Cardio Flashcards
4 phases of cardiomyocyte AP
- RMP (-90)
- Na+ enters, threshold reached @ -70 mV –> rapid/brief depolarization to +10 (L-type Ca channels slowly begin to open)
- Brief repolarization (transiently activated K+ channels–>efflux) –> 0 mV
- Plateau: Outward K+ and inward Ca2+ are balanced; Ca here is not enough to cause contraction triggers Ca-induced-Ca-release
- Repolarization via continued K+ efflux as Ca channels close; Ca efflux through Na/Ca exhanger and Ca-ATPase
Refractory period of cardiomyoctes based on what?
Resetting of Na+ channels (need to move from inactivated –> resting state (different gates)
Explain Ca-induced Ca release
Ca influx in sarcolemma including T-tubules (invaginations close to sarcoplasmic reticulum)
Ca binds RYR receptors on SR –> Ca release
How does a cardiomyocyte return to rest (ionically)
Ca moved back into SR and out of cell
SERCA = Sarco(endo)plasmic reticulum Ca ATPase
Na/Ca secondary active transport
Out of cell via active transport
Why do cardiac muscles have long repolarization phase?
So that the AP (and its refractory period) last most of the contraction time to prevent tetanus/arrhythmia
Gap junctions allow the heart muscle cells to act as a…
Fuctional syncytium
Explain troponin and tropomyosin
Tropomyosin covers myosin-binding sites on actin (thin filaments)
Troponin binds tropomyosin and actin, when Ca binds it releases actin to allow myosin heads to bind
3 subunits of troponin:
TnC - calcium
TnI - actin
TnT - tropomyosin
CO =
SV x HR
BP =
TPR x CO
Impact of catecholarmines on nodal cells
Bind B1AR
G protein cascade –> pKa activation –> phosphorylates and opens Ca channels –> depol, ^ HR
POSITIVE CHRONOTROPIC ACTION
Acetylcholine (Vagus Nerve) impact on cardiac nodal cells
Binds M2 receptors
–> Gi cascade –> K+ channel opening and efflux –> hyperpol/decreased HR
Also inhibits AC/pKa/Ca entry
Negative chronotropic action
Catecholamine impact on cardiomyocytes
Bind B1AR –> pKa activation (G cascade)
Phosphorylates Phospholamban on SR membrane –> Ca influx into SR –> ^ rate of relaxation
(phospholamban inhibits SERCA when dephosphorylated)
Phosphorylation of L-type Ca channels in sarcolemma as well
Term for the fact that the nodal cells can spontaneously trigger themselves
Automaticity
List various pacemaker cells and their spontaneous depolarization rates (4)
SA node = 60-100 bpm
Atria < 60
AV node ~50 (40-60)
Ventricles 20-40
Cardiomyocytes are connected by
Intercalated disks = gap junctions (connexons) + desmosomes (cadherins + plaque proteins, keratin)
3 things that make pacemaker APs unique
1) Phase 4 positive slope (pacemaker current)
2) Maximum diastolic potential =60 mV
3) Phase 0 upstroke is less rapid, lower amplitude (Ca influx not fast Na channels)
Purpose and mechanism of 0.1 sec delay at AV node?
Atrial contraction before ventricular contraction
Fewer gap junctions and smaller diameter fibres
Bundle of His branching
Bundle of His –> RBB and LBB
LBB –> anterior/posterior fascicles
What anchors the AV valves?
Chordae tendinae
Connected to papillary muscles
RMP of cardiomyocytes
-90 mV
Movement of Na/K ATPase
2 K in, 3 Na+ out (hyperpolarizing)
The RMP of cardiomyocytes is approximately the equilibrium potential of…
Potassium (rectifier potasium channels open at rest, pretty much only thing membrane is permeable to)
Explain AP in cardiac nodal cells
- Na+ leaking in through funny channels; RMP -60
- Threshold at -40 mV -> L-type Ca channels open –> depol
- Ca channels shut, K channels open –> repolarization to -60 (no plateau)
Upward inflections on JVP waveform (3)
a = atrial contraction
c = AV valve closure (very small)
v = passive filling during systole
Descents on JVP waveform (2)
x = pressure decline after atrial contraction and tricuspid valve closure
y = opening of tricuspid –> blood empties into ventricle
Describe the hepatojugular reflux
Press on liver -> ^ venous return -> ^RH volume -> if RH dysfunction, visible JV distention (seen via JVP) lasts a few seconds
Stethoscope: bell vs diaphragm for what freqs
Bell for low (lightly)
Diaphragm for high (firm against skin)
Name the 4 heart auscultation areas
Aortic, pulmonic, tricuspid, mitral (apex)
What is a condition that could separate the 2 sounds during S1?
