attention to the following:
* where systole and diastole occur
* 6 stages of the cardiac cycle
* 4 pressure waveforms
* how the pressure waveforms match up to the EKG
* how the valve position changes match up to the EKG
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
you can measure SV, and EDV
How do you calculate ejection fraction
The ejection fraction is a measure of systolic function (contractility). It is the percentage of blood ejected from the heart during systole. Said another way, the EF is the stroke volume relative to end-diastolic volume.
Amount of blood pumped out of the ventricle/total amount of blood in ventricle x 100= EF%
>50% normal
41-49%- mild dysfunction
26-40%- moderate dysfunction
<25% severe dysfunction
(Stroke volume/End-diastolic volume) x 100
- SV is calculated as: EDV-ESV
what is the best TEE view for diagnosing myocardial ischemia?
midpapillary muscle level in short axis.
What is the equation for coronary perfusion pressure?
Coronary perfusion pressure = Aortic DBP- LVEDP
* Aortic DBP is the pushing force
*LVEDP is the resistance to the pushing force
therefore, increasing AoDBP or decreasing LVEDP (PAOP) improves CPP.
Which region of the heart is most susceptible to myocardial ischemia? Why?
The LV subendocardium is most susceptible to ischemia.
The LV subendocardium is best perfused during diastole. As aortic pressure increases, the LV tissue compresses its own blood supply and reduces blood flow. The high compressive pressure in the LV subendocoardium coupled with a decreased coronary artery blood flow during systole increases coronary vascular resistance and predisposes this region to ischemia.
What factors affect myocardial oxygen supply and demand?
Factors that reduce oxygen delivery:
* Decreased coronary flow- tachycardia, decreased aortic pressure, decreased vessel diameter (spasm or hypocapnia), increased end diastolic pressure
* Decreased CaO2- hypoxemia, anemia
* Decreased Oxygen extraction- Left shift of Hgb dissociation curve (decreased P50), decreased capillary density
Factors that increase Oxygen Demand:
Tachycardia, HTN, SNS stimulation, increased wall tension, increased end diastolic volume, increased afterload, increased contractility
discuss the nitric oxide pathway of vasodilation
Nitric oxide is a smooth muscle relaxant that induces vasodilation.
Steps in the nitric oxide cGMP pathway:
* nitric oxide synthase catalyzes the conversion of L-arginine to nitric oxide.
*nitric oxide diffuses from the endothelium to the smooth muscle,
* Nitric oxide activates guanylate cyclase.
*Guanylate cyclase converts guanosine triphosphate to cyclic guanosine monophosphate
* increased cGMP reduces intracellular calcium, leading to smooth muscle relaxation
* Phosphodiesterase deactivates cGMP to guanosine monophosphate (this step turns off the NO mechanism)
Where do the heart sounds match up on the left ventricle pressure volume loop?
S3: May suggest heart failure
S4: May suggest decreased ventricular compliance
Notice the MV opens/closes on the bottom of the loop, and the AV open/closes on the top of the loop
What are the two primary ways a heart valve can fail?
Stenosis:
* there is a fixed obstruction to forward flow during chamber systole
* the chamber must generate a higher than normal pressure to eject the blood
Regurgitation:
* the valve is incompetent (it’s leaky)
* Some blood flows forward, and some blood flows backward during chamber systole
How does the heart compensate for pressure overload? Volume overload?
Aortic valve stenosis (systole)- Pressure overload concentric hypertrophy - sarcomeres added in parallel
Aortic valve regurgitation (Diastole)- Volume overload eccentric hypertrophy- sarcomeres added in series
List the hemodynamic goals for the 4 common valvular defects
Aortic Stenosis-Full, slow, and constricted
Aortic Regurgitation- Full, Fast, and Forward
Mitral Stenosis- Slower, Maintain, maintain
Mitral regurgitation- Full, fast, forward
What is the most common dysrhythmia associated with mitral stenosis?
Atrial fibrillation
List 6 factors for perioperative cardiac morbidity and mortality for non-cardiac surgery.
- High-risk surgery
- History of ischemic heart disease (unstable angina confers the greatest risk of perioperative MI)
- History of CHF
- History of cerebrovascular disease
- DM
- Serum creatinine >2 mg/dL
What is the risk of perioperative myocardial infarction in the patient with a previous MI?
Risk of perioperative MI in the patient with previous MI:
* General population = 0.3%
* MI if >6 months =6%
* MI if 3-6 months= 15%
*MI <3 months = 30%
the highest risk of reinfarction is greatest within 30 days of an acute MI. For this reason, the ACC/AHA guidelines recommend a minimum of 4-6 weeks before considering elective surgery in a patient with a recent MI.
Categorize high, medium, and low risk surgical procedures according to cardiac risk.
