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Acute Care > Acute Care Test1 > Flashcards

Acute Care Test1 Flashcards

1
Q

Diastolic heart failure (DHF)

A

Impaired relaxation of heart
DHF is more common in females and HTN is a more common risk factor,
Although substantial proportion of patients w/ SHF have HTN

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2
Q

Calcium channel blockers

A

Selectively block Ca2+ entry into vascular smooth muscle cells

Mgmt of: HTN, angina, vasospasm

Reduce cardiac contractile force
Used to treat supraventricular arrhythmias

“dipine”
Most common: Amlodipine (Norvase), Diltiazem (Cardizem), Verapamil (Calan)

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3
Q

Limb leads

A

I: Right arm (-)(-) -> Left arm (+)(-)

II: Right arm (-)(-) -> Left leg (+)(+)

III: Left arm (-)(+) -> Left leg (+)(+)

A lead consists of 2 electrodes, 1(+) 1(-)
(Both listed above I-III to know where are)

Limb leads capture different regions of the heart.

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4
Q

“The vicious cycle”

A

Ventricular dysfunction->

Decreased CO ->

Compensations:
Increased SNS, RAS-Aldosterone, arginine vasopressin
->

Excessive vasoconstriction
Excessive Na+/H2O retention
->

Increased afterload
Excessive preload
->
Ventricular dysfunction

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5
Q

ST elevation

A

Indicates cell death

Most common cause: myocardial ischemia and infarction

Threshold values for ST- segment elevation consistent with STEMI are J-point elevation of > 2 mm in leads V2 and V3 or > 1 mm in all other leads

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6
Q

Heart valves- systole

A

Pulmonary and aortic valves open

Tricuspid and mitral valves closed

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7
Q

III
Area of heart?
Which coronary artery?

A

Inferior

PDA: posterior descending artery
(80% RCA- right coronary artery
20% LCx- left circumflex)

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8
Q

Nonischemic T wave

A

Hyperkalemia (elevated K+)

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9
Q

V4
Location of heart
Which Coronary artery

A

Septal / Anteroapical

LAD- left anterior descending

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10
Q

Dependent rubor

A

Blood pooling in maximally dilated capillary

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11
Q

Intermittent claudication pain

A

Cramping type, due to ischemia
Better with rest
Not typically burning
Pain increases with elevation and decreases with dependence arterial disease

Usually in calves, but can be thigh or butt

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12
Q

Cardiac remodeling -

MI / DCM

A

Myocardial infarction/ DCM ->

Cardiac dilation:
Myocyte length increase >> width increase 
Extensive fibrosis 
Myocyte death 
Adv cardiac dysfunction
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13
Q

Wells score PE

A

+3
Clinically suspected DVT
Alternative diag less likely than PE

+1.5
HR > 100
Immobilization 3 or more days or Surgery in previous 4 weeks
History of DVT

+1
Hemoptysis
Malignancy or palliative

> 6 high probability
2-6 moderate probability
< 2 low probability

Score >4 PE likely - consider diag imaging
Score < 4 Pe unlikely- consider d-dimer to rule out

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14
Q

Left bundle branch block

A

R and L ventricules are not same- 1 side slower

Twin peaks

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15
Q

Complications of atherosclerotic plaque

A 
Rupture or ulceration 
Calcification of atherosclerotic plaque
Hemorrhage into plaque -> further narrowing 
Embolization 
Weakening of vessel wall -> aneurysm
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16
Q

Ventricular pacemakers

A

Used for abnormal rhythms
Like Type 2 or grade 3 AV node blocks, or significant A-fib

Wide QRS as pacemaker providing
“Pacer spikes”

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17
Q

Regulation of BP- slow

A

Renin-Angiotensin system (kidneys)

Natriuretic peptides (ANP and BNP)-heart 
Act as counter to RAAS
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18
Q

Systematic approach evaluating rhythm strip

A 
Waveform configurations 
PR intervals 
QRS intervals 
RR intervals 
Rate to assess rhythm disturbance
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19
Q

Augmented leads

A

Termed unipolar leads because single (+) electrode that is referenced against combo of other electrodes

(Machine does calculations and designations)

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20
Q

Atrio-ventricular valves

A

Let side:
Bicuspid (Mitral) valve

Right side:
Tricuspid

Chordae tendinae and papillary muscles prevent inversion ic valves during ventricular systole
(Can become damaged from MI causing backflow “regurgitation”)

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21
Q

Mitral valve prolapse- what expect

A

Volume overload:
LA dilates (A-fib, thrombus formation, pulmonary congestion)
LVH for forward flow

Upon exertion:
Dyspnea

Auscultation:
Holosystolic murmur: regurgitation into LA

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22
Q

Pulse pressure

A

SBP - DBP: Normally ~ 40-60 mmHg

Low: < 40 mmHg may indicate pulse narrowing
Elevated: > 60 mmHg associated with higher CVD morbidity/mortality

Might be better predictor of CV risk than SBP
More reflective of microcirculation dysfunction
Mechanism may be due to endothelial damage from large oscillations in pressure each cardiac cycle

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23
Q

Mitral stenosis- expect

A

Pressure overload:
LA hypertrophy
Limited LV filling (LA thrombus breeding ground, A-fin, pulmonary congestion and HTN)

Upon exertion:
Dyspnea

Auscultation:
Opening snap, diastolic rumble

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24
Q

Composite score chest pain due to CAD

A 
1 point each...
Men > 55 yo/ Women > 65 yo
Known vascular disease 
Pain worse with exercise 
Pain not elicited with palpation 
Patient assumes is cardiac origin

0-1
2-3
4-5 high probability

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25
Q

Mitral valve prolapse

A

2-6 % population

Valve snaps during systole

Mostly asymptomatic, cause unknown

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26
Q

Bigeminy

A

PVC occur every other beat

Premature ventricular contraction

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27
Q

Pericardial effusion

A

Accumulation of fluid in pericardial sac

Causes: similar to pericarditis
Symptoms: pressure pain in chest, dysphagia, dyspnea
Signs: muffled heart sounds, possibly JVD

May progress to a cardiac tamponade (not good)

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28
Q

Hypertrophic cardiomyopathy (HCOM)

A

Strong genetic link
55% familial relative
More common in African-Americans

Ejection murmur changes with position
Softens- sitting
Amplifies- standing/valsalva

Persistent Split S2 - no change w breath hold

Syncope or dyspnea during exercise

Persistent hypertrophy despite detraining

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29
Q

Rhythm: Wide QRS

A

Ventricular rhythm:
Below AV node (ventricles)

Rhythm/impulse generated below atria

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30
Q

V2

A

Unipolar Precordial (chest) lead

4th IC space to the L of sternum
Septal

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31
Q

QRS complex

A

Ventricular depolarization
(Atrial repolarization)

Normal:
0.06 - 0.10 seconds (1.5 - 2.5 small boxes)

Some patients may have wider QRS- absolute cutoff is 0.12 seconds

> 0.5 mV in at least 1 std lead (5 small boxes)
1.0 mV in at least 1 precordial lead (10 small boxes)
Upper limit 2.5 - 3.0 mV (25 small boxes)

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32
Q

Trans-cutaneous valve repairs

A

Typically older patients at high risk for open heart surgery

Promising early results comparing 4 ur clinical outcomes to open heart

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33
Q

V6
Area of heart?
Which coronary artery?

A

Lateral

LCx - left circumflex

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34
Q

Intermittent claudication

Pain in foot

A

Tibial Artery

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35
Q

Rhythm: Narrow QRS

A

Supraventricular:
AV node or above
(SA, AV, atria, nodal tracts)

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36
Q

ACC/AHA - Stage A

A

Patient at high risk for developing HF with no structural disorder of the heart

HTN, Atherosclerotic disease, DM, obesity, metabolic disorder

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37
Q

Anti-arrhythmics

A

Na+ channel blockers

Beta blockers

K+ channel blockers

Ca2+ blockers

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38
Q

Blanching

A

Pressure applied (to nail bed) until turns white. Indicates blood has been forced out of tissue

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39
Q

Late systole murmur

A

Mitral valve prolapse

Clicking sound hallmark

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40
Q

Factors that influence CO

A

Preload
The degree of myocardial distention prior to shortening
Largely depends on amt of ventricular filling

Afterload
Forced against which ventricles must act in order to eject blood
Largely dependent on arterial BP and vascular tone

Contractile state (contractility)

HR

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41
Q

Edema massage

Purpose and contraindications

A

Helps prevent putting edema, which increases likelihood of wounds

Contraindications: uncompensated CHF, untreated infection/cellulitis, active cancer, renal failure, severe pulmonary problems

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42
Q

HF: implications of an abnormal hemodynamic response to exercise

A

Associated pulmonary disorders impair breathing
Reduced gas diffusion in lungs
Increased work of breathing
Contribute to dyspnea and fatigue
Exaggerated redistribution of blood flow away from periphery and to respiratory muscles during exercise- May contribute to enhanced perception of fatigue

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43
Q

V1
Location of heart
Which Coronary artery

A

Anterior / Anteroseptal

LAD- left anterior descending

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44
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Elevation

A

Arterial: worsens symptoms
Venous: lessens symptoms

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45
Q

Auscultation points

A

“All Physical Therapists Move” mnemonic
1. Aortic region
R 2nd intercostal space, parasternal

  1. Pulmonic region
    L 2nd intercostal space, parasternal
  2. Tricuspid region
    L 4th intercostal space, parasternal
  3. Mitral region
    L 5th intercostal space, midclavicular

(There is also: Erb’s point
L 3rd intercostal space (LL sternal border) but n/a for this course)

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46
Q

Exercise testing

A

Cardiopulmonary stress test (gold standard)

