EXAM 4 REVIEW-Old Flashcards
Concentration Gradients Example.
Extracellular Na+ ~142 mEq; intracellular Na+ ~14 mEq
For concentration gradient strong forces
Strong force tends to drive Na+ into cell, down it’s concentration gradient
Transmembrane potential: at rest
At rest inside cell is ~ -90 mV
T/F Strong electrical attraction for Na+ to enter cell
True
Cardiac myocytes have what kind of NA channels
“Fast Na+ Channels”
For cardiac myocytes, when the Na channels are open, important to know that
When activated remain open for only a few thousandths of a second, then close
Inactivated state persists until
membrane is repolarized, providing refractory period
Na channels not active on
Not active on pacemaker cells (SA/AV nodes
• K+ concentration normally greater______ cell due to_________ How many Na in and how many K out?
inside; sodium-potassium pump (3 Na out; 2 K in)
K Inward rectifier channels -
open in resting state allow some K+ to flow out of cell, but overall negative interior charge slows K+ outflow
What happens at equillibrium
At equilibrium, these forces are balanced and there
is zero net movement of K+
• K+ equilibrium potential is ___calculated by____
-91mV; Calculated by Nernst Equation: RT/ZF
For K+, because there is a slight leak of Na+ ions
into cell at rest,
actual resting potential is -90mV
Resting state before depolarization is known as
Phase 4
Phase 4
Rectifier channels leak K+ out
Phase 0
: Fast Na+ channels = rapid Na+ influx
Phase 1
Transient K+ channels open = K+ efflux
Phase 2:
L-type Ca++ channels type Ca++ channels = Ca++ influx
Delayed-rectifier channels = K+ efflux(plateau)
Ryanodine receptors: release Ca++ from S.R.
Phase 3:
Ca++ channels close Delayed-rectifier channels stay open until membrane potential reaches -90mV
“Fibrous Skeleton” of the heart is the
Fibrous connective tissue that surrounds the AV valves
The fibrous skeleton serve as
– Serves as electrical insulator, isolates Atria and Ventricles
What is the only conductor to the ventricles?
– AV node is the only electrical conductor to the Ventricles
What is the purpose of the delay at AV node?
Delay at AV node (0.1sec) allows atria time to contract before ventricles
What serves as an ELECTRICAL GATEKEEPER?
AV Node serves as electrical “gatekeeper” to limit
ventricular stim. during abnormal rapid atrial rhythms
SA node firing rate
60-100
AV node firing rate
40-60
Purkinje Fibers
30-40
Cells of conducting system have different
rates of firing
Normally _____node dominates.
SA
Under abnormal conditions, other pacemakers can
accelerate and overdrive the SA node
What is “Overdrive Suppression?
• Fastest cells preempt all others
Hexaxial (Limb) Leads in what plane?
(look in frontal plane)
Einthoven’s triangle – Leads
I, II, III
Bipolar (+) and (-) poles
I, II, III
Unipolar leads
aVR, aVL, aVF
Precordial Leads looks into what plane?
look in transverse plane)
Precardial leads are
V1 through V6
Lead views I, aVL:
lateral
Lead view II, III, aVF:
inferior
Lead view aVR:
superiomedial
P wave abnormalities: Atrial Enlargement
• Best seen in leads ______
Lead II & V1
RA depol. almost immediately followed by
LA depol. Both superimposed.
Lead II view is _____, which plane?
┴ to axis; Frontal plane
P wave abnormalities Atrial Enlargement
• Lead V1 view which plane?
• Transverse plane
First sign of MI
• STEMI (ST segment elevation myocardial infarction)
Ventricular repolarization very sensitive to
perfusion.
Pathological Q waves develop where ?
Develop in leads overlying infarcted tissue
Permanent evidence of MI
Pathological Q waves
Pathological Q waves occur where?
Occur in groups of leads
Pathologic Q waves do not do this?
Don’t indicate when injury occurred – could be
acute or years ago
Explain pathological Q waves
• Dead infarcted tissue under lead has no electrical
activity, acts as a ‘window’ for lead to see opposite
side of heart depolarizing away from lead
• Causes downward deflecting pathological Q wave
SVT rate
140-250 bpm
Where is SVT initiated?
Initiated by tissue at or above AV node
SVT Symptoms are
lightheaded, dizzy, fatigue, dyspnea
SVT and urine
Polyuria can be assoc’d. w/ SVT 2 to ANP (response to
↑atrial pressure from atrial contraction against closed AV
valve)
Which arrhythmia is associated with polyuria?
