Professional Documents
Culture Documents
Pompe's disease
Hemochromatosis
Amyloidosis (Robbins with that Table)
Heart sounds
Antiarrhythmics
Thrombolytics etc
Notes
Friday, 13 February 2015
3:23 pm
1.
a.
b.
c.
2.
3.
4.
Tension-time index
Myocardial tension x time = oxygen demand.
High bp = high tension
Dilated ventricles = increased duration of contraction
Psf (mean systemic filling pressure)
RAP (Right atrial pressure)
5.
a.
b.
a.
b.
c.
6.
d.
e.
7.
a.
b.
c.
d.
8.
9.
10.
a.
b.
11.
Nicotinic acid:
Most effective method for increasing HDL levels
Can precipitate hyperglycemia hence isn't the best thing for diabetics
HOCM:
a.
b.
i.
c.
12.
MVP:
a.
b.
13.
a.
b.
14.
15.
Increased preload opens up the mitral orifice, hence less noise (less murmurs)
Less preload >> MV orifice is closed, hence jetting of blood (increased murmurs)
Anterior leaflet of the MV closes onto the outflow tract
Best heard over left sternal border
More preload >> dilation of the MV ring, hence less midsystolic click
Less preload >> MV is narrower, hence midsystolic click
Standard lead II
ST elevation = infarction
ST depression = ischemia
a.
b.
16.
17.
18.
19.
20.
Giant cell arteritis associated with Polymyalgia rheumatica (normal CK but joint pain
present)
21.
Rubella infection >> PDA
22.
Verapamil displaces Digoxin from plasma proteins and causes an increase in serum
Digoxin.
23.
a.
b.
24.
Raynaud's disease:
Preganglionic sympathectomy to prevent necrosis of fingers
Overdischarge at stellate ganglion or whatever
25.
26.
27.
a.
b.
c.
d.
a.
b.
c.
Acute bacterial endocarditis + IVDA = Staph aureus (right heart valves - tricuspid)
severe fulminant infection
no history of CHD
Very pathogenic organisms infecting valve
28.
29.
30.
31.
a.
b.
c.
d.
a.
b.
32.
33.
a.
34.
a.
b.
c.
d.
e.
35.
Carcinoid syndrome:
Fibrosis of TV and PV:
i.
Tricuspid regurgitation
ii.
PV stenosis
Williams syndrome:
Basically think the opposite of autism (that kid who begs for food in college)
Highly social with strangers
Elvish features + low nose bridge
Chromosome 7 gene deletions
Supravalvular aortic stenosis
Atherosclerosis:
Causes of endothelial cell injury
i.
Small LDL
ii.
Oxidised LDL
iii.
Homocysteine
iv.
HTN, Tobacco
b.
Inflammation:
i.
Triggered by platelets and macrophages
ii.
Cause hyperplasia of smooth muscles
iii.
Smooth muscle cells enter the intima
iv.
LDL / ox LDL >> macrophages and smooth muscle cells >> Foam cells
v.
Smooth muscle + macrophages >> ECM (collagen, elastin,
proteoglycans)
a.
3.
36.
a.
b.
37.
a.
Serum CRP:
a.
Increased when plaques are disrupted
Mycotic aneurysm:
Does not have to be fungal
Vessel wall weakening due to an infection
i.
Fungi - Aspergillus, Candida, Mucor
ii.
Bacteria - Pseudomonas, Bacteriodes fragilis, Salmonella
Brugada syndrome:
Hereditary channelopathy
i.
Loss of function Na channel
38.
a.
a.
b.
Kussmaul sign:
Increased jvp on inspiration
Sign of pericarditis, restrictive cardiomyopathy, tumour in RA/RV
39.
40.
41.
42.
a.
b.
c.
d.
43.
Ankle-brachial index:
Bp ankle / bp arm
Ratio <0.9 = Peripheral artery disease
a.
b.
U World
Thursday, 26 February 2015
1:46 am
1.
2.
i.
ii.
iii.
b.
i.
ii.
3.
Abdominal pain
Chest pain
Difficulty breathing
Rupture may also involve the ascending aorta (not as common)
Hemopericardium
AV disruption
Aorta anterior to and to the right of the pulmonary artery is diagnostic of transposition
of great arteries (It's quite obvious really: Failure of neural crest cell migration
4.
