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Cardiopulm > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Explain the mechanics of the diaphragm- in which direction does it move, what impairs its function?

A

As we take a breath in, the diaphragm contract and moves in a descending position. It shortens or until stopped by abdominal contents.

Then we relaxdiaphragm and it moves basck up to resting position and passively moves air out causing passive expiration

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2
Q

How to the ribs move?

A

Ribs 1-7 (true ribs)- pump handle, move anterior / post

Ribs 8-10( false ribs) - bucket handle lateral/transverse

Ribs 11,12 free floating

Movement of teh rib cage increases aas go ant and inferiorly

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3
Q

What is the normal breath sequence?

A

Upper abdominals, lateral coastal, upper chest

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4
Q

What causes limitation of rib expansion?

A

Bony deformity, decreased joint mobility

Lumbar brace

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5
Q

Quadriplegic or rib fx breathing pattern

A

Quadriplegic patient with paralysis of inner costals.

Diaphragm contracts, pulls down and a (-) interthoracis pressure is created this time b/c of the lack of stability of the ant rib cage, those ribs are pulled in. Inefficient breathing pattern.

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6
Q

Breathing with a flail chest

A

We have a section of ribs that have bee fractured & separated from the rest of the rib cage. The diaphragm contracts pulls air in & also b/c of the (-) inter-thoracic pressure the flail section of ribs is also pulled in. Inefficient breathing pattern

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7
Q

How do abdominals help in breathing?

A

Stabilize the lower rib cage

Provide visceral support

W/o abdominals the diaphragm is flat

Expand T6-L1

Produce force expiration and cough

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8
Q

What are the accessory muscle and how do they work?

A

Overall they help assist the diaphragm and intercostals

  • SCM: helps anterior chest expansion
  • Pec Major and minor: lift ant chest, substitute for intercostals
  • serratus anterior: post expansion of rib cage
  • scalenes: and and sup expansion Ribs 1,2
  • erector spinae: post stabilization, extension
  • trapezius: with fixed head it lifts clavicles. Stabilizes scapula for serratus ant and pect minor
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9
Q

What do cilia do— what are things that slow their function?

A

Until terminal bronchioles

  • Goblet, serous cells cells secret mucous
  • bottom layer- sol 90% water
  • top layer- gel traps foreign objects.

The cilia move the secretions until they are coughed out.

Paralyzed by cigarette smoke, alcohol, anethesia up to 20 mins.

Helped by coughings

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10
Q

What is the significance of the pores of Khon?

A

Allow for ventilation between 2 adjacent alveoli. Which is important b/c if one alveoli gets plugged with mucous it can’t participate in air exchange. B/c of the Pores of khon air can get from one open alveoli into adjacent one

Tell patient to take a deep breath

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11
Q

Parasympathetic system causes what…?

A

Innervated by vagus nerve

  • bronchial constriction
  • pulmonary artery dilation
  • increased secretions
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12
Q

Sympathetic system causes what…?

A
  • bronchial relaxation
  • pulmonary artery constriction
  • decreased glandular secretions
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13
Q

What is tidal volume?

A

The amount of air that we move in and out normally in each breath avg 500 ml/breath

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14
Q

Inspiratory and expiratory reserve volume and residual volume

A

Inspiratory- on top of the normal inspiration if we breathe in as much as we can 2-3 L.

Expiratory- if we breathe out more at the end of norma tiddal volume ~1L. Beyond that is what we call teh Residual volume ~1L. Air that we cannot mobilize.

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15
Q

Vital capacity and total lung capacity

A

If we add up all the air that we cann breathe in and out, that forms teh Vital Capacity ~5L. If we add to that the residual volume that we can’t move that gives us total Lung capacity ~6L

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16
Q

Respiratory cycle of dead space

A

Dead space= 150 mL

When we take in a breath of air, we take the air from that conducting zone which we call teh dead space area. Even though we say the normal tidal volume is 5L of air not all of that participates in air exchange some of it just sits in dead space area

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17
Q

Ventilation vs perfusion?

