Cardiac Pathology Flashcards
Concentric hypertrophy does what to the LV wall?
Thickens, extra muscle built up to overcome resistance
Eccentric Hypertrophy does what to the LV wall?
dilates out like a balloon, thin wall
Acute Mitral Regurg strains the right side or left side of the heart more
Right Side
What is our hemodynamic goal when it comes to maintaining a patient’s BP and MAP during surgery?
Try to keep BP within 20% of their preop/home blood pressure throughout the periop phase.
Coronary artery autoregulation occurs with a MAP between?
60-140mmHg
For patients with chronic hypertension, their coronary artery autoregulation curve is usually shifted to the ____? What is the significance of this?
Right
Meaning they may need a higher MAP to maintain perfusion
What hypertension medication do we typically try to hold 24 hours before surgery?
ACE inhibitors or ARBs
If the patient takes it at home, what anti-hypertension medication do we want the patient to take before their surgery? If they didn’t take it, what can we do?
Beta Blocker
Give it preop PO or IV. Or intraop if no time.
If the patient took their ACE inhibitor or ARB in the morning before surgery, what might we see intraop?
Refractory Hypotension
What are the two medications we can give intraop to treat refractory hypotension?
Vasopressin(typically all you need) or Methylene Blue
If you have a patient coming in with uncontrolled hypertension, what are some things to consider?
-Assume they have some degree of CAD
-Avoid Ketamine as the sole anesthetic agent because you can see an exaggerated SNS response
-Phenylephrine may have a more exaggerated response than usual
-May be hypovolemic
-“Consider what is an appropriate MAC of anesthesia before incision”
What is the difference between Essential (Primary) HTN and Remedial (Secondary) HTN
Primary: Accounts for 95% of cases and is without an identifiable cause
Secondary: Identifiable cause and potentially curable. ex: renal artery disease, pheochromocytoma, Cushing’s disease, primary aldosteronism
Describe HTN pathophysiology
Can be caused by overactive SNS. SNS dysfunction leads to extra RAAS system activation which increases angiotensin II and Aldosterone levels.
Aging also leads to vascular stiffness which increases SVR
Patients with DBP greater than ______ have a significantly increased risk of cardiac morbidity
110mmHg
consider canceling the case until it is more appropriately managed
What is the most common cause of intraoperative HTN?
Surgical stimulation with too light of anesthetic.
Need an appropriate MAC level before surgical stimulation.
HTN patients are at an increased risk of MI how long after surgery?
24 hours
What variables will increase or decrease cardiac output for patients with chronic constrictive pericarditis?
Increase CO:
-Normal to higher HR. (Ketamine a good choice for these patients)
-Preserve contractility - caution with myocardial depression agents (prop, volatiles)
Decrease CO:
-Bradycardia
-Excessive Positive Pressure Ventilation (can reduce CO by increased intrathoracic pressure, try to keep spontaneous breathing if appropriate)
For patients with chronic pericarditis, Cardiac Output is dependent on? What should be avoided?
Higher dependence on HR.
Bradycardia should be avoided due to impaired diastolic filling and limited Stroke Volume. (The heart is constricted; it can’t fully relax)
What is the most common cause of Acute Pericarditis?
Viral Infection - inflammation of the pericardium
Acute pericarditis that doesn’t resolve over time can lead to?
Chronic constrictive pericarditis
Cardiac Tamponade
Clinical Presentation of Acute Pericarditis
-Sudden onset of chest pain. Different than MI due to postural changes affecting pain.
-Decreased pain by leaning forward
-Fever
-Diffuse ST segment elevation
-Normal cardiac enzymes
Anesthetic management of patient with acute pericarditis? How do you treat?
no change in anesthesia mgmt in the absence of pericardial effusion.
It should resolve on its own. No acute treatment, symptom mgmt.
Brief description of the pathophys of Chronic Constrictive Peridcarditis
stiff, fibrous tissue encircling the heart.
-Limits diastolic filling of both ventricles - so very HR dependent
-Can cause pulmonary and peripheral congestion which can be seen with increased CVP.
Clinical Presentation of Chronic Constrictive Pericarditis
increased fatigue and dyspnea overtime
- Signs on increased venous pressure
such as: JVD, ascites, peripheral edema
-Atrial Dysrhythmias
-Pulses Paradoxes (decreased SBP on inspiration)
How is Chronic Constrictive Pericarditis diagnosed?
Echo and/or CT
What is Beck’s Triad correlated to Cardiac Tamponade
Hypotension, JVD, and muffled heart tones
What areas that we work in do we see Cardiac Tamponade more frequently? Where is it commonly discovered?
Cath Lab / EP Lab
-usually ablations / angios
Commonly discovered/manifests in PACU
How does Cardiac Tamponade impair CO?
impairs diastolic filling due to continual increase in intrapericardial pressure (similar to constrictive pericarditis but more severe)
If the patient is already under general anesthesia and cardiac tamponade is discovered, what action should you take?
