Newman/Nace Flashcards
1
Q
What 3 goals should you keep in mind when treating HTN?
A
- Obtain an accurate assessment of BP (cuff, position, timing, both arms, avoid caffeine/tobacco)
- Assess significance of BP by stratifying CV risk and assessing for target organ damage
1. Vasculature, kidneys, heart, brain, eyes (i.e., increased light reflex) - ID and treat secondary causes of HTN
1
Q
Does loudness have to do with severity of valvular disease?
A
NO
2
Q
What is the clinical significance of this table?
A
- CV events increase continually with increasing BP, but 140 systolic and 90 diastolic are levels at which CV events most significantly increase
- NOTE: for those 60 and over, the tx threshold is now 150/90 (also higher for pts with diabetes and chronic kidney disease -> in ppl with established HTN, little benefit in reducing pressure too much, and can even be dangerous)
3
Q
How do you calculate MAP?
A
- MAP = 2/3DBP + 1/3SBP = CO x TPR
- CO determined by: preload + contractility (SV), HR
3
Q
How does mitral regurgitation affect the stroke volume and EF?
A
Increases them
3
Q
What does aortic regurgitation do to pulse pressure?
A
Widens it
4
Q
Describe and identify.
A
- Supraventricular tachycardia (SVT)
- Ominous rhythm with heart rate around 170-230 bpm
- Has a narrow QRS and regular, very rapid pattern
- Person at rest with SVT can have a rate at 150 bpm
4
Q
Describe and identify.
A
- Ventricular tachycardia (V-Tach)
- Very fast, almost uninterrupted abnormal QRS complexes (>200 bpm)
- Can transition into ventricular fibrillation
- Myocardial ischemia, cardiac drug toxicity, and electrolyte imbalences are common causes
4
Q
What is this?
A
Mitral valve prolapse
5
Q
What are the 2 requirements for and complications of bacterial endocarditis?
A
-
Requirements:
1. Bugs in the blood
2. Damaged heart valve -
Complications:
1. Embolism
2. Destroyed valve -> regurgitation
6
Q
Know these.
A
Good job!
7
Q
What is the difference between hypertensive emergency and urgency?
A
- Emergency: 180/120 with ongoing organ damage
- Urgency: 180/120 with NO ongoing organ damage
- Important tx principle is to treat promptly, but not excessively. Hypertensive emergencies require parenteral administration of drugs that can be rapidly titrated. Reduce mean arterial pressure (MAP) no more than 25% of pretreatment level within the first two hours. BP should then be more gradually reduced over the next 24 hours. This is to avoid compromising perfusion by reducing BP below the lowered threshold established by autoregulation in response to long‐ standing hypertension.
9
Q
Describe and identify.
A
- Atrial fibrillation
- Chaotic rhythm with intermittent normal QRS waves
- Typically has no recognizable P waves; instead has random looking “fibrillatory waves” between the QRS complexes
- Atrial contraction is lost here
- Most common cause of stroke due to increased chance of thrombus formation
10
Q
What are the symptoms of aortic stenosis?
A
- Heart failure (dyspnea)
- Angina
- Syncope
10
Q
With what heart sound does the carotid pulse correlate?
A
1st one
11
Q
What are 3 characteristic features of acute regurgitation?
A
- Murmur
- Lack of hypertrophy
- Sudden pressure rise
13
Q
Identify and describe.
A
- Sinus bradycardia
- Normal EKG waves with a slower heart rate (less than 60 bmp) – not pathologic
- If this if above 50bpm then you’ll tolerate it without symptoms
- Vagal stimulation can produce this
14
Q
How do you decide whether or not to replace valve in aortic stenosis?
A
- Severity of symptoms
- Gradient (as determined by cardiac catheterization)
1. Difference in pressure on either side of the valve (normally 0)
15
Q
What are secondary causes of HTN? What % of the population do these represent?