6MWT (six minute walk test)
Alternative to CPXT to assess
Used extensively in HF studies 1
Predicts morbidity and mortality in patients with HF 2 (< 300 m)

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47
Q

Neuro-hormonal effects of heart failure

A

Kidney isn’t happy with decreased blood flow

Increases Na+/H2O retention to increase perfusion pressure

Increased E, renin, endothelin (all vasoconstrictors) and ANP (produced by heart for vasodilation)

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48
Q

Ventricular tachycardia

A

V-tach
4 or more PVCs (premature ventricular contraction) in a row

NSVT: non-sustained ventricular tachycardia
^ reading this in pt hy is not a contraindication for tx.
IF seen while working with a patient STOP, check vitals and notify RN

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49
Q

PVD

A

Slow and progressive circulation disorder caused by narrowing, blockage or spasms in a blood vessel

Many involve any blood vessel outside heart
Arteries : PAD
Veins: CVI
Lymphatic vessels

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50
Q

Sternal precautious

A

No traction forces on sternum 6-8 weeks (longer if osteoporosis or on steroids)
No shoulder FLEX or ABD > 90*
Lifting restrictions 8-10 lbs 6 wks, then 30 lbs for 3 mo
Minimal push/pull (log roll to get out of bed, edge of chair before standing, use momentum and rocking, look up)
If sternal tissue fails, use rectus or pectoral flaps- severe ROM restriction of 20* FLEX and ABD, no lifting, push or pull
Monitor incision: 30% mortality of opens and becomes infected
Encourage splinting chest with pillow when coughing
Avoid valsalva
No driving (meds) initially- avoid 4-6 wks bc airbags

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51
Q

Exercise training

Acute Cardiovascular

A

Dose determined based on COX results

Moderate intensity aerobic 30-45 min
At least 3-5 x week is general recommendation

Low to mid resistance training recommended with aerobic training

Consider eccentrics !!(BP response)

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52
Q

Atherosclerosis characteristics

A 
Slow, progressive 
Starts 20s-30s
Often undetectable 
Initially plaques are sparsely distributed 
Increase in number and size over time 
Can affect any artery
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53
Q

Heart failure

Complications

A

Impaired exercise tolerance
Increased risk of ventricular arrhythmias
Shortened life expectancy

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54
Q

S/S essential to monitor to help determine the adequacy of mechanical pump function (LVAD)

A

Dizziness

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55
Q

Edema

A

Clinically apparent increase in interstitial fluid volumes

Develops when starling forces are altered so there is increased flow of fluid from vascular system into interstitium

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56
Q

R-R interval

A

Duration between subsequent heart beats
Duration used to calculate HR

Normal:
Should be regular and consistent, especially at rest

Will shorten during exercise as HR increases

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57
Q

____ pain not affected by workload but by posture

A

Neurogenic pain

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58
Q

ECG reviewed to identify 4 areas that require interpretation

A

HR
Heart rhythm
Hypertrophy
Infarction

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59
Q

Thoracotomy

A

Lobectomy

Lung transplant (bilateral AKA clamshell for COPD)

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60
Q

Splitting S1

A

The mitral (M1) and tricuspid (T1) valve sounds are slightly asynchronous

This is a normal finding as mitral closure may precede tricuspid closure by 20-30 msec (0.02-0.03 sec)

Produces 2 audible components
M1-T1 normal or “physiologic splitting” of S1

Wide splitting of 1st sound is almost always abnormal and warrants further medical attention

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61
Q

CVI

A

Chronic venous insufficiency
Vein wall and/or valves don’t work effectively
Impairs ability for blood to return to heart from legs, resulting in venous-stasis

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62
Q

Quadrigeminy

A

PVC (premature ventricular contraction) every 4 beats

Generally less concerning than Bigeminy or Trigeminy (bc within 6 per minute cutoff)

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63
Q

Inpatient PT implications

A

Getting patient moving:
Reduces risk of deconditioning, pulmonary complications (atelectasis and pneumonia), bed sores and DVT

Goals:
Determine stability for ambulation, transfers, stairs, ADLs, assistive device needs, tolerance to activity, return to PLOF or as close to possible

Discharge plans:
Ask if live alone/with family, floors in home, steps to needs

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64
Q

Neuro-hormonal effects of heart failure

A 
Excess vasoconstriction 
Due to increased: 
Aldosterone 
Endothelin
Angiotensin II
Vasopressin 
Norepinephrine

(Not enough/enough effect from: NO, increased ANP, BNP)

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65
Q

Heart wall layers

A 
(Inside-> outside)
Endocardium 
Myocardium
Visceral pericardium 
Pericardial cavity
Parietal pericardium
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66
Q

NYHA - Class I

A

No limitation of physical activity

Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea (shortness of breath)

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67
Q

Nonischemic causes: ST depression

A
  1. RVH (Right precordial leads) or LVH (Left precordial leads, I, aVL)
  2. Digoxin effect on ECG
  3. Hypokalemia
  4. Mitral valve prolapse
  5. CNS disease
  6. 2ndary ST segment changes with conduction abnormalities (ex: RBBB, LBBB, WPW)
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68
Q

Presence of significant Q wave is diagnostic for ____, but ___ cannot be determined from ECG

A

Infarction

Date of infarction cannot be determined by ECG

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69
Q

aVF
Area of heart?
Which coronary artery?

A

Inferior

PDA: posterior descending artery
(80% RCA- right coronary artery
20% LCx- left circumflex)

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70
Q

HF Meds

A

Decrease preload: diuretic
Decrease afterload: ACEI
Control Sympathetic stimulation: beta blocker

Ca2+ blockers NOT used due to adverse effects with HF

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71
Q

Clinical implications for PAD

A

High risk individuals s/b examined for PAD and AAA
Important to monitor hemodynamics during exercise
Patients with intermittent claudication usu have some sort of walking impairments that significantly improves with exercise training
Exercise training as effective as surgical interventions in reducing symptoms and improve walking distances
Instruct in proper foot care, footwear and hygiene
Might improve nocturnal pain by elevating head of bed slightly

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72
Q

Spirolactone (Aldactone)

A

Aldosterone receptor antagonists: blocks aldosterone this interferes with Na-K+ exchange at distal tubule
AKA potassium sparing diuretic

Side effects: volume depletion, frequent voiding

Reduce BP by reducing blood volume via kidneys

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73
Q

Atenolol

A

Beta blocker - specific

Sympatholytic

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74
Q

Intermittent claudication

Pain in hip and butt

A

Aorto-iliac occulusion

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75
Q

Decompensated HF meds

A

Positive inotropes

Afterload reducers

Maintain MAP (IV NorE and E)

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76
Q

Heart failure

Mortality

A

1 in 9 deaths (2009)
5- year mortality is 50%

Most common cause of ED > 65 yo

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77
Q

NSR

A

Normal sinus rhythm

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78
Q

4 cell types of myocardium

A

Working/Mechanical cells
Nodal cells
Transitional cells
Purkinje cells

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79
Q

Endarterectomy

A

Surgical removal of any part of the inner lining of an artery, any obstructive deposits

Most often performed in carotid artery or femoral arteries

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80
Q

T-wave inversions

A

Sign of ischemia

Progresses to S-T segment changes (depression then to elevation)

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81
Q

S-T segment

A

Interval between ventricular depolarization and repolarization

Normal:
Discrete ST segment distinct from T wave is usually absent
(Should be in line with isoelectric line)

At higher HR (exercise) the ST-T segment is a smooth, continuous line beginning at the J-point (end of QRS) slowly rising to the peak of the T-wave

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82
Q

Sympatholytics

A

Beta blockers “olol”

Alpha 1-blockers “zosin”

Alpha 2-agonists

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83
Q

> 180/110 BP

What do you do?

A

Hold exam
Examine for organ damage
Contact PCP
Consider contacting EMS

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84
Q

PEA

A

Pulseless electrical activity
AKA electromechanical dissociation

(Ex: Sustained ventricular tachycardia… can go into v-fib)

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85
Q

QRS “normal” cutoff

A

0.12 seconds or 3 small boxes

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86
Q

T-wave

A

Ventricular repolarization

Normal:
Deflection should be same as largest component of QRS wave (usually R wave)

I.e. if R wave is (+) the T wave s/b (+)

Ex: in lead aVR it is normal for T wave to be (-); since QRS is also (-)

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87
Q

Role of endothelial cells (blood vessels)

A

Normally produce antithrombic molecules
Modulate immune response by resisting leukocyte adhesion and therefore inhibiting inflammation

Laminate shear stress favors:
NO production
KLF-2 mediates immune response, prevents deposition; SOD protects ROS

(Branch points subject to turbulent flow and tend to lack these effects)

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88
Q

Median sternotomy

A

CABG (coronary artery bypass graft)
Valve replacement or repair (Mitral MVR or Aortic AVR)
Heart transplant

One of the most frequent accesses in cardio-thoracic surgery
Vertical inline incision made along sternum
Chest wall is retracted, mediastinum exposed

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89
Q

Patients with nitroglycerin

A

Always have with during exercise sessions

Patients should report symptoms of chest pain and take NTG as directed
If symptoms persist 5 min after NTG, doe can be repeated 2 more times with 5 minute intervals between doses
If symptoms persist seek prompt medical attention
NTG can be used prophylactically 5-10 min before activity

Physiologic responses to activity s/b monitored (HR, BP, RPP)

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90
Q

S2

A

Dub
2nd heart sound
Closure of semilunar valves (aortic and pulmonic)
Marks beginning of ventricular relaxation and end of systole

Shorter duration and higher frequency than S1

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91
Q

Extra heart sounds

A

“Gallops”