AHA/American College of Cardiology Guidelines Based on Surgical Procedure
High (risk >5%):
* emergency surgery (especially in the elderly)
* Open aortic surgery
* Peripheral vascular surgery
* Long surgical procedures with significant volume shifts and/or blood loss
Intermediate (risk 1-5%):
* Carotid endarterectomy
* head and neck surgery
* Intrathoracic or intraperitoneal surgery
* orthopedic surgery
* prostate surgery
Low (risk <1%)
* Endoscopic procedures
* Cataract surgery
*superficial procedures
*breast surgery
* ambulatory procedures
How do you interpret cardiac enzymes in the patient with a suspected ischemic event?
A cell requires oxygen to maintain the integrity of its cell membrane, and a cell deprived of oxygen dies and releases its contents into the systemic circulation
* infarcted myocardium releases 3 key biomarkers: creatine kinase-MB, troponin I, and Troponin T
* Cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction
* These values must be evaluated in the context of the time of the patient’s EKG
How do you treat intraoperative myocardial ischemia?
Treatment of myocardial ischemia should focus on interventions that make the heart slower, smaller, and better perfused.
What factors reduce ventricular compliance?
The diastolic pressure-volume relationship is affected by:
* Age >60
* Ischemia
* Pressure overload hypertrophy (aortic stenosis or HTN)
* Hypertrophic obstructive cardiomyopathy (familial)
* pericardial pressure (increased external pressure)
The clinical take away is that priming the ventricle requires higher filling pressures
What is the difference between HFrER (systolic) and HFpEF (diastolic) heart failure?
HF with reduced ejection fraction (HFREF)- the Ventricle Doesn’t Empty Well
*the hallmark of systolic heart failure is a decreased ejection fraction with an increased end-diastolic volume. Volume overload commonly causes systolic dysfunction.
HF with preserved ejection fraction (HFpEF) - The Ventricle Doesn’t Fill Properly
* Diastolic failure occurs when the heart cannot relax and accept the incoming volume because ventricular compliance is reduced. The defining characteristic of diastolic dysfunction is symptomatic heart failure with normal ejection fraction
Compare the contrast the hemodynamic goals in the patient with HFrEF vs HFpEF.
What is the modified New York Association Functional Classification of Heart Failure?
Class 1: Asymptomatic
Class 2: Symptomatic with moderate activity
Class 3: Symptomatic with mild activity
Class 4: Symptomatic at rest
List 6 complications of HTN.
The problem with HTN is a high afterload that increases myocardial work and an elevated arterial driving pressure damages nearly every organ in the body.
* Left ventricular hypertrophy
* Ischemic heart disease
* Congestive heart failure
* Arterial aneurysm (aorta, cerebral circulation)
* Stroke
*End-stage renal disease
How does HTN affect cerebral autoregulation?
The cerebral autoregulation curve describes the range of blood pressures where cerebral perfusion pressure remains constant.
Chronic HTN shifts this curve to the right. This adaptation helps the patient’s brain tolerate a higher range of blood pressures; howver, this comes at the expense of not tolerating a lower blood pressure. Remember that BP past the range of autoregulation is pressure dependent.
* Malignant hypertension increases the risk of hemorrhagic stroke and cerebral edema
* HoTN increases the risk of cerebral hypoperfusion
As an aside, the texts would lead to believe that the width of the curve remains the same in the hypertensive patient; there is good evidence that the width of the curve (range of autoregulation) becomes narrower
What’s the difference between primary and secondary HTN?
Primary (essential) HTN is more common and has no identifiable cause (95% of all HTN cases)
Secondary HTN is caused by some other pathology (5% of all HTN cases)
List 7 causes of secondary HTN
- coarctation of the aorta
- renovascular disease
- hyperadrenocorticism (cushing’s disease)
- Hyperaldosteronism (Conn’s disease)
- Pheochromocytoma
- pregnancy-induced HTN
What are the 2 major classes of calcium channel blockers? list examples of each
Describe the pathophysiology of constrictive pericarditis
Constrictive pericarditis is caused by fibrosis or any condition where the pericardium becomes thicker.
During diastole, the ventricles cannot fully relax, and this reduces compliance and limits diastolic filling. Ventricular pressures increase, which creates backpressure to the peripheral circulation. The ventricles adapt by increasing myocardial mass, but over time this impairs systolic function
Describe the anesthetic management of constrictive pericarditis
CO is dependent on HR.
* Avoid bradycardia
Preserve HR and contractility.