A 
Ventilation = air exchange
Perfusion = blood flow
  • Neither are consistent throughout the lungs. In upright poture, ventilation is greater in the apices, perfusion greater in bases. V/Q ratio = 0.8
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18
Q

Blood clot affect of perfusion?

A
  • Increase Physiologic dead space

- even if alveolus has “o” ready to be picked up a blood clot blocks teh blood from picking it up

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19
Q

CLosed alveoli affect on ventilation

A

Decreased ventilation from closed alveoli

  • plugged w/ mucous so no oxygen can come down

Creates a Right to left shunt: normally blood is sent from the right side of the heart to the lungs. If blood goes to alveoli and there is no “O” to pick up, no air exchange takes place. It is as though blood is shunted from right side to left w/o “o”

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20
Q

Elastance vs Compliance

A

Compliance- how easy it is for lungs to expand

Elastance- how easily lungs return to normal shape

Small resting lung volumes- high compliance: quite easy to expans - room to grow

Large resting lung volumes- low compliance: already full or air - not easy to expans more Ex: COPD

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21
Q

What is teh significance of surfactant?

A

In the lung we have large alveoli and small ones. Normally if a large alveoli were to expand during inspiration, it would suck all the air out of smaller alveolus. The smaller alveolus would collapse. This does not happen due to production of suurfactant. Surfactant is a mixture of lipoproteins that line themselves up and inc density.

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22
Q

Resistance to air flow and critical closing pressure

A

Low flow is laminar
High flow is turbulent

As lung volume increases air resistance drops off.
- when the volumes are really low i.e. patient is not taking deep breaths we reach a point called the critical closing pressure where the resistance to flow is do great that the airways collapse.

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23
Q

Oxyhemoglobin dissociation curve

A

This shows that the greater the Partial pressure of “O” in solution , the greater the diffusion across teh membrane —

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24
Q

The arterial wall consists of…

A

Adventitia- outer layer: collagen/connective tissue

Media: fibro-muscular, Opens and closes artery

Intime- inner layer: collagen and elastin, permeable to LDL, with age, degenerates and calcifies

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25
Q

When do the A-V valves open of close?

A
  • open in diastole- when ventricles are filling up

- closed in systole- when ventricles contract to prevent blood from going to atria instead of out to lungs or extremity

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26
Q

When do the semilunar valves open or close?

A

Aortic an dpulmonic semilunar valves
- open is systole: as heart contracts and pumps blodd out through teh se valves to the lungs and body

-closed in diastole: we do not want blood from teh lungs and the body to drain back into the heart after pushed out

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27
Q

Left coronary arteries

A

Gives off the anterior interventricular artery and circumflex artery.

  • supplies left ventricle and atrium,
  • ventricular septum
  • 45% of people SA node
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28
Q

Right coronary artery

A

Gives off the posterior inter-ventricular artery, and the right marginal artery

-supplies the right side of heart, AV node and 55% of people SA node

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29
Q

Pulmonary circulation pressure

A

Right and left pulmonary arteries are a low pressure system

20/10mmHg

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30
Q

What happens when we have overloaded Pulmonary veins?

A

Fluid in lungs
Pulmonary edema

CHF: the heart can’t pump enough blood the problem comes from all the extra blood/volume in the pulmonary system, that blood leaks out of capillaries into the interstitium. Extra fluid in the space b/w alveoli and capillary

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31
Q

Normal heart signal conduction

A

The normal wave of depolarization for the heart begins w/ the SA node. SA rate= 60-100bpm
- the SA node fires at its own intrinsic rate, then goes down through the atrium to the AV node from there to the Bundle of His and branches out to the Purkinje network

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32
Q

Characteristic of cardiac muscle celll

A

Automaticity
Rhythmicity
Excitation/contraction coupling

SA node vs ectopic firing

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33
Q

Preload vs afterload

A

Preload: tension on musscle before it contracts (venous return). Amt of fluid we bring from extremities

Afterload: load against which the ventricle has to pump. Resistance to flow which drop CO