ECG physiology:
a.
Ventricular response in AF depends on the AV node refractory period
i.
Narrow QRS
ii.
Irregularly irregular R-R
b.
Bundle branch conductivity - determines duration of QRS
5.
Catheter placement:
a.
Hand washing ensures central lines are not infected
i.
Staph aureus
ii.
Staph epidermidis (coagulase negative)
b.
Use subclavian
c.
Catheter replacement doesnt really work
d.
Antibiotic prophylaxis doesnt work
6.
Amyloidosis
a.
Localised amyloidosis list of precursor proteins:
i.
Senile cerebral - A beta
ii.
Thyroid - Calcitonin
iii.
Pancreatic islets - Amylin
iv.
Heart - ANP
v.
Pituitary - Prolactin
7.
Acute LVF:
a.
Dyspnea
b.
Tachypnea
c.
CXR findings:
i.
Cardiomegaly; LVH (RVF would show RVH)
ii.
Alveolar edema / batwing
iii.
Kerley B lines
iv.
Blunt costophrenic angles (effusion)
1.
COPD - Flat diaphgragm
d.
3rd heart sound due to increased LV end systolic volumes
8.
Atherosclerosis:
a.
Endothelial injury activates platelets
i.
Release of PDGF, and increased expression of VCAM-1 on endothelium
ii.
PDGF from endothelium + platelets + infiltrating macrophages
(monocytes that emigrate)
1.
2.
iii.
b.
c.
9.
10.
Complications of MI
a.
Day 1 : Cardiogenic shock, arrhythmias
b.
Day 1 - 3 : Pericarditis
i.
Serofibrinous
ii.
Localised: over the necrotic myocardium
iii.
Rx: Aspirin, and short lived
c.
Day 3 - 14 : Ventricular free wall rupture, cardiac tamponade
d.
2 weeks: Dressler's pericarditis
i.
New pericardial, pleural effusions
ii.
Autoimmune, diffuse involvement
iii.
Fever, pleuritis, leukocytosis
iv.
Responds to Aspirin, NSAIDS, Glucocorticoids
11.
Sharp pleuritic pain radiating to neck, worsened with swallowing; relieved by leaning
forward - phrenic nerve involvement (close to the heart, and irritated in pericarditis)
12.
13.
14.
A change in O2 saturation while blood moves into the atria to the ventricles - VSD
a.
75% SpO2 = 45mm Hg O2
b.
96% SpO2 = 96 mm Hg O2
15.
Phenoxybenzamine:
a.
Non selective irreversible alpha 1 and 2 blocker.
b.
16.
17.
18.
HOCM:
a.
Asymmetrical septal hypertrophy + dynamic outflow obstruction
b.
AD with variable expression
i.
Mutation in beta-myosin heavy chains
c.
Can lead to sudden death
d.
Increased blood flow (increased preload) = less murmurs
e.
Decreases blood flow (decreased preload) = more murmurs because of AV
closure
19.
Susceptibility to occlusion:
a.
CNS > Heart > Kidney > Spleen > Liver
20.
Atrial Myxoma:
a.
Constitutional symptoms
b.
Mid diastolic rumbling murmur (apex)
c.
Pedunculated mass
d.
Positional dyspnea
21.
Staph epidermidis
a.
Penicillin and Methicillin resistant
b.
Vancomycin
c.
Biofilm production
22.
i.
ii.
iii.
23.
24.
Ageing
Cachexia
Malnutrition
Collagen types
a.
Dermis, bone, tendons, ligament, cornea, dentin, scar tissue
Type 1
Type 2
Type 3
Basement membrane
Type 4
25.
IV drug abusers infective endocarditis: right valves are affected; otherwise 90% are left
sided
26.
27.
Varicose veins:
a.
Superficial veins involved
i.
Dont commonly embolise to the pulmonary arteries (unlike DVT)
ii.
Main complication is skin ulceration and infection
iii.
iv.
1.
2.
3.
4.
5.
28.
Proximal 2-3 cm of pulmonary veins have cardiac muscle, and function as sphincters
during systole.
29.
30.
Heparins - aPTT
a.
Route of administration - sc / iv
b.
Acute management of venous thrombosis (since warfarin takes a while to start
working)
c.
Acute management in the immediate post operative period
31.
