Cardiovascular Flashcards

(76 cards)

1
Q

Stages of HTN

A

Normal - (<120) / (< or equal to 80)
Elevated - (121-129) / (< or equal to 80)
HTN 1 - (130-139) / (<90)
HTN 2 - 140 or greater / 90 or greater

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2
Q

What is the essential workup of newly diagnosised HTN?

A
  1. Fasting glucose - assess risk for DM
  2. Lipid panel - assess for ASCVD
  3. TSH - assess for hyperthyroidism as a secondary cause
  4. CBC - assess for anemia
  5. BMP - assess electrolytes, kidney function
  6. EKG
  7. UA
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3
Q

What are the requirements for a diagnosis of HTN?

A
  • Two elevated readings from two separate occasions.
  • Always check bilateral arms
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4
Q

How is elevated blood pressure treated? What is considered elevated blood pressure?

A

Elevated blood pressure is considered 121-129 systolic / less than 80 diastolic.

Elevated blood pressure is treated in a conservative manner. Initial treatment options include lifestyle modifications with a recheck scheduled in 3-6 months.

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5
Q

What are some lifestyle modifications that are effective in lowering blood pressure?

A
  1. Weight loss - this is the most effective lifestyle modification at lowering the blood pressure
  2. Reducing sodium in the diet - high sodium diet lead to increased fluid accumulation that elevates the blood pressure.
  3. Exercise
  4. Reduce stress
  5. Stop smoking
  6. Eat healthier
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6
Q

How is HTN 1 blood pressure treated? What is considered HTN 1 blood pressure?

A

HTN 1 - is a blood pressure of 130 - 139 / 80-89.

HTN 1 blood pressure is treated with a combination of lifestyle modifications if there are no other risk factors or ASCVD risk. IF there are other risk factors or if ASCVD risk is elevated, then life style modifications in addition to starting a blood pressure medication is the treatment.

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7
Q

What is the overall goal of HTN 2 treatment?

A

To lower the blood pressure to below 130/90

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8
Q

HTN urgency VS HTN emergency

A

HTN urgency is a blood pressure elevated 180-120 without signs and symptoms of end organ damage.

HTN emergency is a blood pressure elevated 180-120 with signs and symptoms of end organ damage.

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9
Q

What are the most commonly seen end organ damage signs and symptoms?

A

End organ damage seen in HTN emergency typically presents with damage to:
- Brain - stroke, ICH - headache, stroke symptoms, AMS, lethargy
- Heart - angina, MI symptoms
- Kidneys - proteinuria, hematuria
- Eyes

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10
Q

What are the two first line treatment options for African Americans with HTN?

A

Thiazide diuretics

CCB

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11
Q

What hormone has a large role in HTN?

A

Aldosterone - the RAAS is an efficient system in elevated the blood pressure when lower levels are detected.

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12
Q

What common antihypertensive is contraindicated during pregnancy?

A

ACEI are contraindicated during pregnancy, they are teratogenic.

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13
Q

What electrolyte abnormalities are most common with thiazide diuretics’ use?

A

Hyponatremia and hypokalemia - Thiazide diuretics remove fluid by inhibiting sodium reabsorption in the distal convoluted tubule. This also results in the removal of potassium.

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14
Q

What two antihypertensive are considered nephroprotective and how does that work?

A

ACEI and ARBs are considered nephroprotective. These two medications reduce the intraglomerular pressure by dilating the efferent arteriole of the glomerulus. This lowers pressure inside which reduces mechanical stress. They also block the RAAS overactivation which can further decrease the inflammation caused by HTN.

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15
Q

What are some common causes of secondary HTN?

A
  1. Hyperthyroidism
  2. Pheochromocytoma
  3. Hyperaldosteronism
  4. Renal artery stenosis
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16
Q

What antihypertensive class is associated with increased peripheral edema? How does this occur?

A

Calcium channel blockers - especially the dihydropyridines (amlodipine, nifedipine, felodipine). These cause arterial vasodilation without corresponding venous dilation. This increases hydrostatic pressure in capillaries which results in fluid leak into interstitial spaces.

This side effect is dose dependent and can be counteracted through the use of a medication that causes vasodilation as well.

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17
Q

Normal values for:
- Triglycerides
- LDL
- HDL
- VLDL
- Total cholesterol

A

Triglycerides - less than 150.
LDL - less than 100
HDL - greater than 40 or 50
VLDL - 150-499
Total cholesterol - less than 200

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18
Q

What are triglycerides? What are they used for?

A

Triglycerides are primarily composed of lipids with a small amount of protein. They are an energy source that the body creates from excess calories, sugar, and alcohol. Too high of levels is associated with MI, stroke, CAD, and metabolic diseases. They are atherosclerotic.