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34
Q

What happens to CO if we…

  1. Increase preload
  2. Increase afterload
    3 increase contractility
A
  1. incr SV
  2. decrease SV
  3. Increase SV
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35
Q

Cardiac reflexes with Baroreceptors

A

Stretch receptors in arteries

- increase pressure—> vasodilation, decr HR

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36
Q

Cardiac reflexes with Chemoreceptors

A

Increase CO2 , increase RR, Inc HR

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37
Q

Dilated cardiomyopathy

A
  • dilation of all 4 chambers with failure
  • muscle is destroyed so more volume collects in ventricles
  • black men, alcoholism
  • 5yrs death unless cardiac transplantation (75% of people diagnosed die unless transplant)
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38
Q

Hypertrophic cardiomyopathy

A

Uni or bilateral
- possible ichemis and sudden death

-left ventricle - rigid
It gets enlarges and does not relax- most common cause of death in young athletes

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39
Q

Pericarditis

A

Inflammation of pericardium around the heart

  • Idipathic (85%)
  • drug induced, autoimmune
  • post MI
  • viral : hepatitis, eptein barr, HIV
  • pericardial effusion - may impede myocardial expansion
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40
Q

Infective Endocaritis

A

Fluid collects in endocardium

  • bacteria - strep,staph
  • damage to mitral valve
  • inflammation followed by vegetation on valve causes stenosis
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41
Q

Rheumatic fever

A

-untreated strep throat infection
-valve swelling, erosion, scarring.
Joint inflammation, fever, truncal rash

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42
Q

Myocarditis

A

Infection of all layers of teh heart- viral

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43
Q

Tetralogy of fallot

A

Ventricular septal defect

Stenosis of pulmonary valve

Aorta in wrong position

R ventricle is larger than left

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44
Q

Valve insufficiency/regurgitation

A

Chamber dilates over time to accomodate increased volume

-increased work of ventricle to maintain flow

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45
Q

Valve prolapsed

A

Leaflets between atrium and ventricle bulge backwards during systole

-leaflets are large and floppy

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46
Q

Mitral valve stenosis

A
  • Post rheumatic heart disease
  • high left atrial pressure
  • pulmonary hypertension, back up to R heart causing failure
  • atrial dysrythmias- fibrillation

As the left atrium tries to push blood through the stenotic valve there is a build up of pressure in the left atrium. Likely a build up of volume of blood that does not get to ventricle can back up to right

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47
Q

Mitral valve regurgitation

A
  • During systole
  • requires extra stroke contractility to compensate for decreased blood going into aorta
  • hypertrophy of left atrium and ventricle
  • The mitral valve does not close well
  • during teh left ventricular systally the left ventricle is contracting to push blood out to teh body instead some of that goes back into left atrium which means less blood going to aorta unless ventricle compensates with extra hard stoke—> leads to hypertrophy
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48
Q

Mitral valve prolapse

A
  • floppy valve
  • balloons back into atria during ventricular systole
  • over time may become insufficient
  • blood can start leaking back
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49
Q

Aortic valve stenosis

A

L ventricle hypertrophy - failure

  • murmur during systole
  • decrased CO
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50
Q

Aortic valve regurgitation

A

Volume overload in L ventricle

Hypertrophy and dilation

Murmur during diastole

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51
Q

Length tension relationship of myocardial muscle

A

Increased blood volume overstretches myocardium= decreased force of contraction and stroke volume

52
Q

Causes of CHF

A
  • Hypertension- LV hypertrophy
  • arrythmias
  • renal dysfunction
  • post MI scarring, weak muscles
  • heart valve abnormalities- stenosis, insufficency
  • cardiomyopathy
  • acute infection-myocarditis,percarditis
  • pulmonary embolism
  • spinal cord injury
  • age related changes
53
Q

What do you see with L ventricular failure?

A

Increased end diastolic volume. Back up to lungs, pulmonary edema

54
Q

What do you see with right ventricular failure?