SVC forms behind the first costal cartilage, Descending aorta echo = rotate TEE
posteriorly
32.
Valve findings:
a.
Aortic regurgitation:
i.
Early diastolic crecendo murmur
ii.
Amyl nitrite reduces preload >> Reduces murmur
b.
HOCM - increases while standing (reduced preload)
c.
AS - decreases while standing (reduced preload)
d.
Non splitting murmur (ASD)
e.
Wide S1 splitting - mitral stenosis/bundle branch block
f.
Mitral / tricuspid stenois - diastolic murmur with presystolic accentuation
33.
Anterior uveitis:
a.
HLA-B27 linked diseases
b.
Lyme disease
c.
Syphilis
d.
Herpes virus
34.
35.
36.
37.
38.
39.
Beta blockers decrease mortality in patients with acute coronary syndrome; watch out
for exacerbation of asthma / COPD due to B2 blockade causing bronchoconstriction
a.
Acute increase in TPR (B2 blockade) but thats transient
b.
Contraindicated in asthma / COPD
40.
Renin is inhibited by (B1 receptors on JG cells) B1 selective beta blockers; reduces ATII,
Aldosterone; useful in hypertension
a.
But - plasma renin levels have little to do with antihypertensive efficacy of beta
blockers. Main mechanism of action is negative chronotropic and inotropic effect
b.
Basically YMMV
41.
Glucagon:
a.
Directly acts on Gs proteins on cardiac myocytes
b.
Increases intracellular cAMP
c.
Bypasses beta receptors, hence useful in beta blocker overdose
i.
Reverses the following - bradycardia, hypotension, CVS collapse
44.
45.
46.
47.
48.
49.
Dose calculations:
a.
Maintenance dose = Plasma conc x (CL / bioavailability)
b.
Loading dose = (Plasma conc / Bioavailability) x Vd
c.
Half life = Vd x 0.7/CL
50.
51.
52.
Erythema nodosum:
a.
Violaceous painful subcutaneous nodules appearing on the legs
b.
S. aureus, Coccidiomycoses, Histoplasmosis, Blastomycosis, Chlamydia
c.
Crohns disease
d.
Sarcoidosis
53.
54.
55.
cAMP
cGMP
4 protein subunits
a.
cGMP:
i.
ii.
b.
56.
57.
58.
FA = produce more ATP than glucose, but uses more O2 per ATP than glucose
Holosystolic murmur - atrioventricular valve regurgitations; VSD
a.
Palpable systolic thrill
Crecendo-Decrecendo: Aortic stenosis; Decrecendo ending before S1: Pulmonary
regurgitation
59.
Action potentials:
a.
Purkinje cells + Cardiomyocytes = Phase 0 1 2 3 4 ; 0 - Na current
b.
Conducting fibres = Phase 0 3 4; 0 - Ca current
60.
61.
62.
Kussmaul's signs:
a.
Paradoxical increase in JVP during inspiration
b.
Causes:
i.
Chronic constrictive pericarditis
ii.
Restrictive cardiomyopathy
iii.
Severe RHF
iv.
v.
Tricuspid stenosis
Cardiac tamponade [rare]
63.
Pulsus Paradoxus:
a.
Decrease in sbp by >10 mm Hg during inspiration
b.
Causes:
i.
Pericarditis
1.
CT may show thickening and calcification of the pericardium
2.
Progressive dyspnea, edema, ascites
3.
Also see Kussmaul's sign: paradoxical increase in jvp during
inspiration
4.
Rapid y descent that is steeper and deeper during inspiration
a.
Causes:
i.
TB
ii.
Irradiation
iii.
Previous cardiac surgery
ii.
Cardiac tamponade
1.
Cardiac tamponade - Can lead to bulging of the intraventricular
septum when the ventricular free wall is prevented from expanding.
Inspiration leads to increased RV preload --> septum bulges into LV -->
Decreased LV filling. Hence pulsus paradoxus
2.
Drop in arterial pressure >10mmHg during inspiration
3.
Force is sufficient to cause collapse of atria (diastolic)
iii.
Croup
iv.
Asthma
v.
Obstructive sleep apnea
64.
Pericardial knock - present in constrictive pericarditis; can be confused for opening snap
of MS
65.
Development of the sinus venosus:
a.
Left side i.
Common cardinal vein --> Oblique vein of RA and coronary sinus
ii.
