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Flashcards in Cardiac Anatomy and Physiology Deck (55):

What are the determinants of myocardial oxygen demand?

Wall tension and contractility


How can myocardial oxygen demand be reduced?

1- Decrease intraventricular pressure
2- Prevent or promptly treat ventricular distention
3- decrease heart rate
4- decrease contractility


What is Laplace's Law?

Laplace's law states that wall tension is proportional to pressure (P) and chamber radius (r) and inversely proportional to wall thickness (h), as represented
by the equation:

Wall tension = (intracavitary pressure) * (ventricular radius) / (2* wall thickness)

This law is applicable to myocardial wall tension. Increased wall tension results in increased myocardial oxygen consumption.

Patients with chronic hypertension (which imposes an increased pressure load on the left ventricle) commonly have left ventricular hypertrophy (ie, increased thickness of the left ventricular wall). The increased wall thickness (increased h in the above equation) results in a decreased wall tension.

In contrast, patients with decompensated systolic heart failure tend to have dilated cardiomyopathy. The increase in ventricular chamber size (increased r) and thin myocardium (decreased h) results in an increase in wall tension. Treatment of congestive heart failure with diuresis or venodilation reduces preload, resulting in a decreased radius, decreased wall tension, and less myocardial oxygen consumption.


How do you meet myocardial oxygen requirements?

Raise coronary blood flow

The principal mechanism for matching oxygen supply to alterations in myocardial oxygen demand is exquisite regulation and control of coronary blood flow.


What critical factors modify coronary blood flow?

1- Perfusion pressure and vascular tone of the coronary circulation
2- time available for perfusion (determined mainly by heart rate)
3- severity of intraluminal obstructions
4- presence of any collateral circulation


Which area of the heart is most vulnerable to ischemia?

The subendocardium of the left ventricle, which is exposed to LV intracavitary pressure and where metabolic requirements are increased because of greater systolic shortening.


When does perfusion of the left and right subendocardium take place?

Left subendocardium: almost entirely during diastole.

Right subendocardium: diastole and systole, assuming pulmonary hypertension is not present.


What determines the LV coronary perfusion pressure?

The gradient between the aortic diastolic pressure and LV diastolic pressure. In the presence of intraluminal obstruction or increased vascular tone, this pressure gradient is reduced. a low LVDP is ideal for improving perfusion (causes higher pressure gradient) and reducing myocardial oxygen demand. On the other hand, increasing perfusion pressure by raising the aortic pressure will also increase myocardial oxygen demand, but this is less important when one considers that tachycardia is the most important cause of intraoperative and perioperative ischemia.


What is coronary vascular reserve?

the difference between autoregulated, baseline flow, and blood flow available under conditions of maximal vasodilation is termed coronary vascular reserve and is normally 3-5x higher than basal flow. As epicardial coronary stenosis becomes more pronounced, progressive vasodilation of resistance vessels allows preservation of basal flow, but at the cost of reduced reserve.


True or False: It is not uncommon for an anesthetized patient to show signs of ischemia without any changes in heart rate, blood pressure, or ventricular filling pressures.

True: in fact, most ischemic episodes are not accompanied by hemodynamic changes.


True or false: anesthetic decisions should be designed to reduce and control factors that increase myocardial oxygen demand (heart rate, contractility, and wall tension).



What are normal PA catheter values for the following:


CVP = RVEDP = 3-8 mmHg
RA= 0-8 mmHg
RV = 15-30 / 0-8 mmHg
PA = 15-30 / 3-12 mmHg
PCWP = 1-10 mmHg


What are normal left-sided heart values?

LA = 1-10 mmHg
LV = 100-140 / 3-12 mmHg
Aortic = 100-140 / 60-90 mmHg


Describe the CVP waveform. Specifically, what do the a, c, and v waves represent? What is the x-descent and what is the y-descent?

Waveform Component Phase of Cardiac Cycle Mechanical Event
a wave End diastole Atrial contraction
c wave Early systole Tricuspid bulging (IVC)
v wave Late systole Systolic filling of the atrium
x descent Mid systole Atrial relaxation
y descent Early diastole Early ventricular filling


What is a normal PR interval? What can cause an increase in a PR interval? What can shorten the PR interval?