S3:
occurs at beginning of diastole after S2.
Lower in pitch than S1/S2 b/c S3 not valvular
Indicative of ventricular/heart failure
SLOSH’-ing-in
S1 S2 S3

S4: 
Occurs prior to S1, produced by sound of blood being forced into stiff/hypertrophic ventricle 
Indicative of LVH or HCOM 
a—STIFF’-wall 
S4   S1       S2
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92
Q

AT (aerobic training) - HF

A

AT is gold standard exercise intervention
Most often “moderate intensity” (60-70% VO2 max)

Improvements: VO2 max, 6MWT, MLHFQ, LVEF, capillary density and peripheral artery diameter

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93
Q

Outer layer of connective tissue that covers heart

A

Epicardium

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94
Q

Angina- visceral pain fibers

A

Internal organs- such as heart or blood vessels, esophagus, visceral pleura- enter SC at multiple levels and map to parietal cortex corresponding to the cord levels shared with somatic fibers

Discomfort, heaviness, aching

Pain difficult to describe and imprecisely located

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95
Q

Medical exam- HF

A

BNP
ECG : wide QRS has higher mortality, dysrhythmias
Interview (symptoms)
Physical exam (signs)
Echocardiogram (EF, chambers and valves, wall motion)
CXR (chest x-ray: fluid, cardiomegaly)
Assess coronary arteries (underlying ischemia)
General chemistry labs

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96
Q

Chronic pain and hemodynamics

A

Diminished tolerance to painful stimuli
Reduced BP response and baroreflex to painful stimuli
Higher HR than heathy subjects at baseline and to painful stimuli

Lower parasympathetic and increased Sympathetic activity
Increased prevalence of HTN

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97
Q

Endothelial dysfunction

A

Increase: Adhesiveness of endothelium (adhesion molecules for leukocytes, T cells, platelets, permeability to oxidized LDL)

Macrophages engulf oxidized LDL and become foam cells

Endothelium becomes pro-coagulant and local adhesions associated with secretion of cytokines and growth factors
Transmigration of molecules (like leukocytes) into wall

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98
Q

Bipolar leads

A

Utilize a (-) and (+) electrode, and record the electrical activity between them

Limb: I, II, III

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99
Q

Mitral regurgitation/incompetence

A

Mitral valve does not close completely during systole (incompetence)
Creates back flow.
Increases to SV to compensate for back flow m
Upstream chamber (L atrium) dilates out
Eccentric hypertrophy to accommodate increased volume

20% >55 yo have some degree of mitral regurgitation (1/3 all cases caused by rheumatic heart disease)

Signs/Symptoms-anxiety and palpitations w/ exercise (if symptomatic- beta blockers)

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100
Q

II
Location of heart
Which Coronary artery

A

Inferior

PDA: posterior descending artery
(80% RCA- right coronary artery
20% LCx- left circumflex)

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101
Q

Pitting edema

A

1+
Barely detectable impression when finger pressed into skin

2+
Slight indentation; 15 sec to rebound

3+
Deeper indentation; 30 sec to rebound

4+
> 30 sec to rebound

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102
Q

ECG

Check PR intervals for…

A

AV blocks

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103
Q

Cardiac remodeling -

Chronic exercise/ Pregnancy

A

Chronic exercise / Pregnancy

Physiological hypertrophy:
Myocyte length increase > width increase
No fibrosis
No cardiac dysfunction

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104
Q

Medical management HF

A

Exercise
Pharmacological
Surgery

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105
Q

ECG systematic analysis

A
  1. Rate (fast or slow)
  2. Rhythm (regular or irregular)
  3. P wave and QRS complex w/ ea cycle
  4. Do P waves look alike
  5. Is there a P wave before every QRS
  6. Is PR interval w/in normal limits
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106
Q

Hydralazine

A

HTN med

Direct-acting smooth muscle relaxant, acts as vasodilator primarily in arteries and arterioles

Reduces BP by reducing TPR

Side effects: may increase Na+ retention and thus fluid retention, often used in conjunction with a diuretic

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107
Q

Chronic HF

Time, cause, effect

A

Time: progressive; weeks to months

Cause: chronic HTN, valve disease, myocardial disease, chronic lung disease

Effects: full compensation, chronic edema, congestion

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108
Q

Modifiable CVD risk factors

A 
HTN
Tobacco 
Elevated blood sugar 
Physical inactivity 
Overweight/Obesity 
Cholesterol/lipids (total <180 mg/dL optimal; HDL 40-60, LDL 100-129)
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109
Q

ACC/AHA - Stage B

A

Patient with structural disorder without symptoms of HF

Previous MI, LV remodeling including LVH and low EF, asymptomatic valvular disease

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110
Q

S1

A

Lub
1st heart sound
Closure of AV valves (tricuspid and mitral)
Occurs with ventricular contraction

Marks beginning of systole

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111
Q

Common end-organ damage associated with HTN emergencies

A 
Acute pulmonary edema 
Acute left ventricular dysfunction 
Acute coronary syndrome (including acute myocardial infarction) 
Cerebral infarction 
HTN encephalopathy
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112
Q

ACC/AHA - Stage C

A

Patient with past or current symptoms of HF associated with underlying structural heart disease

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113
Q

Generalized edema

A 
Heart failure 
Hypo-albumenia 
Nephrotic syndrome 
Cirrhosis 
Sepsis
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114
Q

A patient might be/become symptomatic with any AV node block due to ____.

A dropped or lost QRS indicates ____, which means ___.

A

Loss of CO (cardiac output)

Ventricles did not depolarize, which means
they don’t contract to push blood into systemic circulation for that time point

Ask if symptomatic and check BP

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115
Q

HCTZ (Esodrix)

A

1st drug of choice for essential HTN

Thiazide: block Na+ reabsorption in distal tune of nephron

Side effects: hypokalemia, hyponatremia, volume depletion, frequent voiding

Reduce BP by reducing blood volume via kidneys

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116
Q

ABI < 0.5

A

Indicates critical ischemia

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117
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Skin appearance

A

Arterial: reduces hair, thick/brittle nails, shiny skin

Venous: cellulitis, dermatitis

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118
Q

Irregular rhythm

A

> 1 P wave per QRS

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119
Q

Causes of aortic regurgitation/incompetence

A

Congenital
Rheumatic
Endocarditis
Deterioration with age and long standing HTN

Rarer: Marfan syndrome, ankylosing spondylitis, certain STDs

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120
Q

Carotid bruit

A

Sound made by turbulent flow vibrating against arterial wall

Causes arterial wall to vibrate during systole

Indicates presence of arterial lesion/plaque

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121
Q

P wave

A

Atrial depolarization

Normal:
Duration < 0.12 sec (3 small boxes)
Amplitude < 2.5 mm (2.5 small boxes)

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122
Q

Right ventricular failure manifestations

A 
Progressive failure 
Dependent edema (ankle or pretibial first) 
Jugular vein distention
Abdominal pain and distention 
Weight gain 
R upper quadrant pain (liver congestion)
Cardiac cirrhosis (ascites, jaundice)
Anorexia, nausea 
Cyanosis (nail beds) 
Psychological disturbance
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123
Q

If patients on a beta blocker - use ___ for exercise

A

RPE

Because beta blocker means HR response won’t go up and thus can’t use HR

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124
Q

I
Area of heart?
Which coronary artery?

A

Lateral

LCx - left circumflex

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125
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Skin color

A

Arterial: Cyanotic or pale, dependent rubor

Venous: hyperpigmented, often superior to medial malleolus-hemosiderin

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126
Q

Carotid sinus receptors respond to pressures

A

60-180 mmHg

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127
Q

patient feels like

“Heart skips a beat”

A

2nd degree AV node block

Type 2

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128
Q

Best anatomical place to hear S3 gallop

A

Apex of heart

5th intercostal space
Mid-clavicular line

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129
Q

Unipolar leads

A

Utilize a single (+) recording electrode, and a combination of other electrodes to serve as a composite (-) electrode

Precordial (chest): V1-V6

Unipolar (augmented): aVL, aVR, aVF

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130
Q

PAD findings

A

Intermittent claudication most common symptom but many asymptomatic or a have atypical lesions

Pallor on elevation

Dependent rubor

Impaired capillary refill

Impaired peripheral pulses

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131
Q

Types of aneurysms

A

Saccular AKA Berry
Small, spherical, 1-1.5 cm
Most common in brain tissue

Fusiform
Gradual more progressive

Dissecting
Blood filled channel within aortic wall

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132
Q

Surgical mgmt - HF

A

VAD- ventricular assist device (temp solution)

Heart transplant

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133
Q

In presence of acute injury, the ____, and gradually returns to the level of ___ over a period of 24-48 hours

A

ST segment elevated above isoelectric line

Gradually returns to level of isoelectric line over 24-48 hrs

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134
Q

Aortic incompetence

A

Failure of aortic valve to close tightly causing back flow of blood into L ventricle

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135
Q

Effects of afterload on HF

A

In normal heart, not much decrease in SV with increased afterload

However the effects are much more significant in patients with HF

Why vasodilator therapy- though counterintuitive - is effective with HF

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136
Q

Baroreceptors respond to _____.
___ loop with ___.

If arterial pressure suddenly rises…
If arterial pressure suddenly drops…

A

Stretching of arterial wall

Negative feedback loop with Vagus and Glossopharyngeal nerves

Pressure rises: walls passively expand, increases firing frequency

Pressure drops: decreased stretch of arterial walls, decreases receptor firing

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137
Q

Positive deflection on ECG means…

A

Going ABOVE isoelectric line

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138
Q

Acute HF

Time, cause, effects

A

Time: instant, sudden; hour to days

Cause: acute MI, PE, severe malignant HTN

Effects: no time to compensate, acute pulmonary edema, acute ischemia

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139
Q

Lead aVR

A

“Orphan lead”
Right

(Signal inverted)

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140
Q

VAD

A

Ventricular assist device
Surgical mgmt of HF

Limited organ availability 
Short term solution 
Ability to sense preload
Need Doppler to take pressure- May not have a true HR (use RPE) 
Progressive exercise training indicated
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141
Q

QT interval corrected (QTc)

A

Since duration of QT varies with HR, raw QT interval often not used.