Proximal part of left vitelline vein --> obliterates
1.
Distally - anastomotic vessels formed around the duodenum -->
Portal vein
2.
Hepatic sinusoids
3. Left umbilical vein is left:
a. Proximal part obliterates
b. Distal part carries blood from placenta to liver and ductus venosus
c. After birth:
i.
Ligamentum teres hepatis (umblical vein)
ii.
Ligamentum venosum (ductus venosus)
1. Used for central venous access via the umbilical vein in
neonates
2. Ductus venosus closes in about 1 week (functionally closes in
a few hours after birth though)
2. Right side a. Right common cardinal vein & ACA --> SVC
i.
Anastomosis btw anterior cardinal veins --> brachiocephalic vein
b. Right umbilical vein --> obliterates
3. Right vitelline vein --> IVC
66.
Defect
LV-EDP
Mitral stenosis
Dilated
cardiomyopathy
Restrictive
cardiomyopathy
Cardiac
tamponade
68.
69.
70.
Wedge
Pressure
Aortic stenosis
67.
LV-Systolic Pressure
Angiotensin II - Gq
ADH:
i.
V1 - Gq
ii.
V2 - Gs
71.
i.
ii.
iii.
74.
Atrial fibrillation:
Common in patients with severe aortic stenosis, long standing hypertension,
hyperthyroidism
Excessive alcohol intake 'holiday heart syndrome"
Decreases the preload into the heart
ECG findings:
i.
Absent P waves
ii.
Varying R-R intervals; irregularly irregular rhythm
iii.
Narrow QRS
iv.
F waves (squiggles)
i.
ii.
c.
d.
e.
75.
76.
a.
b.
c.
d.
77.
78.
a.
b.
i.
ii.
iii.
c.
d.
i.
ii.
79.
a.
80.
81.
1.
Oxidative deamination of Tropocollagen
2.
Fucks up collagen and elastin
3.
Can be inhibited by beta aminopropionitrile
Associated with:
Large dose of baclofen
Marfans disease
Beta aminoproionitirle - Angiolathyrism
1.
Mimics marfans disease
Aortic dissections and aortic valve incompetence
Mitral valve prolapse (mid systolic click)
Increase in preload --> Moves it closer to S2
Decrease in preload --> Moves it closer to S1
82.
83.
a.
2. Increase in TPR - reduces the slope of both Venous return and CO curves
a. Veins - decreases the amount of arterial blood entering veins; venous return
decreases
b. Arteries - increases afterload, which decreases SV = Decreased CO.
3. Arteriovenous fistula
a. Acute - only decrease in TPR (since arterioles are bypassed)
b. Chronic
i.
Decreased TPR
ii.
Increased CO (due to sympathetic overdrive and renal fluid retention?)
3.
Increased Psf and Venous return
84.
a.
AV fistula:
Congenital
b.
1.
2.
c.
85.
Antiarrhythmics:
Sodium channel blockade effect:
1.
Ic > Ia > Ib
b.
Class Ia
1.
Moderate Na channel blockade effect
2.
Extend the AP duration
c.
Class Ib
1.
Very weak Na blockade
1.
More selective for ischemia induced ventricular arrhythmias
2.
Associate and dissociate rapidly from Na channels
3.
Reduces AP
d.
Class Ic
1.
Most potent effect
2.
Strongest Na channel blockade
1.
Can promote arrhythmias; speed on conduction slowed more
than the ERP
3.
Slowest dissociation from the channels
iv.
AP duration stays same
a.
86.
88.
Temporal arteritis
a.
Granulomatous (tunica media) + fragmentation of internal elastic lamina
b.
Segmental involvement
i.
Biopsy may not always show inflammation
c.
Patients older than 50
d.
e.
i.
ii.
f.
i.
ii.
g.
i.
h.
i.
ii.
iii.
i.
i.
j.
89.
a.
b.
c.
d.
e.
90.
Takayasu arteritis
Medial granuloma formation, affects the arch of the aorta
Younger age group than Giant cell arteritis
i.
Females < 40 (vs Giant cell arteritis > 60)
May also affect major branches
i.
Coronaries
ii.
Renal arteries
Reduced pulses in the upper extremities (pulseless disease)
Cold / numb fingers
Infective endocarditis:
Doesnt usually affect the aortic valve because of the relatively higher blood
flow
b.
