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Flashcards in Exam 3 -- Cardiovascular System Deck (109):

What are the ocular signs or symptoms that can accompany cardiovascular disease?

Retinal artery or vein occlusion, macroaneurysms, TIA, retinopathy, ocular ischemic syndrome


What are some of the roles of vascular endothelium?

Blood tissue permeability, coagulation/clotting control, vessel repair, blood flow modulation, inflammation and cell growth regulation, oxidation of LDL


True or false: the heart valves have muscles to aid in blood passage through the heart

False; they work on a passive basis


Name the four valves of the heart in the order in which the blood passes through them, along with the structures each valve separates

Tricuspid valve (blood from right atrium --> right ventricle), pulmonic valve (blood from right ventricle --> pulmonary artery), bicuspid/mitral (blood from left atrium --> left ventricle), aortic valve (blood from left ventricle --> aorta)


Normal heart rate is 60-100 bpm. Above 100 bpm is called _______________, below 60 is called _______________

Tachycardia, bradycardia


Systole is contraction of the walls of the ventricles to empty the heart of blood. Which valves are closed during systole?

Mitral and Tricuspid (heart is eMpTying)


Which heart sound corresponds to the closing of the mitral and tricuspid valves?



What is preload? Within limits, what does increased preload do? What is this relationship called?

Amount of blood in the ventricle at the end of diastole (end diastolic volume, EDV). Increased preload (within limits) stretches the ventricle more, which leads to a more rapid and forceful ventricle contraction. This is called the Frank-Starling relationship. (Think of ventricle as a rubber band: more stretch = more energy = further distance when shot; but if too much stretch would not be good.)


What is afterload? What factors affect it?

The force against which ventricles must contract to eject blood. Arterial pressure is the main factor, but thickness of blood and vessel elasticity (among other things) play a role too. (More elastic vessels = decreased afterload = easier to push blood out; think of as a new balloon, which is less elastic than an old balloon; you, the heart, would have to work harder to fill a new balloon than an old balloon)


Contracility is the force of ventricular contraction. It is independent of loading conditions. Calcium and beta-blockers affect contractility.

Free card


What is a normal value for cardiac output?

5-6 L/min


Cardiac index is cardiac output divided by body surface area. What range is the normal range of values?

2.6-4.2 L/min/square meter


Briefly describe conduction of electrical impulses in the heart, starting with the SA node.

SA node fires, sending signals simultaneously to AV node and left/right atria. The atria contract; AV node delays the signal slightly before sending it on through the bundle of His. Bundle of His separates into right and left bundle branches, which each become Purkinje fibers and cause the ventricles of their respective sides to contract.


The sympathetic nervous system affects heart rate and contractility. How does this occur?

It stimulates beta-1 receptors of SA and AV nodes, causing them to pass signals along faster (increased heart rate), also shortening conduction time through the AV node. It also innervates the atria/ventricles and increases their contractility by increasing calcium concentration


The parasympathetic nervous system affects heart rate and contractility. How does this occur?

It decreases heart rate through the nodes. Through the vagus nerve it also innvervates the atria but not the ventricles, causing only a slight decrease in contractility


The atrial and ventricular myocytes form two syncytia. What is this and what does mean?

The cell membrane of the myocytes are fused together, meaning that if one of them depolarizes, they all depolarize. This allows them to all contract together (important for regular heart beats.


Contractility of heart muscle is increased by what?

Increased free (unbound) calcium


Relaxation of heart muscle depends on removal of calcium from the myocyte cytoplasm. How does this occur?

Through exchange with sodium (sodium in for calcium out) and through uptake into sarcoplasmic reticulum and mitochondria


Name a medication that interferes with the sodium-potassium pump in the heart. What effects (including side effects) does this drug have?

Digitalis; slows HR (through delayed AV node signal conduction), increases contractility (through increased inctracellular calcium). SE include blurred vision, color perception alteration, halos on dark objects


Name a medication that interferes with calcium channels in the heart. What effects does this drug have?

Verapamil; decreases afterload (through vasodilation of vascular system via delayed calcium influx into vascular smooth muscle); decreases contractility; delays removal of calcium from pacemaker cells, thus slowing HR (through interfence of SA/AV node repolarization)


What class of medication interferes with the autonomic nervous system innervation of the heart by blocking epinephrine? What is the result of this blockage? You wouldn't want to use this class of drugs in patients with what type of condition?

Beta-blockers; these decrease HR and contracility. They also slow conduction time, so you wouldn't want to use them in a patient with severe heart block (their heart rate is already too slow).