SVT
EKG in SVT have
P wave hidden in QRS
SVT management anesthesia
Avoid precipitating factors: ↑sympathetic tone,
electrolyte imbalances, acid-base disturbances
SVT tx If pt. hemodynamically stable, treat with
Vagal maneuvers and verbal reassurance
SVT If vagal ineffective, pharmacologic treatment should
be directed toward (ABC)
Blocking AV node conduction:
Adenosine, Beta-blockers. Calcium channel blockers
What medication is NOT useful with treatment of SVT?
Digoxin not useful 2o to delayed effect
SVT treatment if unresponsive to drugs
Electrical Cardioversion
Most important clinical consequence of AF is
Thromboembolic event causing stroke
Pharmacological conversion of atrial fibrillation
Normally, Pharm. Cardioversion with Class IC or III
Diseases that cause atrial enlargement promote
AFib
Afib causing diseases
HF, HTN, CAD, pulmonary ds., thyrotoxicosis, EtOH
No P wave; chaotic atria; irregular QRS
Afib
Afib If prior to induction
postpone surgery.
If AFIB occurs during anesthesia/surgery, and if hemodynamically significant,
Cardioversion chemically or electrically (syncd. @ 100-200J).
AFIB Ventricular rate control with drugs if vital signs
stable 3 drugs, drugs choice depends on what?
IV amiodarone, diltiazem or verapamil (drug choice depends on co-existing disease).
AF present for >48 hrs. predisposes to ______what do you have to do before cardioversion?
thrombus. Anticoag. for min. 3 wks. prior to electr.
Cardioversion.
Other alternative to anticoagulation for Afib
TEE to evaluate for thrombus, if none found, then electriccardiovert is lower risk)
MAT most commonly seen in
Most commonly seen in pt.s experiencing acute exacerbation of chronic lung disease.
Rhythm that Can also be assoc’d. w/ methylxanthine toxicity, CHF, sepsis, electrolyte abnormalities
MAT
How do you treat Multifocal Atria Tachycardia (MAT)
Usually responds to treatment of underlying pulmonary
decompensation with bronchodilators and supplemental O2.
Variable P wave morphology; irregular rhythm, what rhythm
MAT
PACs arise from
Ectopic foci in atria
Felt as “fluttering” or a “heavy” heartbeat
PACs
Precipitating factor of PACs
excess caffeine, stress, alcohol, nicotine, rec. drugs, hyperthyroidism
Often occur at rest
PACs
PACs on EKG:
Abnormal early P wave
Mobitz Type I Wenckebach
Caused by
intermittent failure of AV conduction
Progressive prolongation of PR until a QRS is dropped
Mobitz Type I Wenckebach
No PR prolongation, Sudden QRS drop
Mobitz Type II
More dangerous Mobitz
Type II
Mobitz Type I
• Typically
• If symptomatic (2 meds)
no treatment is required
IV ATROPINE or ISOPROTERENOL usually improves AV conduction
If Mobitz type I persists
Permanent pacemaker
Mobitz Type II interventions:
Cardiac Pacing (transcutaneous or transvenous)
Pacemaker warranted, even if pt. is asymptomatic, Mobitz
Type II
Causes of Tachycardia (FI 3H, CIA)
Fever Infection Hypoxemia,hypovolemia, hyperthyroidism, CHF Ischemia Anemia
Usually from ↑ sympathetic tone and/or ↓ vagal EKG: normal waves, but rate >100
Sinus tachycardia
Sinus tachycardia rate
100-180 bpm
The most common manifestation of ischemic heart
disease
Angina Pectoris
Angina Pectoris caused by
Caused by imbalance of O2 supply & demand
Three forms of angina
Stable – Variant – Unstable
What type of angina is Relieved by rest (within a few minutes)
Stable
Stable angina on EKG shows
EKG: temporary ST Depressio
What type of angina is precipitated by physical activity / emotional stress
Stable
Transient type of angina
Stable
What type of angina leads to Pain at rest
”
Variant
Variant angina MAIN cause
Caused by spasm, not ↑O2 demand
For Variant angina on EKG:
ST elevation
a.k.a. “Prinzmetal Angina
Variant
Unstable angina pain is
Increased frequency & duration of Pain at Rest
Complications of Unstable angina pain
High risk of progression to MI if untreated
For unstable angina on EKG
ST depression
Evolution of Plaque (8 steps of formation)
- Various stressors cause endothelial dysfunction
