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136 Cards in this Set
- Front
- Back
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what % of pts undergoing surgery have CAD (diagnosed or undiagnosed) |
30 - 40%
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first indicators of CAD
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angina, MI, cardiac arrest
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primary cause of cardiac arrest
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arrythmias
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what surgical and anesthetic agents cause arrythmias
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epinephrine, cocaine, histamine releasing agents, volatile anesthetics, hypoxia
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volatile anesthetic agents are
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negative inotropes
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risk factors associated with CAD
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male, age, hypercholesterolemia, diabetes, family history, cigarette smoking, hypertension, obesity, sedentary life style
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2 most important risk factors for CAD are
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Male gender and age
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relation between cholesterol and risk of CAD
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linear correlation - a cholesterol value >240 doubles the risk for CAD compared to a value of 180
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the effect of smoking on CAD is the same as
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raising your cholesterol level by 50-100mg/dl
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effects of smoking can be reversed if
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quit smoking early enough - if plaque already laid down, some irreversible damage
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decreased cardiac output leads to ??? SVO2
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decreased SVO2 - because increased time for perfusion due to slow heart rate
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increased CO leads to ??? SVO2
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increased SVO2 because faster heart rate decreases time for perfusion in tissues
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Cardiac Output =
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HR x stroke volume
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SVO2 is an indicator of
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cardiac output
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a septic pt has increased SVO2 because
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toxins prevent cells from uptaking needed oxygen or getting rid of CO2
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SVO2 represents
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returning venous oxygen
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Coronary perfusion pressure is
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DBP-LVEDP
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coronary arteries perfuse
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during diastole
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opposing force to the perfusion of the coronary arteries is the
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left ventriclular end diastolic pressure
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angina is a symptom of a
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supply vs demand problem
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driving force for coronary perfusion is
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diastolic blood pressure in the aortic arch
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4 factors that determine myocardial oxygen demand
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heart rate, afterload (systolic wall tension), preload (diastolic wall tension), contractility
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what affect oxygen demand of the heart muscle the most
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heart rate (secondly SVR)
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why is the heart rate the most important factor in considering myocardial oxygenation |
increases work of the heart, decreases time for coronary artery perfusion, also preload reduced because less time for filling and therefore decreased stroke volume
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5 fators that determine myocardial oxygen supply
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heart rate, LVEDP, aortic diastolic pressure, oxygen content of the blood, oxygen extraction
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blood oxygen capacity predominantly determined by
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hemoglobin level
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oxygen extraction affected by |
sepsis, cyanide
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the oxyhemoglobin curve shifted left means
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holds onto O2 more tightly
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beta blockers work by
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reducing oxygen demand by decreasing heart rate more than they reduce supply
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improve coronary perfusion by
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increasing aortic diastolic blood pressure or decreasing LVEDP
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what % of the CO goes to perfuse the heart
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5%
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if heart rate is too fast then
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pt may become acidotic since there is not enough time for proper perfusion in the capillaries leading to some accumulation of CO2
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if heart rate is too slow then
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supply doesn't meet demand oxygen supply is not enough because all oxygen will be emptied off the hemoglobin before it even gets to all the cells
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preop cardiac evaluation
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evaluate cardiac reserve, identify angina, previous MI, medical interventions (cath, stent, drugs) - also check chest exray, EKG, echos, stress tests, cath lab reports, etc
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goal of taking a pt history with possible cardiac issues is to determine |
the severity, progression, and functional limitations introduced by hypertension or CAD.
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stable factor
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EF40>%, LVEDP < 12mmHG, CI 2.5, no dyskinesia, no CHF, previous MI >6months ago or a CABG to fix, Non Q-wave MI
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unstable cardiac factors
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EF < 40%, LVEDP > 18mmHh, CI < 2, Dyskinesia, episodes of CHF, previous MI < 6 months, Q wave MI
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is a Q wave MI stable or unstable
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arguments can be made both ways
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a Q wave MI is
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complete - the entire thickness of the myocardial wall is damaged
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a Q wave mi is associated with
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areas of dyskinesia
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a non Q-wave MI is
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incomplete - there are some areas of ischemia and infarct but is in danger of reinfarction because vessel may close off again
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what do you ask your patient to assess cardiac function if you can't run all the tests you want
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what kind of work do they do, can they climb 2-3 flights of stairs without pain or severe shortness of breath, do they sleep sitting up or with lots of pillows, have they noticed any changes in activity recently, ever been admitted for CHF?
