Test 1 Flashcards
Explain the mechanics of the diaphragm- in which direction does it move, what impairs its function?
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
How to the ribs move?
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
What is the normal breath sequence?
Upper abdominals, lateral coastal, upper chest
What causes limitation of rib expansion?
Bony deformity, decreased joint mobility
Lumbar brace
Quadriplegic or rib fx breathing pattern
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.
Breathing with a flail chest
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
How do abdominals help in breathing?
Stabilize the lower rib cage
Provide visceral support
W/o abdominals the diaphragm is flat
Expand T6-L1
Produce force expiration and cough
What are the accessory muscle and how do they work?
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
What do cilia do— what are things that slow their function?
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
What is the significance of the pores of Khon?
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
Parasympathetic system causes what…?
Innervated by vagus nerve
- bronchial constriction
- pulmonary artery dilation
- increased secretions
Sympathetic system causes what…?
- bronchial relaxation
- pulmonary artery constriction
- decreased glandular secretions
What is tidal volume?
The amount of air that we move in and out normally in each breath avg 500 ml/breath
Inspiratory and expiratory reserve volume and residual volume
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.
Vital capacity and total lung capacity
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
Respiratory cycle of dead space
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
Ventilation vs perfusion?
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
Blood clot affect of perfusion?
- Increase Physiologic dead space
- even if alveolus has “o” ready to be picked up a blood clot blocks teh blood from picking it up
CLosed alveoli affect on ventilation
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”
Elastance vs Compliance
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
What is teh significance of surfactant?
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.
Resistance to air flow and critical closing pressure
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.
Oxyhemoglobin dissociation curve
This shows that the greater the Partial pressure of “O” in solution , the greater the diffusion across teh membrane —
The arterial wall consists of…
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
When do the A-V valves open of close?
- 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
When do the semilunar valves open or close?
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
Left coronary arteries
Gives off the anterior interventricular artery and circumflex artery.
- supplies left ventricle and atrium,
- ventricular septum
- 45% of people SA node
Right coronary artery
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
Pulmonary circulation pressure
Right and left pulmonary arteries are a low pressure system
20/10mmHg
What happens when we have overloaded Pulmonary veins?
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
Normal heart signal conduction
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
Characteristic of cardiac muscle celll
Automaticity
Rhythmicity
Excitation/contraction coupling
SA node vs ectopic firing
Preload vs afterload
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
What happens to CO if we…
- Increase preload
- Increase afterload
3 increase contractility
- incr SV
- decrease SV
- Increase SV
Cardiac reflexes with Baroreceptors
Stretch receptors in arteries
- increase pressure—> vasodilation, decr HR
Cardiac reflexes with Chemoreceptors
Increase CO2 , increase RR, Inc HR
Dilated cardiomyopathy
- 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)
Hypertrophic cardiomyopathy
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
Pericarditis
Inflammation of pericardium around the heart
- Idipathic (85%)
- drug induced, autoimmune
- post MI
- viral : hepatitis, eptein barr, HIV
- pericardial effusion - may impede myocardial expansion
Infective Endocaritis
Fluid collects in endocardium
- bacteria - strep,staph
- damage to mitral valve
- inflammation followed by vegetation on valve causes stenosis
Rheumatic fever
-untreated strep throat infection
-valve swelling, erosion, scarring.
Joint inflammation, fever, truncal rash
Myocarditis
Infection of all layers of teh heart- viral
Tetralogy of fallot
Ventricular septal defect
Stenosis of pulmonary valve
Aorta in wrong position
R ventricle is larger than left
Valve insufficiency/regurgitation
Chamber dilates over time to accomodate increased volume
-increased work of ventricle to maintain flow
Valve prolapsed
Leaflets between atrium and ventricle bulge backwards during systole
-leaflets are large and floppy
Mitral valve stenosis
- 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
Mitral valve regurgitation
- 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
Mitral valve prolapse
- floppy valve
- balloons back into atria during ventricular systole
- over time may become insufficient
- blood can start leaking back
Aortic valve stenosis
L ventricle hypertrophy - failure
- murmur during systole
- decrased CO
Aortic valve regurgitation
Volume overload in L ventricle
Hypertrophy and dilation
Murmur during diastole
Length tension relationship of myocardial muscle
Increased blood volume overstretches myocardium= decreased force of contraction and stroke volume
Causes of CHF
- 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
What do you see with L ventricular failure?
