Terms in this set (150)
What are the pressures in the heart chambers and great vessels?
Where is S1 heard best?
Lower L sternal border/apex of heart
What makes S1 louder?
-short PR interval (ventricles contracts sooner, AV valves slam shut)
-high CO or tachycardia
-valve leaflets have increased mass (scarred or redundant prolapsing mitral valve)
What makes S1 softer?
-long PR interval (valves float back to closed)
-decreased leaflet mobility from scarring/stenosis
-noncompliant LV (high diastolic pressure precloses leaflets)
Where's the only place you'll hear S2?
pulmonic area (L 2nd intercostal space)
What makes S2 louder?
-leaflets have increased mass
-increased pulm blood flow (S2)
What makes S2 softer?
-decreased mobility in severe valvular stenosis
-calcification of aortic valve
What are some causes of abnl splitting of S2?
-widened splitting (electrical/mech delay of RV delays P2; split during expiration AND inspiration)
-fixed splitting (ASD increases R heart filling, delays P2)
-paradoxical splitting (electrical/mech delay of LV so A2 after P2)
What are ejection clicks?
hearing semilunar (aortic or pulm) valves open
When will a pulmonary ejection click get softer?
Where are ejection clicks heard best?
L sternal border (2nd intercostal space)
What's the etiology of ejection clicks?
-congenitally stenotic semilunar valves
-dilated aorta or PA
What are nonejection clicks?
hearing mitral or tricuspid valves continuing to move (tense) during systole b/c they are prolapsed
What are opening snaps?
hearing mitral or tricuspid valves open
Where are opening snaps heard best?
lower L sternal border or apex
What causes opening snaps?
scarring and fusion of leaflets d/t rheumatic heart disease
What is S3?
low pitched sound heard d/t increased early diastolic ventricular filling or dilated, poorly functioning ventricles
When is it normal to hear S3?
What pathology could cause S3?
LV failure or valve regurg
What is S4?
low pitched sound heard d/t atrial contraction emptying blood into noncompliant ventricle
What's the etiology of S4?
scarring, myocardial ischemia, hypertrophy
What are the 4 causes of heart murmurs?
-flow across partial obstruction (valvular stenosis, hypertrophy, narrowed blood vessel)
-increased flow across nl structures
-ejection into dilated vessel (least common)
-abnl flow when valve doesn't close
-abnl communication b/w high and low pressure chambers or vessels (congenital defects)
What would cause increased flow across nl structures?
Physiologic: kids, athletes, pregnancy, exercise
Pathologic: anemia, CHD - septal defects
What causes a systolic ejection murmur?
aortic or pulmonic stenosis (obstructed flow)
Characteristics of pathologic systolic ejection murmur:
-after S1 (gap d/t isovolumetric contraction)
-grade 3 or 4
-heard at R sternal border - 2nd intercostal space (aortic) or L sternal border - 2nd intercostal space (pulmonic)
Characteristics of physiologic systolic ejection murmur:
-grade 1 or 2
-best heard in aortic or pulmonic areas
-decreases when you're upright (SV goes down)
What causes a pansystolic murmur?
leaky valve (mitral or tricuspid regurg) or VSD
Characteristics of pansystolic murmur:
-continuous b/w S1 and S2
-caused by large pressure diff
-high pitched (best heard w/ diaphragm)
-grade 2 thru 4
What causes a late systolic murmur?
prolapse of mitral valve leaflets during late systole --> regurg
Characteristics of late systolic murmur:
-preceded by at least 1 nonejection click
What causes a diastolic decrescendo murmur?
aortic or pulmonic valve regurg d/t severe pulm HTN
Characteristics of diastolic decrescendo murmur:
-decrescendo b/c pressure diff gradually decreases
-begins right after S2
-heard best at L sternal border w/ diaphragm (high pitched)
What causes a mid-late diastolic murmur?
mitral or tricuspid valve stenosis (partially obstructed flow)
Characteristics of mid-late diastolic murmur:
-after S2 (gap d/t isovolumetric relaxation)
-preceded by opening snap
-low pitched (heard w/ bell at apex for mitral or LLSB for tricuspid)
-crescendo right before systole d/t atrial contraction
What causes a middiastolic low pitched murmur?
-pulmonic valve regurg
-high early diastolic flow across mitral or tricuspid valves (severe regurg)
-preclosure of mitral valve by severe aortic regurg (Austin Flint)
What causes a continuous murmur?
communication b/w high and low pressure chamber/vessel where pressure diff maintained throughout systole and diastole (turbulent flow always in 1 direction)
Characteristics of continuous murmur:
-heard best at L sternal border - 2nd intercostal space
-gets loudest around S2
What causes to and fro murmurs?
combo of stenosis and regurg at any valve
What type of murmurs increase w/ inspiration?