A

Back up into peripheral circulation

-bilateral edema in legs and liver

55
Q

Symptoms of CHF, or cardiac muscle dysfunction CMD

A

Dyspnea
Orthopnea-SOB in supine. W/o gravity heart is overwhelmed
- CXR- interstitial edema

-auscultation- crackles in dependen lung fields. S3 or S4 heart sounds.

Jugular venous distension

Peripheral edema : >/= 2+ pitting

Changes in color or temp of extremities

Rapid weight gain

Inc HR

Decr exercise tolerance (<300 poor prognosis)

3-4 MET capacity

56
Q

Jugular venous distention

A

Increased volume in jugular vein. Back up from right atria.

-patient is lying at 45 deg with head turned. Ou can see slight pulsing of blood. Normal is 5cm aboove angle of louis high is abnormal

57
Q

Intra-aortic balloon pump

A

Catheter inserted into aorta that inflates during diastole

  • inflation during diastole causes back pressure into coronary arteries
  • deflation causes gradient during systole for increasing cardiac output
58
Q

Exercise training with Inta-aortic balloon pump

A

**Do not touch leg that has catheter

Only exercise with upper extremities and non-catheterized LE

59
Q

Patient with CMD

What would you expect their Chief complaint to be?

A

SOB
Fatigue
Trouble at night- orthopnea

Peripheral edema

60
Q

Patient with CMD

What would we expect symptoms to be?

A

Discoloration, edema, suspended jugular,

Decreased aerobic capacity

Decreased MMT—> if not active atrophy

61
Q

What do we doo if we have an acute onset SOB?

A

If at rest- call 911 if unilateral possible pneumothorax, chest trauma , MI

62
Q

Angina vs MI

A

Angina: substernal non-radiating, discomfort, pressure, squeezing, heaviness or indigestion, precipitated by exertion, after meal or emotiona stress, relieved by rest —stop activity

MI: extreme pressure , tightness over sternum, can radiate to jaw, upper back , shoulders (L>R), persists >20 min, OCCURS AT REST accompanied by nausea, diaphoresis, hypotension, dyspnea —> call 911

63
Q

Sputum production

A

-normal 75-100mL secreted daily

  • clear- normal uninfected
  • yellow,green,red- infected

Consistency? If pink and frothy - pulmonary edema

+odor?- infection
+blood? - smoking, infection, tumor, bronchitis, TB

64
Q

Refer immediately if you see these sign for..

  1. Pulmonary embolus
  2. Pneumothorax
  3. MI
  4. Pulmonary edema
A
  1. Embolus- chest pain, anxiety, agitation, tachycardia, hemoptysis, cyanosis
  2. Pneumothorax- acute SOB, unilateral chest pain, absent breath sounds
  3. MI- pain last more than 20 min, occurs at rest with nausea, diaphoresis, hypotension, dyspnea
  4. Pulmonary edema- frothy pink sputum
65
Q

S1 heart sound

A

“LUB”

  • closing of mitral and tricuspid valves
  • beginning of systole
66
Q

S2 heart sounds

A

“DUB”

  • closing of aortic and pulmonic valves
  • end of systole
  • sometimes valves can be heard separately (split) on insp not exp
67
Q

When can you hear S1 or S2 better?

A

S1 louder than S2 at R or L lateral sternal border or apex

S2 louder at the Base

68
Q

Split S1

A

S1 is mitral and tricuspid

  • mitral apex
  • tricuspid LLSB

Sounds can occur separately
Split S1 is normal over Right or Left Sternal Border

69
Q

SPlit S2

A

Aortic and pulmonic valves

  • nomal physiologic split: heard on inspiration, goes away on expiration
  • more likely heard in pulmonic area

Abnormal: heard both on insp and exp
—

70
Q

S3 Ventricular gallop

A

Low frequency sound heard after S2
-best heard at apex Lside-lying

-normal in children and young adults
After 40 pathological

-Heard as AV valve open and blood hits overly dilated L ventricle

1st clinical sound of Heart Failure

-sloshing

Kentucky

71
Q

S4- atrial gallop

A

Heard before S1 during atrial kick

  • normla with ventricular hypertrophy or athlete
  • sound of rapid ventricular filling into a stiff or hypertrophic heart (severe hypertension)
  • heard best in supine or Left side-lying position

Tennesse

72
Q

Murmurs

A

Extra sounds- whooshing, blowing , vibrations

Regurgitation: heart vallve does not close tight and there is retrograde flow

Stenosis: blood is flowing through narrown opening or stiff valve

73
Q

Systolic murmur

WHat pathologies?