- allows entry of lipids into subendothelial space
2&3. Oxidized lipids cause cytokine release from
endothelium = chemoattractant for monocytes - Monocytes take in lipids, become foam cells
- Impaired foam cells produce superoxide anion O2-
and mmp (matrix metalloproteinases) - Smooth muscle cells migrate into intima
- Muscle cells divide and produce matrix, enlarging
plaque - Some muscle cells undergo apoptosis, fibrofatty
lesion forms, lipid core with fibrous fibrous cap
Smooth muscle cells – Synthesize vasoactive inflammatory mediators:
- IL-6
* TNF- α
3 functions of Smooth muscle cells (VIPP)
–Produce extra cellular matrix
–Vasoconstriction/dilation
–Promote leukocyte proliferation
–Induce endothelial expression of LAM (leukocyte adhesion molecule
Complications of Atherosclerosis
Calcification
Rupture/ulceration of plaque
Transmural Hemorrhage
Complications of Atherosclerosis:Calcification
Imparts rigidity,↓ elasticity, ↑ fragility
Complications of Atherosclerosis:Rupture/ulceration of plaque
Leads to thrombus, occlusion, infarct
Complications of Atherosclerosis; Transmural Hemorrhage (FHC)
– From Microvessel growth within plaques
– Hematoma further occludes vessel
– Can cause rupture
Plaque Stability :Inflammatory cytokines stimulate
foam cells to secrete MMP
MMP role
Breaks down collagen & elastin
Weakens fibrous cap predisposing it to rupture
Other complications Complications of Atherosclerosis
Embolization
Aneurysm –>Plaques weaken wall
Angina
MI
Mitral Stenosis (“MS”) • Primarily affects M/F
Females
Almost always rheumatic in origin
Mitral Stenosis (“MS”)
For patients with MS they have hx of
50% of “MS” pts. have pos. Hx. ARF ~ 20 yrs. prior
MS in Elderly pt.s – can be caused by
Calcification of valve
MS congenital?
Congenital (rare)
Pathologic features of MS:
– Fibrous thickening and calcification of valve leaflets
– Fusion of commissures
– Thickening & shortening of chordae tendineae
Normal valve orifice of Mitral
4-6 cm^2
Pathologic valve orifice in Mitral
< 2 cm^2
Mitral Regurgitation Pathology
• Valve fails to close = ↓ SV and C.O.
In MR, there is ____overload can lead to
LA; pulmonary congestion if acute
MR is a structural abnormalities in the
annulus, leaflets, chordae tendineae, papillary muscle
What is MVP?
Billowing of leaflets into LA w/ or w/o regurgitation
What is the most common form of Valvular HD?
MVP
Often asymptomatic; More common in women
MVP
Valve recommended for elderly patients
Biologic
How long does the biologic valve last____advantage (2):
8-10 years; NO AC, no clicks
Valve Recommended for young pts.
Mechanical
How long does the Mechanical valve last____advantage (2):
> 20 years
Anticoagulation needed, Click
↑risk of _____ for all type valve replacements
endocarditis
Fetal Circulation has 3 shunts:
- Ductus venosus
- Foramen ovale
- Ductus arteriosus
BP (bypass) lungs shunt
Foramen Ovale
BP(bypass) liver shunt
Ductus Venosus
Fetal Circulation blood path (UDIRFLA)
Umbilical Vein Ductus Venosus (BP liver) IVC RA Foramen Ovale (BP lungs) LA Aorta
Transitional Circulation:: What maintains PDA?
During fetal life, high levels of PGE-1 maintain PDA
After birth what happens to
PGE 1 levels decline DA constricts closed
Responsiveness to vasoactive substances is
age dependent
With anatomic separation of circulatory paths,
Stroke volume of LV___ and RV ___
↑ ; ↓
ASD Can occur anywhere along atrial septum, most
common
@ Foramen Ovale (failed fusion)
PFO present in __%
~20% of the population
When does the R-to-L shunt occur?
If RA press. ↑ 2o Pulm. HTN or RHF
Termed “paradoxical embolism
PFO with R-to-L shunt can result in systemic embolism
Explain paradoxical embolism
Embolus from systemic vein travels to RA, passes
across PFO to LA into systemic arterial circulation
Tetralogy of Fallot Four anomalies:
- VSD
- Pulmonic Stenosis
- Aorta from both ventricles
- RV Hypertrophy
Tetralogy of Fallot is a ______shunt
Right-to-Left shunt
Aneurysm:
abnormal localized dilation
In aneurysm, what happens to the diameter?