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what is the most striking evidence of decreased cardiac reserve
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exercise intolerance in the absence of significant pulmonary disease
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if a patient answers questions in such a way as to indicate they may have impaired cardiac function - consider |
do they need a cardiac workup, is this an elective surgery? baseline ekg? chest xray? would volatiles be the best? do we need positive inotropes in the room? who will I run my fluids? how will I treat hypotension, hypertension? do I need to pretreat with a beta blocker or something else to make induction smoother?
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is angina stable or unstable
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angina is considered stable if there has been no change in precipitating factors, duration, or frequency in the last 60 days.
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70% of ischemic episodes are not
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associated with angina
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silent MI's account for
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15%
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candidates for silent MI's are |
women and diabetics
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what is the most ominous sign of CAD
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angina at rest
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coexisting diseases that should raise your suspicions of CAD are
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diabetes, untreated hypertension, peripheral vascular disease, COPD, renal dysfunction, and long term smokers
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risk of reinfarcting on the table at 0-3 months after an MI is
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37%
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risk of reinfarcting on the table at 3-6 months after an MI is
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16%
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risk of reinfarcting on the table at more than 6 months after an MI is
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5%
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if a patient has a heart attack, delay the surgery if possible until |
more than 6 months after the MI
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labetalol is contraindicated in
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asthmatics
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labetalol ratio of nonspecific blockers is
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7:1 nonspecific beta: alpha
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B1 block causes
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decreased heart rate
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B2 block causes
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bronchoconstriction
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alpha block causes
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vasodilation and decreased SVR
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esmolol is ??? specific
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B1 specific in smaller doses but will eventually carry over to B2 receptors - so use cautiously in asthmatics
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factors that increase the risk of a perioperative MI
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site and extent of previous MI, hx of CABG, plasty, or stenting, intrathoracic or intraabdominal surgeries lasting more than 3 hours, multiple surgery procedures in same operative setting, and anesthetic technique
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perioperative beta blocker protocol
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a beta blocker started 7 - 30 days prior to surgery and continued 30 days after surgery reduces risk of cardiac morbidities by 90%
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a betablocker started day of surgery
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and continued for 7 days after surgery, reduces risk of perioperative mortality by 50%
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anesthetic goals are
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increase O2 delivery, reduce demand for O2, keep HR WNL, block sympathetic effects (intubation, pain), and avoid anesthetics that suupresses myocardial contractility
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how do anesthetists improve oxygen delivery
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providing oxygen, maintain bp in WNL, obtaining or maintaining a normal preload, maintian normal contractility, maintaining a normal hemoglobin
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how do anesthetists reduce demand for oxygen
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address tachycardia, address high SVR, address excessive HTN, address stress, pain, anxiety, address hemodynamic changes or avoid hemodynamic changes during stimulating times in the surgery
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what can produce tachycardia and hypertension in surgery
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pain, intubation, incision, surgical tugging, light anesthetic,
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when can intubating cause bradycardia
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in small children
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negative inotropy of volatile anesthetics is
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dose dependent - so can be run at a lower MAC with adjunct medication if need to limit negative inotropy effect
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causes of hypertension, tachycardia, and arrythmias in surgery caused by surgeon
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local anesthetics such as epi and cocaine can be absorbed into the systemic circulation
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anesthetic implications to consider when trying to regulate cardiac effect in surgery
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intubation, incision time, surgical tugging, light anesthetic use, post-op pain, volatile anesthetics, epinephrine and cocain local anesthetics, histamine releasing agents, and hypotensive effects of many drugs
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the most common circulatory problem is
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hypertension
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hypertension affects #
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60 million americans - 2/3rds of the people over 60
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essential hypertension
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accounts for 95% of cases and has no identifiable cause