Janeway lesions
i.
Macular
ii.
Painless microemboli (from cardiac valve vegetations) to the palms and
soles
iii.
Subcutaneous hemorrhage
iv.
Bacteria, neutrophils, necrotic tissue
c.
Osler nodes
i.
Painful papulopustules in the pulp of fingers and toes
a.
91.
a.
b.
c.
92.
Internal thoracic artery and veins are between the trasversus thoracis and internal
intercostal muscle.
93.
Pulmonary trunk may be pierced by penetrating injury to 2nd intercostal space at left
sternal border
94.
95.
a.
b.
c.
d.
96.
IVC injury --> Stab to the back, just to the right of the vertebral bodies
Restrictive cardiomyopathy:
Sarcoidosis
Amyloidosis
Radiation damage
Hemochromatosis
97.
a.
b.
c.
98.
Right ventricular overload will lead to widening of S2 split (increased ejection time)
99.
100.
Fibrinolytics are also used for pulmonary embolism, and arterial thrombosis
c.
d.
Dicrotic pulse: Two peaks in the pulse (systole + diastole); extremely low systolic output
114. Hyperkinetic pulse: rapid ejection of a large stroke volume against decreased afterload
[figure this out later?]
a.
PDA
b.
AV fistula (dialysis one)
115. Statins for CVS risk
a.
In patients with a normal HDL profile, use of statins to lower LDL is indicated for
preventing cardiovascular events
i.
Raising HDL doesnt improve CVS outcomes; Niacin is therefore useless
ii.
LDL reduced by 20-25%; increased clearance by increased LDL receptor
expression
1.
Hence decreases circulating Apo B100 (its present on LDL and
VLDL)
2. Indicated for secondary prevention in all patients of atherosclerotic cardiovascular
disease regardless of baseline lipid levels
3. Omega 3 fatty acids - slightly increases HDL, and slightly decreases TG; does nothing
for CVS side effects
116. Group IB antiarrhythmics - most selective to ischemic myocardial tissue
a.
Because ischemic tissue:
i.
Depolarised / rapidly depolarising
b.
Lidocaine
c.
Used to treat post MI Ventricular arrhythmias (DOC is amiodarone)
117.
125.
Cardiac output/Blood flow for left and right heart = same (both rest and exercise)
126.
Pericytes around capillaries regulate the blood flow into that vascular bed
ii.
iii.
b.
i.
c.
i.
ii.
d.
i.
ii.
e.
i.
ii.
b.
Atrial relaxation
b.
Deep in pericarditis
Meckels cartilage
Maxillary artery
Second
Reicherts cartilage
Third
Fourth
Fifth
Sixth
142.
143. Popliteal artery is more likely to be damaged than the tibial nerve or whatever in a
posterior tibial displacement or any other traction force.
a.
The artery is deep in the popliteal fossa
b.
The artery is tightly fixed proximal and distal to the popliteal fossa by: adductor
magnus and the soleus muscles.
c.
Tibial nerve - doesnt pass through the adductor magnus (vs artery)
Third
(S3)
Ventricular gallop;
after S2
Rapid filling of
ventricles
Normal
Abnormal
Kids
Young adults
Pregnancy
Age > 40
Heart failure (Dilated)
High output (anemias)
Restrictive cardiomyopathy
Fourth
(S4)
Concentric ventricular
hypertrophy (long standing
hypertension)
Acute MI
Reduced ventricular
compliance:
- Aortic stenosis
- Hypertensive heart disease
- HOCM
153.
Carvedilol (beta blocker, with alpha blocker) - Improves all cause mortality in CHF
161. Pulmonary artery hypertension leads to RHF, (elevated RH pressures) which can lead to
coronary sinus dilation. Coronary sinus dilation is not a normal finding, and is dilated by any
factor that causes atrial dilation
162.
163. Amiodarone:
a.
Class III antiarrhythmic
b.
Prolongs QT; but has a much lower likelihood of causing Torsades de pointes
i.
Less QT dispersion, whatever the hell that means
c.
Drug of choice for post MI Ventricular fibrillation
d.
Toxicity:
i.
Blue gray discoloration of skin
ii.
Photosensitivity
iii.
Pulmonary fibrosis
iv.
