Cardio - General Flashcards
mitral valve prolapse =
Associated w/
mid systolic click
Marfan’s Syndrome
Cardiac output formula
CO=CVxHR
Total peripheral resistance formula
(MAP - R. Arterial pressure ~0)/CO
Resistance formula
R= ∆P/Q
or ∆P=QR
Resistance in series
R total = sum of Rs
Resistance in parallel
1/R total = sum of 1/R
1st line CHF Rx
ACE inhibitor - prevent cardiac remodeling
-Also beta blockers and ARBs
Loop diuretics is symptom management and HF
CO=
flicks equation
oxygen consumption/( arterial O2 content - venous O2 content)
watch units!!
what divides the R and L embryological atrium? (2)
septum primum -> osteum/foramen secundum
Septum secundom -> foramen ovale
How is blood shunted from the R to L atrium in embryo
foramen ovale (in septum secundum ) and osteum secundum (in the septum primum)
3 possible causes of atrial septal defect?
Common genetic abnormality associated>
osteum secundum overlaps foramen secundum
Absence of septum secundum
neither septum secundum nor septum primum develop
Downs syndrome
6 different aorticopulmonary septal(spiral septal) defects
embryological determination
tetralogy of fallout
persisitant truncus aretiosus
transposition of the great vessels
Dextrocardia
VSD
fenestrae
Neural crest derived
Ascending aorta and pulmonary trunk derived from?
Truncus arteriosus
Smooth outflow parts of L and R ventricles derived from
Bulbus cordis
trabeculated L and R ventricle derived from
Primitive ventricle
Trabeculated L and R atrium derived from
Primitive atrium
Coronary sinus derived from
L horn of sinus venosus
Smooth part of R atrium derived from
R horn of sinus venosus
Superior vena cava derived from
R common cardinal vein and R anterior Cardinal vein
1st aortic arch ->
maxillary artery (branch of the external carotid)
2nd aortic arch ->
stapedial artery and hyloid artery
3rd aortic arch ->
Common carotid
AND proximal part of internal carotid
L 4th aortic arch ->
aortic arch
R 4th aortic arch ->
right subclavian artery
6th aortic arch ->
proximal part of pulmonary arteries and ductus arterioles
ductus venosus shunt
shunts blood from the umbilical vein into the IVC (bypassing hepatic circulation)
foramen ovale shunt
shunts blood from the R atrium to the L
Ductus arteriosus shunt
shunts blood from the the pulmonary arteries to the descending aorta
What is the most oxygenated vessel in the developing fetus?
umbilical veins
What closes the foramen ovale
increased L Atria pressure due to decreased pulmonary vasculature and increased flow through the pulmonary system
What closes the ductus arteriosus
What can be given to close?
breathing -> increased O2 -> decreased prostaglandin E2
Indomethacin
What to give to keep ductus arteriosus open?
PGE1 or 2
KEEEEPs open
most common congenital anomaly
presents as?
VSD
Exercise intollerance
Most common cause of early cyanosis
Tetralogy of Fallot
L to R shunts (3)
seen as?
VSD - holosystolic mumor
ASD ( loud S1 and Fixed spit S2)
PDA - machine murmor
late cyanosis (blue kids
R -> Shunts (5)
seen as?
Persistent Truncus Arteriosus Transposition of the great vessels Tricsupid atresia Tetralogy of Fallot Total anomalous pulmonary venous return
Tricuspid atresia is fatal unless
Persistant ASD and VSD to allow mixing of blood (outflow to the pulmonary circuit is impaired)
Persistent truncus arteriosus pathology
neural crest cells of aorticopulmonary septum fail to divide aorta and pumpnary trunk -> one heart
Total anomalous pulmonary venous return pathology
the pulmonary vein does not return oxygenated blood to the L Atrium but instead back to the R circuit -> closed loop
Eisenmenger syndrome steps (4)
1 - L to R shunt
2. Leads to pulmonary hypertension w/ overuse of pulmonary vasculature
3- leads to hypertrophy of vasculature and resistance
4. Resistance builds and L -> R shunt becomes a R to L shunt (Cyanotic)
4 defects in the tetralogy of fallout
leads to
- Pulmonary valve stenosis
- R ventricular hypertrophy
- VSD
- Over riding aorta over the VSD
Leads to periods of R to L Shunting and cyanosis (get spells)
Crouch down to increase Systemic press to have L to R shunt again
Boot shaped heart think?
Tetralogy of Fallot in infants
R ventricle hypertrophy in adults
Infantile coarctation of the heart concerns and location?
the stenosis is PROXIMAL to the ductous arteriosus leading to the PDA being the only way of blood getting to the lower limbs
Adult coarctation of the heart location
stenosis DISTAL to the ductous arteriosus leading to increased pressure above the stenosis and notching of the ribs
Ebstein animal caused by?