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secondary hypertension
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has an identifiable etiology and is usually renal related
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possible causes of secondary hypertension
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cushings disease, conn's disease, pyelonephritis, pheochromocytoma, coarctation of the aorta, renal disease, renal artery stenosis
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pheochromocytoma is a disorder that causes
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epi secretion
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old definition of hypertension
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two consecutive BPs taken 5 minutes apart in the sitting position with a systolic > 160 mmHg and a diastolic > 90 mmHg
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new definition of hypertension
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115/75
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the risk for cardiovascular disease
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doubles with each increase of the BP by 20/10 mmHg above 115/75 mmHg
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hypertension in older people occurs because
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of loss of elastin in vascular system
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contributing factors to essential hypertension
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sympathetic nervous system, increased renin release by the kideys, too much vasoconstriction, or not enough vasodilation - basically salt and water retention
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significant risk factors for essential hypertension
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ischemic heart disease, angina, LVH, CHF, CVA/TIA, renal insufficiency - all will lead to end organ disease due to poorly controlled essential hypertension
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essential hypertension is a big problem in
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the african american community
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blood pressure =
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CO x SVR
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PIH theorized to be caused by
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imbalance between thromboxane and prostacyclin
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ace inhibitors side effect is
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cough
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cardiac output (as a cause of hypertension) is increased by
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increased extracellular fluid volume, decreased glom filtration rate, impaired sodium excretion, increased renal nerve activity, ineffective natriuresis, increased contraction, increased adrenergic activation
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systemic vascular resistance (as a cause of hypertension) is increased by
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increased vasoconstriction, increased adrenergic stimuli, inappropriate renin endothelin release, increased thromboxane, decreased vasodilation, decreased prostacyclin, decreased nitric oxide
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increased pressure in the renal artery causes (step 1 of the loop)
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pressure diuresis leading to decreased volume which causes the sympathetic system to vasoconstrict leading the kidneys to release renin which causes the formation of angiotensin I which promotes the release of aldosterone
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aldosterone causes
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increased reabsorption of sodium
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increased pressure in the renal artery causes (step 2 of the loop)
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angiotensin I goes to the lungs to be converted to angiotensin II by the angiotensin converting enzyme. angiotensin II is a potent vasoconstrictor which then increases the SVR and BP and causes the whole cycle to begin again
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what does the increasing hypertensive loop mean in a preop context
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a patient may be hypertensive and hypovolemic
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vicious hypertensive cycle
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hypertension causes increased ventricular wall pressure and increased work to unload and increasing oxygen demand. as lvedp and lvedv increase coronary perfusion decreases leading to ischemia, infarction, arrythmias, and heart failure
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coronary insufficiency is created in 2 ways
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shear stress of the coronary arteries lead to CAD and increased LVEDV and LVEDP reduce perfusion during diastole
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infarction and dysrythmias leads to
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heart failure which leads to hypertrophy to compensate which then causes increased myocardial O2 demand and increased myocardial wall tension
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can you have angina without CAD
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yes - a person with sever hypertension can develop angina even if they do not have CAD because the perfusion during diastole is decreased and the oxygen demand is increased
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anesthetic goals in managing pt with hypertension
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fluid management, check electrolytes, keep bp within 20% of normal
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why is fluid management not necessarily obvious in a pt with hypertension
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may be volume depleted even if hypertensive - pt may be on diuretic to keep volume down due to hypertension and may be clamped down too
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why check electrolytes on hypertensive pt
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especially if on diuretic - may have elevated or low K+ level based on whether or not K+ sparing diuretic
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autoregulation curves shift in a hypertensive pt
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to the right - therefore need to keep bp within 20% of normal which for a chronic htn patient will be higher than a healthy normal - in order to keep organs perfusing
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what bp meds do you take and what bp meds don't you take before surgery?