A

Between S1 and S2 when ventricles are contracting

Pathologies:

  • aortic or pulmonary stenosis
  • mitral valve prolapse or regurgitation
  • atrial or ventricular septal defect
74
Q

Diastolic murmur

What pathologies?

A

Between S2 and S1 when heart is relaxed and filling

Pathologies?

  • aortic or pulmonic regurgitation
  • mitral or tricuspid stenosis
75
Q

Cholesterol levels

A

We want <200mg/Dl

High cholesterol (>240 mg/dL)
LDL shoul be <160 or <130if more than 2 risk factors or <100 if CAD

Triglycerides <200 mg/dL

Total /HDL <3.5

HDL > 60 lowers risk

76
Q

Process of atherosclerosis

A

Injury or irritation to endothelium. Intima is permeable to LDL. Macrophages covered with lipids
Lodge and grow to break endothelium

Platelets , clots, plaque

-sclerosis= decreased compliance, predisposition for heart disease, stroke

77
Q

Symptoms of unstable ANgina

A

Unpredictable, may occur at rest or exercise
Anywhere in the epigastric area, the jaw, the back

Administer prinzmetal, variant- vasospasm

*We do NOT treat people with unstable angina

78
Q

Direct causes of Myocardial ischemia, injury, and necrosis

A

Coronary thrombosis- about 90% of cases.

Coronary artery spasm

79
Q

Indirect causes of Myocardial ischemia, injury, and necrosis

A
  • decr coronary arterial blood flow
  • incr myocardial workload
  • hypoxemia
  • toxic exposure to cocaine or ethanol
80
Q

EKG signs of a MI trasnmural vs Non-transmural

A

Non-Q wave . Inverted T wave. MI non-transmural, just the inside lower endocardium

Q wave - MI transmural - the entire wall of teh myocardium

81
Q

Differences in ischemia , injury, infacrtion?

Reversible or not?

A

1st stage- Ischemia- reversible

2nd stage- injury Reversible. Happens if we were not able to restore blood flow

3rd stage- infarction- irreversible. Cells do not recover, even if we restore blood flow to the area the tissue is dead.

82
Q

Extent of necrosis in a Myocardial infacrction

A

Injury begins from inside out

Onset- 0% necrosis
<20 min - 0% necrosis we see injury
30 min- 10%
1hr-  30%
2Hr- 50 %
83
Q

Serum enzymes

A

When the tissue is damages. It will release certain enzymes. We can look at theses enzymes to determine the extent of damage and where we are in the process.

CPK- diagnostic for heart ischemia and damage

Myoglobin- peak 3-15 hours

Troponins- peak 5-7 days

LDH- most conclusive

84
Q

Mean arterial pressure EQ

A

((2* D) + S)/ 3

85
Q

Atrial receptors and

Atrial Natiuretic peptide -ANP

A

-respond too an increase in pressure in the atrium

—> occurs if too much blood comes in when they are stretched they release atrial natiuretic peptide which causes us to get rid of water & sodium…pee

86
Q

Renin-angiotensin-aldosterone system pathology in chronic hypertension

A

Body perceives that there is a drop of blood coming to the kidney it causes the kidney to release Renin.