The PR interval includes the P wave as well as the PR segment. It is measured from the beginning of the P wave to the first part of the QRS complex.

Normal time: 0.12-0.2 sec

The PR interval is shorter at faster heart rates due to sympathetically mediated enhancement of AV nodal conduction; it is longer when the rate is slowed as a consequence of slower AV nodal conduction resulting from withdrawal of sympathetic tone or an increase in vagal inputs. Long PR intervals are usually seen in first degree AV block, but there may be other causes


What is the QRS complex? What is the duration of a normal QRS complex?

The QRS complex represents the time for ventricular depolarization.

The entire QRS duration normally lasts for 0.06 to 0.10 seconds (1½ to 2½ small boxes) and is not influenced by heart rate


What is the length of a normal QT interval? What can prolong a QT interval?

The QT interval consists of the QRS complex, the ST segment, and T wave. Thus, the QT interval is primarily a measure of ventricular repolarization. The time for ventricular repolarization and therefore the QT (or JT) interval is dependent upon the heart rate; it is shorter at faster heart rates and longer when the rate is slower. Thus, a QT interval that is corrected for heart rate (QTc).

The normal value for the QTc in men is ≤0.44 sec and in women is ≤0.45 to 0.46 sec

Bundle branch block can increase the QT interval.


EKG paper and length of the tics:
1- one full box
2- the tiny tics

Each 1 mm (small) horizontal box corresponds to 0.04 second (40 ms), with heavier lines forming larger boxes that include five small boxes and hence represent 0.20 sec (200 ms) intervals


How do you approach EKG interpretation?

Step 1- Calculate the rate.

Step 2: Rhythm — Are P waves present? Is there a P wave before every QRS complex and a QRS complex after every P wave? Are the P waves and QRS complexes regular? Is the PR interval constant?

Step 3: Axis — Is there left or right axis deviation?

Step 4: Intervals — What is the PR interval? Short PR intervals are suggestive of WPW syndrome. Long PR intervals are usually seen in first degree AV block, but there may be other causes. What is the QRS interval? Long QRS intervals represent a bundle branch block, ventricular preexcitation, ventricular pacing, or ventricular tachycardia. What is the QT interval? Short and long QT intervals may be present.

Step 5: P wave — What is the shape and axis of the P wave? The P wave morphology should be examined to determine if the rhythm is sinus or from another atrial location

Step 6: QRScomplex — Is the QRS wide? If so, examination of the morphology can determine if there is left or right bundle branch block or pre-excitation present. In addition, increased voltage may indicate left or right ventricular hypertrophy. Are Q waves present, suggestive of infarction?

Step 7: ST segment-T wave — Is there ST elevation or depression? Are the T waves inverted?


Describe 1st degree AV block.

Prolonged PR interval (> 0.2 seconds), usually clinically insignificant


Describe 2nd degree AV block, Mobitz Type 1.

P-wave normal , PR interval progressively lengthens with each cycle until QRS complex is dropped. PR interval following dropped beat is shorter than normal. Commonly seen in trained athletes.


Describe 2nd degree AV block, Mobitz Type 2.

P waves normal, but some are not followed by QRS complex. In contrast to Mobitz type 1, the PR and RR intervals are constant and the dropped QRS occurs without warning.


Third degree AV block, complete heart block.

Represents complete failure of conduction form the atria to the ventricles. Immediate treatment with atropine (if sinus bradycardia) or isoproterenol (to increase ventricular rate) is required if cardiac output is reduced.


Left bundle branch block.

Complete LBBB means QRS > 0.12 s
Incomplete LBBB means QRS 0.1-0.12 sec

Does not occur in healthy patients and usually indicateds serious heart disease with a poor prognosis. In patients with LBBB, insertion of a PA catheter may lead to complete heart block.


Right BBB

Complete RBBB means QRS > 0.12 s
Incomplete RBBB means QRS 0.1-0.12 sec

In the presence of RBBB, Q waves may be seen with an MI.


What key information is gained from a PA catheter?