diameter increase of at least 50%
“True aneurysm” =
dilatation of all three wall layers
“True aneurysm” = 2 types
fusiform or saccular
Fusiform –
. –
more common – symmetrical dilation of entire circumference of a segment
Saccular aneurysm –
localized outpouching involving on a portion of the circumference
• Pseudoaneurysm “False aneurysm” =
contained rupture of wall, blood leaks out of vessel through hole in intima and media, but contained by adventitia or perivascular thrombus
Develop at sites of vessel injury:
infection – trauma – puncture of vessel during surgery or percutaneous catheterization – Very unstable, prone to complete rupture
Majority of Aneurysms involve
•
Ascending thoracic aorta 65%
• Descending thoracic aorta 20%
• Aortic arch 10%
• Abdominal aorta 5%
Aortic dissection classified as
Commonly classified as Type A or Type B
Aortic Dissection
Immediate DX necessary with Contrast CT (CTA),
TEE, MRA or Constrast A-gram
Coarctation of the Aorta Symptoms:
– Claudication in lower extremities following exercise
•
• HF if severe
Coarctation of the Aorta: Differential Cyanosis if PDA present
– Upper half of body perfused; lower half cyanotic
Coarctation of the Aorta• If less severe:
Claudication in lower extremities following exercise
If Asymptomatic, coarctation suspected 2o to
• Treatment: Surgical correction
upper extremity HTN later in life
Treatment of Coarctation of the aorta
Surgical Treatment
Virchow’s Triad: Factors that predispose to
Venous thrombosis
Stasis of blood flow
Hypercoagulable states
Vascular damage
Ex. Dental procedures or IVDA
Endocarditis
90% of endocarditis cases are
G(+)
Infected vegetations are source of
continuous bacteremia
Thrombotic or septic emboli –
Infarct target organs (or vasa vasorum causing aortic
aneurysm)
Antigen-Antibody complex deposition –
Glomerulonephritis, arthritis, vasculitis
• Erosion into conduction system –
Manifest as heart block or other new arrhythmias
• Acute Bacterial Endocarditis (ABE)
- Fulminant infection
- Highly virulent AND invasive
- Staph aureus usual causative organism
- May occur on previously healthy valves
Subacute Bacterial Endocarditis (SBE)- LSO
• Less virulent
• Strep viridans usual causative organism
• Often occurs in pts. w/ prior underlying valve
damage
• Staph epidermidis commonly causes
prosthetic valve endocarditis; (rarely on a native valve)
IVDA often involves
right-sided heart valves
Ventricular Hypertrophy and Remodeling
However, hypertrophied wall =
↑ stiffness, causes ↑ diastolic pressures, translated back to atria and pulmonary vasculature.
• Pattern of remodeling depends on whether ventricle subjected to
chronic volume or pressure overload.
Volume overload causes “eccentric hypertrophy”
– Results in synthesis of new sarcomeres in series with the old, causing myocytes to enlongate.
– Chamber radius enlarges in proportion to wall thickness.
• Pressure overload causes “concentric hypertrophy
”
– Results in synthesis of new sarcomeres in parallel with the old, causing myocytes to thicken instead of elongate.
–
Wall thickness increases without proportional chamber dilation = substantially ↓ wall stress.
Pressure overload “concentric hypertrophY”
Effects of ↑ Preload
↑ SV, but constant ESV
Effects of↑ Afterload result in
ESV, SV, EDV, ventricular pressure
↑ Ventricular pressure
↑ ESV
↓ SV
EDV remains constant
Primary glomerulonephritis: 4 conditionw
– Minimal change disease (MCD)
– Focal segmental glomerulosclerosis (FSGS)
– Membranous glomerulonephritis (MGN)
– Membranoproliferative glomerulonephritis (MPGN)
Minimal change disease (MCD
• Most common cause of nephrotic syndrome in children
Focal segmental glomerulosclerosis (FSGS)
Most common cause of nephrotic syndrome in adults
Membranous glomerulonephritis (MGN)
• Antibodies bind to basement membrane
Membranoproliferative glomerulonephritis (MPGN)
• Damage to mesangium
Post-streptococcal glomerulonephritis
• Anti-streptococcal antibodies
– antigen-antibody complexes deposit in glomeruli
– Activate complement MAC = vessel damage
– Increased capillary permeability – leakage of protein and large numbers of erythrocytes
Treatment of post streptococcal glomerulonephritis
• Tx: BP meds, Diuretics, ABX if needed
well-defined rounded deposits of immune
complexes outside capillary walls appear as humps
Post Streptococcal glomerulonephritis
Renal Vein Entrapment Syndrome
a.k.a.
“nutcracker syndrome” due to similarity of
vessel position to a nutcracker:
Renal vein Entrapment syndrome involves
– Aorta
– Superior Mesenteric Artery
– Renal Vein
In renal vein entrapment
Venous hypertension causes rupture of thin-walled
veins into the collecting system with resultant
hematuria.