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19
Q

What are VLDLs?

A

VLDLs are lipoproteins that have a higher ratio of fats to protein. They transport triglycerides around the body and deliver to peripheral muscle and fat. As they lose triglycerides they turn into LDL.

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20
Q

What are LDL?

A

Low density lipoprotein - “bad cholesterol” - these fellas deliver cholesterol to cells for use in membrane synthesis and hormone production. Too much LDL is associated with atherosclerosis and increased risk for cardiovascular disease.

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21
Q

What are HDL?

A

High density lipoproteins - “good cholesterol” - reverse transport, take cholesterol from the tissues and transport it back to the liver for removal. Cardioprotective, anti-inflammatory.

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22
Q

What are lipoproteins?

A

A combination of lipids and proteins that work to transport hydrophobic materials like cholesterol and triglycerides throughout the body.

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23
Q

How long to fast before a lipid panel? What lipid panel value is most affected by recent food consumption?

A

Fasting should be done for 8-12 hours before getting labs collected.

Triglycerides are most affected by recent eating

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24
Q

What physical assessment finding indicates long-standing HTN?

A

Long-standing HTN can cause shifting of the PMI as the LV hypertrophies to adjust for the increased afterload it has to work against

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25
How do high triglycerides increase the risk for pancreatitis?
High triglyceride levels increase the risk of pancreatitis by overwhelming the pancreatic microcirculation. When triglycerides exceed 1000 mg/dL, large lipoprotein particles—especially chylomicrons—accumulate and impair capillary flow within the pancreas, leading to localized ischemia. This ischemia triggers inflammation, which further obstructs pancreatic ducts. Meanwhile, pancreatic lipase breaks down the excess triglycerides into free fatty acids, which at high concentrations are cytotoxic and exacerbate tissue damage. This toxic and obstructive environment can cause premature activation of pancreatic digestive enzymes, resulting in autodigestion of the pancreas, as the enzymes are unable to reach the small intestine.
26
Describe S1, S2, S3, S4
S1 - caused by the closure of the AV valves (tricuspid and mitral). This marks the beginning of systole. A normal heart sound. S2 -caused by closure of the semilunar valves (pulmonic and aortic). This marks the beginning of diastole. A normal heart sound. S3 - Location: Heard best at the apex with the bell of the stethoscope, in left lateral decubitus position. Timing: Occurs just after S2 during early diastole — when blood rapidly fills the ventricles. Normal heart sound in younger patient populations caused by vigorous relaxation and rapid filling. Pathologic in older adults caused by volume overload or ventricular dysfunction. S4 - Know as atrial gallop. Heard just before S1. Associated with atrial contraction against a stiff, noncompliant ventricle. Always pathologic. Seen with ventricular hypertrophy, aortic stenosis, hypertrophic cardiomyopathy.
27
The bell is best for hearing what kind of sounds?
The bell of the stethoscope, the small circle, is best used to hear low sounds.
28
Mitral Stenosis - Where? - Results in? - Murmur
Where - the mitral valve is located between the LA and the LV. Results in? - the narrowed lumen of the valve puts strain on the atrium. This strain can cause dilation of the atrium resulting in disconnection of the normal electrophysiology of the heart in this area resulting in increased risk for AFIB and other arrhythmias. Decreased ability to push blood forward results in backing up of the blood causing pulmonary congestion. Murmur - diastolic rumbling, low-pitched, best heard at the apex in the left lateral decubitus position
29
Mitral Regurgitation - Where? - Results in? - Murmur?
Where - between the LA and LV What is going on? - the valve does not completely shut, allows backflow of blood from the ventricle to the LA Results in? - allowance of the blood to backflow from the ventricle to the atrium decreases CO since not as much is going forward to the body. Increased blood volume in the LA can result in dilation of the atrium and the associated increased risk for AFIB. Increased blood in the LA can result in backup into the pulmonary system. Murmur - holosystolic murmur (pansystolic). High-pitched as the high pressure ventricles push blood through the incompetent valve. Radiates to the L. axilla. Caused by connective tissue defects (Marfans), rheumatic heart disease.
30
