Cardio/Pulm Flashcards
Normal BP:
Pre-HTN BP:
Stage 1 HTN:
Stage 2 HTN:
Normal BP: 120/80
Pre-HTN BP: 120-139/80-89
Stage 1 HTN: 140-159/90-99
Stage 2 HTN: >/= 160 / >/= 100
Primary HTN no known cause
Secondary HTN usually due to renal
95th percentile children for HTN
TV: 10% IRV: 50% ERV: 15% RV: 25% VC: 75% (IRV+TV+ERV) IC: 60% (TV+IRV) FRC: 40% (ERV+RV) TLC: 100%
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ABI = systolic blood pressure at ankle and arm for PAD.
Use Brachial artery and post tib artery.
= Higher ankle systolic / Higher brachial systolic
Values:
> /= 1.30 rigid artery, need US to test for PAD
- 0 - 1.3 normal, NO BLOCKAGE
- 8 - 0.99 mild blockage, intermittent claudiation p ! during ex
- 4-0.79 moderate, p! during ex
Cardiac conduction pathway:
SA node - normal pace maker of heart.... AV node... Bachaan Bundle (RA to LA)... Bundle of His... ////IV SEPTUM//// R and L bundle branches.... Purlinje fibers... ventricular walls
Normal ABG Values: PH PaCO2 PaO2 HCO3 SaO2
PH: 7.35 - 7.45 PaCO2: 35-45 mmHg PaO2: 80-100 mmHg HCO3: 22-26 mEq/L SaO2: 95-98% Eucapnia: normal level of Co2 in arterial blood mild Hypoxemia: Pa02 60-79 mmHg Mod: 40-59 Severe:
Premature atrial contraction (PAC):
impulse before SA node (p wave immature, abnormal config). Can progress to atrial flutter, atrial tachy
Atrial flutter:
250-350 BPM, atrial tachy
saw-tooth p waves
A-fib:
350-600 BPM
.
Borg Dyspnea Scale:
Borg Dyspnea scale: 0 = no breathlessness 0.5 = very, very slight 1 = very slight 2 = slight 3 = moderate 4 = somewhat severe 5= severe breathlessness 6 = 7 = very severe 8 9 = very, very severe 10 = max breathlessness
Heart sounds
S1 (lub) close mitral and tricuspid, beginning of systole (decreased in 1st degree heart block)
S2: (dub) close aortic and pulmonary, end of systole (decreased in aortic stenosis )
S3 (vibration of distended ventricle walls) due to passive blood flow from atria into ventricles during rapid filling of diastole phase *normal in children, abnormal in adults b/c associated with CHF (“ventricular gallop”)
S4 (ventricular vibration c ventricular filling and atrial contraction), pathological; associated with HTN, MI, stenosis, MI (“atrial gallop”)
Phases of BP sounds:
Phase 1 - clear tap, appearance of pulse systolic
Phase 2 - soft and louder
3 - crisper and louder
4 - muffled and softer
5 - disapears completely (last beat is diastolic)
**Deflate BP cuff 2-3 mmHg/second
BP in children:
Age 3-17, BP is by percentiles %
SBP and DBP = 90-95%
stage 1: SBP and/or DBP >/= 95 - = 99% plus 5mmhg
stage 2: > 99th % plus 5 mmhg SBP and/or DBP
1st deg AV block:
PR > 0.2 second
constant beat to beat, NO symptoms
2nd deg AV block
AV conduction between atria & ventricles fail intermittently
2 types:
a) Mobitz type 1 (Wenckebach block) - progressive prolongation of PR until impulse not conducted, benign
b) Mobitz type 2 - MORE serious, dec in CO due to consecutive/normal PRs followed by nonconduction of
>/= 1 impulses; can progress to 3rd deg AV block