RBBB
Delayed R ventricular contraction/tricuspid closure
Explain how leaflet drifting impacts S1 sound
The leaflets passively drift throughout ventricular filling. The less drift –> louder sound when forced closed by V > A pressure
What might increase S1 sound? (3)
Short PR interval (less drifting)
Mild mitral stenosis (reduced flow means prolonged diastolic dP which keeps valves more open)
Rapid HR (short diasole, less drifting)
What might decrease S1 sound (4)
1st-degree AV block (prolonged PR interval, ^ drifting)
Mitral regurgitation (leaflets don’t fully contact on closure)
Severe mitral stenosis (leaflets never open much)
“Stiff” L ventricle (high ventricular pressure at end of diastole ^ drift)
S1 and S2 are high or low sounds? Best heart with what part of stethoscope?
Both high, diaphragm
S1 and S2 best heard in what auscultation areas?
Apex (mitral) and pulmonic repectively
S2 insensity is impacted by what? Examples? (2)
Velocity of blood coursing back twd SL valve after ventricle contracts (hypertension –> LOUDER)
Suddenness of closure (stenosis –> valves don’t move much –> softer)
What is physiological splitting of S2?
A2 and P2
On inspiration, pulmonary vascular capacitance is increased, resulting in less pressure on the pulmonary valve –> late P2
A1 is earlier because less venous return from pulmonary circulation reduces ventricular pressure and emptying time
S2: Widened splitting
A2 and P2 separate during exp and even more during insp
Delayed closure of pulmonic valve (RBBB, stenosis)
S2: Fixed splitting
Abnormally wide interval thorughout resp cycle due to chronically increased pulmonary circulation capacitance (e.g. chronic R volume overload)
Paradoxical splitting (S2)
P2 before A2 on exp and single sound on insp
Delayed AV closure (LBBB, aortic stenosis)
2 types of extra systolic heart sounds
1) Early ejection clicks: opening of SL valves after S1 (e.g. valve stenosis)
2) Mid/Late: systolic prolapse of AV valves into atrium –> regurgitation
Extra diasolic heart sound:
Opening snap
AV valve (usually mitral) stenosis –> “snaps” when opening
(third sound on inspiration! Comes after P2)
S3 sound
AKA?
Early diastole after AV valves open
Tensing of chordae tendinae due to rapid ventricular filling/expansion
Ventricular gallop when pathological (can be normal in children)
Ventricular gallop can be caused by what?
What is the “word” representing the sound
Dilated ventricle (systolic HF), AV valve regurgitation increasing flow
Ken-TuCky
S4
AKA?
Word rhythm?
Examples?
Late diastole before S1. Ejecting blood into a stiff ventricle
Atrial gallop
Tenne-ssee
Ventricular hypertrophy, myocardial ischemia
Quarduple rhythm
S1 + S2 + S3 + S4
Summation gallop
Quadruple rhythm + tachycardia –> S3/4 overlap (short diastole) so becomes a long middiastolic low/loud sound
S3 and S4 frequencies
Dull/low (bell!)
Contrast with high freq S1/S2
Murmurs are caused by ____?
5 mechanisms
Turbulent blood flow
- Flow across partial obstruction
- Increased flow through normal structures
- Ejection into dilated chamber
- Valve regurgitation
- Blood shunting into lower-pressure chamber
How to describe murmurs? (7)
- Timing (systole, diastole, continuous)
- Intensity (grading systems)
- Pitch
- Shape (intensity changes, cresc/decrsc)
- Location (loudest)
- Radiation (direction!)
- Response to maneuvers
Grading scales for murmur intensity
Systole: 1/6 –> 6/6
Diastole: 1/4 –> 4/4
Define systolic ejection murmur
2 types?