Increased end diastolic volume. Back up to lungs, pulmonary edema
What do you see with right ventricular failure?
Back up into peripheral circulation
-bilateral edema in legs and liver
Symptoms of CHF, or cardiac muscle dysfunction CMD
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
Jugular venous distention
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
Intra-aortic balloon pump
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
Exercise training with Inta-aortic balloon pump
**Do not touch leg that has catheter
Only exercise with upper extremities and non-catheterized LE
Patient with CMD
What would you expect their Chief complaint to be?
SOB
Fatigue
Trouble at night- orthopnea
Peripheral edema
Patient with CMD
What would we expect symptoms to be?
Discoloration, edema, suspended jugular,
Decreased aerobic capacity
Decreased MMT—> if not active atrophy
What do we doo if we have an acute onset SOB?
If at rest- call 911 if unilateral possible pneumothorax, chest trauma , MI
Angina vs MI
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
Sputum production
-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
Refer immediately if you see these sign for..
- Pulmonary embolus
- Pneumothorax
- MI
- Pulmonary edema
- Embolus- chest pain, anxiety, agitation, tachycardia, hemoptysis, cyanosis
- Pneumothorax- acute SOB, unilateral chest pain, absent breath sounds
- MI- pain last more than 20 min, occurs at rest with nausea, diaphoresis, hypotension, dyspnea
- Pulmonary edema- frothy pink sputum
S1 heart sound
“LUB”
- closing of mitral and tricuspid valves
- beginning of systole
S2 heart sounds
“DUB”
- closing of aortic and pulmonic valves
- end of systole
- sometimes valves can be heard separately (split) on insp not exp
When can you hear S1 or S2 better?
S1 louder than S2 at R or L lateral sternal border or apex
S2 louder at the Base
Split S1
S1 is mitral and tricuspid
- mitral apex
- tricuspid LLSB
Sounds can occur separately
Split S1 is normal over Right or Left Sternal Border
SPlit S2
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
—
S3 Ventricular gallop
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
S4- atrial gallop
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
Murmurs
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
Systolic murmur
WHat pathologies?
Between S1 and S2 when ventricles are contracting
Pathologies:
- aortic or pulmonary stenosis
- mitral valve prolapse or regurgitation
- atrial or ventricular septal defect
Diastolic murmur
What pathologies?
Between S2 and S1 when heart is relaxed and filling
Pathologies?
- aortic or pulmonic regurgitation
- mitral or tricuspid stenosis
Cholesterol levels
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
Process of atherosclerosis
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
Symptoms of unstable ANgina
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
Direct causes of Myocardial ischemia, injury, and necrosis
Coronary thrombosis- about 90% of cases.
Coronary artery spasm
Indirect causes of Myocardial ischemia, injury, and necrosis
- decr coronary arterial blood flow
- incr myocardial workload
- hypoxemia
- toxic exposure to cocaine or ethanol
EKG signs of a MI trasnmural vs Non-transmural
Non-Q wave . Inverted T wave. MI non-transmural, just the inside lower endocardium
Q wave - MI transmural - the entire wall of teh myocardium
Differences in ischemia , injury, infacrtion?
Reversible or not?
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.