3rd deg AV block
ALL impulses blocked @ AV node
none transmitted to ventricles
atrial rate > ventricular rate
***requires pacemaker, EMERGENCY
Premature ventricular complex (PVC):
P wave absent, QRS wide/weird shape
Bigeminy, normal sinus rhythm followed by PVC
Trigeminy, PVC occurs after every 2 normal sinus impulses
V-tach: >/= 3 PVCs consecutively with ventricular rate of > 150 BPM; leads to cardiac arrest
EKG abnormalities:
ST dep, ST elev, T-wave inversion
ST depression - subendocardial ischemia, or digitalis toxcity or hypokalemia
ST elevation - EARLIEST sign of acute MI
T-wave inversion - occurs hours or days after MI due to delay in repolarization
Homans sign:
Passively DF ankle with Knee STRAIGHT, positive produces pain in calf or popliteal space
Absolute indications to stop cardiac exercise test:
Decrease in SBP >/= 10mmHg
moderate angina (3 out of 4 on angina scale)
Increase of nervous system sxs (dizziness, ataxia etc)
Signs of poor perfusion (pallor, cyanosis)
Sustained v-tach
1.0 mm ST elevation (without Q waves)
Relative indications to stop cardiac exercise test:
Decrease in SBP > 10 mmHg > 2mm ST depression Arrhythmia, bundle branch block Fatigue, SOB, claudication, increase in chest pain HTN response (>250 SBP and/or > 115 DBP)
Normal HR values:
normal infant: 100 - 130 BPM
normal child: 80 - 100 BPM
normal adult: 60-100 BPM
*stop activity if SpO2 drops below 85% in COPD or 88% in critically ill
Grading of pulses, and FEV1/FVC
Grading of pulses: 0 = absent pulse 1 = small, reduced pulse 2+ normal 3+ large, bounding
FEV1 / FVC 80% (normal) BUT if decrease in FVC then demonstrates restrictive lung disease (due to dec lung volumes)
Hematology: RBCs: WBCs: Platelets: PTT: Hematocrit:
Hematology: RBCs: 4.3 - 10.6 M ; 4.0 - 5.2 F WBCs: 3.54 - 9.06 neutro: 0.4-0.70 lympho: 0.20 - 0.50 mono: 0.04-0.08 eosino: 0.00-0.06 baso: 0.00 - 0.02 Platelets: 165 - 415 PTT: 26.3 - 39.4 sec Hematocrit: 0.388 - 0.464 M , 0.354 - 0.444 F
More lab values: Hb: Total cholsterol: LDL: HDL: Triglycerides:
More lab values: Hb: 13.3 - 16.2 M ; 12.0 - 15.8 F Total cholsterol: 240 high) LDL: 160-189 high) HDL: 60 high Triglycerides: >200-499 high
claudication test:
2.0 mph treadmill, 0-12% incline grade.
initial claudication distance = pain free distance
absolute = max distance, terminated due to pain
grade 1 = initial discomfort
grade 2 = moderate discomfort, can divert attention away
grade 3 = severe, cannot distract from pain
grade 4 = excruciating, unbearable
alpha adrenergic antagonist:
ace inhibitor:
A2 receptor antagonist:
alpha adrenergic antagonist: decreases peripheral vascular tone by blocking Alpha 1 adrenergic receptors
(causes vasodilation, dec BP)
(for HTN, BPH)
ace inhibitor:for HTN, CHF
(decreases BP and preload by suppressing A1 to A2 enzyme conversion)
A2 receptor antagonist: block alpha2 receptors by limiting vasoconstriction and stimulation of vascular tissue
Antiarryhthmic drugs:
class 1: sodium channel blocker, controls cardiac excitation and conduction.