Reduce concentration on anesthetic to reduce the myocardial depression effects
If the patient is in PACU and extubated, and cardiac tamponade is discovered, what steps do you take?
-Do not induce general anesthesia. (Myocardial depression and PPV can be detrimental to SV and CO.)
-Maintain spontaneous ventilation
-Stabilize by maintaining HR, contractility, and afterload (epi a good choice)
Pericardiocentesis is done under local anesthesia.
Clinical presenation of cardiac tamponade: intraop and postop
Intraop: Hypotension and Tachycardia are most often seen
Postop: Becks triad, Pulsus Paradoxes, Decreased voltage across all leads on ECG
CXR has an enlarged cardiac silhouette.
What is the difference between Primary and Secondary Valvular Dysfunction
Primary: valve leaflets or anchoring structures are damaged.
Secondary: Valve is normal, but function altered due to another disease process such as ventricular dilation, papillary muscle infarct, aortic dissection
What is the clinical definition of severe mitral stenosis?
Valve Orifice < 1.0cm^2
For Mitral Stenosis and Aortic Stenosis, how do we generally want to manage them?
Slow to Normal, Regular HR with patients with stenotic lesions because it allows more time for diastolic filling. Allow more time for chambers to fill to overcome stenotic lesion.
For stenotic lesions, how do we want to manage preload and afterload?
Maintain or slightly increase.
For patients with regurgitant lesions, what will bradycardia do to your regurgitant fraction and stroke volume?
Increase regurgitant fraction and reduce overall stroke volume
For patients with stenotic lesions, what will tachycardia do to your filling time, SV, and oxygen demand?
Shorten filling and ejection times
Reduce SV
and Increase oxygen demand
Describe the pathophys effects of Mitral Stenosis on the left atrium.
Decreased blood flow into LV across MV. Leading to an increase in volume and pressure in LA. LA becomes stretched increasing risk of Afib.
What is the significance of afib in patients with mitral stenosis?
Loss of atrial kick creates a more pronounced drop in cardiac output in MS pts than in normal patients. CO is already reduced and dependent on atrial kick to push blood across the valve.
How does mitral stenosis effect the RV?
Blood backing up into LA can back up further and increase pulmonary venous pressure and volume. Can create pulmonary congestion and hypertension which increases the work load of the RV leading to failure (cor pulmonale).
How does the body compensate for the chronically undefilled LV in mitral stenosis?
Due to the lower EDV,SV, and CO, body compensates with increased SVR to maintain MAP.
Compared to a normal LV pressure/volume loop, how will the pressure volume loop of mitral stenosis compare?
Decreased SV
Decreased LV Volume
Decreased LV Pressure
What kind of anesthesia is an absolute contraindication for a patient with severe Aortic Stenosis? What might you do if youre planning on doing this kind of anesthesia?
Spinal Anesthetic (as a sole anesthetic) because the sympathetic blocking can cause profound hypotension, decreased coronary perfusion pressure, and CV collapse
You’re planning on doing a spinal anesthetic for a noncardiac surgery procedure. What action should you take in your preop assessment?
Listen to heart sounds for the presence of a murmur. Severe aortic stenosis is contraindicated for spinal. Listen to ensure no murmur is detected.
Many patients with cardiac conditions are on anticoagulants d/t hx of afib. What INR level is necessary before considering regional anesthesia?
consider regional only if INR is less than 1.5
To maintain afterload in mitral stenosis patients, what agents are the best choice? Pick 3.
- Phenylephrine
- Norepi
- Vasopression
(ephedrine not the best choice)
What are some things to avoid to reduce increases in PVR?
Avoid acidosis, hypercarbia, hypoxia, nitrous oxide, and Trendelenburg position
What are the clinical triad of symptoms for Aortic Stenosis?
Syncope, Angina, and Heart Failure
SevereAortic Stenosis is characterized by?
AV orifice less than 1cm^2
(normal 2.5-3.5)
Describe how Aortic Stenosis causes left ventricular hypertrophy
LV must increase force of contraction to generate adequate stroke volume through stenotic valve. Pressure overload and increased LV wall tension leads to concentric hypertrophy (LVH).
Why does left ventricular hypertrophy increase myocardial oxygen demand?
More stretching of the now larger muscle requires more oxygen and can cause subendothelial compression of vessels.
Afterload in Aortic Stenosis is ____ on the stenotic lesion
Fixed. Decreasing SVR won’t help much because the valve stenosis has not changed.
How does the LV pressure volume loop of Aortic Stenosis change from a normal LV loop
Large increased pressure and moderate increased volume
Anesthetic considerations for aortic stenosis
similar to Mitral Stenosis
maintain low-normal and regular HR
-Normal to a slight increase in preload
-Maintain to slight increase in SVR (may augment preload venous return)
-Maintain PVR
-Avoid spinal anesthesia in severe AS
Describe the pathophys of chronic aortic regurg
Blood ejected from the LV re-enters the LV during diastole via an incompetent aortic valve. Cardiac Output drops because blood volume to the systemic circulation is down.