Serum enzyme tests are done to detect enzymes released by dying heart muscle. Creatinine phosphokinase (CK-MB), lactate dehydrogenase (LDH-1), and troponin I are three such tests. Levels of these substances start increasing how long after the myocardial infarction (MI)? When do levels peak? When do they return to normal?

CK-MB: increased 2-6 hours after, peak at 12-24 hours, normal in 3 days; LDH-1: increased in 24-72 hours after, peak at 2-5 days, normal in 14 days; Troponin I: increased 4-6 hours after, peak at 10-24 hours, normal in 10-15 days


Of the serum enzyme tests, which is probably most specific?

Troponin I


An EKG doesn't indicate anything about heart disease; it only analyzes the electric circuitry of the heart. How many peaks/deflections should show on a normal EKG? What is indicated by each peak?

5 peaks: P (atrial cell depolarization), QRS (ventricle depolarization), and T (ventricular repolarization). [FYI: PR interval measures AV conduction time, or the time from the onset of atrial depolarization to the time of onset of ventricular depolarization.]


What is the purpose of a stress test?

A stress test determines the heart's response to physical exertion by measuring ECG, BP, and pulse during exercise. Changes in the ECG during the exercise as compared to rest indicate presence and severity of the ischemia.


True or false: cardiac catheterization is used to detect pressures and patterns of blood flow.

True. You can also inject contrast for angiography


A coronary calcium scan is a CT used to evaluate calcium buildup in coronary arteries. Generally, people with risk but no symptoms are evaluated with this test. What is the range of possible scores on this test? What kind of score is more likely to be indicative of coronary artery disease?

Score range: 0-400; greater than 100 means likely to have CAD


Ultrasonography shows structure and movement of the heart, and doppler is a special form of ultrasonography used for blood vessels to show bloodflow.

Free card


Multiple-gated acquisition scan (MUGA scan) is a radioactive test. What part of the heart is monitored, and what is being measured?

The left ventricular wall is monitored for the left ventricle's ability to eject blood. This tests the function of the heart and the heart's cardiac output


Stress thallium (DIP-thal) is a test that involves injection of thallium 201. It is used to image the heart. What types of tissue take up the radioactive thallium?

Healthy myocardial tissue, but not infarcted or scarred tissue, and not blood.


Define: arrhythmia

Irregularity in rate or rhythm


Cardiac arrhythmias can be accompanied by several symptoms. What are some of these symptoms?

Palpitations, dizziness, lightheadedness, syncope, anxiety, chest or neck discomfort, dyspnea, weakness.


True or false: cardiac arrhythmias are always accompanied by some amount of lightheadedness

False; arrhythmias can in fact be asymptomatic.


Diagnosis of arrhythmias may involve case history, clinical exam, EKC, echocardiogram, even monitor, and what other type of device?

Holter monitor (24-48 hour time period in which patient wears the device and it monitors for irregularities of heart beat)


What are different ways an arrhythmia could be classified?

Tachyarrhythmia (too fast) vs. bradyarrhythmia (too slow); supraventricular (atrial or nodal) vs. ventricular; regular vs. irregular


How would you describe the heartbeat of a patient with a regular arrhythmia?

One that is either too fast or too slow, but still a predictable beat with the two heart sounds.


How would you describe the heartbeat of a patient with a irregular arrhythmia?

The beat is still predictable but the heart sounds are abnormal (could be three heart sounds, for example).


How would you describe the heartbeat of a patient with a irregularly irregular arrhythmia?

The rhythm is completely unpredictable.


Sinus tachycardia is due to an increased rate of the SA node. It can be caused by exercise, fear, fight, stress, etc (due to catecholamine release). What are some diseases or conditions that might cause sinus tachycardia?

Anemia, hyperthyroidism, heart failure


How would you treat sinus tachycardia?

Treat the underlying condition (i.e., treat the hyperthyroidism, if that is the cause) or use a med that slows AV node: beta blockers or calcium antagonists.


Atrial fibrillation is the most common sustained rhythm disturbance and is what type of arrhythmia? (i.e., regular, irregular, or irregularly irregular)

Irregularly irregular


The constant depolarization of the atria in atrial fibrillation is based down to the ventricles as well, though these beat at a much slower rate. (Atria = 300-600 bpm, ventricles = 120-170 bpm). Where does the signal come from causing the constant atrial depolarization?

Usually near the pulmonary vessels


What are the three "classic" causes of atrial fibrillation? What are the most common causes of atrial fibrillation?