What murmurs increase w/ leg raising?
What murmurs get louder after long R-R interval?
How long is a nl PR interval?
What would cause an abnl PR interval?
short: abnl connection b/w atria and ventricles
long: delayed conduction thru AV node
How long is a nl QRS interval?
less than 120 msec
What would cause a short QRS interval?
abnl sequence of ventricular depolarization or increased ventricular mass
How long is a nl QT interval?
less than half the RR interval
What would cause a prolonged QT interval?
delayed ventricular repolarization (puts you at risk for torsade)
What EKG leads look at inf wall of the heart?
II, III, aVF
What EKG leads look at the septum?
What EKG leads look at the ant wall LV?
What EKG leads look at LV (lateral)?
I, aVL, V5, V6
How do you calculate HR from EKG?
HR = 300 / # of big boxes b/w beats
for irreg HR... HR = # of beats across EKG x 6
What is the range of the nl QRS axis?
-30 degrees to +90 degrees
What is the QRS axis?
avg direction of electrical activity in heart during ventricular depolarization (measured in frontal plane)
Quadrant Approach to QRS axis:
Lead I pos, Lead aVF pos --> Normal
Lead I pos, Lead aVF neg --> could be nl or L axis deviation (look at Lead II - if QRS pos, it's nl; if QRS neg, it's L axis deviation)
Lead I neg, Lead aVF pos --> R axis deviation
Lead I neg, Lead aVF neg --> extreme deviation
Equiphasic Approach to QRS axis:
What lead has most equiphasic QRS complex?
Which lead is 90 degrees away from this lead?
If QRS complex in 2nd lead is pos, direction of this lead approximates QRS. If it's neg, QRS axis is 180 degrees away.
What EKG findings suggest R atrial enlargement?
P wave axis shifted R of +75 degrees
P wave taller than 2.5 mm (lead II)
R atrial part of P wave bigger than 1 small box (V1)
What EKG findings suggest L atrial enlargement?
P wave axis shifted L of +30 degrees
P wave greater than 120 msec w/ 2 peaks (lead II)
L atrial part bigger than 1 small box (V1)
What changes happen to QRS complex in leads V1 and V6 w/ ventricular hypertrophy?
RVH: QRS is inverse of nl
LVH: QRS more exaggerated than nl
What secondary repolarization abnormality happens in ventricular hypertrophy?
downsloping ST segment and T wave inversion
What are the diagnostic criteria for LVH?
S wave (V1) + R wave (V5 or V6) greater than 35 mm
R wave (V5 or V6) greater than 26 mm
What are the diagnostic criteria for R bundle branch block?
QRS duration greater than 120 msec
M shaped QRS complex (V1)
prominent S wave in leads I and aVL
secondary repolarization abnormalities in V1 and V2
What are the diagnostic criteria for L bundle branch block?
QRS duration greater than 120 msec
Broad R wave in leads I, aVL, V6
Lack of q waves in I and V6
ST depression and inverted T wave (I, aVL, V6)
deep S wave, upsloping ST elevation, prominent T wave (V1, V2, V3)
How long are incomplete bundle branch blocks?
What are the etiologies of RBBB?
-iatrogenic during R heart cath
What are the etiologies of LBBB?
-acute MI (ant heart)
What EKG findings are present in LAFB?
L axis deviation
small q in leads I and aVL
small r in leads II, III, aVF
intrinsicoid deflection in aVL greater than 45 msec
What EKG findings are present in LPFB?
R axis deviation
small r in leads I and aVL
small q in leads II, III, aVF
instrinsicoid deflection in aVF greater than 45 msec
What is bifascicular block?
RBBB + either LAFB or LPFB
What causes bifascicular block?
-CAD (most common)
-degenerative disease of conduction sys
Equation for minute ventilation:
VE = RR x (Valveolar + Vdeadspace)
What values from ABG would be nl?
pH = 7.4
pO2 = 80-100
pCO2 = 40
HCO3 = 24
SaO2 = 100%
What values define respiratory acidosis?
pH less than 7.4, elevated pCO2
What's the compensation for respiratory acidosis?
kidneys retain bicarb
Acute: for every 10 mmHg rise in pCO2, bicarb rises 1 mEq
Chronic: for every 10 mmHg rise in pCO2, bicarb rises 3.5 mEq
What are some causes of respiratory acidosis?