Thyroid dysfunction
164. Procainamide - increased risk of torsades (QT prolongation; IA)
a.
283pg FA for more
165. Infective endocarditis:
a.
Valvular scarring and damage is a risk factor for infective endocarditis
b.
Fibrin and platelet deposition at site of bacterial colonization --> vegetations
166. Cocaine
a.
Reuptake inhibitor
i.
Hypertension
ii.
Tachycardia
iii.
Mydriasis
iv.
CNS activation
b.
Vasoconstrictor
i.
MI, Coronary artery vasospasm
ii.
Intranasal use --> Mucosal atrophy, nasal septal perforation
167. Heart blocks
a.
Complete 3rd degree heart block:
i.
SA node --> Atria
ii.
AV node --> Fires the ventricles; QRS is narrow
b.
The P wave and QRS waves are totally out of sync
c.
QRS will be prolonged and wide when:
i.
Impulses are generated below the AV node
ii.
Purkinje system, ventricles etc
d.
Mobitz type II and 3rd degree heart blocks may be the result of transmural
septal ischemia
168. Causes of PDA
a.
Prematurity
b.
Patent ductus arteriosis
c.
Congenital rubella
d.
169.
170.
171. RCA - gives off the posterior descending artery in 90% of the population; 10% LCX
a.
Right dominant circulation
b.
AVF, II, III - ST elevations + Sinus node dysfunction (bradycardia) = RCA
thrombosis
i.
Rx Bradycardia:
1.
Atropine (inhibits Vagal influence)
a.
Toxicities - Can precipitate acute angle glaucoma in pts
with shallow anterior chambers
172. Anticholinergic drugs - reduce pain & prevents adhesions of iridocyclitis (uveitis)
173. Coronaries:
a.
LCX - runs between the left atrium and ventricle (AV groove, kinda close to the
rear of the heart)
b.
LAD - runs in the anterior interventricular groove
c.
Remember the heart apex is tilted
174. Capillary hemangioma (juvenile strawberry hemangioma)
a.
Very common benign congenital vascular tumour
b.
Thin walled loose aggregate of capillaries
c.
May be multiple;
i.
Skin, subcutaneous tissue, oral mucous membranes, lips
ii.
Compressible plaques; dusky if deeper
iii.
Initially increase in size, then regress
d.
Most begin to fade by 1-3 years of age and then fade completely by age 7
175. Cherry hemangioma
a.
Benign vascular proliferation in adults; present in the papillary dermis
b.
Dont regress
176. Thromboangiitis obliterans (Buerger's disease)
a.
Heavy smokers, young age of onset
b.
Nicotine antigens, smoke antigens whatever
177. Urokinase
a.
Treatment for myocardial infarction and pulmonary embolism
b.
Plasminogen --> Plasmin; Plasmin degrades Fibrin into its degradation products
178. Concentric hypertrophy of LV:
a.
Increased afterload
b.
Chronic hypertensive heart disease
c.
Aortic stenosis
d.
High voltage ECG
179. Restrictive cardiomyopathy --> mcc of death is CHF that develops due to it
a.
Decreased ventricular compliance (dV/dP)
180. Eccentric hypertrophy of LV in Mitral regurgitation
a.
Because increased regurgitant flow during systole = amount of blood returning
to the LV during diastole
b.
Volume overload
181. Hypertrophic cardiomyopathy - important cause of VF in individuals <30 and mcc of
sudden cardiac death in young athletes.
a.
Massive cardiac hypertrophy
b.
Septal involvement
c.
Normal coronaries
182.
183. Alpha 1 selective agonists - Dont cause much reflex tachycardia (wha?)
184. Adult type aortic coarctation:
a.
Post-ductal coarctation
b.
Hypertension in head + upper extremities
i.
LVF
ii.
Berry aneurysms - rupture due to htn
iii.
Aortic aneurysms
c.
Hypoperfusion in lower extremities
i.
Low exercise tolerance / muscle weakness
d.
Large palpable intercostal vessels
i.
Sign of development of collateral circulation
ii.
Notching of ribs
185. Sydenham chorea
a.
Restlessness and purposeless movements; 3 mo post sore throat
b.
Mcc acquired chorea in childhood
i.
Autoimmune reaction involving anti-streptococcal antibodies to basal
ganglia
c.
Hyperkinetic defect
186. Maintaining cardiac output in aortic regurgitation
a.