Rheumatic heart disease, excessive alcohol, and thyrotoxicosis are the "classic" causes but aren't very common due to these conditions being treated before they tend to cause fibrillation. Hypertension and heart failure are the most common causes.


Atrial fibrillation increases a patient's risk for what other conditions?

Ischemic stroke (due to poor cardiac output), embolization, and non-stroke dementia (poor blood flow)


How would you treat atrial fibrillation?

Treat any underlying cause; use beta blockers or calcium channel blockers (slow ventricle contractions); use amiodarone or dronedarone (prolong action potential); radiofrequency ablation (of the cells causing the irregular stimulation); possible electrical cardioversion


Anticoagulation medications are used in atrial fibrillations because clots can easily form in the left atrial appendage. Which medications might be used? Which of these can be offset with vitamin K should an overdose occur?

Warfarin, dabigatran, apixaban, rivaroxaban. Warfarin OD can be treated with vitamin K; the other three would need blood transfusion in case of OD.


From an eyecare point of view, why should a patient on amiodarone be monitored carefully?

SE include corneal microdeposits (in 90%, but doesn't cause vision loss), lens opacities, disc edema (concerning), optic neuritis (very concerning;)


What sorts of ocular side effects might a patient on warfarin experience? What tests should be performed to check how their clotting times are affected by the medication?

Subconjunctival hemmorage, retinal or vitreous hemorrhage, spontaneous hyphema, cerebral hemorrhage. Patient should have PT and INR done


AV nodal re-entry tachycardia is more common in which gender?



Briefly describe mechanism of AV nodal re-entry tachycardia.

In some individuals, there are two paths through the AV node, when normally there is only one. The "extra" path depolarizes slower but repolarizes more quickly than the normal path. Normally, signals sent through the AV node go through the normal path and any depolarization of the extra path is cancelled out. However, if the AV node is stimulated again while the normal path is still in its refractory period, the signal will get passed through the extra path into the AV node, then the signal travels retrograde back to cause the atria to contract. This contraction passes a new signal back to the AV node, where the second (extra) path is again stimulated since it repolarizes more quickly and the normal path has not yet repolarized. This cycle continues until it is stopped by very good timing of the normal path repolarization (to stop the extra signal) or extraneous methods by health care professionals.


How would you treat AV nodal re-entry tachycardia?

Increase vagal (parasympathetic) stimulation to the SA/AV nodes so they can reassert control. This can be attempted through mechanical maneuvers (carotid sinus massage, valsalva maneuver, head immersion in cold water) and/or with medication (adenosine). You can use long-acting beta-blockers, calcium channel blockers, and digitalis to prevent AVNRT episodes. Radiofrequency ablation can be done to block signals going down the "extra" (slow) AV pathway.


Wolff-Parkinson-White syndrome is more common in which gender?



True or false: Wolff-Parkinson-White syndrome is inherited

True, but not 100% true; it can random (doesn't have to be inherited)


In Wolff-Parkinson-White syndrome, there is an accessory pathway between the atria and the ventricles that allows impulses to quickly travel between the atria and the ventricles (in either direction). This syndrome is more prone to atrial fibrillation than is AVNRT. Atrial fibrillation can lead to life-threatening ventricular fibrillation.

Free card


Premature ventricular contraction (PVC) is extremely common and usually does not effect the eatria or the SA node. Which factors may incrase the frequency of PVC?

Age, infection, emotional stress, caffeine, tobacco, alcohol.


Sustained ventricular tachycardia is when the ventricles beat between 120-220 bpm but have a regular rhythm, for longer than 30 seconds. What is the cause? How does this effect cardiac output? What is done to correct this condition?

Cause is unknown; cardiac output is decreased; direct current cardioversion helps correct


True or false: ventricular fibrillation is associated with a very rapid and irregular heart rate.



Patients with ventricular fibrillation have no cardiac output, requiring CPR or defibrillation to sustain life. Survivors are at risk for sudden cardiac death and have cardioverter-defibrillators implanted.

Free card


Bradycardia usually results from ________________ or _________________.

Inadequate SA node activity (sinus bradycardia), blocked conduction (AV block)


True or false: sinus bradycardia can occur in response to cardiovascular conditioning of athletes, hypothyroidism or drugs, and is highly concerning.

False; it can indeed occur in response to cardiovascular conditioning of athletes, hypothyroidism or drugs, but it is typically of limited concern.


Treatment of sinus bradycardia, if needed, may consist of what?