QTc = measured QT interval % square root of R-R interval

Normal < 0.44 seconds

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142
Q

CVI May result from

A

Vein wall degeneration
Post-thrombotic valvular damage
Chronic venous obstruction
Dysfunction of muscular pumps

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143
Q

Valvular replacement/repair

A

Can be mechanical or biological
Typically require by-pass and median sternotomy

Mechanical lasts lifetime but require lifelong anticoagulant meds.
Mechanical: higher risk for infection, thrombus or emboli
Younger pt may be better candidate for mechanical bc limited life of biological valve

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144
Q

V3

A

Unipolar precordial (chest) lead

Between V2 and V4
(Anterior wall)

75*

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145
Q

5 ECG mnemonic for electrode colors

A

“White on right”
“Snow over grass”
“Smoke over fire”
“Everyone loves chocolate”

RA- white 
RL- green 
LA- black 
LL- red 
V1- brown
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146
Q

V4

A

Unipolar precordial (chest) lead

Midclavicular line, 5th IC space
(Anterior wall)

60*

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147
Q

Murmur:
Decreases with standing
Increases with squatting
S1 sound

A

Aortic stenosis- ejection Type

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148
Q

R wave progression

A

Small R waves begin in V1/V2 and progress in size to V4/V5
The R in V6 is usually smaller than V5

In reverse, the S-waves begin in V6 or V5 and progress in size to V2
The S in V1 is usually smaller than V2

Transition from S>R to R>S usually occurs at leads V3 or V4

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149
Q

PVC

A

Premature ventricular contraction

Wide spontaneous funky QRS
Can be benign
Ectopic pacemakers/focus

Unifocal if similar
Multifocal if different

Cutoff 6 per minute
Check BP

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150
Q

ECG- what looking attire determine regular or irregular

A

P-P, R-R intervals

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151
Q

For every 10 bpm increment over a RHR of 75, mortality increases by…

A

All-cause 9%
Cardiovascular 8%
Especially if HR >90

Normal is 60-100 bpm

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152
Q

HTN crisis

A

76% urgencies
BP > 180/110
No signs of organ damage

24% emergencies
BP > 180/120
Showing signs/symptoms of organ damage

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153
Q

Wells score DVT

A

+ 1 points for each…

  1. Active cancer
  2. Calf swelling >= 3 cm
  3. Swollen unilateral superficial veins
  4. unilateral pitting edema
  5. Previous DVT
  6. Swelling of leg
  7. Local tenderness along deep venous system
  8. Paralysis, paresis or recent cast immobilization of LE
  9. Recently bedridden >=3 days, or major surgery in past 12 weeks

-2 for “alternative diag likely”

> 2 high probability
1-2 moderate probability
< 2 low probability

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154
Q

Venous network in LE commonly affected by CVI divided into …

A

Superficial (lesser and greater saphenous)

Deep (ant and post tibial, peroneal, popliteal, iliac, deep and superficial femoral)

Perforating or communicating veins

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155
Q

Normal HR

A

60-100 bpm

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156
Q

> 160/100 BP

What do you do?

A

Hold resistance exercise, consider aerobic exercise
Contact PCP
Monitor closely

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157
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Symptoms

A

Arterial: aching, cramping that is predictable with activity or elevation

Venous: aching, burning, heaviness, fatigue while standing

158
Q

NYHA class III

A

Marked limitation of physical activity
Comfortable at rest
Less than ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath)

159
Q

V3
Location of heart
Which Coronary artery

A

Septal / Anteroapical

LAD- left anterior descending

160
Q

> 140/90 BP

What do you do?

A

Proceed with usual care
Contact PCP
Monitor closely

161
Q

What BP range hold exam?

A

> 180/110

162
Q

Clopidogrel (Plavix)

A

Anti-platelets

ADP inhibitor

163
Q

V5

A

Unipolar precordial (chest) lead

Anterior Axillary line at level of V4
(Lateral wall)

30*

164
Q

Blood lab to assess for MI

A

Cardiac enzymes: troponins and creatine kinase

165
Q

Angina- stable

A

Discomfort gradually builds
Occurs with exercise at a predictable and consistent intensity
Gradually subsides with rest
Typically lasts 2-5 min, rarely more than 5-10

Improve with nitroglycerin

166
Q

Pain and BP

A

Normal:
Systolic increase 15-25 mmHg
Diastolic increase 10-20 mmHg

Hyper-reactive if higher
Increased risk of developing HTN RR

167
Q

Intermittent claudication

Pain in thigh

A

Iliofemoral occlusion

168
Q

Most common leads for clinical setting

A

3-lead and 5-lead

169
Q

3 lead ECG

A 
3 electrodes:
Right arm (white)
Left arm (black)
Left leg (red)

Bipolar limb leads (I, II, III)

Basic monitoring/research purposes

170
Q

Mitral stenosis

A

Hypertrophy occurs in chamber upstream from stenosis, concentric type

Stretch of L atrium creates multiple foci causing arrhythmias

At risk for thrombus due to pooling in L atrium and increased turbulence

Body may compensate early on with little to no symptoms
May advance to R side heart failure

Medical mgmt: anticoagulant, anti-arrhythmics, surgery

171
Q

Beta blockers

A

Primarily target Beta-1 receptor sites

Reduces: HR, BP primarily by reducing contractility, Sympathetic tone

Has anti-arrhythmic properties
In low doses actually function as anti-anxiety med

Limits adverse ventricular remodeling (dilation) after MI

Cautious with patients with kidney/renal dysfunction, pulmonary dysfunction or asthma
2 categories: specific and non-specific

172
Q

P-R > 0.2 sec

A

AV block present

173
Q

Trigeminy

A

PVC (premature ventricular contraction) every 3 beats

Generally less concerning than Bigeminy (bc within 6 per minute cutoff)

174
Q

Splitting S2

A

S2 is shorter duration and higher frequency than S1

S2 has 2 audible components: aortic closure sound (A2) and pulmonic closure sound (P2)

Normal or physiologic splitting is demo during inspiration in normal healthy, since the splitting interval widens primarily due to the delayed P2 (common in kids and well conditioned athletes)

Persistent splitting S2 May occur in supine or recumbent position- however split should resolve on expiration following sitting, standing or valsalva
If splitting of S2 does not change w/ these are is in adults…further medical attention

175
Q

Regulation of BP- fast

A

Baroreceptors (aortic arch and carotid sinus)

176
Q

Effects of CHF in heart/blood

A

Decreased CO (SV, EF)

Cardiac remodeling; increased LVEDP

Increased systemic vasoconstriction (SNS, humoral, reflex, structure)

Impaired cardiac output distribution, pro-inflammatory state

Anemia -> decreased O2 content

177
Q

HTN medications

A

Majority of patients will require 2 meds

Thiazide-Type diuretics usual initial med.

Depending on co-morbidities..,
ACEI (ace inhibitor) 
ARB (aldosterone receptor blocker) 
BB (beta blocker) 
CCB (calcium channel blockers)
178
Q

Aneurysms

A

Localized abnormal dilation by at least 50% compared to normal

Causes: atherosclerosis, congenital infections, Marfan’s

Risk factors: CVD and CVD risk factors (esp smoking), male, genetics (Marfan’s), 40-60 yo, HTN prevalent

179
Q

Symptoms of cardiac valvular disease

A 
Easy fatigue 
Dyspnea 
Palpitations 
Murmur 
Chest pain
Putting edema 
Orthopnea 
Dizziness
180
Q

Mean arterial pressure is normally regulated…

A

Within a narrow range

Mean arterial pressure typically 85-100 mmHg in adults

181
Q

NYHA class IV

A

Unable to carry on any physical activity without discomfort
Symptoms of heart failure at rest
If any physical activity is undertaken, discomfort increases

182
Q

ST depression types

A

Normal
Upsloping
Horizontal
Downsloping

183
Q

Intermittent claudication

Pain in proximal 2/3 calf

A

Superficial femoral artery

184
Q

Ischemia- causes of increased demand

A

Exercise
Cold weather (increased vascular resistance)
Mental/emotional stress
Spontaneous changes in HR and BP

185
Q

Complications cardiac post surgery

A 
DVT and/or PE
Intra- or Peri-operative MI
Pericarditis 
Infection 
Sternotomy failure 
Pulmonary complications 
Reduced bowel motility 
Deconditioning 
Neurocognitive decline 
Chest wall pain and mobility issues
186
Q

___ receptors have high threshold pressure and are less sensitive that ____ receptors

A

Aortic arch receptors higher threshold and less sensitive than carotid sinus receptors

187
Q

Intermittent claudication

Pain in distal 1/3 calf

A

Popliteal Artery

188
Q

CVD defined by presence of ___.

3 major causes

A

Stenosis

Atherosclerosis
Thrombo-embolism
Vasculitis

189
Q

Ejection fraction (EF)

A

EF = (EDV - ESV) % EDV

Normal value 55-75%

Mild 40-50.%
Moderate 30-40%
Severe < 30%

EF does NOT correlate with functional capacity

190
Q

Blood lab to assess and track severity of heart failure

A

BNP

Brain natriuretic peptide

191
Q

Presence of ___ in ____ indicates an anterior infarction and probable involvement of ___ Artery.

