Apex Unit 3 Flashcards Cardiac
Define the following terms: chronotropy, inotropy, dromotropy, and lusitropy.
Chronotropy = Heart rate
Inotropy = Strength of contraction (contractility)
Dromotropy = Conduction velocity (how fast the action potential travels per time)
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 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. see photo
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 SEE PHOTO
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 SEE PHOTO
What process determines the intrinsic heart rate, and what physiologic factors alter it?
Heart rate is determined by the rate of spontaneous phase 4 depolarization in the SA node. 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. SEE PHOTO
What is the formula for pulmonary vascular resistance?
[(MPAP - PAOP) / CO] x 80 Normal = 150 - 250 dynes/sec/cm^5
List 3 conditions that set afterload proximal to the systemic circulation.
- Aortic stenosis 2. Hypertrophic cardiomyopathy 3. Coarctation of the aorta
How do you calculate ejection fraction?
The ejection fraction is a measure of systolic function (contractility). It is the percentage of blood that is ejected from the heart during systole. Said another way, the EF is the stroke volume relative to the end-diastolic volume. (Stroke volume / End-diastolic volume) x 100 Normal EF = 60 - 70% LV dysfunction is present when EF < 40% SV is calculated as: EDV - ESV
Describe the Frank-Starling relationship.
The Frank-Starling relationship describes the relationship between ventricular volume (preload) and ventricular output (cardiac output): ↑ preload → ↑ myocyte stretch → ↑ ventricular output ↓ preload → ↓ 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. SEE PHOTO
What factors affect myocardial contractility?
Contractility (inotropy) describes the contractile strength of the heart. Just remember that Chemicals affect Contractility - particularly Calcium. Nearly every example 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. SEE PHOTO
Discuss excitation-contraction coupling in the cardiac myocyte.
The myocardial cell membrane depolarizes. During the plateau of the ventricular action potential (phase 2), Ca+2 enters the cardiac myocyte through L-type Ca+2 channels in the T-tubules. Ca+2 influx turns on the ryanodine-2 receptor, which releases Ca+2 from the sarcoplasmic reticulum (this is called calcium-induced calcium-release). Ca+2 binds to troponin C (myocardial contraction). Ca+2 unbinds from troponin C (myocardial relaxation). Most of the Ca+2 is returned to the sarcoplasmic reticulum via the SERCA2 pump. Once inside the sarcoplasmic reticulum, Ca+2 binds to a storage protein called calsequestrin. The next time the cardiac myocyte depolarizes, the whole process repeats. SEE PHOTO
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. SEE PHOTO FOR EQUATIONS
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
What is the difference between systolic and diastolic heart failure?
Systolic Heart Failure – 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. Diastolic Heart Failure – The Ventricle Doesn’t Fill Properly Diastolic failure occurs when the heart is unable to relax and accept the incoming volume, because ventricular compliance is reduced. The defining characteristic of diastolic dysfunction is symptomatic heart failure with a normal ejection fraction.
List 6 complications of hypertension.
The problem with hypertension: A high afterload 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
What’s the difference between primary and secondary hypertension?
Primary (essential) hypertension is more common and has no identifiable cause (95% of all HTN cases). Secondary hypertension is caused by some other pathology (5% of all HTN cases).
List 7 causes of secondary hypertension.
Coarctation of the aorta Renovascular disease Hyperadrenocorticism (Cushing’s syndrome) Hyperaldosteronism (Conn’s disease) Pheochromocytoma Pregnancy-induced hypertension
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 a backpressure to the peripheral circulation. The ventricles adapt by increasing myocardial mass, but over time this impairs systolic function.
What is Kussmaul’s sign?
Kussmaul’s sign indicates impaired right ventricular filling due to a 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 that limits 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 10 mmHg during inspiration). This finding suggests impaired diastolic filling. Negative intrathoracic pressure on inspiration → ↑ venous return to RV → bowing of ventricular septum toward LV → ↓ SV → ↓ 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: Hypotension (decreased stroke volume) Jugular venous distension (impaired venous return to right heart) Muffled heart tones (fluid accumulation in the pericardial space attenuates sound waves)
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 congenital heart disease Repaired congenital heart defect 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 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 our interpretation of blood gas results during CPB. As temp decreases, more CO2 is able to dissolve in the blood. By extension, this affects the pH. Knowing this poses an interesting question about how to best manage blood pH during CBP with hypothermia. Should the temperature of the sample be corrected or not? Alpha-stat does not correct for the patient’s temperature. This technique aims to keep intracellular charge neutrality across all temperatures. It is associated with better outcomes in adults. pH-stat corrects for the patient’s temperature. This technique aims to keep a constant pH across all temperatures. It is associated with better outcomes in peds.