*Ketamine
*Pancuronium
* Volatile agents with caution
*Opioids, benzodiazepines, and etomidate are okay
Maintain afterload
Aggressive PPV can decrease venous return and CO
Describe the pathophysiology of pericardial tamponade
Cardiac tamponade occurs when fluid accumulates inside the pericardium. What separates it from a pericardial effusion is that the excess fluid exerts external pressure on the heart, limiting its ability to fill and act as a pump
CVP rises in tandem with pericardial pressure. As ventricular compliance deteriorates, left and right sided cardiac diastolic pressure (CVP and PAOP) begin to equalize. TEE is the best method of diagnosis, and the best treatment is pericardiocentesis or pericardiostomy
What is Kussmaul’s sign
Kussmaul’s sign indicates impaired right ventricular filling due to poorly compliant RV or pericardium. Since RV filling is affected, the blood essentially “backs up”, which causes jugular venous distention and an increased CVP. It is most pronounced during inspiration
List 2 conditions commonly associated with Kussmaul’s sign.
Although it can occur with any condition limiting RV filling, make sure you associate Kussmaul’s sign with constrictive pericarditis and pericardial tamponade
What is pulsus paradoxus?
Pulsus paradoxus represents an exaggerated decrease in SBP during inspiration (SBP falls by more than 10mmHg during inspiration). This finding suggests impaired diastolic filling.
* negative intrathoracic pressure on inspiration -> increased venous return to RV -> bowing of ventricular septum toward LV-> decreased SV-> Decreased CO-> SBP
List 2 conditions commonly associated with pulsus paradoxus
Like kussmaul’s sign, you should also associate pulsus paradoxus with constrictive pericarditis and pericardial tamponade
What is Beck’s triad? what conditions are associated with it?
Beck’s triad occurs in the patient with acute cardiac tamponade.
Signs include:
* HoTN (decreased SV)
*JVD (impaired venous return to the right heart)
* Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)
What are the best anesthetic techniques for the patient with acute pericardial tamponade undergoing pericardiocentesis?
Because hemodynamics are minimally affected, local anesthesia is the preferred technique for pericardiocentesis.
If a general anesthetic is required, your primary goal is to preserve myocardial function. Severely decreased SV and increased SNS tone (increased contractility and increased afterload) provide compensation. Any drug that depresses the myocardium or reduces afterload can precipitate a cardiovascular collapse.
Drugs to avoid: Halogenated anesthetics, propofol, thiopental, high dose opioids, neuraxial anesthesia
Drugs that are safer to use: Ketamine (activation of the SNS makes this the best choice), nitrous oxide, benzodiazepines, opioids
List 7 patient factors that warrant antibiotic prophylaxis against infective endocarditis.
The following conditions are associated with the highest risk for developing infective endocarditis:
* previous infective endocarditis
* prosthetic heart valve
* Unrepaired cyanotic heart defect , or if the repair is < 6 months old
* Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site
* Heart transplant with valvuloplasty
List 3 surgical procedures that warrant antibiotic prophylaxis against infective endocarditis.
High-risk procedures are thought to be “dirty” procedures where the risk of transient bacteremia outweighs the risk of antibiotic therapy
* Dental procedures involving gingival manipulation and/or damage to mucosa lining
* respiratory procedures that perforate the mucosal lining with incision or biopsy
* Biopsy of infective lesions on the skin or muscle
What are the 3 key determinants of flow through the left ventricular outflow tract?
Systolic LV volume
Force of LV contraction
Transmural pressure gradient
What factors reduce cardiac output in the patient with obstructive hypertrophic cardiomyopathy?
Things that distend the left ventricular outflow tract (LVOT) are good for cardiac output, while things that narrow the LVOT are bad.
How long should elective surgery be delayed in the patient after a percutaneous coronary intervention?
Previous intervention duration to wait for elective
Angio without stent: 2-4 weeks
Bare metal stent: 30 days (3 months preferred)
Drug eluting stent:
*stable ischemic heart dx -first gen DES= 12 months
- current gen DES= 6 mths
*Acute coronary syndrome 12 months min
CABG 6 weeks (3 months preferred)
This chart reflects the changes for DES included in the 2016 ACC/AHA guidelines. The old guidelines said a minimum of 12 months for all drug-eluting stents
What is the difference between alpha-stat and pH-stat blood gas measurement during cardiopulmonary bypass?
because the solubility of a gas is a function of temperature. it should make sense that hypothermia complicates out interpretation of blood gas results during CPB. As temperature decreases, more CO2 will dissolve in the blood. By extension, this affects the pH. Knowing this poses an interesting question about how best to manage blood pH during CBP with hypothermia. Should the temperature of the sample be correct or not?
- Alpha-set- does not correct the pts temp. This technique aims to keep intracellular charge neutrality across all temperature. It is associated with better outcomes in adults.
- pH-stat- corrects the pts temperature. This technique aims to keep a constant pH across all temperature. It is associated with better outcomes in peds.
Why is left ventricular vent used during CAPB
A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt)