A

Significant Q waves in V1-V4

LAD (left anterior descending coronary artery)

192
Q

HTN subdivided into…

A

Essential HTN-
Cause unknown, 95-99% of cases
Interaction between genetics and environment

Secondary HTN-
1-5%
Result of biochemical or mechanical pathology, potentially reversible

193
Q

Regulation of arterial blood flow

A

Sympathetic: NE
(NE binds to alpha-1 causing vasoconstriction)

Circulating: E
Circulating hormone: angiotensin II

Local metabolites: prostaglandins

Mechanical: muscle contraction, vessel stretch (CA2+ influx)

194
Q

4 groups most likely to benefit from statins

A
  1. Any form of ASCVD
  2. Primary LDL-C levels of 190 mg/dL or greater
  3. DM, 40-75 y/o, with LCL-C levels 70-189 mg/dL
  4. W/O DM, 40-75 y/o, with estimated 10-year ASCVD risk >= 7.5%
195
Q

Depolarization of cell membrane allows influx of ___ into cell and efflux of __.

A

Na+ in

K+ out

196
Q

Intermittent claudication- manifests

A

Predictable time and intensity, reproducible, doesn’t change with posture

Location of the diseased artery determines location of claudication

Walking test

197
Q

Sinus rhythm

A

Normal

198
Q

ARBs

A

Angiotensin 2 receptors “sartan”
Similar effects as ACEI, used when patients don’t tolerate ACEI (“coughing”)

Most common: Losartan (Cozar),Valsartan (Diovan)

Also used to treat patients with obstructive sleep apnea

199
Q

Heart disease (CDC facts)

A

~ 610,000 Americans die annually (25% of deaths)

Coronary heart disease is most common (370k annually)

In US, heart attack every 43 seconds; death every minute from heart-related event

AKA: CAD (coronary artery disease); ASHD (atherosclerotic heart disease)

200
Q

Aystole

A

Flat line

No electrical activity to heart

201
Q

Special exercise considerations- HF

A

Avoid exercise after eating and vasodilator meds
Use VO2max instead of HRmax
Initial exercise intensity should be 10 beats below significant symptoms

Signs of cardiac decompensation: pulse narrowing, arrhythmia, fluid changes (3lbs on 24 hrs; 5lbs in a week)

Goal writing: increased intensity/duration; functional activities and independence

202
Q

Pallor on elevation

A

Insufficient arterial pressure to perfuse when leg elevated above level of heart
Limb drains of blood, turns pale

203
Q

Chronic HTN shifts baroreceptor curve to ____.

A

Right
(Mean arterial pressure increases x-axis; receptor firing y-axis)
Baroreceptor sensitivity decreases, the higher pressure is “new normal”

204
Q

Couplet

A

2 PVCs (premature ventricular contraction) in a row

Concerning

205
Q

Effects of CHF on gut/splanchnic organs

A

Hyperconstricted

206
Q

When subjected to various stressors, endothelial cells can also produce….

A

Prothrombotic molecules

In response to injury or infection, secrete chemokines and produce cell surface adhesion molecules

207
Q

Elevated BP

A

Systolic 120-129

Diastolic <80 (79 or less)

208
Q

Irregularly irregular rhythm

A

RR interval and ectopy variable with no pattern- totally irregular

209
Q

12-lead ECG is used primarily for ___. Single-lead monitoring is for ___.

A

12- lead: determining ischemia or infarction

Single-lead: evaluating heart rhythm

210
Q

Stage 1 HTN

A

Systolic 130-139

Diastolic 80-89

211
Q

Mitral valve prolapse sound

A

Click mid-systole (between S1 and S2)

Followed by a murmur

212
Q

Heart failure with reduced ejection fracture (HFrEF)

A

EF = < 40%.

AKA systolic HF (SHF)

213
Q

When contraction increases within a given chamber of the heart ___

When contraction ends …

A

Chamber pressure greater than downstream pressure, the valve opens

When contraction ends, pressure decreases below downstream pressure, the valve closed

214
Q

Heart valves- diastole

A

Pulmonary and aortic valve closed

Tricuspid and Mitral valves open

215
Q

On ECG, wave of depolarization is recorded as ___ when moving toward a (+) electrode on the skin

A

An upward deflection

216
Q

Heart transplant

A

Native SA node
No longer innervated
Different mechanisms for CO regulation during exercise

Immunosuppressive agents needed-
Side effects HTN, osteoporosis, muscle weakness, liver damage

217
Q

CHF etiology

A 
Ischemic heart disease (most common in US)
HTN
Idiopathic cardiomyopathy 
Infections (viral myocarditis, Chagas) 
Toxins (alcohol or cytotoxic drugs)
Valvular disease 
Prolonged arrhythmias (A-fib)

Lifetime risk is greater if BP remains > 160/90

218
Q

Exercise considerations-

Valvular stenosis

A

Close monitoring with RPE
Low muscle perfusion may limit exercise
Suppressed BP response to exercise, possibly exaggerated HR
Low cardiac output

Pt with symptomatic aortic stenosis typically not candiofor exercise programs

Asymptomatic: intensity low and progressed gradually
Angina may be a symptom

219
Q

Raynaud’s syndrome

A

Vasospasm causing reduced blood flow
Primary- more common in women (15-30 yo) more typical in cold climates, family history, no underlying disease
Secondary- less common, more serious. Usually appears around 40 (scelerodema, lupus, RA, repetitive trauma, smoking, atherosclerosis)
Severe- rare, could result in permanent hypoperfusion of digits

220
Q

A significant Q wave is

A

1 mm wide
OR
1/3 size of QRS complex

221
Q

P-R interval

A

The propagation of the cardiac AP from atria -> AV node -> ventricles

Normal:
0.12 - 0.2 seconds (3-5 small boxes)

(Will shorten during exercise as heart rate increases)

222
Q

Hypertrophy is detected on a 12-lead ECG by looking at…

A

Waveforms- particularly P-wave and QRS complex for voltage (> 3 mV) or configuration

223
Q

Pericarditis and ST elevation

A

Concave upwards ST elevation in most leads except aVR

No reciprocal ST segment depression (except maybe aVR)

T waves are usually low amplitude and HR usually increased

May see PR segment depression- a manifestation of atrial injury due to compression

224
Q

Neuropathic ulcers

A

Plantar location
(Metatarsal heads- esp 2nd; sole of foot, balls of toes)

“Punched out” margins, usu correspond to pressure points

Insensate- often diabetic w/ peripheral neuropathy

May have arterial insufficiency signs/symptoms

225
Q

Regular rhythm

A

1 P wave per QRS complex

RR interval constant

226
Q

V2
Location of heart
Which Coronary artery

A

Anterior / Anteroseptal

LAD- left anterior descending

227
Q

Mitral stenosis - etiology

A

Primarily females (66%)

Valve leaflets don’t open easily or completely
Decreases area and increases resistance to flow between A-V

Main cause: rheumatic heart disease
Other etiologies: congenital mitral stenosis such as parachute mitral valve; marked mitral annual calcification and infective endocarditis with large vegetations (often fungal)

228
Q

Aortic stenosis

A

Calcific aortic stenosis and congenital bicuspid aortic valve stenosis account for majority of cases

Mild thickening, calcification, or both of a tri-leaflet aortic valve w/o restricted leaflet motion

~25% of the population older than 65 years

229
Q

Q-T interval

A

Time taken for ventricular depolarization and repolarization

Shortens during faster HR,
Lengthens during slower HR

Normal:
Men: 0.4 - 0.44 sec (10-11 small boxes)
Women: 0.44 - 0.46 sec (11 - 11.5 small boxes)

230
Q

Heart failure

A

Complex clinical syndrome from any structural/functional cardiac disorder that results in inability of heart to eject blood to meet the demands of the body while maintaining normal pressures in its chambers and lungs

231
Q

Angiotensin-converting-enzyme inhibitors OR Angiotensin antagonists

A

Vasodilator

Decreases remodeling

232
Q

Ectopic pacemakers/foci

A

Abnormal pacemaker sites located outside SA node that display automaticity

Normally their activity is suppressed via overdrive suppression- by the higher rate SA node

Can occur within atria or ventricles

233
Q

ECG sinus rhythm

A

P wave followed by QRS
QRS preceded by P wave

P upright in leads I, II, III

PR interval > 0.12 sec (3 small boxes)

234
Q

Murmurs classified on…

A

Shape (crescendo, decrescendo, plateau…)

Location (site where originates: A P T M)

Timing (murmurs longer than heart sounds. Systolic, diastolic, continuous)

Intensity (graded 1-6; 6 is so loud no stethoscope needed; “Thrills”associated w/ murmurs grade 4-6)

Pitch (high, med, low)

235
Q

Aldosterone

A

Decrease fibrosis
Na retention
Antagonist remodeling
Aldosterone release

236
Q

Polymorphic

A

2 different morphologies

237
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Pulses

A

Arterial: May be decreased or absent; bruits

Venous: normal but may be difficult to palpate

238
Q

ECG
Rhythm
Check for…

A

P before each QRS
QRS after each P

PR intervals- for AV blocks
QRS intervals- for BBB

239
Q

Typical post op progression and goals

A

Day 0: transfers to chair with RN in am

Day 1: transfer sit->stand, gets to doorway, pre-gait
Afternoon ambulation

Day 2-3: chest tubes and cardiac pacer d/c
Patient must be supine and remain still for 1 hr with d/c
Stairs and independent ambulation assessments

240
Q

Ventricular rate vs Atrial rate

A

Should be 1:1

241
Q

Phase 2

Cardiac AP

A

Influx of Ca2+ through L-Type Ca2+ channels

Electrically balanced by K+ efflux through delayed rectifier K+ channels

242
Q

Angina- somatic fibers

A

Usually easily described, precisely located, and usually experienced as a sharp sensation

243
Q

Effects of CHF on lungs

A 
Increased:
Pulmonary vascular pressure 
Stiffness 
VA/Q mismatch 
Alveolar- arterial O2 gradient 
Respiratory muscle work

Decreased:
Diffusing capacity

244
Q

Aortic stenosis- what expect

A

Volume overload:
LV dilates out
LVH

Upon exertion:
Dyspnea

Auscultation:
Diastolic murmur “blowing”

245
Q

Phase 0

Cardiac AP

A

Rapid Na+ influx

Through open fast Na+ channels

246
Q

Statins

A

HMG-CoA reductase inhibitors

Blocks LDL synthesis
Increases HDL
Some anti-inflammatory properties

Common: Lovastatin (mevacor), Simvastatin (Zocor), Atorvastatin (Lipitor), Rosuvastatin (Crestor)

247
Q

Heart failure

Compensation

A 
Neurohormonal mechanisms (SNS and RAAS) to Increase CO (SV x HR); 
Natriuretic peptides
248
Q

Digoxin or Dobutamine or PD3

A

Positive inotrope

249
Q

The heart in general depolarizes and conducts from ….