After S1 until before/during S2
Crescendo-decrescendo
Delay after S1 (isovolumetric contraction of L ventricle)
Pulmonary or aortic valve stenoses
Pansystolic (holosystolic) murmur
Regurgitation across incompetent AV valve or through VSD
Uniform intensity throughout systole, directly connected to S1 (as soon as pV > pA backflow occurs)
Murmur intensity in VSD is greater in smaller or bigger hole?
Smaller
Late systolic murmur: when is it heard and what causes it?
Mid/late systole to S2
Caused by mitral valve prolapse into atrium
2 ways to do echocardiography
(bonus points for examples of why you’d use echo)
Transthoriacic (TTE)
Transesophageal (TEE)
Evaluate murmurs, valve function, myocardial contractility, septal defects, aneurysms, thrombi…
What causes a continuous murmur?
Presistent pressure gradient
Patent ductus arteriosus = abnormal communication b/w aorta and pulmonary artery; aortic pressure always higher
Early diastolic murmur =
Regurgitant flow through SL valve (aortic or pulmonic)
Descrescendo because pressure gradient reduces as blood backflows and the aortic/pulmonic pressure decreases
Mid-to-late rumbling diastolic murmurs
2 reasons and describe (including shape)
Across AV valves (stenotic or increased flow)
- Stenosis* –> OS then descrescendo-crescendo (lowering gradient then atrial contraction)
- Flow* –> fever, anemia, hyperthyroidism, exercise
4 main parameters of CO
Heart rate
Preload
Afterload
Contractility
(Co = HR x SV, and SV determined by the latter 3)
Cardiomyopathy
Definition + 2 risk factors
Disease in the heart muscle
Alcohol (dilated cardiomyopathy)
Diabetes mellitus (diabetic cardiomypoathy or via CAD/atherosclerosis)
Isometric vs isotonic contractions
Relations to preload/afterload?
Isometric: staying same length; preload = ventricular V (stretch) at end of diastole
Isotonic: staying same tension; afterload = fixed load, determines final length
Preload impacts are represented through what curve?
Preload approximated via?
Frank-Starling
Ventricular EDV or EDP
Afterload =
Proxy?
Ventricular wall tension during contraction (force that must be overcome for ventricle to eject contents = wall stress)
~systolic ventricular (or arterial) pressure
Ventricular wall stress (afterload) is proportional to what?R
Ventricular pressure
Ventricular radius (dilated chamber ^ stress)
1/thickness of wall (distribution over greater area)
What shifts the Frank-Starling curve?
Contractility (inotropic state)
Impacted by hormones/chemicals –> change cross-bridge cycling rate
Cardiac output denominator
min
Define ejection fraction
Normal range?
Fraction of EDV ejected during systole
= SV/EDV
Usually 55-75%
Describe the ventricular P-V loop
Which part represents the afterload?
c-d = afterload
Continue at page 3 HF
Atropine
Anticholinergic, ^HR
Define Arteriosclerosis + 2 subtypes
Hardening of arterial walls
Atherosclerosis = hardening due to atheromatous plaque formation in endothelium
Arteriolosclerosis = hardening of artioles
3 tunics of blood vessel walls
- Tunica intima = endotheium + subendothelium
- Tunica medica = SM + elastic fibres
- Tunica externa = collage, vasa vasorum (large BVs)
Basic steps of atherosclerosis plaque formation
- Endothelial damage
- LDL buildup in intima
- LDL oxidation –> inflammatino
- Recruitment of monocytes, differentiate into macrophages
- Macrophages eat lipids –> foam cells –> fatty streak
- Foam cells –> inflammation –> SM (media) proliferation and migration into intima
- Formation of lipid core + fibrous cap (CT) –> atheroma
- May calcify, may rupture
What common hormone is a protective factor for atherosclerosis?
Estrogen
Prognosis/phenotype of atherosclerosis is highly dependent on
Plaque stability (bursting = bad)
Risk factors for atherosclerosis
Dyslipidemia, Smoking, Hypertension, Diabetes Mellitus
Smoking doubles the risk of ___ in patients with CAD
Stroke
Serum measure associated with atherosclerosis
CRP (inflammation)
Why do atheromas tend to form in bifurcated vessels (e.g. common carotid, L conary arteries)?
Laminar flow –> superoxide dismutase (antioxidant), NO production (vasodilation, platelet inhib, anti-inflamm)
Name 5 ways that physical/chemical stressors impact endothelial function and predipose to atheroma formation
- ^cell-surface adhesion molecules
- Impairement of permeability barrier
- Inflammatory cytokines
- Altered release of vasoactive substances (NO, prostacyclin)
- Interference with antithrombotic properties
Does early atherosclerotic plaque formation narrow the artery?
