EKGs and heart failure Flashcards

(30 cards)

1
Q

Where can rhythm for the heart come from? How would you refer to this medically?

A

SA node- “sinus”
AV node- “Nodal”
Ventricle- “ventricular”

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2
Q

What is the standard speed of paper in an EKG? How does this allow you to calculate the HR?

A

25 mm/sec

Each little box is .04 of a second so 1500/# little boxes b/wn beats = HR

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3
Q

How long should a normal PR interval be? A QRS complex? A QTc interval?

A

PR- less than .2 seconds (1 big box)
QRS- less than .1 seconds (3 little boxes)
QTc- about .45 seconds (this is a correction FYI)

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4
Q

Electrical activity towards a lead results in ______ deflection. Electrical activity away from a lead results in ______ deflection.

A

Towards- upward

Away from- downward

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5
Q

What should the P wave look like in leads I, II and III? What is going on if it looks different?

A

It should be upright.

The P wave is not coming from the SA node

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6
Q

What does a right bundle branch block appear as? A left bundle branch block? What does this mean physiologically?

A

RBBB- late upward deflection in right side leads (V1, aVR) and late downward deflection on left (I, V6)
LBB- late upward deflection in left leads (I, V6, aVL), and late downward deflection in right (V1)
Ventricular depolarization takes longer

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7
Q

What does it mean if QRS complexes are close together? Or far apart?

A

The patient is tachycardic or bradycardic

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8
Q

What does first degree heart block mean? What does it look like on an EKG?

A

The AV node is taking longer to conduct the signal to the ventricles. Prolonged PR interval

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9
Q

What does 3rd degree heart block mean? What does it look like on an EKG?

A

There is no conduction at the AV node. This is always associated with an escape rhythm. QRS waves do not follow P waves, although both may be present

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10
Q

What is second degree heart block? What are the 2 types? What do they look like on EKGs?

A

Only some of the atrial depolarizations are conducted by the AV node (defect in the His-Purkinje system). Mobitz type 1- PR interval gradually lengthens then a beat is skipped. Mobitz type 2- P waves are randomly not conducted

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11
Q

Which of the types of 2nd degree heart block is more serious?

A

Type 2. It’s hard to predict and can easily become third degree heart block

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12
Q

What do premature ventricular or atrial beats appear as on EKG? Why is this?

A

A longer P to P interval. A beat happens and the AP reaches the AV node/ventricular cells before they were repolarized so the AP wasn’t conducted

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13
Q

When an EKG shows tachycardia, what does the QRS tell you?

A

A narrow QRS indicates that it is a supraventricular tachycardia and interventricular conduction is intact
A wide QRS indicates either V. tach or supraventricular rhythm with impaired IV conduction (i.e. bundle branch block)

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14
Q

Which is more dangerous, V tach or A tach?

A

V tach. It can degenerate into V fib which is life threatening

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15
Q

Define: heart failure

A

An inability of the heart to meet the metabolic needs of the body

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16
Q

What are some causes of heart failure?

A

A decreased circulatory supply to the body (maybe b/c of an MI or valvular disease) or an increased circulatory demand from the body (i.e. hypertension)

17
Q

What are 4 adaptive mechanisms the body uses to compensate for heart disease or to meet increased demand? How rapid are they?

A

Frank-starling law (within seconds)
Neuro-hormonal (hours to days)
Renin-angiotensin (hours to days)
Hypertrophy (days to years)

18
Q

How does the heart use the Frank-Starling law to increase cardiac function?

A

It increases EDV which increases CO

19
Q

How is using the Frank-Starling law problematic?

A

Eventually, as heart function declines, the curve shifts down/to the R and for a given change in EDV, you get less of an increase in CO. Also, when LA pressure exceeds 25 mm Hg, you risk developing pulmonary edema

20
Q

How does the body increase plasma norepi levels? What is this associated with?

A

It releases more at the synapse and takes up less. It also degrades less. And the heart produces some too. Increased blood norepi is associated with worse prognosis

21
Q

What negative effects does increased norepi in the plasma have on the heart?

A

The heart is less sensitive to SNS stimulation and downregulates expression of the B1 adrenergic receptors

22
Q

What stimulates renin production? What does it stimulate in the body?

A

Stimulated by decreased glomerular filtration rate and renal blood flow; also increased aldosterone. Renin stimulates salt and water retention, ADH and aldosterone secretion, norepi release, thirst and vasoconstriction.

23
Q

What does ANP do? How about BNP? Where are they made?

A

Made in the heart. Both suppress renin and promote vasodilation and peeing out salt

24
Q

What does endothelin-1 do?

A

It vasoconstricts

25
Why does the ventricle hypertrophy? Does this work?
It can't move the amount of blood it needs to move so it adds muscle to increase contractility. It kind of works- the muscle is contractive but not as much as normal muscle
26
How does hypertrophy from volume overload differ from that of pressure overload?
Volume overload- need a bigger lumen so add sarcomeres in series. Wall size stays the same Pressure overload- need stronger walls so add sarcomeres in parallel. Lumen stays same size
27
What are some downsides to ventricular hypertrophy?
It decreases coronary reserve and eventually, LV function worsens
28
Give an example of Right heart failure. Left heart failure. Is heart failure ever truly 1 sided?
R- pulmonary embolism, mitral stenosis L- aortic stenosis, mitral insufficiency, hypertension No, there will be an element of heart failure in both ventricles
29
What is the difference b/wn systolic and diastolic heart failure?
Systolic- heart has a low forward CO (maybe from an MI) Diastolic- EF is ok so CO is fine but heart can't relax quickly or is too stiff to acquire the blood it needs to pump to the body (from hypertension or early ischemia)
30
Atrial fibrilation is associated with what type of contraction?
Not coordinated contraction of the atria