Cardio Flashcards
(145 cards)
1
Q
^ contractility (&SV)
A
Big picture
1. ^intracellular Ca
2. ^ sarcomere length
-Catecholamines
Inhibit phospholamban --> ^Ca into SR
-^intracellular Ca
-Decrease extracellular Na
(decrease Na/Ca exchanger)
-Digitalis
blocks Na/K pump --> ^ intracellular Na --> stops Na/Ca exchanger (too much Na to bring in more) --> ^ intracellular Ca
2
Q
Decrease Contractility (& SV)
A
- B1 blocker (decrease cAMP)
- Systolic HF
- Acidosis
- Hypoxia/hypercapnia
- Non-dihydropyridine CCB (verapamil, diltiazem)
- loss of myocardium (MI)
- dilated cardiomyopathy
3
Q
Decrease pre-load
A
PrE-load = VEnodilators
-nitroglycerin
ACEi, ARB: pre & after
4
Q
Decrease afterload
A
Afterload= VAsodilators (hydralazine)
ACEi, ARB: preload & afterload
5
Q
Pompe Disease
A
=Type II glycogen storage dz
-primarily affects heart: "Pompe trashes the pump"
-Lysosomale a-1,4-glucosidase deficiency
-fxn: hydrolysis of glycogen branches
-->glycogen deposits in myocardium
6mo:
-developmental delays
-feeding probs
-HF
-hypotonia
-hepatomegaly
-Biventricular hypertrophy
-short PR interval, wide WRS
-^Serum creatine kinase
-decreased leuk acid maltase
6
Q
Fabry Disease
A
Lysosomal storage dz
- a-galactosidase deficiency
- ->ceramide trihexoside accumulates
- Peripheral neuropathies: hands & feet
- *Angiokeratomas (benign cutaneous lesion of caps)
- CV dz
- renal dz
7
Q
Gaucher Disease
A
Lysosomal storage dz B-glucocerebrosidase deficiency -hepatosplenomegaly -aseptic necrosis of femur -bone crises -Gaucher cells
8
Q
Large Vessel Vasculitis
A
Giant cell (temporal) arteritis Takayasu Arteritis
9
Q
Giant cell (temporal) arteritis
A
-Mostly affects br of carotid artery
Epidemiology/Presentation:
-elderly females
-unilateral headache (temporal a)
-jaw claudication
-possible permenant blindess (ophthalmic a)
Labs/path:
-focal granulomatous inflam
-^ESR
Tx:
-Corticosteroids
Tx before biopsy to prevent blindness
Asc: polymyalgia rheumatica (inflam disorder, muscle pain & stiffness)
10
Q
Takayasu Arteritis
A
Granulomatous thickening & narrowing of aortic arch & great vessels
Presentation/Epidemiology:
-Asian females,
11
Q
Medium Vessel Vasculitis
A
Polyarteritis Nodosa Kawasaki Dz (mucocutaneous lymph node syndrome) Buerger Dz (thromboangiitis obliterans)
12
Q
Polyarteritis Nodosa
A
Presentation:
-Youngins
-Hep B (30%), HepC, Hair cell leuk
-Fever, wt loss, malaise, headache
-GI: abdominal pain, melena
-HTN, neuro dysfxn
-cutaneous eruptions
-renal damage
Path/Labs:
-renal & visceral vesels- NOT pulm arteries
-Immune complex mediated
-Transmural inflammation + fibrinoid necrosis
-Diff stages of inflam coexist in diff BV
-Rosary sign: lots of little aneurysms
Tx:
-corticosteroids
-cyclophosphamide
(forms cross links in DNA--> apoptosis)
13
Q
Kawaski Dz = mucocutaneous lymph node syndrome
A
Presentation:
-Asian children desquamating)
-CRASH & BURN
-Conjunctival injection
-Rash
-Adenopathy (cervical)
-Strawberry tongue