No - compensatory outward remodelling of the arterial wall preserves diameter (no ischemic symptoms).
Later that isn’t enough, vessel restricted –> ischemia, anging/claudication
How does atherosclerosis typically beget acute coronary syndrome?
Fibrous cap of plaque ruptures –> prothrombotic molecules exposured –> acute thrombus
What is a consequences of atheroma calcification?
Increases rigidity/fragility –> bursting
What happens when an atherosclerotic plaque ruptures?
Thrombogenic materials in core exposed –> thrombus formation –> vessel occulation –> infarction (tissue death due to obstructed bloodflow)
Do atherosclerotic symptoms correlate with disease severity?
Not consistently
What are bruits?
Sounds indicating turbulant bloodflow
Summarize treatment of CAD
Risk factor control (smoking!!!)
Restore perfusion or decrease O2-demand by heart
Stents, CABG
Thrombolytic/anti-platelet/anti-coagulant drugs
Most patients given drugs that reduce myocardial oxygen demand (via reducing HR, contractility, preload/afterload) - Beta/Ca-blockers, nitrodilators
For variant angina treat with drugs to prevent vasospasm
What is the “widow-maker”?
Anterior interventricular artery (commonly occluded by atherosclerosis plaques)
AKA Left anterior descending artery = LAD
Ischemic heart disease
Imbalance in myocardial O2 supply/demand
Angina pectoris
Uncomfortable sensation in the chest (may radiate) due to myocardial ischemia
Stable angina
Chronic pattern of transient angina pectoris
Precipiated by physical activity or emotional upset. relieved by rest in a few min
Temporary ST depression but no permanent myocardial damage
Variant angina
ECG?
AKA?
Anginal discomfort at rest due to coronary artery spasm
Causes ST elevation
AKA Prinzmetal angina
Unstable angina
Increasing freq/duration produced by less exertion –> commonly progresses to MI
Myocardial infarction
Prolonged lack of blood supply –> myocardial necrosis
(usually due to acute thrombus at site of atherosclerotic stenosis)
Describe myocardial oxygen supply (2 main components) & demand (3)
Supply:
1) O2 content of blood
2) Coronary blood flow (perfusion pressure + vascular resistance; Q = P/R)
Demand:
1) Wall stress
2) HR
3) Contractility
Coronary perfusion pressure is estimated how?
Aortic diastolic pressure (coronary vessels not perfused during systole!)
Name the main intrinsic mediators of coronary artery tone (3 categories + examples)
1) Metabolic: adenosine –> vasodilation
2) Endothelial factors: NO, prostacyclin, EDHF (all dilation), Endothelin 1 (constriction)
3) Neural factors: SNS –> constriction via alpha receptors, dilation via beta receptors
Explain why endothelial changes lead to ischemia
- Loss of antithrombotic properties (NO/prostacyclin)
- No longer secrete vasodilatory mediators in response to Ach, sheer stress, serotonin, thrombin. SNS effects not opposited. Impacts of metabolites (adenosine) reduced)
__ vessels in heart tend to get plaques, while ____ ones acts as what?
Proximal
Distal –> reserves (“resistances vessels”, modulate tone)
Explain levels of diameter restriction and their impacts on coronary flow
<60% -> no impairment at rest and compensate during exertion
60-~80% –> max flow reduced even with full resistance vessel dilation (exertional ischemia)
>90 –> ischemia even at rest
What impacts do Ach, sheer stress, platelet products (serotonin/thrombin) have on vascular diameter?
Direct –> SM contraction
Indirect –> release of endothelial factors –> SM dilatino
What might you see in patients with cardiac risk factors before plaques form?
Endothelial dysfunction
Consequences of anaerobic metabolism during ischemia
Low ATP –> less systolic contraction & diastolic relaxation –> ^LV pressure –> pulmonary congestion
Metabolic product buildup –> pain and arrhythmia
Differentiate stunned vs hibernating vs infarcted myocardium
What is the clinical significance of this?