If the condition is extreme enough to cause symptoms, you can use atropine to increase the sinus rate. A pacemaker can also be implanted.


AV block occurs when not all of the signals generated by the SA node make it to the ventricles. Three degrees of AV block were discussed in class. Which degree features a pulse that feels normal but would every so often skip a beat?

Second degree; this is due to intermitten failure of the signal to reach the ventricles.


What treatment might be considered for a patient with second degree AV block?



AV block occurs when not all of the signals generated by the SA node make it to the ventricles. Three degrees of AV block were discussed in class. Which degree features an overall slower HR that is otherwise normal?

First degree; this is due to the AV node sending signals on more slowly.


AV block occurs when not all of the signals generated by the SA node make it to the ventricles. Three degrees of AV block were discussed in class. Which degree seldom has symptoms or requires treatment?

First degree.


AV block occurs when not all of the signals generated by the SA node make it to the ventricles. Three degrees of AV block were discussed in class. Which degree involves none of the atrial impulses reaching the ventricles?

Third degree (aka complete)


In third degree AV block, what mechanism compensates for the block?

AV node can take over the pacemaker job, or the ventricles can start to spontaneously depolarize.


Since severe bradycardia can occur in third degree AV block (15-40 bpm), a pacemaker should be implanted in these patients.

Free card


What are the two most common cause of preventable deaths in the US?

Smoking is #1, hypertension is #2


Risk factors for hypertension include family hx, obesity, renal disease, increased age, alcohol abuse, cigarette smoking, diabetes mellitus, lack of sleep, some medications. Which gender has a higher prevalence for hypertension?

Males, but once women hit menopause the prevalence evens out between the genders.


Which factors can affect a blood pressure measurement?

Time of day, level of anxiety, recent activity, caffeine intake, etc.


What is the systolic/diastolic BP measurement for the normal category?

Adults: <90th percentile


What is the systolic/diastolic BP measurement for the pre-hypertension category?

Adults: 120-139/80-89; younger than 18 years: between 90th-120/80


What is the systolic/diastolic BP measurement for the hypertension stage 1 category?

Adults: 140-159/90-99; younger than 18 years: >= 95th percentile to 5 mmHg above 99th percentile


What is the systolic/diastolic BP measurement for the hypertension stage 2 category?

Adults: >=160/>=100; less than 18 years: >5 mmHg above 99th percentile


What qualifies a patient as in the hypertensive urgency category?

BP >180/>110 (which is stage 2 HTN)


What qualifies a patient as a hypertensive emergency?

Urgent BP (>180/>110) with organ damage


If a patient's systolic BP is <80 (i.e., normal), what is the recommended follow up plan?

Recheck in two years


If a patient's systolic BP is 120-139 or their diastolic BP is 80-89 (i.e., pre-hypertensive), what is the recommended follow up plan?

Recheck in 1 year, discuss lifestyle modifications


If a patient's systolic BP is 140-159 or their diastolic BP is 90-99 (i.e., stage 1 hypertension), what is the recommended follow up plan?

Confirm within two months


If a patient's systolic BP is 160-179 or their diastolic BP is 100-109 (i.e., stage 2 hypertension prior to the urgent point), what is the recommended follow up plan?

Refer to PCP within one month


If a patient's systolic BP is 180-219 or their diastolic BP is 110-119, what is the recommended follow up plan?

Refer to PCP within one week


If a patient's systolic BP is >220 or their diastolic BP is >120, what is the recommended follow up plan?

Refer to PCP within 24-48 hours if there are no end organ effects; refer within a few hours if end organ effects are present


What conditions are considered end organ effects of hypertension?

Cardiovascular (atherosclerosis, coronary artery disease, heart failure, left ventricular hypertrophy, MI, unstable angina, aneurysm); brain (hemorrhagic stroke, Alzheimer's, confusion), CKD, pulmonary edema, eye (retinopathy, optic nerve head edema), peripheral artery disease


Review the chart for management hypertension in patients younger than 18 years.

Free card (kind of)


Truly or false: untreated hypertension reduces life expectancy by 10-20 years



Increasing either peripheral resistance or cardiac output increases blood pressure. What factors increase peripheral resistance?

Vessel size (vasoconstriction increases BP), vessel elasticity (decreased elasticity increases BP), blood viscosity (increased viscosity increases BP)


Increasing either peripheral resistance or cardiac output increases blood pressure. What factors increase cardiac output?

Blood volume (increased blood volume, for example through renin release increases BP); heart rate (increased HR increases BP)


Primary hypertension is the most common form of HTN in adults. What is its cause?