A

Right -> Left
Superior-> Inferior
Internal-> External

(Repolarizes in opposite direction)

250
Q

V6

A

Unipolar precordial (chest) lead

Mid Axillary line at level of V4
(Lateral wall)

0* (left lateral)

251
Q

HTN med considerations

A

Alpha blockers, Calcium channel blockers or vasodilating drugs may lead to sudden hypotension post-exercise

Avoid suddenly stopping exercise and undertake an extended cool down of light activity

Beta blockers and diuretics may impair thermoregulation

252
Q

As cell becomes positive on interior, the myocardial cells …

A

Are stimulated to contract

Excitation coupling

253
Q

Beta blockers

A

Decreased HR
Decreased remodeling (block SNS)
Anti-arrhythmic

254
Q

Renin release stimulated by…

A

Sympathetic nerve activation (beta1 adrenoreceptors)

Renal Artery hypotension (caused by systemic hypotension or renal artery stenosis)

Decreased sodium delivery to distal tubules of kidney

255
Q

Murmurs

A

Extra sounds during the cardiac cycle, such as whooshing or swishing made by turbulent blood flow often due to a faulty valve or structural changes in myocardium

256
Q

V1

A

Unipolar precordial (chest) lead

4th IC space to R of sternum
Septal

257
Q

aVL
Area of heart?
Which coronary artery?

A

Lateral

LCx - left circumflex

258
Q

Afib vs Aflutter

A

Aflutter P-wave- distinct sawtooth
Afib P-waves- variable, hard to detect or not demonstrated at all

Aflutter Rhythm- usually fairly regular, Ltd R-R variability
Afib Rhythm- usually very irregular, high R-R variability, with isoelectric line variability

Aflutter usually has a fixed/consistent conduction block pattern

259
Q

Infarction

ECG

A

Q waves
Inverted T waves
ST segment elevation or depression

260
Q

Pericardium

A

Fibrous - outermost later, firmly bound to central tendon of diaphragm, sternum and mediastinal pleura

Serous - inner surface of fibrous pericardium (parietal) and reflected onto heart as visceral layer (epicardium)

Pericardial space - filled with fluid to lubricate/reduce friction

261
Q

S3 occurs

A

At beginning of diastole

262
Q

Ventricular fibrillation

A

Not pumping effectively
No pulse
Probably passed out
High risk of death (code blue)

263
Q

Low-molecular weight heparin (LMWH)

A

Anti-coagulant

Fast acting (3-5 hrs) 
Used in patients with better kidneys

Often injected

264
Q

Diuretic

A

Decreases fluid volume

Relives dyspnea

265
Q

Acute HF

4 things

A
  1. Blood flow- vessels constrict, vital organs are not perfused with enough blood
  2. Kidney function- in response to insufficient blood feeding kidneys, their function deteriorates leading to fluid build-up
  3. Fluid buildup- fluid starts to leak out of vessels into surrounding tissues, causing body to swell and add weight
  4. Breathlessness- fluid builds up in lungs and alveoli, difficulty breathing and congestion (drowning in own body)
266
Q

ST- depression

A

ST depression > 1 mm at J point

Significant for ischemia

267
Q

Evolution of atherosclerotic plaques - developmental stage 2

A

Fibrous plaque

Lipoproteins transport/deposits LDL into arterial intima
Fatty streak covered by collagen and calcium deposits forming a fibrous plaque that appears grayish/whitish

Result = narrowing of lumen

268
Q

Percutaneous coronary intervention (PCI)

A

Formerly known as angioplasty with stent
Non-surgical procedure
Catheter and balloon to place a stent to open up blood vessels in heart that have been narrowed by plaque buildup

2 types stents: bare metal and drug eluting

269
Q

What must consider when monitoring the response to exercise for a patient with aortic stenosis

A

BP might not increase much during exercise

270
Q

Furosemide (Lasix)

A

HF and patient’s with CAD with CKD

Loop diuretic: block Na+/K+/Cl- reabsorption

Side effects: hypokalemia, hyponatremia, volume depletion, frequent voiding

Reduce BP by reducing blood volume via kidneys

271
Q

Exercise for claudication

A

Exertion to the point of leg pain is required for maximum benefits

For more severe cases: arm ergometry also improves walking performance

Leg strength training improves walking time- but not as much as treadmill

Interval training with short rest periods for relief is most effective

At least 3x week (for 12 weeks)
Intensity should induce claudication within 3-5 min; continue until pain is moderate (5/10)
Goal 30-35 min

272
Q

NYHA- class II

A

Slight limitation of physical activity
Comfortable at rest
Ordinary physical activity results in fatigue, palpitation, dyspnea (shortness of breath)

273
Q

AV node blocks

A

1st degree AV block PR > 0.20 seconds

2nd degree AV block: 2 types
Type 1: Mobitz I or Wenckeback
Increasing PR interval until a QRS complex is dropped (usually benign)
Type 2: Mobitz II
QRS dropped w/o any progressive increase in PR interval

274
Q

TAVR/TAVI

A

Transcatheter aortic valve replacement

Accessed through femoral artery

275
Q

Regularly irregular rhythm

A

RR interval variable but with s pattern

Normal and ectopic beats grouped together and repeating over and over

276
Q

Nonischemic causes: ST elevation

A
  1. LVH (Left precordial leads, I, aVL)
  2. Conduction abnormalities (ex: LBB, WPW and non-specific intracardiac delay)
  3. Early repolarization pattern
  4. Aneurysm/old MI
  5. Pericarditis/myocarditis
  6. Brugada pattern
  7. Takotsubo (apical ballooning) syndrome
  8. Hyperkalemia
  9. Hypercalcemia
277
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Ulcers

A

Arterial: pale base, discrete borders, high-pressure sites like heel or toes

Venous: near medial malleolus, irregular border, pink base

278
Q

Heart failure

Symptoms

A 
Shortness of breath 
Fluid retention 
Fatigue 
Orthopnea 
Paroxysmal nocturnal dyspnea
279
Q

Myopathy and statins

A

Myalgia up to 25%

Myagliga and weakness (7%)

Rhabdo assoc w statin possible but rare (<0.1% muscle pain, weakness, dark urine; more prominent muscle groups)

280
Q

Murmur:
Increases with standing
Decreases with squatting
S1 sound

A

HCOM - ejection Type

Hypertrophic cardiomyopathy

281
Q

Most common cause of HF in US?

A

Ischemic heart disease

282
Q

MI

A

Myocardial infarction

Cell death in the heart muscle caused by complete and prolonged occlusion of a coronary artery

283
Q

Phase 1

Cardiac AP

A

Transient K+ channels open

K+ efflux returns TMP to 0mV

284
Q

Evolution of atherosclerotic plaques - developmental stage 1

A

fatty streaks
Lipid-filling smooth muscle cells
Potentially reversing

285
Q

PAD findings

A

Affected limb may show signs of cyanosis
Feels cool to touch
Numbness or tingling reported in affected area
Skin may appear shiny, thin, pale and hairless
Nails become thickened and brittle

286
Q

Semilunar valves

A

Aortic and pulmonary

3 leaflets of each side
NO papillary muscles or chordae tendinae

Do NOT lie back against walls of aorta or pulmonary artery

287
Q

12 lead ECG

A

Diagnostic and stress testing

10 electrodes:
All 4 limbs (RA, LL, LA, RL)
6 Precordium (V1-V6)

Monitors 12 leads: V1-V6, I-III, aVR, aVF, aVL

Allows interpretation of specific areas of heart

288
Q

You note elevated troponins in a patient chart and see comment “demand ischemia”- this can be due to…

A

Poor cardiac output and does not represent MI

Patient may be at risk for additional ischemia related to activity, so proceed cautiously

289
Q

Composite score chest pain due to CAD

A 
1 point each:
Male > 55 / Female > 65
Known vascular disease 
Pain worse with exercise 
Pain not elicited with palpation 
Patient assumes pain is cardiac origin

4-5 high +LR

290
Q

Unfractionated heparin

A

Anti-coagulant

Blocks clotting factors in blood, traditionally IV

24 hours to effect

Used post-op to prevent clots, DVT

291
Q

Myocardial oxygen demand determinants

A

Wall stress
HR
Contractility

292
Q

Systolic heart failure (SHF)

A

Impaired contractile function of heart

SHF most common etiology = ischemic heart disease, although many patients with DHF have CAD

293
Q

Aortic regurgitation/incompetence

What expect

A

Eccentric hypertrophy
Late stages may include LA concentric hypertrophy
No pulmonary symptoms until very advanced