-Hand & foot: edema, erythema
-Fever
Complications:
-Anneurysms
Tx:
-IVIg
-Aspirin (only time give kids aspirin)
14
Q
Buerger Dz = thromboangiitis obliterans
A
=progressive; recurring inflammation; thrombosis of medium BV in LE
Presentation:
-Heavy smokers (after a big burger, you want to smoke)
-males, gangrene, autoamputation
of digits, superficial nodular phlebitis
Tx:
Smoking cessation
15
Q
Small Vessel Vasculitis
A
Granulomatosis w/ Polyangiitis (GPA)
Microscopic Polyangiitis
Churg-strauss (eosinophilic GPA)
Henoch-Schonlein Purpura
16
Q
Granulomatosis w/ Polyangiitis (GPA)
A
Presentation: -Upper respiratory tract: sinusitis, otitis, mastoiditis -Lower respiratory: hemoptysis, cough, dyspena -Renal: hematuria, RBC casts Triad: -focial necrotizing vasculitis -necrotizing granulomas in lung -Necrotizing glomerulnephritis c-ANCA (PR3) Tx: -cyclophosphamide -corticosteriods
17
Q
Microscopic Polyangiitis
A
Necrotizing
Presentation:
Lung, kidneys, skin- NO nasopharnyngeal (unlike GPA)
Kidneys: pauciimune nephritis
Skin: palpable purpura
Path/Labs:
No granulomas
p-ANCA (anti-myeloperoxidase)
Tx:
Cyclophosphomide
Corticosteroids
18
Q
Churg-Strauss
A
Eosinophilic GPA
Presentation
Lungs, spleen, heart, GI, CNS
Lungs:
Asthma, sinusitis
Skin:
Purpura, skin nodules
CNS:
Neuropathy: wrist/foot drop
Kidney:
Pauci immune nephritis
Labs:
p-ANCA
^ IgE
19
Q
Henoch-Schonlein Purpura
A
=most common childhood systemic vasculitis
Presentation:
Often follows URI
ASC: IgA nephropathy (Berger Dz)
Triad:
-Skin: palpable purpura legs
-Arthralgias
-GI: abd pain
Path:
-Due to IgA immune complex deposition
20
Q
Baroreceptors: increased P
A
Vagal response (carotid massage)
- stretch baroreceptor–> ^ firing
- ^AV node refractory period
- decreased HR
21
Q
Cushing Reflex
A
Response to ^intracranial P (CSF)
- ->compression of cerebral arterioles --> ischemia - ->^cerebral PCO2 -->^ symp stimulation - ^BP (to force blood in head) - bradycardia (initially tachy until vagal response) - respiratory depression (impaired brainstem fxn)
22
Q
A wave meaning for JVD mapping
A
Absent a wave: A-fib
Giant a wave: RA contracting against RV resistance
-tricuspid stenosis
-RV hypertrophy
-pulmonic stenosis
-pulm HTN
-RA myxoma
Cannon a waves (large a + sharp ascent & descent)
-RA contracting against closed tricuspid valve
-jxnal arrhythmias- 3rd degree heart block
23
Q
Tricupid Valve Endocarditis
A
-asc: IV drug use Bacteria: -S. Aureus -Pseudomonas -Candida
24
Q
S. Aureus Endocarditis
A
=Acute endocarditis
-Vegetations: large, rapidly destroy valve
25
Strep Viridans Endocarditis
=Subacute endocarditis
- Indolent presentation
- Vegetations: Small, don't destroy valve
26
S. Epidermidis Endocarditis
asc: prosthetic valve
27
E. Coli Endocarditis
Nosocomial endocarditis (esp urinary catheters)
28
Culture Neg Endocarditis
- Coxiella Burnetii
| - Bartonella spp
29
Endocarditis Symps
```
FROM JANE
Fever
Roth spots (retinal hemorrhages w/white centers)
Osler lesions (tender)