Increased EDV due to regurgitant blood - Increases Preload
i.
Heart rate increases transiently, then comes back to normal as heart
adapts to volume overload
ii.
Increased ventricular stroke volume
b.
Afterload is already high; medical stabilization of acute AR might need to be
reduced with vasodilators + inotrope (to ensure CO is maintained)
i.
Vasodilation - Decreases afterload; hence improves stroke volume
c.
Eccentric hypertrophy
187. Place filter in the IVC in patients with DVT treatment complications (GIT bleeds)
a.
Renal veins join IVC at L1/L2
b.
ii.
d.
i.
ii.
iii.
iv.
v.
vi.
vii.
ii.
Decreases hypertension
6. Nicardipine
a. Causes some tachycardia
b. Longer half life than other drugs
200. Orthopnea
a.
Supine dyspnea that is relieved by sitting up; specific sign of LHF
b.
LHF progresses to:
i.
Pulmonary interstitial edema, widening of alveolar septa
ii.
Intra alveolar accumulation
201. Cardiac asthma - exercise induced wheezing in LHF. Exercise = increased venous return
to the heart, but failing heart cant increase CO appropriately. Hence pulmonary pressures
rise.
a.
Not a specific sign
b.
Seen in COPD and Asthma
202. Aortic stenosis
a.
Congenital bicuspid valve --> calcification in 50s [you may get endocarditis, but
thats rare]
b.
Calcification of normal valve
i.
Occurs at a greater age > 65
c.
Rheumatic heart disease
203.
204.
205.
206. Isoproterenol - b2 agonism can cause increased blood flow in skeletal muscles, renal and
mesenteric vascular beds. Not useful for increasing perfusion in the skin though.
207.
208. Adjust dose of Digoxin in the elderly, since renal function decreases with age and can
lead to digoxin toxicity.
a.
Only a 1/3 of the drug is actually protein bound (so protein binding isn't really a
big deal)
b.
Not accompanied by increase in creatinine; since muscle mass also falls with age
c.
Muscle mass - lean body weight (important for dosing calculations of digoxin;
just not as important as renal function)
d.
Symptoms:
i.
Changes in colour vision [neurological sign]
ii.
Fatigue and weakness [hyperkalemia]
iii.
Delirium
iv.
Diarrhoea, nausea, vomiting
v.
Arrhythmias
209.
210. Isoproterenol - increases cardiac contractility (b1) and decreases peripheral venous
resistance (b2) at low doses; [understand the axes of the graph and then figure out if effect
increasing or decreasing with x]
211. Labetalol (alpha + beta blocker)
a.
Vasoconstriction (increased PVR)
b.
Decrease in contractility (b1 blockade)
212. Intermittent claudication (muscle pain with exercise that remits with rest)
a.
Result of atherosclerosis of large arteries, fixed stenotic atheromatous plaques
that bulge into the arterial lumen
i.
Blood flow to muscle cant increase during exercise
b.
Pain relieved by resting; exacerbated by minimal exercise (ischemic muscle pain)
c.
Thigh claudication:
i.
Ipsilateral external iliac artery or common femoral artery
ii.
Common femoral and profunda femoris artery
213. Isolated systolic hypertension
a.
Common form of hypertension in the elderly
b.
First line in non-diabetics and non CHF patients
i.
Thiazide diuretics
ii.
DHP Calcium channel blockers
c.
In diabetics - Use ACE inhibitors; anti proteinuric effect.
i.
ACE inhibitors dont cause pedal edema, it may however cause
angioedema and hyperkalemia
ii.
ACE inhibitors are useful in CHF as it inhibits the AT-II mediated
myocardial hypertrophy and remodeling.
214.
e.
Right sided S3 and S4 develops as LHF progresses to cause RHF. Very severe
state.
i.
Left sided S3 and S4 doesnt happen because there is impaired left
ventricular filling because of MS.
LDL receptors functions by receptor mediated endocytosis; (clathrin pits yada yada)
Accentuated P2 - Pulmonary hypertension; Accentuated S2 - Systemic hypertension
234. Muscarinic receptors are present on the endothelium; on stimulation trigger the release
of NO (EDRF) --> Smooth muscle relaxation.
235. Cholinergic action on the heart:
a.
M2 muscarinic receptors
b.