Pulmonary artery systolic pressure, diastolic pressure, CVP, and cardiac output. Pulmonary artery wedge pressure is usually similar to pulmonary artery diastolic pressure (in patients with high pulmonary vascular resistance, there may be a large gradient between the pulmonary artery diastolic and the pulmonary artery wedge pressure).


What is the most common valvular disease in the US?

Aortic stenosis


What is the normal AV diameter? Normal AV area?

Normal AV diameter: 1.9-2.3 cm
Normal AV area: 2-4 cm2


What is the normal diameter of the LVOT?

2.2 +/- 0.2 cm


What clinical factors are associated with aortic sclerosis?

older age, male gender, smoking, hypertension, HLD

Pts with bicuspid AV (increased mechanical stress) or altered mineral metabolism (Paget disease, renal failure) have a higher prevalence of calcific AS.


What are classic symptoms of AS

- angina, syncope, and dyspnea are harbingers of death within 5, 3, and 2 years respectively.


How does the heart compensate for narrowing of the AV orifice?

The progressive narrowing of the AV orifice results in chronic obstruction to LV ejection. Intraventricular systolic pressure increases to preserve forward flow. Concentric ventricular hypertrophy, in which the LV wall gradually thickens but the cavity size remains unchanged, is the compensatory response that normalizes the concomitant increase in LV wall tension. Contractility is preserved and EF is maintained at a normal range until late in the disease process.


At what AV orifice size do signs and symptoms of AS usually occur?

AV orifice < 0.8-1.0 cm2


Discuss myocardial oxygen supply and demand in the setting of AS.

The costs of concentric LV hypertrophy are decreased LV compliance and a precarious balance between myocardial oxygen supply and myocardial oxygen consumption. Hypertrophy-induced impairment of diastolic relaxation ("stiff" LV) impedes early LV filling, and LA contraction becomes critical for maintaining adequate ventricular filling and subsequent stroke volume. In AS, the "atrial kick" may account for up to 30-40% of LV end-diastolic volume. The ventricular filling pressure, as reflected by the pulmonary capillary wedge pressure, may vary widely only with small changes in ventricular volume.

The hypertropied muscle mass has increased basal myocardial oxygen consumption. Because the capillary density is often inadequate for the hypertrophic muslce, a reduction in perfusion pressure, as when aortic diastolic pressure is decreased and/or ventricular filling pressure is increased, may compromise supply and total vasodilator reserve. The situation is compounded in the presence of coronary obstruction.


List anesthetic considerations for AS. Preload, afterload, contractility, rate, rhythm, MVO2, CPB.

Preload: full

Afterload: maintain coronary perfusion gradient to prevent hypotension-induced ischemia, subsequent ventricular dysfunction, and worsening hypotension.

Contractility: usually not a problem, may require inotropic support if hypotension persists

Rate: avoid bradycardia (will decrease cardiac output) and tachycardia (causes ischemia and decreases duration of diastolic coronary perfusion)

Rhythm: sinus

MVO2: avoid tachycardia and hypotension

CPB: contractility augmentation may be required 2/2 myocardial stunning.


Why do you not want bradycardia in the setting of AS?

Bradycardia is a common cause of hypotension in the patient with AS. Slowing the heart rate and increasing diastolic time will not increase stroke volume in the LV with concentric hypertrophy, and rather it will induce a fall in total cardiac output and systemic arterial pressure. THIS IS ESPECIALLY PERITNENT IN THE ELDERLY AND DIABETIC PATIENT, in whom sinus node disease and reduced sympathetic responses may predispose to significant bradycardia.


What is the most important cause of intraoperative and perioperative ischemia?

Tachycardia- treat with esmolol or metoprolol


Cardiac autonomic innervation is provided by the right and left vagal nerves. What provides autonomic innervation to the SA and AV nodes?

SA node: right vagal nerve
AV node: left vagal nerve


Cardiac parasympathetic innervation comes by way of the: A

Cardiac sympathetic innervation comes by way of the: B

a) vagus nerve
b) arises from T1-T4 and innervates the heart by way of the stellate ganglion


During SVT treatment, what are the effects of massaging the right vs left vagal nerves?