Murmur
Janeway lesions (non-tender)
Anemia
Nail bed hemorrhage
Emboli
```
30
Endocarditis Complications
Chordae Tendinaea rupture
GN
Suppurtive Pericarditis
Septic Emboli
31
Wide Splitting (A2-P2)
Conditions that delay RV emptying
- Pulm stenosis
- RBBB
32
Fixed Splitting (A2-P2)
ASD
| ^vol that delays P2 regardless of breath
33
Paradoxical Splitting (P2-A2)
```
Delay Aortic valve closure
-Aortic stenosis
-LBBB
P2-A2
Inspiration: P2 closes later --> paradoxically removes split
```
34
Aortic Stenosis
```
=Crescendo-decrescendo systolic ejection murmur
+/- ejection click
-Heart @: base (esp aortic area)--> carotids
-Symps: SAD
-Syncope (decreased flow to brain)
-Angina (decreased flow to carotids)
-Dyspnea on exertion
Causes:
-BAV
-Calcification
-Chr. rheumatic fever
```
35
Tricuspid Regurg
Holosystolic, high pitched, blowing
Heard @: tricuspid area, radiates to R sternal border
Cause:
RV dilation
Rheumatic fever & infectiveendocarditis
36
Mitral Regurg
```
Holosystolic, high pitched, blowing
Heard at: apex --> axilla
Cause:
-ischemic heart dz (MI)
-MVP
-LV dilation
-Rheumatic fever, infective endocarditis
```
37
Mitral Valve Prolapse
Late systolic crescendo (S2 loud & long) + mid systolic click= dun NA dun NA
Heard: apex
-Can predispose to infective endocarditis
Cause:
-myxomatous degeneration
primary
or secondary to Marfans or Ehlers-Danlos
-Rheumatic fever
-Chordae rupture
38
VSD
Holosystolic, harsh
| Heard @ Tricupsid area
39
Aortic Regurg
```
Early diastolic decrescendo, high pitched, blowing
Hyperdynamic pulse
Head bobbing
Wide pulse P
Cause:
Aortic Root dilation
BAV
Endocarditis
Rheumatic fever
Progresses to LHF
```
40
Mitral Stenosis
S2--> Opening snap (abrupt halt in leaflet motion)
Delayed rumbling late diastolic murmur
(^ interval btwn S2 &OS: ^ severity)
Cause:
-Rheumatic fever
41
Patent Ductus Arteriosus
```
Continuous machine like murmur
Loudest @ S2
Heard @: L intraclavicular area
Cause:
-Congenital rubella
-prematurity
```
42
Marfans (mut)
Chr15: fibrillin (AD)
43
MI EKG
ST elevation: transmural infarct
Q: transmural infarct
ST depression: subendocardial
(NSTEMI, unstable angina)
44
Lipofuscin
Atrophic heart + lipofuscin accumulation --> brown atrophy
Wear & tear pigment (in eldery):
-deposits in:
-hepatocytes
-spenocytes
-myocardial cells
Composition: oxidized & polymerized membrane lipids from autophagocytosed organelles
Hematoxylin & eosin stain: brown perinuclear pigment
45
Hemosiderin
-hemoglobin derived
-Fe containing pigment- aggregates of ferritin
-Normal:
-small amts in macros of bone marrow, liver, etc
-Excess amts:
Due to hemochromatosis
-in: hepatocytes, cardiac, pancreatic islet cells
-Microscope:
brownish granules
Prussian blue stain: turn blue
-Cardiac complications:
-restrictive cardiomyopathy
-arrhythmias
46
Dig Tox
```
Cause:
-Quinidine (Class IA)
Signs/Symps
Nausea/Vomiting
Atrial tachycardia
AV block
```
47
INR
Normal:
48
Warfarin
```
Anticoagulant
Mech:
Inhibits synth & y-carboxylation of vit K dependent
clotting factors: VII, X, IX, II
Metabolized by CYP450 system (CYP2C9)
```
49
Griseofulvin
Tx: superficial fungal infections
DDI: CYP450 inducer
50
Erythromycin
Macrolide antibiotic
| DDI: CYP450 antagonist
51
Isoniazid
Antibiotic
tx: TB
DDI: CYP450 inhibitor
52
Ketoconazole
Antifungal
| DDI: CYP450 inhibitors (like all azoles)
53
Ritonavir
Protease inhibitor
Tx: HIV triple therapy
DDI: CYP450 inhibitor
54
Hypertrophic Cardiomyopathy
=hypertrophy w/asym septal enlargement w/o free wall enlargement
Asc:
-mut in myosin-binding protein C (AD)
55
Causes of Dilated CM
- Enterovirus (coxsakie B)- myocarditis
- Alcohol abuse
- wet beriberi
- cocaine
- Chagas dz
- doxorubicin toxicity
- hemochromatosis
- peripartum CM
56
Clonidine
```
a2 receptor agonist
Side Effects:
-depression, drowsy
-Dry mouth
-constipation
-erectile dysfunction
-disturbance of sleep cycle
-confusion
```
57
Class IA Antiarrhythmics
```
"Queen Proclaims Diso's pyramid"
Quinidine
Procainamide
Disopyramide
Mech:
^: AP duration, refractory period, QT
Use: Atrial & ventricular arrhythmias
*esp re-entrant & ectopic SVT & VT
Side Effects:
Quinidine: cinchonism, dig tox
Procainamide: SLE like syndrome
Disopyramide:HF
-HF
-thrombocytopenia
-Torsades de pointes
```
58
Class IB Antiarrhythmics
```
"I'll Buy Liddy's Mexican Pinatas"
1B= Lidocaine, Mexiletine + Phenytoin
Mech:
decrease AP duration
Preferentially: ischemic or depolarized purkinje & ventricular tissue
Use:
-acuteventricular arrhythmias (esp post MI)
-Dig induced
Side effects:
-CNS stimulation/depression
-CV depression
```
59
Class 1C AntiArrhythmics
```
"Fries Please"
Flecainide
Propafenone
Mechs:
slow phase 0, ^ refractory time in AV
No affect on AP
No affect on refractory time in purkinje & ventricle
Tx:
-SVT (Afib)
Adverse:
-Proarrhythmic
-NO for structural or ischemic heart dz (post MI)
```
60
MI Markers
```
Troponin I:
-4 hrs -1wk
-most specific
CK-MB (creatine-kinase myocardial bound)
-increased for 6hrs-2 days
-also in skeletal muscle
-best for re-infarction
```
61
Class I antiarrythmics
Decrease phase 0 slope, decrease conduction v
State dependent
IA/C: increase refractory period
62
Antiarrhythmics: Increase refractory period
IA, IC (AV node only)
| III
63
Antiarrhythmics: decrease conduction velocity
I, III, amiodarone
64
ENa
ECa
EK
```
ENa= +25 (wants IN cell)
ECa= +124
EK= -90 (wants OUT of cell)
```
65
Absolute Refractory Period
Effective Refractory Period
Relative Refractory period
Absolute Refractory Period:
=Phase0-after plateau: NO AP can initiate
Effective Refractory Period
=slightly longer than ARP
Phase0-right before Phase 3 ends
AP can't be initiated by a local non-propagated
response can-only local (a few Na are open)
Relative Refratory Period
AP can be initiated but must be stonger
end tail of phase 3
*Determined by reactivation of Na channels that are inactivated after phase 0
*why don't give electrical shock in relative refractory period!!