A
- Secondary causes accounts for only about 5%
- Secondary HTN more likely in pts with:
1. Age of onset of HTN 50 years
2. Target organ damage at presentation
3. Features of specific secondary causes:
a. Abdominal bruit, extensive vascular disease (renal artery stenosis)
b. Unprovoked hypokalemia (primary, secondary hyperaldosteronism)
c. Labile pressures with tachycardia, sweating, and tremor (may suggest pheochromocytoma)
d. Known personal or family history of renal disease (renal parenchymal HTN)
4. Poor response to combos of antihypertensive agents known to be generally effective -> often translated into poor control in spite of 3+ drugs - These pts still may have advanced essential HTN
16
Q
What are the 4 causes of mitral regurgitation?
A
- Mitral valve prolapse (most common)
- Papillary muscle rupture (MI)
- Dilated left ventricle
- Rheumatic fever
17
Q
Is concentric hypertrophy a risk factor for sudden death?
A
YES
18
Q
How was the “normal” BP level determined?
A
Based on least CV risk from evidence-based studies (optimal pressure: generally
19
Q
At what age should pulse pressure be widest? Why?
A
- Old age
- Due to decreased compliance
21
Q
Identify and describe.
A
- Normal sinus rhythm (NSR)
- Most common adult rhythm (60-100 bpm)
- This is our typical EKG
22
What is essential HTN?
- 90-95% of HTN pts for whom a single, reversible cause of elevated BP cannot be identified (genetic predisposition)
- GOF in pathways that promote vasoconstriction, Na retention, or LOF in vasodilation, Na excretion (most have normal CO)
- Idiopathic, but may be related to:
1. Congenital decrease in nephron numbers
2. Primary defect of renal Na excretion
3. Chronic stress (acting through prolonged activation of SYM)
4. Genetic changes in renin/angiotensin system
24
Describe and identify.
- Normal sinus rhythm (NSR) with premature ventricular complexes (w/PVCs)
- May be caused by increased ventricular automaticity or re-entry
- Typically a string of normal QRS complexes with a random extra abnormal one thrown in
- Can be benign; but does indicate ventricular irregularity
25
What is this?
- Bundle branch block: width of QRS normally about 2mm, but this one is clearly 4-5mm wide (always abnormal, but not specific)
- Can occur in ischemic, valvular heart disease, after taking certain drugs, etc. (unlike ventricular hypertrophy)
26
Why should people with HTN avoid NSAIDs?
- May blunt response of some anti-HTN responses (same with decongestants and sympathomimetic drugs)
27
What is the significance of HTN treatment goals?
- Reduces all end-points, complications, which is the goal, even more so than reducing the actual HTN
- Not treating #'s -\> treating below goals appears to not provide much additional benefit
28
What can you see on an echocardiograph?
- Diseased valves
- Hypertrophy
- Flow of blood
29
Describe and identify.
- Sinus tachycardia
- More narrow EKG waves with a faster heart rate (greater than 100 bmp) – not pathologic
- This is limited to 150 bpm usually; but that’s pretty darn fast don’t you think?
- Sympathetic stimulation will produce this
31
Who is affected by essential HTN?
- Identifiable behaviors contribute: increased salt intake, alcohol, obesity
- Obesity estimated to account for up to 60% of new cases (sleep apnea may contribute)
- More prevalent in AA, and also starts at earlier age, tends to be more severe, and causes more target organ damage, premature disability, and death
32
What is the most common preventable cause of death in developed countries?
HTN
33
How is the dx of aortic stenosis best made?
- History and physical
- Echocardiography
- Cardiac catheterization
34
Describe and identify.
- 3rd degree (complete) heart block
- Ominous rhythm with very low heart rate (around 30 bpm)
- Can progress to ventricular stand still
- Some characteristic EKG findings: P- waves without QRS (“lonely P-wave”), non-regular P-R intervals, prolonged QRS
36
Describe and identify.
- Ventricular fibrillation
- Muted random unrecognizable waves (0 bmp) with no cardiac output
- Primary rescue = AED shock
- Secondary prevention = ICD
37
What is this showing?
Aortic stenosis
38
Describe and identify.
- Atrial flutter
- Due to establishment of a reentry circuit within atria (flutter rate of around 250-300 bpm)
- Characteristic “sawtooth baseline” on the EKG
- Typically normal QRS complexes either at every 2nd or 4th impulse