Renin causes

  • vasoconstriction to inc blood pressure
  • release of aldosterone to save sodium and water
87
Q

Phase 1 cardiac patient

A

Inpatient <7-10 days
-begin when hemodynamically stable

GoaL: Able to safelt do ADLs, walk around house, optional stairs, able to complete 20 min of aerobic work first

Education: lifestyle recommendations

88
Q

Phase II cardiac patient

A

6wks- 6 months

-supervised in hospital, center, community-based program or 1:1 session

-physician exercise test as screen
Can begin within 1-2 wks of D/C
3x/wk 6-8 wks

-small groups

Education:review risk factors, lifestyle behaviors and changes

89
Q

Length of Phase II for cardiac patient

A

Low risk- uncomplicates MI or CABG need at least 1 month outpatient program

Moderate risk- CHF or can’t self monitor 2-3 months

High risk- survived sudden death, BP compromise, or arrhythmias - 3 or more months

90
Q

Phase III cardiac patient

A

6-12 months

  • supervised in hospital, center , community-based program or 1:1 session
  • large groups
  • minimal monitoring
  • 1x/wk
91
Q

Phase IV cardiac patient

A

> 12 months

  • self-management
  • maintenace/oreventon for high risk
  • plan for follow -up
92
Q

CEdar sinai Phase I cardiac Rehab

In bed with HOB 45

A

Level I

Ankle circels- 
heel slides
hip abduction
Bicep curls
Shoulder flexion
Shoulder abduction
93
Q

CEdars Sinai Phase I cardiac rehab Level II

Sitting EOB or in chair

A 
Ankle pumps
Long arc quads
Marching
Bicep curls
Bilateral shoulder flexion with hands together to shld level

Shrug shoulders
Neck circles

94
Q

Cedar-Sinai Phase I cardiac rehab

Level III- sitting

A

Add:
hands behind head, point elbows forward and back

Trunk rotation

Trunk side bends

95
Q

Cedars-sinai Phase I cardiac rehab

Level IV- standing

A 
ADD:
Toe raises
Mini squats
Marching in place
Trunk rotations
Trunk side bends
96
Q

Progression to ambulation for a cardiac rehabb patient

A

2-4x/day

2-3 minutes warm-up, in bed or sitting (cedars 1-4 exercises 10 reps)

-short intermittent 3-5 min bouts of ambulation with 1-2 minute rest

Accumulate up to 20 minutes

97
Q

Stop exercise if these symptoms…

A 
Chest pain
Severe dyspnea
Dizziness, lightheadedness
Markes apprehension,mental cunfusion
Ataxia
Pallor, diaphoresis, sweting
Nausea
Pt unwilling to continue
Severe fatigue
98
Q

Stop exercise if you see thse vital signs…

A

Maladaptive BP or HR: failure to rise with excessive fall

Post MI, cardiac surgery: HR should not increase >20-30bpm above resting

EKG changes- ischemia, dysrythmias

O2 saturation drops >3-5%

  • BP systolic drop >20 mmHG
  • BP diastolic drop >10mmHG
99
Q

Phase II exercise Prescription

A

Modality: Rhythmic, large muscle group aactivities- cycling, walking

Goal: accumulate 30-45 minutes/ session
—start: use short bouts 3-10min intervals
—

100
Q

Resistance training for home or Phase II center-based exercise

A

Must be 5 weeks post MI with 3 weeks of rehab program participation.

Must be 8 weeks post CABG with 3 weeks of rehab participation

8-10 exercises, major muscle groups

  • 2-3x/wk
  • proper breathing no valsalva

Start low weight and incr when able to do 155 reps easily

101
Q

Medications that wil decrease cardiac workload

A
  • decrease preload- diuretics
  • decrease afterload: calcium channel blocckers, ACE inhibitors

-reduce excessive sympathetic stimulation (decr HR and contactility ) Beta blockers

102
Q

Cardiac Medication to increase contractility , CO

A

-glycosides

103
Q

How do diuretics decrease preload?