66
Resting membrane potential of cardiac myocytes
-90 (Ek=-90)
67
Cardiac AP Conduction pathway
Sa node --> atria --> AV node --> bundle of His --> R & L bundle branches --> purkinje fibers
-->Left bundle br-->L anterior & L post fasicles
68
AV node blood supply
RCA
| post. inf. interatrial septum
69
Normal Sinus Rhythm
60-100 bpm
1,500/#small boxes
Large boxes: 300-150-100-75-60-50
=P precedes each QRS by normal PR (
70
Sinus Arrhythmia
Normal
HR changes due to reflux changes in vagal tone during
respiration
Inspiration: decrease vagal tone --> ^ HR
71
A-fib
```
=regularly irregular heart beat
-jagged baseline
-no discrete P
-irregular QRS intervals (RRs don't match up)
RF:
-hypertension
-CAD
Complications:
-thromboembolic --> stroke
*LA dilated --> atrial clot
Tx:
-anticoag
-Rate control
-Rhythm control
-&/or cardioversion
```
72
Atrial Flutter
```
Sawtooth
-indentical atrial depolarizations
-even RR btwn QRS
Tx:
//A-fib
-anticoag
-Rate control
-Rhythm control
Best: catheter ablation
```
73
V-Fib
Completely erratic
Fatal
Tx:
CPR & defibrillation
74
AV block: 1st degree
PR (>.2s, 4 boxes)
| -benign
75
AV Block: 2nd degree
| Mobitz 1 & 2
Mobitz 1:
-increasing PR until P w/o QRS --> starts again
Mobitz 2:
-Constant PR, Some P w/QRS
76
AV Block: 3rd degree
Complete block (his-purkinje)
Atria & ventricles beat independently
P-P constant
R-R cosntant, slower
77
ANP (atrial natriuretic peptide)
```
Atrial myocytes release ANP due to:
^Blood vol, atrial P
Causes:
-Vasodilation
-Causes diuresis
-afferent arteriole: dilate
-Efferent arteriole: constrict
-decrease Na reabsorption (& water too)
```
78
BNP (B type natriuretic peptide)
From ventricular myocytes due to ^tension
//ANP but longer half-life
-Used for diagnosing HF
-Recombinant form (nesiritide): Tx HF
79
What changes QT length
QT= ventricular contraction
^QT:
-prolonged Phase 3
-low Ca
80
What changes PR
Normal PR:
81
Delta on EKG
Wolf-Parkinson-White
82
Aortic Arch baroreceptor action
Responds to BP --> vagus nerve (X) --> solitary nuc of medulla
^BP: ^ firing (parasymp)
Decreased BP: decrease firing --> symp takes over
83
Carotid sinus Baroreceptor path
Carotid sinus -->glossopharyngeal n (IX)-->solitary nuc of medulla
84
Peripheral Chemoreceptors
-Carotid & aortic bodies
Mediate changes in ventilation in response to:
-Low O2
-^CO2
-pH
1. Low O2 (altitude)
-doesn't kick in until hypoxic drive to ^ventillation
2. ^Co2: fast, seconds
eg. climbing stairs
3. ^[H]:
-fast
-only mediator of response to metabolic acid/base
insults (ketoacidosis)
-bc metabolic doesn't create CO2 to cross BBB
85
Central Chemoreceptors
Ventral medulla
H+ can't cross BBB
CO2 crosses --> special carbonic anhydrase converts
--> H+ binds H+ receptor (CSF has low buffer)
Slow response (minutes)
-day to day regulation
eg. bronchitis, pathological V/Q mismatch
86
RA P
87
RV P
25/5
88
Pulm Artery P
25/10
89
LA P
90
LV P
130/10
91
Aortic P
130/90
92
Net fluid Flow (Jv)
Net Fluid Flow = Kf [(Pc-Pi) -c(oncoticc - oncotici)]
Kf: permeability of cap to fluid
C: permeability of cap to protein
93
Edema Causes
^cap P: ^vol, HF
Decreased Plasma proteins:
-nephrotic, liver failure, malnurition
^Cap Permeability (Kf): toxin, infection, burn
^interstitial osmotic P: lymph blockage
94
Causes of Torsades de Pointes
-Congenital long QT
-Hypokalemia
-hypomagnesemia
-hypocalcemia
-Diarrhea
-Alcoholism
ABCDE
Anti Arrhythmics
-Class IA anti-arrythmics
-Quinidine, Procainamide, Disopyramide
-Class IIII (except amiodarone)
-Ibutilide, Dofetilide, Sotalol
Anti-Biotics (macrolides)
Anti-Cytoics (haloperidol)
Anti-Depressants (TCAs)
Anti-Emetics (ondansetron)
95
Strep Pyogenes
```
2 autoimmune complications:
i. Rheumatic Fever
Risk decreases w antibiotics
-->rheumatic heart dz
Rheumatic Heart dz causes:
-mitral stenosis
-Afib
ii. Glomerulonephritis
**Risk does not decrease w antibiotics
-immune complexes
```
96
Libman-Sacks Endocarditis
=due to non-bacterial vegetations on both surfaces of mitral valve
- may cause regurg
- asc: SLE
97
Non-bacterial Thrombotic endocarditis: Causes
- libman-Sacks Endocarditis
- Mucin producing adenocarcinoma
- Hypercoagulative state
- SLE
98
Fetal shunts
1. Ductus Venosus (-->ligamentum venosum)
-bypass liver
Umbilical v -->ductus venosus -->ICV
2.Foramen Ovale (-->Fossa Ovalis)
-bypass lungs
-RA-->Formaen ovale -->LA
3. Ductus Arteriosus (-->Ligamentum Arteriosum)
-bypass lungs
-Pulm a -->Ductus arteriosus --> desc aorta'
-Keep PDA open: PGE1,2
-Close PDA: Indomethacin
99
AllaNtois becomes..