Decreases contractility and conduction velocity
i.
More in atria than ventricles (since ventricles are more richly supplied
with adrenergic receptors)
236. Milrinone - increases cardiac contractility by preventing the degradation of cAMP within
the myocytes [PDE-3 inhibitor]
a.
Increased cAMP --> Calcium conductance increases
237. Wolf-Parkinson-White syndrome (WPW)
a.
Causes sudden cardiac death
b.
Accessory AV impulse conduction pathways anatomically distinct from the AV
node
238.
239. ACE inhibitor therapy - causes characteristic dry cough [you know why]
a.
ARBs dont inhibit bradykinin degradation, hence dont cause dry coughs
240. Atherosclerosis, neointimal hyperplasia, aneurysmal disease - shear stresses induced by
turbulent blood flow has something to do with these.
241. Fatty streaks are present in kids, may not always progress to atherosclerosis. But they
will be made of foam cells.
242. DCM causes
a.
Idiopathic
b.
Cardiotoxic substances (alcohol)
c.
Peripartum state
d.
Viral myocarditis
i.
Lots of inflammatory interstitial infiltrate
e.
Mitochondrial / cytoskeletal defects
243. Aortic regurgitation
a.
Large pulse pressure (high systolic, low diastolic)
i.
Waterhammer pulse
b.
Head bobbing with carotid pulsations (de Musset); transfer of momentum from
the large LVSV
c.
Intensity of murmur is highest when the pressure gradient between the aorta
and LV is maximum; (ie as soon as the aortic valve is supposed to close)
i.
High pitched blowing decrescendo murmur
ii.
Holodiastolic [best heard with the patient leaning forward @ left sternal
border]
Decrease LDL
Fibrates
Decrease TG
Niacin
Increase HDL
256. Cyanotic toe discoloration + renal failure after invasive vascular procedure
a.
Atheroembolic disease of renal arteries
b.
Cholesterol debris gets pushed from larger arteries into the smaller ones -->
Ischemia of the organs and tissues.
c.
Other sites:
i.
Livedo reticularis
ii.
Cholesterol emboli on retinal examination
iii.
Skin infarcts
257. Hibernating myocardium
a.
Repetitive ischemia, or persistent hypoperfusion
b.
Metabolism is reduced, but sufficient ATP is present to prevent contracture
i.
Increased TNF and NOS (inhibitors of contraction)
c.
REVERSED BY:
i.
Revascularization with CABG or a balloon angioplasty
ii.
Basically this is the opposite of reperfusion injury (heart recovers in
hibernation, after revascularisation)
258. Ischemic preconditioning - development of resistance to infarctions due to prior
repetitive non-lethal ischemia.
259. Ventricular remodeling - chronic change in mass, volume, shape & myocyte composition
of the heart. Usually adjacent to the ischemic dysfunctional myocardium.
260. DVT risk is high in patients who are undergoing hip/knee replacements and are nonambulatory:
a.
261.
262.
263. Ivabradine - slows heart rate by blocking sodium channels from the cytoplasmic side,
prolongs the Na+ funny current.
a.
No effect on contractility
b.
Decreases heart rate
c.
Rx for HF with reduced ejection fraction
264. Coronary sinus blood - most deoxygenated blood in the body. Myocardial oxygen
extraction (75 - 90%) is the highest in the body.
a.
Mixes with slightly less deoxy blood from the rest of the body at the RA before
entering the PA.
265. Pacemaker wires (3 leads): Enter the SVC
a.
RA
b.
RV
c.
RA --> Coronary sinus --> lateral venous tributaries (for pacing the LV)
266.
267.
268.
269.
Infective endocarditis
Diagnosis by Dukes criteria:
1.
2 major clinical criteria
2.
1 major + 3 minor
3.
5 minor
Immunological complications:
Glomerulonephritis
Janeway lesions (non tender lesions on palms and soles; septic embolism)
b.
Small vegetations (1-2mm)
c.
Fibrinoid necrosis along closure lines of cusps
d.
Subendocardial lesions (McCallum plaques); Left atrium
# Erythema marginatum:
the presence of pink rings on the trunk and inner surfaces of the limbs which come and go for as long as several months. It is
found primarily on extensor surfaces.
Aortic Stenosis
Leads to acquired Von- Willebrand's disease and Factor VIII:c depletion.