A

First lline of treatment
-increase renal secretion of water and sodium

-decr fluid volume in vascular system which decreases BP-HTN and reduces preload

104
Q

Potassium sparing vs depleting

A

Potassium depleting- encourage to eat banana
-thiazides eg Diuril, loop diuretics Lasix

Potassium sparing

Watch for side effects of weakness and fatigue, PVCs from electrolyte imbalance, orthostatic hypotension

105
Q

ACE inhibitors

A
  • Prinvil
  • inhibits conversion of angiotension I to angiotensin II

-decrease vasoconstriction decrease afterload- used for HTN, heart failure, post-MI

Angiotensin II leads to incr Na+ and H2O retenstion hich leads to more blood volume and incr BP
—blocking this process = decr vasocronstriction and decr BP

106
Q

ACE inhibitors side effects

A

Persistent dry couch
GI discomfort, chest pain- minimal

Dizziness, lighheadeness- expecially with exercise. Or hot weather

107
Q

Positive ionotropes

A

Increase contractility

-glycoside- Digoxin,digitalis, Slows HR, increase electrical delay at AV node (treat Afib), toxicity common

Sympathomimetics- epinephrine- emergency situation- side effect is tachycardia

108
Q

What are 2 types of vasodilators>

A

Calcium channel blockers

Nitrates

109
Q

Calcium channel blockers

A

-block calcium entry into smooth muscle cells, prevent contraction

Vasodilation-mostly on arterial side leads to Decreased BP

Drug of choice for variant (prinzmetal) angina

110
Q

Common side effect of calcium channel blockers

A

Orthostatic hypotension,dizziness,headache
-ankle/peripheral edema

GI upset

Tahcycardia

111
Q

Nitrates

A

Act on arteriole & venous side of sysstem

Act on smooth muscle to inhibit contrcation

-Decreased peripheral resistance, decr afterload (arteriodilator) decr preload (venodilator)

Nitroglycerin
- side effects headache,hypotension dizziness, tachycardia

112
Q

Beta 1 stimulation

A

Stimulation causes increased force of contraction and HR

113
Q

Beta 2 stimulation

A

Stimulation causes skeletal an dsmooth muscle relaxation, vasodilation of vessels in heart and skeletal muscle, nronchodilation

114
Q

Alpha 1 and 2 stimulation

A

Causes vasoconstriction and bronchoconstriction

115
Q

Betaa blockers

A 
Decrease HR
Decrease contractility
Decrease CO
Decrease BP
====Decreased work of heart
116
Q

How do we treat HTN? With medication

A
  • decrease preload and afterload- diuretics, ACE inhibitirs , CA channel blockes
  • inhibit vasoconstriction : alpha 1 blocker
117
Q

How do we treat CAD, myocardial ischemia with medication?

A
  • decrease myocardial demand- Bblockers, CA channel blocker, nitrates
  • increase myocardial O2 supply- Ca channel blocker, blood thinners
  • lipid management
118
Q

Anti-arrythmic drugs Class I

A

Act on Na channel to slow depolarization/repolarization

Side effect: skin rask,hearing or vision changes, bruising

Xylocain,norpace

119
Q

Class II anti-arrythmic drugs

A

Beta blockers
- slows sympathetic stimulation, decrease HR

Atenolol,metoprolol

120
Q

Class III anti-arrythmic drugs

A

Inhibit K an dNa channels
-prolong repolarization to prevent re-entry

Side effect: lung,liver damage, restlessness, heat/col intolerance, thinning hair

Cordarone,pacerone

121
Q

Class IV anti-arrythmic drugs

A

Act on calcium channels
-block CA channel

Side effect: dizziness, coughing, LE edema

Verapamil

122
Q

EKG norms for
PR interval

QRS complex

ST segment

A

PR interval = 0.12-0.2 sec 3-5 small boxes

QRS - 0.04-0.12 <3 small boxes

ST segment on isoelectric line

123
Q

St segment elevation vs derpression

A

Significant >1mm (small box) displacement from baseline

  • Elevation = myocardial injury, infacrtion
  • Depression = myocardial ischemia (reversible)
124
Q

EKG bradycardia

A

Slow heart rate <60 bpm

125
Q

Tachycardia EKG

A

Fast heart rate >100

Cardiopulm (4 decks)

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