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60 Cards in this Set
- Front
- Back
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Heart Failure can be a _____ or _____ disorder.
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Heart failure can be a structural or a functional disorder.
IT can also be an acute or a chronic disorder. It impairs the ability of the ventricle to eject blood. |
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Acute HF is due to _______.
Chronic HF is due to _______. |
Acute HF Is due to some other disorder.
Chronic HF is due to chronic HTN. |
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The leading cause of HF is
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Chronic HTN
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Classic S/S of heart Failure
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Fatigue
Shortness of breath Pulmonary congestion Periperal Edema |
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What kinds of pathologies leads to systolic heart dysfunction?
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Ischemic Dilated Cardiomyopathy (reduced contractility).
Hypertensive Dilated Cardiomyopathy CAD/ Ischemic Heart Disease HTN (first leads to diastolic dys. and then systolic dys) Primary myopathy from Infections, Toxins, Idiopathic, Familial (cause loss of inotropy). Valvular dysfunction ---> Aortic Stenosis (pressure overload, concentric hypertrophy...first diastolic dys, and then systolic dys.) ---> Aortic regurgitation (volume overload, eccentric hypertrophy). Congenital heart Defects (loss of inotropy) High Output Failure: due to ischemia ---> Anemia ---> Thyrotoxicosis ---> Systemic AV fistulas/ shunts ---> Padget's Disease (cancer) ---> Beriberi disease (thiamine deficiency) |
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What are some pathologies that cause diastolic heart failure?
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(When you have a stenosis, you get so hypertrophied that you can't fill. Your diastolic function if impaired.)
Hypertrophic Cardiomyopathy (Obstructive and non-obstructive) Hypertension (causes concentric hypertrophy) Ischemic Heart Disease (Ischemia due to the hypertrophy) Restrictive Cardiomyopathies (Sarcoidosis, Amyloidosis, Subendocardial Fibrosis) Aortic Stenosis: (pressure overload- causes concentric hypertrophy) Constrictive Pericarditis Chemotherapeutic Agents (cause stiffness of the left ventricle) |
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American Heart Association Stages of Heart Failure
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STAGE A
---> High risk factors (chronic HTN) with no symptoms. Goal is to reduce risk factors (statin therapy, lifestyle changes) STAGE B ---> Stuctural Heart Disease with no Symptoms ---> Tx: ACEIs or ARBs in all pts. BBs in SELECTED pts. STAGE C ---> Structural Disease with previous or current symptoms. ---> Tx: ACEI's, BB's in ALL pts. ---> Dietary Na restriction ---> Diuretics ---> Digoxin ---> Cardiac resynchronization if bundle branch block present ---> Revascularization, mitral valve surgery ---> Consider Multidisciplinary team ---> Aldosterone Antagonist, Nesiritide (a naturetic peptide...reduces blood volume) STAGE D ---> Refractory symptoms requiring special intervention ---> Tx: Inotropes, ---> VAD, or transplantation ---> Hospice |
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New York Hearts Association Classes of Heart Failure
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CLASS 1
--->Asymptomatic heart failure. EF < 4-% CLASS 2 ---> Mild symptomatic HF with ordinary exertion. (SOG w/ exertion). CLASS 3 ---> Moderate symptomatic heart failure with less than ordinary exertion. Can't do more than 4 mets of metabolic activity without SOB. CLASS 4 ---> Symptomatic heart failure at rest. |
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What is the most common type of heart failure?
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Combined HF
Systolic and Diastolic HF. |
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What is a sign of systolic heart dysfunction?
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A low ejection fraction < 45%.
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Systolic heart failure is due to a loss of _________.
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Systolic heart failure is due to a loss of inotropy. Stroke work decreases.
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What are the two type of Ventricular Hypertrophy
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ECCENTRIC HYPERTROPHY: Chronic volume overload stresses the ventricle. The ventricle responds by adding new sarcomeres in-series with existing sarcomeres (i.e., the sarcomeres lengthen rather than thicken). This results in ventricular dilation - the heart can expand to receive a greater volume of blood. There is a decrease in wall thickness relative to the ventricular radius. Can cause systolic heart failure.