Four Types of stones: –
Calcium oxalate (70%)
Uric acid (15%)
Struvite (15%)
Cystine (~1%)
• Most common type of stone
Calcium oxalate
Uric acid associated with
High purines
Struvite stone associated with
Infection with ↑ pH
Cystine associated with
Genetic disorder
Uric acid is a by-product of
purine metabolism via xanthine oxidase pathway
Normal uric acid in BLOOD is
2-7 mg/dl (blood);
Normal uric acid in Urine
600 mg/dl
95% people with ↑ uric acid are
asymptomatic
High levels of uric acid due to 2 things
– Decreased excretion (90%)
– Over production (10%)
Necrotic cells produce “muddy brown casts
Acute Tubular Necrosis (ATN)
Most common cause of ARF (AKI)
Acute Tubular Necrosis (ATN)
Classified as Toxic or Ischemic
Acute Tubular Necrosis (ATN)
Tx: ATN
Treat underlying cause
Hydration
Stop offending drug
Drugs/Toxins that cause ATN: CAMASREH
Cisplatin Aminoglycosides Methotrexate – Amphotericin B Statins Radiographic contrast Ethylene glycol Heavy metals
Toxic ATN Involves
PCT only- casts form downstream of necrosis
IgA Nephropathy
• a.k.a.
Berger’s Disease
Most common cause of Nephritic Syndrome worldwide
IgA Nephropathy
• a.k.a. “Berger’s Disease
Genetic predisposition to form Abnormal IgA after a
triggering event (ie. Infx or other allergin)
IgA Nephropathy
• a.k.a. Bergers Pathophysiology
Abnormal IgA binds mesangium of glomerulus activating complement MAC damaging vessel wall
• “Cola” colored hematuria
IgA Nephropathy • a.k.a. Bergers
What is Fibromuscular Dysplasia
• Fibrous or fibromuscular thickening of artery wall
Fibromuscular dysplagia shows alternating
Alternating pattern of stenosis and neurysms causes
“string of beads” appearance:
3 types of Fibromuscular dysplagia
• 3 types:
– Intimal “focal”
– Medial “multi-focal” most common
– Adventitial
Fibromuscular Dysplasia
• Multiple factors contribute to development:
GEMESOM
Genetic Estrogen Mechanical stress Environmental factors Smoking ↓ Oxygen supply Hormone
Goodpasture’s Syndrome
- Autoimmune disorder
* Antibodies attack basement membrane of Kidney and Lung
Causes hemoptysis and hematuria
Goodpasture’s Syndrome
• Causes of Good pasture syndrome
– exposure to organic phosphates – metal dust inhalation – certain gene mutations HLA-DR15 – treatment w/ monoclonal antibodies
Henoch–Schönlein purpura
• a.k.a. “IgA Vasculitis” USUALLY IS
Usually self-limiting
• Common cause of nephritic syndrome in children
Henoch–Schönlein purpura
a.k.a. “IgA Vasculitis”
Malignant Nephrosclerosis
• a.k.a. “
QUICK or slow process
Hypertensive Nephrosclerosis”
Process occurs very quickly
Vessel walls lose elastic fibers, become fragile,
rupture easily
Malignant Nephrosclerosis
In Malignant Nephrosclerosis, you see
- Pinpoint hemorrhages seen throughout kidney
* 2o to malignant HTN• (ex. 180/120 mmHg)
GLOMERULONEPHRITIS
Inflammation of the glomerulus leads to ↑permeability and dysfunction
Nephrotic syndrome:
proteinuria
Nephritic syndrome:
proteinuria and hematuria
GLOMERULONEPHRITIS
Causes include
both infectious and non-infectious processes.
Urine protein normally
60-100 mg/day
Urine protein >______ = Nephrotic Syndrome
3.5 g/day
Nephrotic syndrome is characterized by:
- massive Proteinuria
- HYPOalbuminemia
- Anasarca (Usually begins in the face)
Nephrotic Syndrome
There is Hyperlipidemia why?
– Liver increases lipoprotein production in response to low plasma proteins
Nephrotic Syndrome• Hyponatremia (dilutional)
Occurs with low fractional sodium excretion
Nephrotic Syndrome Thrombophilia
– Due to loss of Antithrombin III in the urine
Nephrotic syndrome other signs
Pitting edema
Pleural effusion
Muehrcke’s nails
Scleroderma Renal Crisis (SRC)
uncontrolled accumulation of collagen and widespread vascular lesions
Scleroderma Renal Crisis (SRC) causes
Causes thickening of the vascular wall and narrowing of lumen
Arteries thickened in SRC
Intimal thickening of the interlobular and arcuate arteries