Cause is unknown, though there may be some influence from environment/genetic factors (excess salt intake, obesity, lack of exercise, abnormal peripheral resistance, renin-angiotensin-aldosterone abnormalities, impaired natriuresis [naturiuresis = ability to remove salt from body])


Secondary hypertension is attributable to a known cause. What are some of these causes? Which cause is the most common in individuals younger than 20 years?

CKD, endocrine disorders, sleep apnea or sleep deprivation, meds (contraceptives, cold remedies or appetite suppressants, NSAIDs). CKD is the most common cause of hypertension in individuals less than 20 years old


Lifestyle modification for hypertensive patients includes what?

Smoking cessation, dietary sodium less than 2.3g/d (6g NaCl), maintenance of adequate dietary potassium, calcium, magnesium, and vitamin D, limitation of alcohol intake


True or false: milk chocolate can lower BP about as much as one medication (5.2 mmHg systolic and 1.8 mmHg diastolic)

False; dark chocolate has this effect, not milk chocolate


Laughter can help decrease BP through decreasing sympathetic activity and dilating blood vessels

Free card.


Antihypertensive drugs usually work through decreasing cardiac output and/or peripheral resistance. Which categories are suggested as first line by the JNC8?

Thiazides, ACE inhibitors, angiotensin receptor blockers, calcium channel blockers. Beta-blockers and renin inhibitors can also be used but are not on the JNC8 first line list.


How many medications do most hypertensive patients require to achieve control?



None of the hypertensive medications is inherently superior to the others. What factors can influence the choice of medication? Which medication should be avoided in African Americans?

Comorbidities (CKD), ethnicity, cost, tolerance/compliance. ACE inhibitors should not be used in African Americans.


Reminder: get the drug chart on Moodle; learn the action of the major categories, specific indications, optometric interests, and mechanism of action

Not-so-free card


What is the JNC8 guideline for general nonblack population in terms of first line hypertensive medication?

Thiazide, calcium channel blocker, ACE inhibitor, angiotensin receptor blocker


What is the JNC8 guideline for general black population in terms of first line hypertensive medication?

Thiazide, calcium channel blocker


What is the JNC8 guideline for patients with CKD and HTN in terms of first line hypertensive medication?

ACE inhibitors, angiotensin receptor blocker


What glaucoma concerns should be considered for patients being treated for hypertension?

If patient is already on an oral beta-blocker, a topical beta-blocker won't help with IOP; nocturnal hypotension increases risk of progression of POAG and NTG (some people's IOP naturally drops overnight, so taking HTN meds at night may make this worse).


Marfan syndrome is a connective tissue disorder. It is an autosomal dominant disease. If a person with this condition is untreated, around what age might they die?

Fourth or fifth decade


What non-ocular findings could a patient with Marfan's syndrome have?

Narrow face, long legs/arms/fingers, tall/slender, loose joints, narrow high-arched palate, curvature of spine, chest deformities, dimished reflexes and muscle tone, skins folds/stretch marks with no previous weight gain or loss.


What ocular findings could a patient with Marfan's syndrome have?

Axial myopia, bilateral ectopia lentis* (lens pulled up superior temporal), strabismus, iris transillumination, retinal detachment, glaucoma, cataracts, peripheral retinal degenerations, blue sclera


What cardiovascular concerns would you have about a patient with Marfan's syndrome?

Ascending aortic dilation*/aneurysm/dissection, aortic regurgitation, mitral valve prolapse


What pulmonary concerns would you have about a patient with Marfan's syndrome?

Pneumothorax, obstructive sleep apnea


What are key features in diagnosing Marfan sydrome?

Family history (fam hx + bilateral ectopia lentis or fam hx + ascending aortic dilation is enough to make diagnosis), ophthalmologic exam, echocardiography/EKG, CT/MRI to assess aorta size, physical exam. DNA analysis of fibrillin gene on chromosome 15 can also be done.


Since there is no cure for Marfan syndrome, what can you do to reduce the potential for morbidity and mortality for a patient with this condition?

Decrease cardiac contractility and blood pressure to lower pressure on aorta (with beta blockers, ACE inhibitors, ARBs), grafts to replace aortic valve and region with aneurysm, avoid contact sports and strenuous exercise, pain meds for aches and pains


When would you refer a patient with Marfan syndrome?

If their condition is undiagnosed, for annual cardiac evaluation, moderate scoliosis, pregnancy, genetic counseling. Severe or unusual chest pain development, send patient to hospital in case of pneumothroax and aortic dissection.