CONCENTRIC HYPERTROPHY --->Chronic pressure overload (VC), the chamber radius may not change; however, the wall thickness greatly increases as new sarcomeres are added in-parallel to existing sarcomeres. This type of ventricle is capable of generating greater forces and higher pressures, while the increased wall thickness maintains normal wall stress. Concentrically hypertrophied ventricles become "stiff" (i.e., compliance is reduced), which can impair filling and lead to diastolic dysfunction. |
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Explain systolic heart failure
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Loss of inotropy
EF < 45% ESV increases. Eccentric Hypertropy occurs...causing the myofibrils to grow in series (not parallel). The ventricle dilates. EDV and EDP increase. Relative wall thickness decreases. Decreased inotrophy leads to a fixed SV. A fixed SV results in a decreased CO. The body compensates by increasing heart rate. Eventually the heart cannot compensate and you get decreased perfusion to organs. Eventually the organs cannot autoregulate and start to shut down. Can happen with ischemia and with dilated cardiomyopathy (eccentric hypertrophy). |
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Explain Diastolic Heart Failure
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DECREASED COMPLIANCE
Concentric ventricular hypertrophy causes a stiff left ventricle. This causes a loss of compliance. Preload decreases. Initially you have a normal to increaed EF (d/t the high inotropy). ESV is normal at rest but increased with exercise (decompensates with exercise). But the heart eventually decompensates. (So eventually diastolic heart failure turns into systolic heart failure). This can occur in combination wtih systolic heart failure. |
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With systolic HF EF is ________.
With diastolic HF, EF is __________. |
Systolic HF, EF is decreased (<45%).
Diastolic HF, EF is normal or increased. (due to increased contractility). |
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Explain the pathophysiology of heart failure
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* Impaired LV Function is caused by either primary myocardial injury (ischemia/MI, valve dysfunct, etc) or increased afterload. Both cause cardiac remodelling...leading to a geometric change in the left ventricle (hypertropy/ dilation). Eventually, with both systolic and diastolic HF you will have a decreased EF and hypoperfusion.
* Decreased EF causes decr CO and pulmonary congestion. * Decreased cardiac output causes increase SNS VC and HR, RAAS stimulation, ADH release, Incr AngII and endothelin levels (VC). This VC increases afterload, which only worsens the LV function. * The combo of the above causes Na and H20 retention, causing an increased preload, which worsens the pulmonary congestion. * RAAS stimulation also causes Hypokalemia (aldosterone effects), Hyponatremia (ADH effects)..which can both lead to arrythmias and sudden death. (These pts usually die from Vtach or Vfib). * Increased preload also causes ANP release from the right atria and naturesis/ vasodilation. |
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Neurohumoral changes act as a compensatory mechanism, but exacerbate CHF in what two ways?
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Increasing afterload that decreases SV
Increasing preload that results in pulmonary and systemic edema |
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Explain what causes mitral regurgitation
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* Effects of remodeling
* Dilatation of left ventricle and heart * Papillary muscles and mitral leaflets change in geometric relation to ventricular wall…become pulled wider and wider apart..valve does not close and you get M. regurg. * Dilatation of annulus of mitral valve, * Result is mitral regurgitation with increase LV volume overload Can also be caused by left main artery occlusion, causing left ventricle papillary muscle ischemia. |
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Explain Combined Systolic and Diastolic Heart Failure
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You have reduced inotropy AND reduced compliance (can't fill)
So: ---> Preload (EDV) is decreased (no compliance). ---> Ejection Fraction is decreased (no inotropy). ---> Stroke work is decreased (no inotropy) ---> End systolic volume is increased b/c of decreased SV (Kristi is wrong.) DRAMATIC decrease in SV causes a DRAMATIC decrease in CO. This causes RAAS to be HEAVILY STIMULATED. You get a DRAMATIC increase in blood volume, causing pulmonary congestion, HIGH heart pressures, and peripheral edema. If you put a swan in these pts, you should expect high heart pressures, if they are normal, that means the pt is dehydrated. Here is a great explanation:...... It is not uncommon in chronic heart failure to have a combination of both systolic and diastolic dysfunction. Therefore, the slope of the end-systolic pressure-volume relationship (ESPVR) is decreased and the slope of the passive filling curve (reciprocal of compliance) is increased in the ventricular pressure-volume loop. When this occurs, there is a dramatic reduction in stroke volume because end-systolic volume is increased and end-diastolic volume are decreased. Both ejection fraction and stroke work are also decreased. This combination of systolic and diastolic dysfunction, coupled with compensatory volume expansion, can lead to very high end-diastolic pressures that can cause pulmonary congestion and edema, as well as systemic edema and ascites (particularly when the right ventricle is in failure). Therefore, diuretic drugs are commonly used in these patients. |
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T/F
The clinical manifestations of systolic and diastolic HF are the same. |
TRUE
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Clinical Manifestations of HF
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Dyspnea (on exertion)
-->Pulmonary congestion -->Non-productive cough Orthopnea Pulmonary Edema – LV failure Organomegaly – RV failure Peripheral Edema – RV failure On an EKG you will see signs of ventricular hypertrophy: * RIGHT SIDE HEART FAILURE --->V2-V3 Tall P waves (P pulmonale) ---> V2-V6 Tall R waves ---> RBBB * LEFT SIDE HEART FAILURE ---> Afib with a LBBB --->V1-V2 R waves > 15mm ---> V5,V6 S waves > 20mm ---> Ventricular Arrythmias * CXR ---> Pulmonary congestion ---> Cardiomegally (systolic HF) ---> Pleural/ pericardial effusion * Echocardiogram: Will show low EF (systolic), increases wall thickness (systolic), valve dysfunction (diastolic), etc. |
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Anterior leads
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Lead II
Lead V5 |
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Brain natriuretic peptide is release in response to _______.