-thoracic cage abnormality (scoliosis, kyphosis)
What values define respiratory alkalosis?
pH greater than 7.4, low pCO2
What's the compensation for respiratory alkalosis?
kidneys excrete more bicarb
Acute: for every 10 mmHg drop in pCO2, bicarb drops 2 mEq
Chronic: for every 10 mmHg drop in pCO2, bicarb drops 5 mEq
What could cause respiratory alkalosis?
What values define metabolic acidosis?
pH less than 7.4, low bicarb
Equation for anion gap:
Na - (Cl + HCO3)
Nl value is 12
What's the compensation for metabolic acidosis?
hyperventilation (blow off CO2)
Tip: last 2 digits of pH = pCO2
What causes increased anion gap metabolic acidosis?
-methanol or ethylene glycol poisoning
What causes non anion gap metabolic acidosis?
-diarrhea (most common)
-renal tubular acidosis
What values define metabolic alkalosis?
pH greater than 7.4, elevated bicarb
What's the compensation for metabolic alkalosis?
hypoventilation (lungs retain CO2)
for every 1 mEq of elevated bicarb, pCO2 rises 0.6 mmHg
What differentiates chloride responsive and chloride unresponsive metabolic alkalosis?
Cl responsive: urine Cl less than 10 mEq/L
Cl unresponsive: urine Cl greater than 10 mEq/L
What are the causes of Cl responsive metabolic alkalosis?
What are the causes of Cl unresponsive metabolic alkalosis?
Flow = change in pressure / resistance = change in pressure x radius^4 x pi / viscosity x tube length x 8
What's the most impt factor in determining vessel resistance?
What factors regulate organ blood flow?
-hormonal (only under stress)
Equation for compliance:
Compliance = change in volume / change in pressure
Equation for mean arterial pressure:
MAP = diastolic pressure + 1/3 (systolic - diastolic)
Phases of cardiac AP:
0: upstoke d/t opening of fast Na channels
1: dip d/t Na channel inactivation and transient K efflux
2: plateau d/t Ca influx
3: repolarization d/t closed Ca channels and increased K conductance
4: resting, determined by K
Equation for cardiac output:
CO = HR x SV
Equation for stroke volume:
SV = end diastolic volume - end systolic volume
Equation for ejection fraction:
EF = (end diastolic - end systolic) / end diastolic volume x 100
Nl is 55-75%; heart failure is less than 40%
Tension = chamber blood pressure x radius / 2 x wall thickness
What factors affect myocardial O2 consumption?
What differentiates cardiac muscle from skeletal muscle?
-T tubules at Z discs
Blood vessel layers:
Intima - endothelium and subendothelial collagen
Media - int elastic layer, smooth muscle cells, elastic fibers, ext elastic layer
Types of capillaries:
Continuous - transport occurs by diffusion and caveolae
Fenestrated - found in glomerulus and intestine, have cytoplasmic pores
Discontinuous - found in liver and spleen, have gaps in basement membrane
Layers of trachea:
Mucosa - resp epithelium, loose CT, lympathics
Submucosa - dense CT, smooth muscle, mucous and serous glands
Cartilaginous - C shaped rings of cartilage
Adventitia - loose CT
Layers of bronchi:
Mucosa - resp epithelium (basal lamina now has 3 layers), loose CT, lymphatics
Submucosa - dense CT, smooth muscle, glands
Cartilaginous - irreg shaped cartilage plates
Adventitia - connects to accompanying branch of pulm a
Where's the last place in the airway Goblet cells, glands, and hyaline cartilage are found?
Where's the last place in the airway ciliated cells are found?
What are the ways CO2 is transported in the blood?
-bound to Hb
What are the nl O2 sats for the heart chambers and great vessels?
R heart and pulm a: 70-80%
L heart, pulm veins, pulm capillary wedge: 93-100%
What is the Fick method?
CO = O2 consumption / arteriovenous O2 diff
Equation for pulm vascular resistance:
PVR = mean pulm a pressure - LA pressure/CO x 80
Equation for systemic vascular resistance:
SVR = MAP - RA pressure/CO x 80
What roles do diff areas of the brainstem play in ventilation?
Medulla: rhythm of breathing
Apneustic (pons): unclear; if transected, long inspiratory gasps
Pneumotaxic (pons): fine tuning of breathing
What do central chemoreceptors (medulla) respond to?
pH of CSF
More impt in controlling ventilation
What do peripheral chemoreceptors (carotid and aortic bodies) respond to?
arterial pO2 and pH
What's the function of J receptors?
stimulation causes rapid shallow breathing in assoc w/ capillary distention (CHF)
What are some conditions where you'd see Cheynes Stokes respiration?
-high altitude (esp while asleep)
-brain damage (injury, stroke)
-severe heart disease (heart failure, cardiomyopathy)
What do the colors in Color Doppler mean?
red = blood flowing towards probe
blue = blood flowing away from probe
pressure diff (b/w 2 chambers) = 4 x velocity sq
How is Fick's law applied to diffusion of air in the lung?