Early VS Late diastole heart sounds
Early - S3 Late - S4
31
Aortic Stenosis - Results in? - Murmur?
Aortic stenosis is narrowing of the aortic valve. This narrowing results in increased resistance the LV has to pump against. This increased workload can result in LV hypertrophy which will decrease CO due to decreased volume held and pumped with each contraction. This can have the most profound effects when the patient is exercising and there is an increased demand for CO. Unable to meet this demand, the patient can experience (SAD) syncope, angina, and dyspnea. The murmur of aortic stenosis is high pitched and considered a systolic ejection murmur. Cresendo-decresendo.
32
Pulmonic stenosis - Results in? - Murmur?
Results in? - narrowing of the pulmonary valve that results in increased afterload applied on the RV. This increased afterload can result in RV hypertrophy, right sided heart failure. Can cause increased fatigue, dyspnea, DOE. Murmur - systolic ejection murmur. Best heard at the left upper sternal border. May radiate to the back or neck. Often accompanied by an ejection click.
33
Heart murmur best heard at the R2nd ICS and radiates to the neck?
Aortic stenosis
34
Blowing, holosystolic heart murmur best heard at the apex of the heart
Mitral regurgitation. Mitral stenosis is mid-diastolic.
35
What heart sound is commonly absent with AFIB?
S4 - caused by blood being forcefully pushed from the atria into a stiff, noncompliant ventricle. There is no atrial kick with AFIB, so there is no forceful push from the atria into the ventricles.
36
What is a abdominal aortic aneurysm? What are the signs and symptoms? What is the normal size of the abdominal aorta?
An abdominal aortic aneurysm is an outpouching of the aorta starting below the diaphragm and ending at the aorta bifurcation. The condition is typically asymptomatic and is only found secondary to coincidence. The normal abdominal aorta size is 2.5-3cm.
37
When are AAA treated?
AAA that are larger than 5.5 cm in diameter are to be treated
38
What are risk factors for AAA?
1. Male 2. Smoking 3. HTN 4. HLD 5. Family hx 6. Atherosclerosis 7. Connective tissue disorders
39
What is the goal of treatment for AAA that are too small for surgery?
The goal is to prevent rupture and slow or stop the growth progression of the AAA
40
What are the signs and symptoms of a ruptured AAA? What is the prognosis of a ruptured one?
Severe abdominal or back pain. Hypotension. Tachycardia.
41
What type of drugs are Terazosin (Hyrtin) and Tamsulosin (Flomax)? What are these drugs used to treat? What is the difference between the two?
These are both alpha-blockers that prevent catecholamines from binding to alpha 1 receptors in the prostate and bladder neck. These drugs are used to treat BPH. Selective - target urinary alpha 1 receptors. Decreased risk of hypotension and decreased effect on blood pressure. Nonselective - target alpha 1 receptors but have a broader area of action causing increased risk for hypotension (particularly orthostatic). Tamsulosin is selective. Terazosin is non-selective.
42
Mitral Regurgitation - Timing - Location - Radiation - Quality - Symptoms
Timing - Holosystolic Location - at the apex of the heart (L 5th ICS) Radiation - L axilla Quality - high pitched, blowing Symptoms - DOE, SOB, orthopnea
43
S3 and S4 - Quality - Causes
Quality: - S3 - made by increase volume of blood rushing into a compliant or volume-overloaded ventricle. Low-frequency lub-dub-ta. Occurs early in diastole, just after S2. - S4 - made by ejection of blood from the atria (atrial kick) into the ventricles, striking a non-compliant ventricle resulting in the sound. Low pitch soft. Heard late in diastole, just before systole.
44
What heart murmur is seen with Marfan Syndrome? - Where is it best heard? - Describe the murmur
Mitral regurgitation - mitral valve prolapse Mid-systolic click heard best at the apex Marfan + Mitral + Mid-systolic
45
Lipid screenings guidelines - Adult patient without ASCVD - Adult patient with risk factors for ASCVD - Adult patient whose previous screenings were borderline
- Adult without ASCVD - no regular screenings needed - Adult with risk factors for ASCVD - every 5 years - Borderline - every 3 years
46
What is acute coronary syndrome? What is the most common presenting signs and symptoms of acute coronary syndrome? What is the most common cause of acute coronary syndromes signs and symptoms?
A spectrum of clinical presentations including STEMI, N-STEMI, UA, and chest pain. Chest pain is the most common presenting issue. SOB and fatigue should be considered equivalents to chest pain in certain patients. The chest pain can be described as tightness, pressure, discomfort that occurs in the shoulders, arms, neck, back, upper abdomen, or jaw. S&S associated with ACS are caused by a mismatch between supply and demand of oxygen. The heart requires a good deal of oxygen to keep working and blockages or narrowings in the vasculature can reduce the amounts of oxygen being delivered to the heart.