AllaNtois -->urachus --> mediaN umbilical lig
| btwn blatter & umbillicus
100
Notochord becomes...
nucleus pulposus
101
UmbiLical arteries become...
MediaL umbilical ligaments
102
Umbilical vein becomes...
Ligamentum Teres hepatis
| w/in falciform ligament
103
SA & AV nodes: Blood supply
R coronary artery
| -MI causes bradycardia, heart block
104
Dysphagia (difficulty swallowing) & hoarseness caused by:
compression of L recurrent laryngeal n (part of vagus)
105
CO=
CO = SV x HR
CO= rate of O2 consumption (ml/min)/
arterial [O2] - venous [O2]
CO = MAP/SVR
Early exercise: CO maintained by ^HR & ^SV
Later exercise: CO maintained only by ^HR
^HR: shortens diastole
106
^ Pulse Pressure (systolic P - diastolic P): Causes
- Hyperthyroidism
- Aortic Regurg
- Aortic stiffening
- Obstructive sleep apnea (^ symp tone)
- Exercise (transient)
107
Decreases Pulse Pressure (systolic P - diastolic P): Causes
- Aortic Stenosis
- Cardiogenic shock
- Cardiac Tamponade
- Advanced HF
108
Aortic area: systolic Murmur
- Aortic Stenosis
| - Aortic valve sclerosis
109
Pulmonic area: systolic ejection murmur
- Pulmonic stenosis
| - flow murmur
110
Tricuspid area:
i. Holosystolic murmur
ii. Diastolic Murmur
i. Holosystolic murmur
- Tricuspid murmur
- VSD
ii. Diastolic Murmur
- Tricuspid stenosis
- ASD (^ flow across tricuspid valve)
111
Mitral Area:
i. Holosystolic murmur
ii. Diastolic Murmur
i. Holosystolic Murmur
- Mitral regurg
ii. Diastolic Murmur
- Mitral stenosis
112
Left Sternal Border
i. Systolic Murmur
ii. Diastolic Murmur
i. Systolic Murmur
- Hypertrophic CM
ii. Diastolic Murmur
- Aortic/pulmonic regurg
113
Handgrip:
```
^afterload
^:
Mitral regurg
Aortic regurg
VSD
Decrease:
Hypertrophic CM ( equalizing pressures)
Mitral valve prolapse: later onset of click/murmur
```
114
Inspiration PE for murmurs
^ venous return to RA
| ^: R heart sounds
115
Valsalva Phase II, Standing up
Decrease preload
Decrease: most murmurs (including AS)
^:Hypertrophic CM: bc ^outflow obstruction w/low vol
MVP: later onset
116
Rapid Squatting
^venous return, ^ preload, ^ afterload
Decrease: Hypertrophic CM
^AS
MVP: Later onset
117
Drug Induced Long QT
```
ABCDE
Antiarrhythmics (Ia, III)
AntiBiotics (macrolides)
Anti-"C"ychotics (haloperidol)
Anti-Depressants (TCAs)
Anti-Emetics (ondansetron)
```
118
Primary HTN TX
- Thiazide diuretics (decrease blood vol)
- ACEi/ARBs (vasodilate, decrease blood vol)
- Dipine CCB (vasodilate)
119
HTN + HF TX
- Diuretics (decrease vol)
- ACEi/ARBs (decrease vol, vasodilate)
- Aldo receptor antagonists (decrease vol)
- B blockers** (decrease HR, ..)