Atrial natretic peptide is released in response to _______. |
Brain natriuretic peptide is release in response to volume and pressure overload in the VENTRICLE.
Atrial natretic peptide is released in response to volume overload in the ATRIA. |
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What elevated serum level can diagnose heart failure, monitor the severity of heart failure, and monitor the effectiveness of treatment?
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Brain Naturitic Peptide
NORMAL: 0–99 picograms per milliliter (pg/mL) ABNORMAL: 80–100 pg/mL indicates possible heart failure >=100 pg/mL indicates DEFINITE heart failure BNP is released in response to pressure and volume overload of the ventricles. |
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Is relative wall thickness with systolic heart failure increased or decreased?
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Decreased
The myofibrils grow in series, not in parallel (the muscle grows in length and not width.) |
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Diastolic HF is seen most in what population?
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women over the age 65
Eldely Females |
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Diastolic has _______ hypertrophy.
Systolic has ________ Hypertrophy. |
Diastolic has concentric hypertrophy.
Systolic has Eccentric Hypertrophy. |
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Systolic HF is seen most in what population?
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Males Age 50-70
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Explain Hypertrophic Cardiomyopathy
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Hypertrophic cardiomyopathy is a GENETIC disease of the myocardium in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause. It is perhaps most well known as a leading cause of sudden cardiac death in young athletes.
The hypertrophy is uneven. (non concentric), it occurs only in the septal and anterolateral walls. The hypertrophy causes high velocity flow though the ventricle. This causes a venturi effect and pulls the anterior leaflet of the mitral valve into the left ventricle outlet...blocking the flow of blood to the aorta. This motion is called SAM (systolic anterior motion), and blockage can cause sudden cardiac death either due to a) low cardiac output/ ischemia or b)arrythmias. This obstruction due to SAM is also called idiopathic hypertrophic subaortic stenosis (IHSS) |
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Describe treatment and management of Hypertrophic Cardiomyopathy
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DECREASE MYOCARDIAL CONTRACTILITY.
* Avoid events that increase myocardial contractility ---> Avoid inotropes. ---> Avoid SNS stimulation ---> Give BB's, volatiles, CCB's * INCREASE PRELOAD (this prevents increases in contractility). ---> Give volume (IVF) ---> AVOID NITRATES! ---> Avoid hypovolemia * INCREASE AFTERLOAD (to maintain CPP ...pvts ischemia). --->Alpha selective agonists: neosynephrine, levophed --->Avoid inotropes!! Epi, NE, Ephedrine, etc. ---> Avoid vasodilation |
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Sudden death from dilated cardiomyopathy occurs from what?
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SVT
VT Conduction abnomalities (LBBB) |
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What can cause a mural thrombus?
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Dilated cardiomyopathy.
Hypokinetic wall aneurysms out and a mural thrombus forms. This can break off and form an embolii. |
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What area of the heart is hypokinetic with dilated cardiomyopathy?
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Everywhere - global.
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Treatment for dilated cardiomyopathy
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Anticoagulation to pve mural thrombus formation.
ICD (implantable cardiac defibrillator) placement Amiodarone thereapy to pvt SVT, VT, and conduction abnormalities (LBBB). Bi-ventricular pacing - resynchonization therapy Cardiac transplantation. |
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What is the required EF to place an ICD in someone with dilated cardiomyopathy?
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They have to have an EF < 30%.
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How you you anesthetically manage someone with dilated cardiomyopathy?