class 2: beta blocker, inhibits symptathetics by blocking beta adrenergic receptors
class 3: potassium and sodium channel blocker, prolongs repolarization, MOST effective
class 4: calcium channel blocker, depress depolarization, decrease conduction through AV node
Lymphedema, cardiac tamponade:
Lymphedema: 2 types
a. primary - rare, inherited due to lymph vessel problem
b. secondary - condition/procedure damaged lymph vessel
* achiness, fibrous, heaviness, brawny, fullness, NONPITTING EDEMA
Cardiac tamponade: fluid in pericardium puts pressure on heart (prevents heart from filling properly), less blood leaves heart (decreases BP, can be fatal)
rheumatic fever, acute respiratory distress syndrome, atelectasis:
rheumatic fever:from group A steptococcocus due to poorly treated strep throat. can damage heart valves and cause HF
Acute respiratory distress syndrome (ARDS): sudden respiratory failure secondary to fluid accumulation in alevoli, fatal 25-40%
Atelectasis: area of lung does not inflate properly or collapses. Caused by factors that prevent deep breathing (post-op pain etc)
bronchiectasis, chronic bronchitis, COPD:
bronchiectasis: progressive, OBSTRUCTIVE, abnormal dilation of bronchus. irreversible, chronic infection weakens bronchial walls (dilate bronchi and bronchioles)
- seen in cystic fibrosis
chronic bronchitis: productive cough for 3 Month over 2 consecutive years
COPD (chronic bronchitis, emphysema):
- block airflow due to narrowing of bronchial tree
- alevolar destruction, air trapping (increases TLC and RV)
types of breathing:
biot’s: irregular depth and rate vary with periods of apnea (due to increased ICP, damage to medulla)
bradypnea: 20)
cheyna-stokes (periodic): decreasing rate and depth of breathing with periods of apnea (CNS damage)
eupnea - normal rate and depth
(hyperpnea - increased rate/depth, hypopnea - decreased rate/depth)
Kussmaul’s - deep and fast breathing (metabolic acidosis)
paradoxical - chest wall moves in with inhalation and out with exhalation (opposite of normal. chest truama, paralysis of diaphragm)
FEV, VE, PEF:
FEV: forced expiratory volume. amount of air exhaled in specified amount of time.
VE: minute volume ventilation. Volume of air expired in one minute (VE = TV x RR)
PEF: Peak expiratory flow. Max flow of air during forced expiration.
3 types of cardiomyopathy:
- dilated cardiomyopathy: require ace inhibitors, beta blockers, digoxin, diuretics, pacemaker.
- hypertrophic cardiomyopathy: meds decrease HR, stabilize rhythm, lopressor and calcium channel blockers
- restrictive cardiomyopathy: improve sxs, use diuretics, anti HTN, and anti-arryhtmia meds
Anticoagulants, antithrombotics, beta blockers:
anticoagulants: for post surgery. Ex: heparin, comoudain (warfarin).
Antithrombotics: inhibit platelet aggregation and clot formation, for post - MI. Ex: bayer (aspirin), plavix
Beta blockers: decrease myocardial O2 demand (decreases HR and Heart contractility) by blocking beta adrenergic receptors For HTN, angina, arryhtmia, HF. -olols med names. “*WATCH FOR OTHO HYPOTENSION side effect
Ca channel blockers, diuretics:
calcium channel blockers: decrease entry of Ca into smooth muscle which leads to decreased myocardial contraction, dec’d O2 demand of heart, and inc’d vasodilation. For HTN, angina, CHF, arryhtmia.
Diuretics: increase excretion of sodium and water (urine) which leads to decreased plasma volume, decreased preload, and ultimately dec’d BP. For CHF, edema, HTN, pulmonary edema.
nitrates, positive inotropic agents:
nitrates: decrease ischemia via smooth muscle relaxation and dilation of peripheral vessels (for angina)
positive inotropic agent: increase force and velocity of myocardial contraction to decrease HR, decrease conduction velocity of AV node, decrease degree and activation of sympathetics. (For HF, atrial fib) ex: lanoxin (digoxin)
thrombolytics:
breaks up clot (via plasminogen -> plasmin), plasmin breaks down clots and allow occluded vessels to maintain bloodflow. For: MI, PE, ischhemic stroke.
ex: activase
types of airways:
nasopharyngeal: nasotracheal suctioning
oral pharyngeal: maintains airway
endotracheal: for mech ventilation
traceostomy: prolonged mech vent
heart sympathetics versus paraympathetics
heart sympathetics: achieved with release of epinephrine and norepinephrine. Chambers beat faster (chronotropic effect) and with greater force of contractility (inotropic effect).
Heart Parasympathetics: via ACh from vagusn erve, slows heart rate (chronotropic) via ACh release from vagus nerve on SA node
absent breath sounds = pneumothorax, lung collapse.
words faint in normal lung, if hear voice sounds this indicates consolidation (atelectasis, fibrosis )
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