* *careful in decompensated HF
* *NOT in cardiogenic shock
120
HTN + DM Tx
- ACEi/ARB
* protects against diabetic neuropathy
- CCB
- Thiazide diuretics
- B-blockers
121
HTN in preg
- Hydralazine
- Labetalol
- Methyldopa
- Nifedipine
122
Rheumatic Fever
Cause: Pharyngeal: B-hemolytic strep
Can lead to:
-Rheumatic heart dz (Mitral>aortic>>>>tricuspid)
-Aschoff bodies (granuloma w/giant cells)
-Anitschkow cells (large macros w wavy rod like nucs)
-^ASO titers (anti-streptolysin)
Jones Criteria:
-Joint (migratory polyarthritis)
-
123
Pulsus Paradoxus
```
-Decreased systolic BP >10 during inspiration
In:
-Cardiac tamponade
-Asthma
-Obstructive sleep apnea
-pericarditis
-Croup
```
124
GERD vs MI
Both present as angina
- GERD:
- usually w/large meals
- ^es when laying down
- MI:
- respiratory symps
- neg cardiac enzymes
125
Bupivacaine
- local anesthetic
- Amide based
- cardiotoxic:
- arrhythmias
- Hypotension
126
Normal WBC count
4,500-11,000 WBC/uL
127
Normal Platelet Count
150,000-450,000 plats/uL
128
Normal PCWP
PCWP = 4-12 mmHg
* PCWP & CVP (central venous P) correlate with eachother
129
Drugs that cause coronary vasospasm
- Cocaine
- Sumatriptan
- Ergot Alkaloids
130
Drugs that cause cutaneous flushing
VANCE
- Vanco
- Adenosine
- Niacin
- CCB
- Echinocandins
131
Norepinephrine: side effect
```
Reflex Bradycardia:
Stimulate
a1: ^BV contract --> ^BP--> ^ venous return --> ^SV
B1: ^inotrope, ^HR
CO= HR x SV
Can maintain CO by decreasing HR
```
132
alpha 1 receptor actions
- BV contraction
- Pupillary dilator m contraction (mydriasis)
- Intenstinal & bladder sphincter m contraction
133
alpha 2 receptor actions
- Decrease
- sympathetic outflow
- insulin release
- lipolysis
- aqueous humor production
- Increase:
- plat aggregation
134
B1 receptor actions
```
Heart:
Increase:
-HR
-contractility
Kidney: renin release
Increase Lipolysis
```
135
Beta 2 receptor actions
-BV dilation
-bronchodilation
-lipolysis
-insulin release
-ciliary m. relaxation
-aqueous humor production
Decrease:
-Uterine tone (tocolysis)
136
Beta 3 receptor actions
- lipolysis
| - thermogenesis in skeletal m
137
Dopaminergic (D1) receptor actions
-renal BV dilation
138
Dopaminergic (D2) receptor actions
-modulates transmitter release (esp brain)
139
Histamine (H1) receptor actions
- nasal/bronchial mucus production
- BV permeability
- bronchiole contraction
- pruritus
- pain
140
Histamine (H2) receptor actions
-gastric acid secretion
141
Muscarinic (M1) receptor actions
- CNS
| - enteric nervous system
142
Muscarinic (M2) receptor actions
- decrease HR
| - decrease atria contractility
143
Muscarinic (M3) receptor actions
- exocrine gland secretions (lacrimal, seat, salivary, gastric)
- gut peristalsis
- bladder contraction
- bronchoconstriction
- pupillary sphincter m contraction (miosis)
- ciliary m contraction (accomodation)
144
Vasopressin (V1) receptor actions
-BV contraction
145
Vasopressin (V2) receptor actions
-H2O permeability/reabsorption in collecting tubules
| V2 is in the 2 kidneys