Volume overload:
LV dilates out
LVH

Exertion: dyspnea
Auscultation: diastolic murmur “blowing”

294
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Skin temp

A

Arterial: cool

Venous: normal

295
Q

Left ventricular failure manifestations

A 
Progressive dyspnea (exertions first)
Paroxysmal nocturnal dyspnea 
Orthopnea 
Productive spasmodic cough 
Pulmonary edema: Extreme breathlessness, anxiety, frothy pink sputum, nasal flaring, accessory muscle use, rales, tachypnea, diaphoresis
Cerebral hypoxia: irritability, restlessness, confusion, impaired memory, sleep disturbance 
Fatigue, exercise intolerance 
Muscular weakness 
Renal changes
296
Q

Condition of imbalance between myocardial O2 supply and demand often caused by atherosclerosis of coronary arteries

A

Ischemia

297
Q

Palpation of abdominal aorta

A

Relax abs- flex hips and support head and legs with pillow
Start left and superior to umbilicus
Apply first pressure with flattened fingers of both hands
Width > 2.5 cm (~2 finger widths) warrant further medical examination

298
Q

Angina

A

Chest pain or discomfort due to cardiac ischemia

3 major types: stable, unstable, printzemental

Heaviness, tightness, pressure 
Discomfort gradually builds 
Gradually subsides 
Episode lasts 1-5 min 
Often confused with digestive disturbances
299
Q

Stage 2 HTN

A

Systolic 140 or higher

Diastolic 90 or higher

300
Q

Hemodynamics

A

Blood flow parallels CO
BF
CO = HR x SV

CO = driving pressure % resistance to flow…
or CO = (MAP - CVP) % TPR

301
Q

Localized edema

A

MSK injury

DVT

302
Q

CVD is

A

Disease and dysfunction to the myocardium and blood vessels, includes numerous problems, many of which are related to process of atherosclerosis

303
Q

Arterial ulcers

A

Dorsal or distal location (toes)
Sharp margins
Painful
Pallor, loss of hair, nail dystrophy

304
Q

Afib

A

Atrial fibrillation
Atrial activity poorly defined; may see course or fine undulations or no atrial activity at all

Cause by multiple ectopic pacemakers in atria

Ventricular response: irregularly irregular
Can be rapid, moderate or slow

Adequate control (HR < 110 bpm) 
Inadequate control (HR > 110 bpm)
305
Q

PAC

A

Premature atrial contraction

Usually benign

306
Q

ACE-Inhibitors

A

Angiotensin converting enzyme inhibitors “pril”

Blocks conversion of Ang 1 to Ang 2
Lowers BP
Few adverse side effects other than orthostasis

Decrease afterload and improves survival in HF

Increases survival and prevents LV dilation post-MI

Most common: Lisinopril (Zestril), Captopril (Capoten) and Enalapril (Vasotec)

307
Q

EKG leads: the (+) terminal

A

The “eye”

Captures/receives the signal

308
Q

Overlap of atherosclerotic disease

A

Coronary artery disease
Cerebrovascular disease
Peripheral artery disease

Patients with one often have coexistent disease in other vascular beds

309
Q

HTN causes about 50% of ___ and increases risk of ___.

A

Ischemic CVA

Increased risk of hemorrhagic stroke

310
Q

Ankle-Brachial Index (ABI)

Procedure

A
  1. Patient in supine
  2. Measure brachial artery pressure using Doppler US
  3. Apply same BP cuff to ankle on same side of body
  4. Palpate for posterior tibial artery- take SBP reading
  5. Palpate for dorsalis pedis artery- take pressure
  6. Repeat other side/arm-ankle

ABI = ankle pressure % brachial pressure
(Using highest value from L or R side)

311
Q

Structure of artery walls

A 
Intima: endothelial cells
Internal elastic membrane 
Media: smooth muscle cells
External elastic lamina 
Adventia
312
Q

___ is due to increase in capillary pressure usually from an elevation of venous pressure caused by obstruction to venous and/or lymphatic drainage

A

Edema

313
Q

Evolution of atherosclerotic plaques - developmental stage 3

A

Complicated lesion/Instable plaques

Continued inflammation can result in plaque instability, ulceration and rupture
Lipid core is exposed to blood stream, platelets accumulate, and thrombus forms

Result = narrowing of lumen or thrombo-embolotic event

314
Q

Lead aVL

A

Lateral wall

315
Q

ABI 0.5-0.8

A

Patients with claudication

316
Q

Temporary epicardial pacer

A

Epicardial pacing wires common after open heart surgery, wires exit through mediastinal incision

Cardiac surgery makes myocardium irritable and prone to arrhythmia

Pacer used to control heart rate due and rhythm

317
Q

ST-segment depression that develops during exercise is

A

An ischemic response to activity and following rest should return to baseline

318
Q

ECG paper:

___ = 1 mV

A

10 mm

2 thick lined boxes; each thick box has 25 thin line boxes total, so 10 small boxes in a row is 1mV

319
Q

Normal EF

A

> 55%

From echocardiogram

Is NOT related to functional capacity and tolerance to exercise

320
Q

Coumadin (Warfarin)

A

Long-term Anti-coagulant

A-fib, chronic DVT

Blocks effect of Vit K-epoxide reductase

321
Q

Effects of CHF - respiratory muscles

A

“Steal” blood from locomotor muscles

322
Q

Lead =

Electrode =

A 
Lead = signal
Electrode = sticker placed on skin
323
Q

___ is leading risk factor for CVD mortality.

Only __% are compliant with ___.

A

HTN
13% global deaths
Leading cause of CVD worldwide

Only about 50% compliant with medication

324
Q

RT (resistance training) - HF

A

Once considered unsafe

Most often in form of a PRE (progressive resistance exercise)
60-80% 1RM

Most protocols emphasized LE muscles

Improvements: “muscle hypothesis” attenuated the loss of muscle mass, improved functional mobility and ADLs, 6MWT and WoL (SF-36)

325
Q

3 types of ulcers

A

Atrial
Venous
Neuropathic

326
Q

Capillary refill test

A

Blanch nail bed
Remove pressure
Count time until normal pink color returns
Normal refill fingers/toes is < 2 seconds

327
Q

Ankle-Brachial Index (ABI)

Interpretation

A

ABI = ankle pressure % brachial pressure (Using highest value from L or R in equation)

Normally ABI = or > 1
ankle BP is as high as brachial

ABI = < 0.9 diagnostic of PAD
ABI 0.5-0.8 found in claudication
ABI < 0.5 critical ischemia

An ABI of 0.9 or lower has SpIN 83-99% and SnOUT 68-73% in detecting stenosis greater than 50%
(SnOUT of ABI less than 1.0 approaches 100%)

328
Q

ECG paper:
Thin lines
Thick lines

A

thin:
1 mm intervals or 0.04 seconds
0.1 mV

Thick:
5 mm intervals or 0.2 seconds
0.5 mV

329
Q

Aspirin

A

Anti-platelets

COX1 and COX2 inhibitor
Often used in low doses

Given larger doses during MI

330
Q

V5
Area of heart?
Which coronary artery?

A

Lateral

LCx - left circumflex

331
Q

Monitoring guidelines- 5 things “hold exercise”

A
  1. QRS widening > 0.12 sec
  2. > 6 PVC per min or couplet
  3. Glucose >250 or below 60
    (Make sure they have a snack prior)
  4. Resting 90mmHg > SBP > 180mmHg
    OR DBP > 110 mmHg
  5. RHR >100 or with A-fib > 110 bpm
332
Q

Calculating HR on ECG paper- method 2

A

Count number of QRS complexes in a 6 second interval and multiply by 10 (30 thick lined boxes)

Ex: 8 QRS complexes x 10 = 80 bpm

(5 thick boxes = 1 sec)

333
Q

Tissue plasminogen activators (TPA)

A

Thrombolytic

Facilitate breakdown of clots that have already formed by converting plasminogen to plasmin

Used in acute MI, if used w/in 1 hr of symptoms reduces mortality by 50%

Most common: Streptokinase (Streptase), UroKinase (Abbokinase)

334
Q

Sustained ventricular tachycardia

A

Does not revert back to normal rhythm after ~30 sec

335
Q

Left ventricular hypertrophy is present if

A

The depth of S-wave in V1 + height of R wave in V5

> 35 mm

336
Q

Non-modifiable risk factors of CVD

A

Gender (male > female)
Age (male > 40; female >50)
Race (African-American or Asian)
Family history

337
Q

Heart failure with preserved ejection fraction (HFpEF)

A

EF = > 50%

AKA DHF (diastolic heart failure)

41-49% borderline
> 40% improved

338
Q

Pathophysiology - valvular disease

A

Congenital- genetic, maternal exposure

Acquired- rheumatic fever, endocarditis, gradual fibrosis

339
Q

Phase 4

Cardiac AP

A

Na+ and Ca2+ channels closed

Open K+ rectifier channels keep TMP stable at -90mV

340
Q

Factors that increase likelihood of MI (top 3)

A

Assoc with exertion
Radiation to L arm
Described as pressure

341
Q

ST-segment depression at rest associated with chest pain may indicate…

A

Acute injury to subendocardial wall

342
Q

Phase3

Cardiac AP

A

Ca2+ channels close
Delayed K+ rectifier channels remain open
Return TMP to -90mV

343
Q

Venous ulcers

A

Maleolar location (usually medial)
Irregular margins
Hemosiderin staining (brown)
Varicose veins and pitting edema

344
Q

Ischemic changes -ECG

A

Reduced blood flow ->
Reduced ability to conduct AP

Membrane potential changes

T-wave inversions
Progresses into S-T segment changes (depression then to elevation)

345
Q

Pathologic Q waves

A

Scar tissue (prior tissue death)

346
Q

J point

A

Initiation of ventricular repolarization
Junction between termination of QRS complex and beginning of ST segment

Normally, should be in line with isoelectric line

347
Q

Presence of ___ in ____ indicates an inferior infarction and probable involvement of ___ Artery.