LV becomes volume overloaded and leads to LV dilation (aka eccentric hypertrophy) to allow extra volume to compensate but eventually becomes to dilated and begins to fail.
Describe acute pathology of aortic regurg
LV becomes Acutely Dilated, leading to increased wall tension and decreased function. Myocardial ischemia results and rapid hemodynamic instability.
Regurgitant volume in aortic regurg is increased via?
Bradycardia increased SVR. and larger valvular orifice
Anesthetic Considerations for Aortic Stenosis - HR, Preload, Contractility, and Afterload
“Fast, Forward, Full”
-Higher HR between 80-100 because faster reduces the regurgitant volume
-Maintain or increase preload because more volume increases overall SV and CO
-Decrease Afterload bc it promotes forward flow, reducing regurg volume
-Avoid myocardial depression
What pressor might be the better choice for Aortic Regurg?
Ephedrine might be better here because you don’t want too high of an SVR
Is regional anesthesia, such as a spinal, a good option for Aortic regurg pts?
Yes, sympathectomy will reduce afterload. Not contraindicated like severe aortic stenosis
Describe the pathophysiology of Mitral Regurg.
Blood reenters the left atrium through incompetent MV during ventricular systole.
SV is directed in two directions (aorta and LA) during systole, reducing SV and CO and leading to volume overload in the LA and LV.
How does Mitral Regurg cause pulmonary edema
Increased LA volume, increases LA pressure, which increases the risk of pulmonary edema
How does mitral regurg cause LV dilation
Increased volume in LV from regurg volume increases LVEDV and causes LV dilation (eccentric hypertrophy)
Acute Mitral Regurg Pathology
Acute increases in LVEDP lead to an acute increase in PAP and pulmonary edema, pulm htn, and RV failure. No time for compensatory changes.
How does acute mitral regurg pressure/volume loop differ than normal LV loop
-Pressure decreased in LV (pressure builds in LA, not LV)
Volume increased in LV.
Mitral Regurg Anesthetic Considerations
-Increase HR (80-100), faster rate decreases time in systole and less regurgitant volume.
-Maintain or increase preload
-Slight Decrease in Afterload - promotes forward flow from aorta.
Acute Mitral Regurg can cause?
More pronounced symptoms. RV failure d/t pulmonary congestion. No time for LA and LV to make compensatory changes.
The eccentric hypertrophy associated with chronic aortic regurg and/or mitral regurg allows the LV to?
Allows the LV to dilate/balloon out to hold a bigger volume without increasing pressure too much in the LV.
What is Hypertrophic Cardiomyopathy? What is its key characteristic?
A genetically transmitted disorder that causes left ventricular hypertrophy, resulting in decreased size of LV chamber and LV Outflow Tract Obstruction due to asymmetric hypertrophy of the interventricular septum.
Hypertrophic Cardiomyopathy causes systolic, diastolic, or both LV dysfunction
Both.
D: Thickened/Smaller chamber doesn’t fill as well.
S: Ejection compromised due to outflow tract obstruction.
What anatomic changes can patients with hypertrophic cardiomyopathy have that further complicate issues associated with HCM
SAM - systolic anterior motion - of the anterior mitral valve leaflet that further obstructs the LVOT. Not all pts with HCM have SAM.
What is unique about the anesthetic management of patients with Hypertrophic cardiomyopathy?
Myocardial Depression is desirable. Decrease in contractility to minimize outflow tract obstruction.
-Limit the use of Ephedrine, Epi, etc
-Consider BBs and CCBs
Anesthetic Considerations for HCM
(HR,preload, contractility, afterload)
HR: avoid tachycardia. Maintain slow - normal rate and SR.
Preload: Adequate/Increase since LVOT obstruction limits ejected SV.
Afterload: Maintain/Increase since LVOT obstruction limits CO.
Contractility: Decrease to minimize LVOT obstruction severity.
What is the most common form of cardiomyopathy?
Dilated Cardiomyopathy
Dilated cardiomyopathy causes what kind of dysfunction?
-Cause eccentric hypertrophy of both ventricles.
-Systolic and Diastolic Dysfunction - leads to a decrease in contractility and CHF
-Correlated with Mitral Valve and/or Tricuspid valve regurg
-Increased myocardial oxygen consumption
Anesthetic Considerations for Dilated Cardiomyopathy
Reduce afterload
Avoid large fluid bolus
Chose an anesthetic technique that will reduce overall myocardial depression.
-maybe keep awake
-low dose epi for inotropy
Anesthetic management for a patient with restrictive cardiomyopathy would be similar to the treatment of what other condition?
Cardiac Tamponade
Described Restrictive Cardiomyopathy
Rare form. Caused by the genetic predisposition of stiffening ventricles.
One or both ventricles become stiff and non-compliant, leading to impaired diastolic filling, decreased stroke volume
Anesthetic Considerations for Restrictive Cardiomyopathy
-Possible IV inotropic support - double diluted epi (10mcg/mL)
-Consider the use of TEE and hemodynamic monitoring
-Choose an anesthetic that doesn’t cause as much myocardial depression.