Stunned: prolonged systolic dysfunction after blood returns
Hibernating: prolonged low blood supply and ventricular contractile dysfunction
Infarction: necrotized tissue (permanent)
Former 2 can regain function, latter would not. E.g. don’t do coronary revascularization on necrotized myocardial tissue
2 types of stable angina
1) Fixed threshold: mostly due to stenosis, constant level of activity required to precip symptoms
2) Variable-threshold: vasoconstriction; diff levels of exertion @ diff times trigger discomfort
Unstable angina is a type of ____ and is usually due to ____
Acute coronary syndrome
Rupture of an unstable atherosclerotic plaque
Why does variant angina frequently cause symptoms at rest?
Issue with supply not demand
Silent angina is more common in what populations?
Women
Elderly
Diabetics
How long does an angina attack usually last?
More than a few seconds, less than 5-10 min
Name some symptoms that may accompany angina
Whare are “anginal equivalents”?
Tachycardia, diaphoresis, nausea
Dyspnea (LV dysfunction –> pulmonary congestion)
Fatigue, weakness
“Anginal equivalents” if no chest discomfort but just these symptoms during ischemia
How long should angina take to relief after stopping the aggravating activity?
A few min
(3-5 min after taking nitroglycerine)
Carotid bruits are a sign of
Cerebrovascular disease
2 signs of peripheraly artery disease on physical exam
Femoral bruits
Decreased pulses in lower extremities
Name 5 physical exam signs for myocardial ischemia and why they are present
Dyskinetic apical impulse (abnormal bulge on palpation) - systolic dysfunction
Rales/Crackes - Pulmonary edema
S4 - Reduced diastolic complicance
Mitral regurgitation - papillary muscle dysfunction
Diaphoresis, elevated HR/BP - SNS tone
Name 4 cardinal symptoms of myocardial ischemia (to help with differential)
- Brought on by exertion, relieved by rest/nitroglycerin
- Lasts <10 min
- Retrosternal tightness/pressure, radiating to neck/jaw/L shoulder/arm
- ECG: transient ST depression/elevation, or flattened/inverted T waves
Name 3 possible differentials for chest pain and how to tell them apart from angina
Pleuritis –> longer-lasting, worse on inspiration
GI issues (e.g. GERD) –> precipitated by certain foods, may improve with antacids
Musculoskeletal –> more superficial/localized, point with finger!
What is the Levine Sign?
Clenched fist over sternum when patient describing anginal pain
ECGs in angina patients
Between attacks: ~50% patients normal, some have chronic changes (e.g. pathological Q waves from past MI)
During attack: transient ST-depression and T-wave flattening/inversion
ST-elevation possible in severe transmural ischemia or Prinzmetal’s angina (similar to STEMI)
What tests do you do to look for angina in a patient not in an acute attack? (4 subtypes)
Stress tests:
- Standard exercise testing
- Nuclear imaging (+exercise)
- Exercise echocardiography
- Pharmalogical stress tests
What are some signs indicating a positive exercise test for myocardial ischemia? (5)
Iscemic ECG changes
Exercise intolerance <2 min for cardiopulmonary reasons
High-grade ventricular arrhythmia
Drop in systolic BP
Replication of chest discomfort
Why would nuclear imaging (IV radionuclide injection) be indicated in an exercise stress test for ischemia?
What are “cold spots”?
Patient has baseline abnormalities of ST segments (e.g. LBBB)
If standard ex test doesn’t align with clinical suspision
Radionuclide accumulates proportionally to viable myocardial cells; cold spots = ischemic or infarcted (repeat @ rest to see if it fills back in)
When is echo-exercise stress testing indicated for ischemic testing?
Baseline ST- or T-wave abnormalities
Standard ex test results don’t match clinical suspision
Describe pharmacologic stress tests for ischemia (2 types)
When are they indicated?
If patient can’t exercise
Coronary vasodilator (e.g. adenosine) - shunts blood away from ischemic regions which are already fully dilated
Inotrope (dobutamine) - if patient took caffeine/theophylline (adenosine antagonists), reactive airway disease (adenosine –> bronchospasm)
Can couple w/ echo or nuclear imaging!
What is the gold standard test for CAD diagnosis? Is this used in all patients?
Coronary angiography
- inject radiopaque contrast (invasive)
No - only use in patients who are not responding to meds or very unstable
What does coronary angiography show?
(include added possible test)
Anatomical issues (not functional consequences which are important to guide treatment!)