47
What is considered unstable angina?
1. Rest angina that is prolonged (20+ minutes) 2. New-onset angina that limits physical activity 3. Increasing angina (occurs more frequently, lasts longer, occurs with less exertion).
48
What is an NSTEMI?
Non-ST elevation MI - myocardial necrosis (evidenced by cardiac markers trop) without ST segement elevation or Q waves. ST depression, T wave inversion may be present.
49
What is a STEMI?
ST elevation MI - myocardial necrosis with ECG changes and cardiac biomarkers elevated. And/or new left bundle branch block.
50
Why do women more commonly receive delayed care when presenting to the ER with ACS symptoms?
ACS symptoms in women are more atypical than men. Women can present with CP, severe fatigue (acute onset), nausea, and/or pain in the jaw, arm, or back.
51
Recommended time frame for EKG when presenting to the ER or outpatient clinic?
If a patient presents with chest pain they should get an EKG done within 10 minutes of presentation.
52
What is the diagnostic workup of chest pain?
1. EKG - within 10 minutes 2. Trop 3. Lab: PT, INR, CBC, glucose, CMP, lipids, TSH 4. Chest X-ray: looking for cardiomegaly, HF, pulmonary disease 5. Angiography: visualize the blood vessels 6. Echo
53
Time frame of treatment for STEMI VS NSTEMI and UA
STEMI - PCI within 90 minutes door-to-balloon time. If this time frame is unachievable then provide fibrinolysis. NSTEMI and UA - 24-48 hours to provide angiography to visualize the lesions.
54
Nitrate use during ACS - MOA - Side effects - Drug-to-drug - Monitor
Nitrates provide symptomatic relief during acute coronary syndrome (ACS) by inducing vascular smooth muscle relaxation, leading to venodilation and arterial dilation. This reduces preload and afterload, thereby decreasing myocardial oxygen demand and alleviating ischemic chest pain. Nitrates may also enhance collateral coronary blood flow, improving perfusion to ischemic areas. Side-effects: headache, hypotension, orthostasis, flushing, nausea Drug-to-drug: Avoid concurrent use with phosphodiesterase type 5 inhibitors due to risk of severe hypotension Monitor blood pressure
55
What are the dosing rules for short-acting nitrates?
Sublingual - 1 dose at onset, repeat q5 minutes for a max of 3 doses. Spray - 1-2 sprays at onset, repeat q5 minutes for a max of 3 sprays. If unrelieved after 15 minutes ER
56
Isosorbide mononitrate
Long acting nitrate. Takes 30-60 to start working. Lasts 12-24 hours. Used for chronic angina prevention. Works by causing vasodilation, decreasing preload and afterload which reduces myocardial oxygen demand.
57
Ranexa (Ranolazine)
Long acting nitrate that does not affect blood pressure significantly like other nitrates. Improves the myocardial relaxation and efficiency leading to reduced ischemia and angina, especially during exertion. Side effects - dizziness, constipation, nausea, QT prolongation
58
Beta-blockers - MOA - Indications - Side-effects - Contraindications - Drug/Drug - Monitor
MOA - BBlockers work by antagonizing beta-1 receptors or beta-1 and beta-2 receptors if they are non-selective. Blocking these receptors results in decreased HR, decreased BP, reduced inotropy. This decrease in overall heart work reduces the hearts oxygen consumption. Indications: HTN, ACS, post-MI, tachycardia Side-effects: Hypotension, bradycardia, SOB (beta-2 involvement), fatigue, dizzy, orthostatic Contraindications: hypotension, bradycardia, cardiogenic shock, 2nd or 3rd degree heart block, asthma, emphysema, PVD Drug/Drug - CYP2D6 Monitor - BP, HR (do not stop treatment abruptly, taper to avoid rebound HTN)
59
Younger patients (45 years and younger) and how they present with MI
- 31% of this demographic does not present with prior chest pain at time of MI - ST elevation in only 1/3 of cases - most cases are caused by plaque rupture
60
What is the definitive diagnostic test to diagnosis right heart failure? What are the signs and symptoms of right heart failure?
Cardiac cath. JVD, hepatosplenomegaly, peripheral edema, dyspnea, chest discomfort, abdominal distention.
61
Arrhythmia that can occur with fluoride toxicity
Vtach
62
What is the gold standard treatment for post-MI HTN?
Beta-blockers - negative chronotropic and inotropic agents that reduce myocardial oxygen demand ACEI or ARBs - prevent cardiac remodeling and lower BP. These two medications are avoiding in conjunction due to the increased risk of renal dysfunction and hyperkalemia.
63
Post-MI must prescribes and why for each