-lower pressure diff slows diffusion
-thicker membrane slows diffusion
-lower surface area impedes diffusion
-less soluble, bigger MW gases have harder time diffusing
What's an example of perfusion limitation?
Nitrous Oxide - gas uptake only limited by available blood flow
What affects perfusion limitation?
-rate of blood flow
-# of vessels involved
What's an example of diffusion limitation?
Carbon Monoxide - gas uptake depends only on how fast gas diffuses across membrane
When will O2 become diffusion limited?
-exercise at high altitude
Equation for Diffusing Capacity of lung:
DL = VCO / PACO
How fast is CO taken up in a pt that's inhaling known CO conc?
Nl value: 25 mL/min/mmHg (increases during exercise)
What factors affect DLCO?
-area and thickness of blood/gas barrier
-volume of blood in pulm capillaries
-distribution of diffusion properties
What are the mechanisms of edema formation?
-increased pulm capillary hydrostatic pressure
-decreased plasma oncotic pressure
-disruption of alveolar capillary basement membrane
-obstruction of pulm lymphatics
What's the mech of cardiogenic pulm edema?
LV failure --> blood backs up in LA --> increased LA pressure --> blood backs up in pulm veins and capillaries --> increased pulm capillary hydrostatic pressure! --> fluid leaks into alveoli (edema)
What's the mech of hypoproteinemic pulm edema?
blood protein level drops (kidney or liver problem)--> capillary oncotic pressure drops (can't balance out capillary hydrostatic pressure) --> fluid leaks into alveoli
What's the mech behind edema in ARDS?
contents of granules from neutrophils damage capillary basement membrane --> plasma leaks into alveoli
d/t sepsis, acid aspiration, massive trauma
What are some functions of the lungs?
How does diet affect the respiratory quotient?
R increases w/ a carb heavy diet and decreases w/ a fat heavy diet
Alveolar Air Equation:
PaO2 = FiO2 (Pb - 47) - PaCO2/R
R is usually 0.8
What's the value for nl Tidal Volume and what are its components?
Vt = 500 mL
Anatomic dead space = 150 mL
Alveolar air = 350 mL
VT = VD + VA
What are the values for nl minute ventilation and alveolar ventilation?
Minute ventilation = 7500 mL / min
Alveolar ventilation = 5250 mL / min
Equation for minute ventilation:
VE = RR (VA + VDS)
What factors contribute to lung compliance?
Characteristics of lung
-stiffer w/ scarring/fibrosis, pneumonia, pulm edema
-stretchier w/ emphysema, aging
Surface Tension - smaller alveoli want to collapse and push their air into bigger alveoli
*counteracted by surfactant
What factors determine airway resistance?
-size and numbers (mostly medium bronchi)
-smooth muscle constriction
-density and viscosity of inspired gas
What is the equal pressure pt?
when intrapleural pressure becomes greater than pressure inside the airway
What makes the equal pressure pt happen sooner?
-low lung volumes (idiopathic pulm fibrosis)
-high airway resistance (asthma, bronchiolitis, emphysema)
-poor airway traction (emphysema)
Normal Hb values:
Male: 15 g/dl
Female: 13 g/dl
When should you suspect methemoglobinemia?
-blood is chocolate brown
-O2 sats are 85% (pulse ox)
-O2 sats nl on ABG
-pO2 is nl
Dx: measure metHb % on ABG
When should you start supplemental O2?
-if pO2 (arterial blood) less than 55 mmHg
-if O2 sats less than 89%
Diagnostic criteria for CO poisoning:
Symptoms: HA, confusion, nausea
-low O2 sats
-CO blood level greater than 25%
What causes R shift of O2/Hb dissociation curve?
-increased DPG (high altitude, chronic lung disease)
What causes L shift of O2/Hb dissociation curve?
-decreased DPG (stored blood)
Equation for mean pulm arterial pressure:
mPAP = [(2 x diastolic pressure) + systolic pressure] / 3
Nl values for SVR and PVR:
SVR: 900-1200 dyn x s / cm^5
PVR: 100-120 dyn x s / cm^5
What factors determine pulm vascular resistance?
-blood viscosity and hematocrit
How does endothelin affect its 2 receptor types?
Endothelin A receptors: stimulates arteriolar smooth muscle contraction and vasoconstriction
Endothelin B receptors: stimulates endothelial smooth muscle to make more NO, causing vasodilation
Definition of pulm HTN:
mPAP greater than 25 mm Hg at rest (greater than 30 w/ exercise)