Can use catheterization –> functional flow reserve (=Pdistal to stenosis/Paorta)
Types of revascularization for treatment of myocardial ischemia (2 + 2 subtypes each)
Percutaneous Coronary Intervention (PCI)
- Percutaneous transluminal coronary angioplasty
- Coronary stents
Coronary Artery Bypass Graft Surgery
- Saphenous vein or internal mammary artery
Why are coronary stents preferable to percutaneous coronary angioplasty?
PCA (stretch artery via balloon) –> recurrance common in 6 mo
Coronary stents reduce restonosis
Describe 2 problems with coronary stents and how they are dealt with
- Thrombogenic - must take aspirin + P2Y12 receptor antagonist
- Neointimal proliferation (migration of SM cells + ECM production) –> drug-eluting stents w/ antiproliferate med; but also slow protective endotheliazation making anticoagulants all the more important!
Why might PCI be preferable over CABG?
Less invasive, faster recovery
Do PCIs reduce MIs/death in stable CAD?
NOPE
What medical treatment is essential after CABG?
What BV is preferred for the same reason?
Lipid-lowering to prevent atherosclerosis
Internal mammary artery (anastomose it) more resistent than saphenous vein
In what patients is the survival benefit of CABG > medical therapy and PCI
- Large amounts of myocardium at ischemic risk (>70% stenosis in all 3 major coronary arteries)
- >50% stenosis of L main coronary artery
- Diabetes with multivessel disease
- Critical narrowing of LAD
What are the 4 classes of angina pectoris (Canadian Cardiovascular Society)
- Class I* - Only during strenuous/prologed exertion
- Class II* - Slight limitation in ordinary activities
- Class III* - marked limitation in ordinary activities
- Class IV* - can’t do any activity without angina, inclds angina @ rest
New-onset Class III-IV –> hospitalization indicated
Name 4 types of therapies for prevention of acute cardiac events
(not to treat symptoms, but to actually reduce risk of MI/death!!)
Include brief description of treatment plan/goal
- Antiplatelet therapy (aspirin) - continue indefinitely in all CAD patients unless otherwise indicated
- Platelet P2Y12 ADP receptor agonists (clopidogrel) if allergic to aspirin, or use combo) - prevent platelet activation/aggregation
- Statins = HMG-CoA reductase inhibitors (goal =50% LDL reduction)
- ACE-inhibitors (reduce MI/stroke/death)
How do venodilation and arteriodilation impact wall stress?
Both reduce it
(veno –> reduces preload; arterio –> reduces afterload)
Why wouldn’t you want to combine Beta-blocker and Ca-blocker in a patient? What particular patients should this especially be avoided in?
Both are negative inotropes and decrease contractility
Especially avoid in patients with L ventricular dysfunction
Name 4 common meds that are used for symptomatic relief in stable angina (no HF or LV dysfunction) but don’t actually reverse atherosclerosis or increase longevity
Organic nitrates
Beta-blockers
Ca-channel blockers (dihydropyridines, non-DHP e.g. verapamil)
Ranolazine
Mechanism of action of organic nitrates for myocardial ischemia
Side effects?
Decrease demand: reduce preload via VENOdilation
Increase supply: ^perfusion, decrease vasospasm
ADR: Headache, reflex tachycardia (combine w/ BB!), hypotension
Beta blockers mechanism of action for myocardial ischemia
Side effects?
Demand: Decrease O2 demand by decreasing HR and contracility
Supply: Increases time in diastole –> ^coronary perfusion
ARD: Fatigue, bradycardia, reduce LV contraction, bronchoconstriction, hypoglycemic symptom-masking
Ca-channel blockers mechanisms of action (overall, although they vary b/w types) and ARDs
Decrease demand: reduce proload (venodilation), wall stress/BP, contractility, HR
Increase supply: ^ perfusion and decreased vasospasm
ADRs: headache, decrease LV contraction, bradycardia, edema, constipation
*Use long-acting (once per day) as 2nd line to nitrate and BBs!
What does ranolazine do?
Decreases late-phase inward Na current (which is enhanced in ischemia leading ot Ca overload and reduced relazxation)
No impacts on HR or BP!
Can you use B1-selective BBs in patients with obstructive airway disease?
NO! Not fully despective, still can cause bronchospasm
(Recall: B1AR on myocardium, B2AR in bronchial tree/BVs)