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1 - DECREASE PRELOAD Preop
---->Fluid Restriction ----> Furosemide ----> ACEIs 2 - AVOID ARRYTHMIAS ----> Get preop K and Mg levels ----> Give lidocaine or amiodarone intraop. 3 - ADEQUATE MONITORING ----> Arterial line ----> Swan Ganz ----> TEE (earliest signs of myocardial ischemia). 4 - MAINTAIN CPP (Avoid VD!!!) ----> Vasopressors: Neo, NE, Vasopressin 5- MAINTAIN CONTRACTILITY ----> Inotropic agents: Epinephrine, Digoxin VOLATILES: ---> Risks: Will depress the myocardium, cause bradycardia, and vasodilation...be careful to monitor HR and BP. ---> Benefits: Precondition the heart to tolerate ischemic events. INDUCTION ---> Etomidate is the DOC. ---> Opiods are okay ---> Ketamine depends on how bad off the pt is...pt is usually beta blocked so it might be okay. Reserve ketamine for aortic ruptures. |
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When does peripartum cardiomyopathy occur?
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Anytime from the 3rd trimester until 5 MONTHS Post partum.
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Explain Peripartum Cardiomyopathy, the risk factors, cause, tx, and anesthesia implications.
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This is cardiomyopathy that occurs from the 3rd trimester until 5 months postpartum.
RISK FACTORS: ---> Multiparity ---> Age ---> Preeclampsia TX: Treat the symptoms ANESTHESIA: ---> Regional anesthesia is preferred. ---> Careful monitoring of preload and afterload. ---> Maintain cardiac output and metabolic needs. |
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What is the first line of tx in heart failure?
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ACEI's and ARBs
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Medical Therapy for Heart Failure
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Diuretics
ACE inhibitors or Angiotensin Receptor Blockers Beta Blockers Digoxin (inotropic) Aldosterone Antagonists Nitrates, ASA (anticoags), Satins(antiinflammatory) |
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ACEIs and ARBs for heart failure...explain their therapeutic and adverse effects.
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First Line Therapy for Heart Failure
CAUSE * Vasodilation (no AngII) * Blunting of SNS response * Inhibit neuroendocrine response (no ADH) * Decrease Preload * Augment kinin mediated prostaglandin production THERAPEUTIC EFFECTS * Improved Survival * Reduced Disease Progression * Favorable for MYOCARDIAL REMODELLING * Enhances overall sense of well-being ADVERSE EFFECTS * Renal Dysfunction * Hypotension * Hyperkalemia * Contraindicated in Pregnancy * Angioedema |
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Aldosterone Antagonists
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End in "-one"
Spironolactone and Epleone Therapeutic Effects" ---> Improvement in functional class ---> Reduction in HF hospitalizations Adverse Effects: ---> Hyperkalemia ---> Renal dysfunction. |
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When is hydralazine used in heart failure?
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When the pt is intolerant to ACEI's. (AA and geriatric pts)...don't ahve renin.
Adverse effects: it can cause rebound tachycardia and can induce lupus. It also can cause tolerance. |
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Phosphodiesterase Inhibitors...what are they and when are they used in heart failure?
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They end in -one
Milrinone and Amrinone. These are phosphodiesterase III inhibitors (the enzyme that degrades cAMP in the heart). Therefore, they increase cAMP in the heart and cause vasodilation by increasing Ca ATPase activity. So these drugs are positive inotropes (but minimal chronotrophic effects). They VD the CA's. Not used for chronic therapy due to risk of dysrhythmias. ADVERSE EFFECTS: ---> Enhanced mortality with chronic therapy ---> HOTN ---> Thrombocytopenia |
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Chlorothiazide
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Thiazide Diuretic
Blocks the Na/Cl cotransporter in the distal convoluted tubule. Improves cardiac function in heart failure by decreasing preload. ADVERSE EFFECTS: ---> Azotemia (high Nitrogen levels) ---> Hypercalcemia |
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Furosemide
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Loop Diuretic
Used in HF to decrease preload. Side Effect is hypovolemia. |
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Bumetanide
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Loop Diuretic
Used in HF to improve exercise tolerance. Side Effects is HOTN |
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Nesiritide (Natrecor)
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Diuretic used in ACUTE HF
A B-type natruretic peptide (decreases preload). Also causes vasodilation. |
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Levosimendan
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Calcium sensitizer used in Acute decompesated heart failure.
Causes vasodilation of the CA's. "Sounds like "leave him" alone. Imagine a "sensitizer" to an outcast group urging people to leave them alone and not harrass them. This is a calcium sensitizer. Causes VD. When you are left alone you VD. VD's the CA's. |
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Dobutamine
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B-Agonist used in Acute Heart failure to increase Inotrophy.
Also cause VD and decreased PVR. SIDE EFFECTS: tachycardia, tachyarrythmias. |
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Digoxin
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Used in chronic therapy for heart failure.