Right: inhibits sinus discharge
Left: slows AV node conduction


Mitral Stenosis:

Represents an obstruction to blood leaving the atrium for the ventricle --> causes high atrial volumes and pressures and an underfilled ventricle.


Aortic Stenosis:

A high afterload state, necessitating an increase in preload to maintain cardiac output. Furthermore, concentric hypertrophy associated with aortic stenosis requires increased pressures for a given volume.


What are hemodynamic changes during aortic cross-clamping? Address the following:
- arterial blood pressure
- segmental wall motion abnormalities
- left ventricular wall tension
- ejection fraction
- cardiac output
- renal blood flow
- pulmonary artery occlusion pressure
- central venous pressure
- coronary blood flow

- increase in arterial blood pressure
- increase in segmental wall motion abnormalities
- increase left ventricular wall tension
- decrease in ejection fraction
- decrease in cardiac output
- decrease in renal blood flow
- increase or decrease in pulmonary artery occlusion pressure
- increase in central venous pressure
- increase in coronary blood flow


What can cause aortic regurgitation?

Processes that affect the aortic valve leaflets (eg rheumatic fever, infective endocarditis, congenital bicuspid aortic valve) or the aortic root and valve-supporting structures (aortic dissection, systemic hypertension, cystic medial necrosis, Marfan syndrome)


With aortic regurgitant lesions, what range heart rate is sought?

A slightly higher yet still normal heart rate is sought to compensate for the heart's inability to maintain sufficient forward stroke volume, subsequently placing a greater volume load on the left ventricle.

In response, a rise in sympathetic tone increases heart rate and contractility, resulting in a proportional decrease in diastolic time when the regurgitation is occurring, thus decreasing the amount of regurgitation time.

Avoid anything that would increase diastolic blood pressure.


What is the ideal hemodynamic management for a patient with acute MR? Address:


- promote vasodilation and mild tachycardia, which allows for afterload reduction and effective forward flow of blood from the left ventricle to the aorta versus regurgitation from the left ventricle to the left atrium.

Preload- increased
Afterload- decreased
Contractility- decreased
Rate- increased
Rhythm- controlled

The management goal, therefore, is to improve cardiac output by reducing systemic vascular resistance and increasing heart rate. Several pharmacologic agents, including dobutamine and low-dose epinephrine (at a dose range where beta2 effects predominate), improve cardiac output by increasing heart rate and/or decreasing systemic vascular resistance.


What is the calculation for SVR?



Describe BNP.

BNP changes rapidly in response to worsening HF and studies have demonstrated that levels of BNP correlate with the severity of HF. Despite the long list of alternate cardiac, pulmonary, and other causes for BNP elevations, BNP is the primary test used to confirm the diagnosis of HF and monitor its progression. Depending on the laboratory, BNP may be reported as pg/mL or ng/L. In either case, the normal value is 0–99, and a value in excess of 100 is consistent with HF.


T or F: caused by papillary rupture, acute MR can present itself with CHF, hypotension, increased pulmonary congestion.

True- in the patient with acute severe MR and cardiogenic shock from ischemic rupture of a papillary muscle, pharmacologic support of the left ventricle, often accompanied by mechanical support from IABP counterpulsation, may be necessary.


Apart from ischemic heart disease, what are other causes of an elevated troponin?

Although troponin has a very high sensitivity and specificity for ischemic heart disease, a number of conditions may elevate troponin levels in the absence of a myocardial ischemia or infarction, including

chest trauma
percutaneous coronary intervention
electrical cardioversion, defibrillation, and ablation procedures
cardiac surgery
heart failure
renal failure
severe asthma
drug toxicity (eg, high-dose chemotherapy)
inflammatory heart disease (eg, Kawasaki disease, myocarditis)
acute neurologic catastrophe (eg, cerebrovascular accident, subarachnoid hemorrhage).


A wave

atrial contraction


C wave

bulging of the tricuspid valve into the atrium during the beginning of systole



occurs during systole and corresponds to atrial relaxation



represents filling of the atrium while the tricuspid valve is closed


Y descent

occurs when tricuspid valve opens and the atrium starts to empty