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do take beta blockers and Ca++ channel blockers. Don't take diuretics. ACE inhibitors? If take, watch for low BP
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hypertrophic cardiomyopathy is aka
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obstructive hypertrophic cardiomyopathy and
idiopathic hypertrophic cubaortic stenosis |
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cardiomyopathy is
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a compensatory enlargement of the heart
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hypertrophic cardiomyopathy is caused by
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a genetically transmitted disease
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hypertrophic cardiomyopathy can cause
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CAD, valve dysfunction, arrhythmias, hypertension, and myocardial hypertrophy because the myocardial cells become hypertrophic and disorganized.
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anesthetic goals for patient with hypertrophic cardiomyopathy are
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increase preload, decrease heart rate, decrease contractility, maintain or increase SVR
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physical differences in heart with hypertrophic cardiomyopathy
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thickened septum wall, narrowed outflow tract, and leaky mitral valve
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what is critical to patients with hypertrophic cardiomyopathy
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RSR - because they rely on the atrial kick for as much as 75% of the LV preload
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describe the problem with functioning of the hypertrophic cardiomyopathic heart
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the thickened septum bulges into the ventricle, narrowing the outflow so when blood ejects through the narrowed outflow it causes a venturi effect that sucks the mitral valve leaflet into the outflow tract making it even more difficult to get the blood out.
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additional problems with hypertrophic cardiomyopathy are
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a stiffened ventricle produces abnormally high LVEDP but still has a low LVEDV, and passive filling is difficult.
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in a pt with hypertrophic cardiomyopathy you want to avoid
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increasing contractility, increasing heart rate, and decreasing preload
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example of the venturi effect
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the winter wind sucking the air out of you
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describe the pressure volume loop of IHSS (hypertrophic cardiomyopathy)
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the loop is tall and narrow and shifted way left - long isovolumetric phases, short ejection phase and small stroke volume (like this on boards)
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stiffer chamber in IHSS causes
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decreased volume
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types of pericardial disease
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inflammatory acute pericarditis, pericardial effusions, chronic pericarditis, constrictive pericarditis
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possible causes of pericardial inflammation are
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viral infections (often), an acute MI, post cardiotomy, metastatic disease, irradiation, tuberculosis, rheumatoid arthritis
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Dressler's syndrome is
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a delayed form of pericardial inflammation that may follow an acute MI
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the inflammation of the pericardium can cause
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fusion of the two pericardial layers leading to pericardial effusions.
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the normal pericardial space holds
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20 - 25 ml
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with constrictive pericarditis the CVP and PAOP will
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even out (some books say at 20 mmHg)
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historically the most common cause of restrictive pericarditis was
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tuberculosis - now is idiopathic
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treatment for chronic pericarditis with hemodynamic compromise is
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pericardiectomy (remove the pericardial sac)
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pericardiectomies are
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associated with high level of intraoperative mortality, arrhythmias, and massive bleeding
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chronic pericarditis is associated with
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constrictive pericarditis an dcardiac tamponade with impaired filling and decreased cardiac output
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causes of cardiac tamponade are
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penetrating trauma, blunt trauma, dissecting aortic aneurysm, cardiac surgery, pericardial effusion and pericarditis
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a reduction in preload and subsequent CO in a patient with cardiac tamponade leads to
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SNS vasoconstriction and tachycardia
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pulsus paradoxus is a sign of
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cardiac tamponade
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pulsus paradoxus is
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this is a reduction in blood pressure with inspiration
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a 12 lead will show on a patient with cardiac tamponade that
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the axis or vector has changed because the heart is torqued
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why do you get hypotension with cardiac tamponade
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because of increased pressure on the heart makes it difficult to fill the heart so you will have decreased cardiac output
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why do you have distended neck veins with cardiac tamponade
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because the increased pressure on the heart will make it more difficult for the blood to return to the heart
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why do you get distant heart sounds with cardiac tamponade
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because the heart is torqued and you have to listen to it through a bunch of fluid (like listening to something under water)
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if patient with cardiac tamponade is viewed as too risky to fully sedate, second option is
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to have local sedation and do a pericardial window under local or a fluoro guided pericardiocentesis
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why not pavulon in a cardiac tamponade case
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good for increased heart rate but lasts way too long for the short pericardial window procedure
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cor pulmonale is |
pulmonary hypertension caused by a lung problem (cover in pulmonary lecture) |