Inhibits Na/K ATPase. This increases intracellular Ca via another channel due to changes in membrane potential. This increase inotrophy. Decreases central SNS tone, which inhibits compensatory neurohumoral effects. ADVERSE EFFECTS * Arrythmias * Conduction disturbances * GI Symptoms * Neurologic complaints (visual disturbances, confusion). |
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Acute Heart Failure Treatment
What is the first line of tx? |
INOTROPIC SUPPORT!!
---> Epi, Dopamine, Dobutamine, NE ---> Phosphodiesterase inhibitors block the breakdown of cAMP (Milrinone, Amrinone) (the second are better because of less side effects). Also: ---> Nitrates and vasodilators ---> Diuretics (reduce preload) ---> B-type natriuretic peptide ---> Nesiritide (Natrecor) ---> Mechanical devices ---> IABP-intraaortic balloon pump. ---> LV or RV assist device |
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Describe anesthetic management of ACUTE heart failure
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* Etomidate is the induction med of choice. NMB's and benzo's are okay.
* Opiods provide CV stability and decrease tachycardia * Milrinone for inotrophic support. * Treatment of ischemia * Optimization of BP * Maintain sinus rhythm (amiodarone, lidocaine) * Optimize intravascular volume (diuresis) (restrict IVF) * Regional vs General: Both will venodilate and reduce preload..which is good. * Volatiles provide dose dependent depressant effects..be careful. * AVOID N2O - will increase PVR secondary to sympathetic stimulation. * MAC anesthesia * Monitoring depends on type and complexity of the surgery and the perioperative risk factors |
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Indications for ICD placement with heart failure...ie what makes you a candidate?
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* Survivors of a cardiac arrest
* Life expectancy of > 1 yr * Patients with sustained ventricular tachycardia or inducible ventricular tachycardia * LVEF <30% following a myocardial infarction (Cardiac resynchronization therapy can be combined with an ICD as a single case) |
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What is Cardiac Resynchronization Therapy and what makes a pt a candidate?
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Biventricular pacing combined with ICD
*Re-coordinate the action of the right and left ventricles in patients with heart failure. It improves the left ventricular function and favors REVERSE REMODELING! * There are THREE LEADS: 1) Right atrial lead (defibrillating ability) 2) Left Atrial Lead (defibrillating ability) 3) Coronary sinus lead: Allows the right and left ventricle to fire at the same time. Sits in the coronary sinus. CANDIDATES: End-stage CHF (Stage 3 or 4) Maxed out Medical Therapy (refractory) Left or right BBB by ECG |
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What is persistant superior left vena cava and what problem does this pose when someone needs a biventricular pacer (cardiac resynchronization) with HF?
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The left brachiocephalic vein does not develop fully and the left upper limb and head & neck drain into the right atrium via the coronary sinus.You can't get the coronary sinus lead into the coronary sinus.
The pt needs a mini thorocotomy done to place the lead through the left ventricle. |
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What is a Dor Procedure?
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Ventricular Reconstruction Surgery after Severe HF.
* Coronary artery bypass grafting, * Mitral and tricuspid valve repair * Resection of left ventricular scar or aneurysm * Reshaping the left ventricle from an spherical to an elliptical shape ( Epicardial left ventricular pacing lead placement |
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What is an LVAD (Left Ventricular Assistive Device?)
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A mechanical circulatory device that is used to partially or completely replace the function of a failing heart. THIS IS NOT AN ARTIFICIAL HEART.
Consists of pulsatile or non-pulsatile flow pumps. Ex: HeartMate II, Abiomed devices These can be used to sustain life for a period of time if a pt is not a candidate for a heart transplant. They can also be used to treat acute heart failure. |
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How do you select a candidate for a left ventricular assistive device?
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FUNCTIONAL ASSESSMENT:
--->Class III or IV --->Inability to walk one block without SOB --->Maxed out medical therapy: Intolerant or refractory to ACE inhibitors, ARBs or Beta-blockers --->One heart-failure related hospital admission in the past 6 months --->Failed cardiac resyncronization therapy --->High diuretic dose LAB VALUES: Serum Na < 136 mmol/L BUN > 40 mg/dl or serum creatinine > 1.8 mg/dl Hct < 35% |
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What makes someone a candidate for a heart transplant?
Who is NOT? |
Reserved for otherwise healthy patients with end-stage congestive heart failure with severely impaired function despite optimal medical therapy
Excluded for transplantation if they have chronic medical co-morbidities, pulmonary hypertension, active infection, psychosocial contraindications, or medical non-compliance, or if they do drugs. |