Statins - cholesterol and LDLs are atherosclerotic. Atherosclerosis accounts for 70-80% of MIs. Statins aim to reduce this plaque formation to reduce subsequent MI risk. B-blockers - ideally initiated within 24 hours of diagnosis. Reduce the infarction size and early mortality and also decrease overall mortality when continued long-term. Reduce the risk of subsequent MIs when combined with ACEI or ARBs. ACEI/ ARBs - cardio and renal protective medications. Reduce remodeling secondary to increased RAAS activity by blocking it. This reduces blood pressure, circulating volume, and reduces mechanical stress on the kidneys by dilating the efferent arterioles. Antiplatelet medications - to thin the blood, preventing further clot formation to reduce the risk of recurrent heart attacks. Will be on dual antiplatelet for awhile then just ASA indefinitely.
64
What is an ARNI medication? What is it used for?
Angiotensin Receptor-Neprilysin Inhibitor - the most commonly used one is sacubitril/valsartan (Entresto). These medications are used in HFrEF. They prevent the breakdown of natriuretic peptides, bradykinin, and other vasodilatory substances. This promotes vasodilation, natriuresis, and anti-fibrotic effects.
65
What are 3 ways to reduce cholesterol levels?
1. Exercise 2. Weight loss 3. Increase fiber intake
66
At what age does age become a risk factor for CAD?
Men - around 45 years old Women - around 55 years old
67
What lab monitoring should be done for a patient on HCTZ?
Thiazide diuretics can cause: - Hyperglycemia - Hyperuricemia - Hypertriglyceridemia - Hypercholesteremia - Hypokalemia - Hyponatremia
68
Coarctation of the aorta - What is it? - What are its characteristics?
Congenital heart condition where there is a narrowing of the aorta around the ductus arteriosus. This narrowing obstructs blood flow and increases pressures in the upper body. Overtime, this need to overcome the stenosis leads to left ventricular hypertrophy and persistent hypertension. Characteristic findings include a higher blood pressure in the upper body and a lower blood pressure in the lower body.
69
What is abnormally connected with PDA? How are PDAs treated?
PDA has an abnormal connection between the pulmonary artery and the aorta. Small PDAs are left alone and may close spontaneously. Larger PDAs need to have surgical ligation. These can cause CHF and a murmur. The murmur is harsh and machine-like.
70
What effect does alpha-1 stimulation cause?
1. Vasoconstriction 2. Mydriasis - pupil dilation 3. Closure of the bladder sphincter
71
If a patient experiences myalgia, or muscle toxicity associated with statins. What should be done?
The statin should be stopped until the myalgia goes away and then restarted at a lower dose. If it happens again then a different medication should be started to control LDLs.
72
Dihydropyridines VS Non-dihydropyridines - What medication class? - Differences
These are the two types of CCB Dihydropyridines are selective for vascular smooth muscle. This type of calcium channel blockers causes vasodilation (also applies to arteries which is the main target of the medication) which results in decreased afterload and decreased blood pressure. These do no effect cardiac muscle. Dihydropyridine medications - Amlodipine, Nifedipine, Felodipine Non-dihydropyridines are selective for cardiac muscle. These cause negative chronotropic and inotropic effects. Used to treat HTN, arrhythmias, and angina. Medications - verapamil, Diltiazem
73
Alpha-1 agonist VS alpha-1 antagonist - Medications of each class
Alpha-1 adrenergic receptors cause vasoconstriction, mydriasis, bladder sphincter contraction, vasoconstriction of cutaneous vessels. Medications: + Phenylephrine - pure alpha 1 agonist resulting in strong vasoconstriction. + Oxymetazoline - topical nasal decongestant Alpha-1 adrenergic antagonist block vasoconstriction, cause miosis, relax the bladder sphincter. Medications: + Prazosin, Terazosin - vasodilation to control BP + Tamsulosin (Flomax) - BPH medication that helps voiding
74
What is the flow of blood with a PDA? What was the flow of blood before the baby was born? Why?
PDA - patent ductus arteriosus. This allows oxygen rich blood to transfer from the aorta (higher pressure) to the pulmonary artery (lower pressure). Characterized by a machine like murmur and an increased for heart failure if large and untreated. The flow inside the womb before the baby is born goes from the pulmonary artery to the aorta. The lungs do not need blood flow because they are nonfunctional.
75
What are characteristics of an innocent murmur in a young child? Signs of a pathologic murmur?
Innocent murmurs increase in intensity during activity, fever, activity, and anxiety. Pathologic - persistence during positional changes. Splitting of S2. Occurrence in patients with chromosomal trisomy
76
What antihypertensive medications are associated with ED? What medications can improve ED?
Diuretics, specially HCTZ, are associated with erectile dysfunction. Alpha blockers (Tamolusin and Doxazosin) can improve these symptoms.