Extent of necrosis in a Myocardial infacrction
Injury begins from inside out
Onset- 0% necrosis <20 min - 0% necrosis we see injury 30 min- 10% 1hr- 30% 2Hr- 50 %
Serum enzymes
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
Mean arterial pressure EQ
((2* D) + S)/ 3
Atrial receptors and
Atrial Natiuretic peptide -ANP
-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
Renin-angiotensin-aldosterone system pathology in chronic hypertension
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
Phase 1 cardiac patient
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
Phase II cardiac patient
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
Length of Phase II for cardiac patient
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
Phase III cardiac patient
6-12 months
- supervised in hospital, center , community-based program or 1:1 session
- large groups
- minimal monitoring
- 1x/wk
Phase IV cardiac patient
> 12 months
- self-management
- maintenace/oreventon for high risk
- plan for follow -up
CEdar sinai Phase I cardiac Rehab
In bed with HOB 45
Level I
Ankle circels- heel slides hip abduction Bicep curls Shoulder flexion Shoulder abduction
CEdars Sinai Phase I cardiac rehab Level II
Sitting EOB or in chair
Ankle pumps Long arc quads Marching Bicep curls Bilateral shoulder flexion with hands together to shld level
Shrug shoulders
Neck circles
Cedar-Sinai Phase I cardiac rehab
Level III- sitting
Add:
hands behind head, point elbows forward and back
Trunk rotation
Trunk side bends
Cedars-sinai Phase I cardiac rehab
Level IV- standing
ADD: Toe raises Mini squats Marching in place Trunk rotations Trunk side bends
Progression to ambulation for a cardiac rehabb patient
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
Stop exercise if these symptoms…
Chest pain Severe dyspnea Dizziness, lightheadedness Markes apprehension,mental cunfusion Ataxia Pallor, diaphoresis, sweting Nausea Pt unwilling to continue Severe fatigue
Stop exercise if you see thse vital signs…
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
Phase II exercise Prescription
Modality: Rhythmic, large muscle group aactivities- cycling, walking
Goal: accumulate 30-45 minutes/ session
—start: use short bouts 3-10min intervals
—
Resistance training for home or Phase II center-based exercise
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
Medications that wil decrease cardiac workload
- decrease preload- diuretics
- decrease afterload: calcium channel blocckers, ACE inhibitors
-reduce excessive sympathetic stimulation (decr HR and contactility ) Beta blockers
Cardiac Medication to increase contractility , CO
-glycosides
How do diuretics decrease preload?
First lline of treatment
-increase renal secretion of water and sodium
-decr fluid volume in vascular system which decreases BP-HTN and reduces preload
Potassium sparing vs depleting
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
ACE inhibitors
- 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
ACE inhibitors side effects
Persistent dry couch
GI discomfort, chest pain- minimal
Dizziness, lighheadeness- expecially with exercise. Or hot weather
Positive ionotropes
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
What are 2 types of vasodilators>
Calcium channel blockers
Nitrates
Calcium channel blockers
-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
Common side effect of calcium channel blockers
Orthostatic hypotension,dizziness,headache
-ankle/peripheral edema
GI upset
Tahcycardia
Nitrates
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
Beta 1 stimulation
Stimulation causes increased force of contraction and HR
Beta 2 stimulation
Stimulation causes skeletal an dsmooth muscle relaxation, vasodilation of vessels in heart and skeletal muscle, nronchodilation
Alpha 1 and 2 stimulation
Causes vasoconstriction and bronchoconstriction
Betaa blockers
Decrease HR Decrease contractility Decrease CO Decrease BP ====Decreased work of heart
How do we treat HTN? With medication
- decrease preload and afterload- diuretics, ACE inhibitirs , CA channel blockes
- inhibit vasoconstriction : alpha 1 blocker
How do we treat CAD, myocardial ischemia with medication?
- decrease myocardial demand- Bblockers, CA channel blocker, nitrates
- increase myocardial O2 supply- Ca channel blocker, blood thinners
- lipid management
Anti-arrythmic drugs Class I
Act on Na channel to slow depolarization/repolarization
Side effect: skin rask,hearing or vision changes, bruising
Xylocain,norpace
Class II anti-arrythmic drugs
Beta blockers
- slows sympathetic stimulation, decrease HR
Atenolol,metoprolol
Class III anti-arrythmic drugs
Inhibit K an dNa channels
-prolong repolarization to prevent re-entry
Side effect: lung,liver damage, restlessness, heat/col intolerance, thinning hair
Cordarone,pacerone
Class IV anti-arrythmic drugs
Act on calcium channels
-block CA channel
Side effect: dizziness, coughing, LE edema
Verapamil
EKG norms for
PR interval
QRS complex
ST segment
PR interval = 0.12-0.2 sec 3-5 small boxes
QRS - 0.04-0.12 <3 small boxes
ST segment on isoelectric line
St segment elevation vs derpression
Significant >1mm (small box) displacement from baseline
- Elevation = myocardial injury, infacrtion
- Depression = myocardial ischemia (reversible)
EKG bradycardia
Slow heart rate <60 bpm
Tachycardia EKG
Fast heart rate >100