Why is a left ventricular vent used during CABG surgery?
A left ventricular vent removes blood from the LV. This blood usually comes from the Thebesian veins and bronchial circulation (anatomic shunt).
How does the intra-aortic balloon pump function throughout the cardiac cycle? How does it help the patient?
The intra-aortic balloon pump is a counter pulsation device that improves myocardial oxygen supply while reducing myocardial oxygen demand. Diastole: Pump inflation augments coronary perfusion. Inflation correlates with the dicrotic notch on the aortic pressure waveform. Systole: Pump deflation reduces afterload and improves cardiac output. Deflation correlates with R wave on the EKG.
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 holds the heart together (it counterbalances intraventricular pressure)
Wall stress is reduced by:
Decreased intraventricular pressure
Decreased radius
Increased wall thickness
A patient is undergoing carotid endarterectomy with EEG monitoring. What does this monitor tell you, and what conditions can lead to false conclusions?
Describe the DeBakey and Stanford classification systems of aortic dissection.
Describe the DeBakey and Stanford classification systems of aortic dissection.
Describe the Crawford classification system of aortic aneurysms.
Describe the Crawford classification system of aortic aneurysms.
How long should elective surgery be delayed in the patient with a bare metal stent? Drug eluting stent? s/p angioplasty? s/p CABG?
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.
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.
Can calculate the stroke volume and/or ejection fraction with a pressure volume loop?
If you are given a pressure volume loop, you should be able to calculate the stroke volume as well as the ejection fraction.
SV = Width of the loop
EDV = Right side of the loop at the x-axis
Enter both variables into the equation in the previous question.
What is the best TEE view for diagnosing myocardial ischemia?
Midpapillary muscle level in short axis
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 subendocardium coupled with a decreased coronary artery blood flow during systole increase coronary vascular resistance and predisposes this region to ischemia.
What factors affect myocardial oxygen supply and demand?
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 ventricular pressure volume loop?
S1: Closure of mitral and tricuspid valves (marks onset of systole)
S2: Closure of aortic & pulmonic valves (marks onset of diastole)
S3: May suggest systolic dysfunction (normal in kids and athletes)
S4: May suggest diastolic dysfunction
Notice that the MV opens and closes on the bottom of the loop, and the AV opens and 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 backwards during chamber systole.
How does the heart compensate for pressure overload? Volume overload?
Match each pressure volume loop with its pathophysiology (notice there are 6 loops).
List the hemodynamic goals for the 4 common valvular defects.
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 time 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 years
Ischemia
Pressure overload hypertrophy (aortic stenosis or HTN)
Hypertrophic obstructive cardiomyopathy
Pericardial pressure (increased external pressure)
The clinical take away is that higher filling pressures are required to prime the ventricle.
Compare and contrast the hemodynamic goals in the patient with systolic- vs diastolic heart failure.
How does HTN contribute to CHF?
How does hypertension affect cerebral autoregulation?
The cerebral autoregulation curve describes the range of blood pressures where cerebral perfusion pressure remains constant.
Chronic hypertension shifts this curve to the right. This adaptation helps the patient’s brain tolerate a higher range of blood pressures, however this comes at the expense of not being able to tolerate a lower blood pressure. Remember that BP past the range of auto regulation is pressure dependent.
Malignant hypertension increases the risk of hemorrhagic stroke and cerebral edema.
Hypotension increases the risk of cerebral hypoperfusion.
As an aside, the texts would lead you to believe that the width of the curve remains the same in the hypertensive patient, however there is good evidence that the width of the curve (range of autoregulation) becomes narrower.
What are the 2 major classes of calcium channel blockers? List examples of each.
Describe the anesthetic management of constrictive pericarditis.
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 an external pressure on the heart limiting its ability to fill and act like 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 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. SV is severely decreased and increased SNS tone (increased contractility and increased afterload) provide compensation. Any drug that depresses the myocardium or reduces afterload can precipitate cardiovascular collapse.
What factors tend to 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.