A

Significant Q-waves in II, III, aVF

Right coronary artery

348
Q

Normal BP

A

Systolic <120 (91-119)

Diastolic <80 (61-79)

349
Q

Turgor

A

Normally skin springs back to its resting position right away

In dehydrated patients this return to resting is delayed
May also observe hypotension, tachycardia, orthostasis, irregular HR and ECG

350
Q

Myocardium oxygen supply determinants

A

O2 content

Coronary blood flow 
Coronary perfusion pressure 
Coronary vascular resistance: 
(External- compression 
Internal- intrinsic regulation: local metabolites, endothelial factors, neural innervation)
351
Q

Cardiovascular diseases, including stroke and heart disease, account for ___% or ____ of all US deaths.
And ____.

A

1/3 or 33.6% deaths

Among leading causes of disability in US (nearly 4 million people)

352
Q

5 lead ECG

A
  1. Right arm (WHITE- below clavicle)
  2. Right leg (GREEN- lower edge rib cage)
  3. Left arm (BLACK- below clavicle)
  4. Left leg (RED- lower edge rib cage)
  5. Chest (BROWN- V1)

Monitor displays bipolar leads (I, II, III) AND a single chest/precordial lead (can be V1-V6 depending on position)

Commonly used in acute care

353
Q

Torsades de pointes

A

Code blue

Ventricular fibrillation

354
Q

3rd degree AV node block

A

AKA Complete heart block
Atria and ventricles are electrically dissociated
P-waves and QRS complexes occur independent of each other

As always use QRS complexes to determine HR

355
Q

S4 occurs

A

Late diastole

356
Q

Ischemic contracture of myocardium

A

Insufficient or no ATP delivered to break cross myofilament cross-bridge

357
Q

ECG paper:

Tick marks on rhythm strip = ?

A

3 seconds

358
Q

Overview of pathophysiology of atherosclerosis

A

Endothelial dysfunction
Inflammatory process involving many cellular markers within the lesion
Deposits of fatty streaks initiating event
Lesions occur in large and medium sized vessels

May be present throughout lifetime

359
Q

Angina- special populations

A

Elderly patients:
More likely to present with atypical symptoms (SOB, AMS)

Diabetics: may not be able to accurately sense or describe pain

Women: more commonly report nausea, emesis, jaw pain, neck pain, back pain

Presence of multiple RX, drugs and alcohol will also alter perception to perceive discomfort

360
Q

Abdominal aortic aneurysm

A

Dull, tearing ache/pain in low back, groin or mid-abdominal left flank
Chest pain
Weakness or transient paralysis of legs
Palpable, pulsating abdominal mass (> 3cm)
Inter-arm systolic BP difference > 20 mmHg
Absent or decreased peripheral pulses (pulse deficit)
Tachycardia

361
Q

Metoprolol (Lopressor)

A

Beta blocker - specific

Sympatholytic

362
Q

Rhythm: No P wave but normal QRS

A

AV node

363
Q

3 properties of cardiac muscle

A

Automaticity
Rhythmicity
Conductivity

364
Q

Neurohumoral activation

Compensatory mechanisms in heart failure

A

Decreased CO ->
Renal sodium and water retention->
Restoration of organ perfusion

And/or

Decreased CO ->
Increase vascular resistance->
Restoration of organ perfusion

365
Q

Factors that decrease likelihood of MI

A

Described as positional
Not associated with exertion
Reproducible with palpation
Described as sharp

366
Q

Warning s/s of ltd exercise tolerance

A
  1. Resting tachycardia
  2. Lack of HR or BP increase with exertion (10 mmHg/MET)
  3. Exaggerated HR or BP response to exertion
  4. > = 10 mmHg fall in SBP with increased workload
  5. Low angina threshold
  6. Excessive dyspnea
  7. Slow HR recovery from activity
367
Q

ACC/AHA - Stage D

A

Patients with end-stage disease who requires specialized treatment strategies

368
Q

Coronary artery bypass graft

A

320k annually in US
1-2% mortality but 5-10% risk of MI during procedure

Graft vessels sewn to coronary arteries beyond blockage and attached to aorta

Triple, quadruple or quintuple bypasses are not routine

Most commonly used vessel for grafts is saphenous vein

369
Q

Palpate pulse when auscultation:
When you feel pulse and hear a sound indicates ____
When

A

Systole (feel pulse and hear sound) - AV valves (M1, T1)

End of systole/beginning diastole (don’t feel pulse and hear a sound) - semilunar valves (A2, P2)

370
Q

Types of Remodeling

A

Eccentric hypertrophy-Normal wall thickness with LV increased mass

Concentric hypertrophy- increased wall thickness and LV mass

Concentric remodeling- increased wall thickness, normal LV mass

371
Q

Cardiac Remodeling - HTN

A

Chronic HTN->
Aortic valve stenosis

Pathological hypertrophy: 
Myocyte length increase < width increase 
Fibrosis 
Maybe cardiac dysfunction 
-> 
Cardiac dilation: 
Myocyte length increase >> width increase 
Extensive fibrosis 
Myocyte death 
Adv cardiac dysfunction
372
Q

Calculating HR on ECG paper - method 1

A

60 % 0.2 = 300 bpm
(60 seconds per minute divided by thick line box of 0.2 seconds)

60 % 0.4 = 150 bpm
(60 sec % 2 thick line boxes)

60 % 0.6 = 100 bpm
(60 sec % 3 thick line boxes)

(Note: each thick line box = 0.2 sec)

373
Q

Stage A patient

Therapy goals

A

Heart healthy lifestyle
Prevent vascular, coronary disease
Prevent LV structural abnormalities

374
Q

Atrial flutter

A

Aflutter

Regular atrial activity with a saw-tooth appearances
Ventricular rate usually 60-100 bpm
Conduction ratio usually between 2:1 and 4:1

Supraventricular Rhythm
Not frequently encountered

375
Q

In ventricular aneurysm… (ECG)

A

ST segment remains elevated and does not return to isoelectric line over time

376
Q

Normal blood flow

A

5 L/min

Heart failure 3.5 L/min

377
Q

Alpha-1 blockers

A

Block alpha-1 receptors on vascular smooth muscle, reducing TPR and BP

Effective treating: Benign prostate hypertrophy

Most common:
Doxazosin (cardura)
Prazosin (minipress)

Sympatholytics

378
Q

Atherosclerosis

A

“Hardening of arteries”
Dynamic chronic inflammatory condition
Pathogenesis involves lipids, thrombosis, elements of vascular wall, and immune cells

379
Q

ECG paper:
1 thick lined box
5 thick lined boxes

A

1 thick lined box (5 small boxes)
5 mm or 0.20 seconds

5 thick lined boxes (25 small boxes)
= 1 second
= 0.5 mV

380
Q

Pericarditis

A

Swelling and inflammation of pericardium

Common causes: viral infections > bacterial infections > fungal infections

S/S:
Sharp retrosternal pain w/ radiation to back (lasting hours), fever
Pain worsens w/ deep breathing, coughing, laying flat
Pain improves sitting up and leaning forward
Friction rub on auscultation

381
Q

HTN contributors

A 
Diet (salt sensitivity)
Inactivity 
Obesity 
Abnormalities of adrenal cortex 
Sleep apnea 
Sympathetic nervous system activity 
Kidney disease 
Congenital vascular disorders 
Recreational drugs and alcohol
382
Q

Epicardium is outed later of connective tissue that covers heart, contains …

A

Variable amounts of adipose tissue that tends to aggregate along vessels and in the grooves on the surface of the heart

383
Q

Effects of CHF in skeletal muscles

A

Decreased:
Blood flow, endothelial function, muscle pump, vasodilation, mitochondrial volume, capillary (% flow, RBC reflux), O2 diffusing capacity, micro vascular O2 pressure, intracellular O2 pressure, NO bioavailability (extracellular), glycogen

Increased:
Vasoconstriction, vascular stiffness, Atrophy Type 2 fibers, glycolytic stimulation/glycogen depletion, VO2 requirement

384
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Walking

A

Arterial: aching begins at specific time/distance; improves with rest

Venous: lessens symptoms

385
Q

Angina- Unstable

A

Recent or acceleration of angina threshold
New onset < 2 months

Symptoms at rest > 15-20 min
Gradually worsens in a crescendo like pattern

May not respond to nitro or rest
Often precursor to MI

386
Q

Acute vs Chronic HF

A

Acute:
Immediately life threatening, in acute pulmonary edema and acute ischemia, medical emergency. End sequela of an MI

Chronic:
Can exist in compensated failure for many years, cardiac dilation, poor pump quality, chronic peripheral edema and congestion

387
Q

Clinical manifestations: Difference between Arterial and Venous disorders
Limb size

A

Arterial: decreased due to muscle wasting

Venous: swollen in chronic disease

388
Q

For LVAD

RPE, HR or BP?

A

RPE

Bc continuous flow, no pulse and can’t take HR and BP

389
Q

Lead aVF

A

Inferior wall

390
Q

SVT

A

Supraventricular rhythm

Common ectopic pacemaker

No P wave
> 150 bpm

391
Q

Alpha-2 Agonists

A

Reduces vascular tone by centrally mediated methods by stimulating Alpha 2 receptors

Suppresses Sympathetic outflow to vasomotor centers from brainstem
Not as commonly used

Most common: Clonidine (Catapres)

Sympatholytic

Acute Care (4 decks)

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