Presents as (3)
Lithium use in mothers
Descent of tricuspid valves into the R ventricle. often have patent foramen oval.
See wide S2 split and tricuspid regurgitation
Congenital heart defects w/ digeorge’s syndrome(2)
truncus arteriosus
Tetralogy of Fallot
Down syndrome congenital heart defects?
ASD, VSD or AV septal defect
Congenital Rubella heart defect?
PDA
Pulmonary arterial stenosis as well
Turner syndrome heart defect (2)
Coarctation of the aorta Bicuspid valve (aorta)
Marfans congenital heart concerns
Aortic regurgitation -> dissection
Infantile diabetic mother concerns (2)
Big baby and associated delivery complications
Transpositions of great vessels
MAP =? (2 formulas)
2/3 diastolic pressure + 1/3 systolic pressure
CO x TPR
~P= QR
SV =
CO/HR
EDV - ESV
Why does CO decrease in ventricular tachycardia?
The diastolic filling is incomplete - too fast of HR
Pulse Pressure=
systolic - diastolic BP
Stoke volume is affected by (3)
COntractility
Preload
afterload
Role of Verapamil and contractility?
nondihydropyridine Ca2 channel blocker that lowers Ca intracellularly and contractility
Diltiazem also
Preload is the same as?(3)
Atrial pressure
end diastolic pressure
central venous pressure
hydralazine
decreases afterload w/ arterial dialation
nitrates
decrease preload w/ venous dialation
Ejection fraction =
Normally?
Stroke volume / End Diastolic Volume
> 55%
Viscosity of blood may increase in (3)
leads to?
polycythemia
hyperproteinemic states - multiple myeloma
hereditary spherocytosis
leads to increased resistance
X intercept of cardia venous function curve =
mean systemic filling pressure
normal L Atrial pressure
<12mmHg
Pulmonary wedge pressure measures?
L Atrial pressure
~ diastolic pressure of LV
BNP is released when from where?
Causes what?(2)
released from myocytes when they are stretched (like in CHF)
Leads to
vasodilatation
increased excretion of Na and water
Right sided heart signs (3)
Hepatomegaly (nutmeg liver
peripheral edema
JVD
Left sided Heart failure (5)
Pulmonary edema - with hemosiderin laden macrophage -> crackles and rales
- paroxysmal nocturnal dyspnea
- Othopnea
- DOE -dypnea on exertion
- Cardiac dilation
Renin secretion stimulated by what 3 mechanisms
sympathetic nervous system ( Beta 1 receptors -> CHF and compensation)
macula densa - senses low Na in glomerular filtrate
JG Apparatus - senses low BP
Leads to AT II
- > (vasoconstriction
- > Aldosterone secretion
Chronic CHF Rx (7)
First 4 improve surival and minimize heart remodeling
- ACE inhibitors
- ARBs
- Aldosterone inhibitors - spironolactone, eplereonone,
- beta blockers (metoprolol, carvediol, brisprolol)
Digoxin
Diuretics (loops and thalazides)
Vasodilators (Nitrate and Hydralazine)
Rx for Acute decompensated CHF
NO LIP
Nitrates Oxygen Loop Diuretics Inonotropics (stop beta, give dobutamine or phosphodiesterase) Position - upright
Blurry yellow vision, confusion, bradycardia, N/V and EKG changes?
Think of of Digoxin toxicity
Digoxin decreases conduction through the AV node
3 factors predisposing to Digoxin toxicity?
Renal failure - decreased excretion
Hypokalemia -
Quinidine - displaces digoxin from binding sites
Rx for Digoxin toxicity (3)
normalize the [K]
Mg
anti-digoxin FAB
–Atropine or pacemaker if not available
Examples of increased capillary pressure
leads to ?
heart failure, CHF, Thrombosis, tumor clothing, cast, Na/H2O retention
Edema
decreased plasma proteins examples
leads to ?
nephrotic syndrome, liver failure, protein malnutrition, protein losing enteropathy
edema
Uncreased capillary permeability pathological causes (3)
permeability also known as
burns, sepsis and extotoxins
Kf
increased interstitial fluid colloid osmotic pressure due to ?
Leads to?
blocked lymphatics
nonpitting edema, leaked proteins have no where to go, water mixes leading to a jello like mass
net filtration pressure formula
Pnet = (Pc-Pi) - (Pi c - Pi i)
low cardiac output and increased systemic vascular resistance indicative of what?(2)
Shock
Hypovolumetric or cardiogenic
Rx for Cardiogenic shock
Dobutamine and other ionotropics
Sepsis is characterized by what presentation?(3)
Systemic vascular resistance?
CO?
Rx? (3)
Presents w/ fever and warm to the touch skin
May be lactic acidotic due to low O2 and anaerobic metabolization
DIC
high output shock w/ 1st vasodiation (leak capillaries) -> increased CO (Tachy)
Rx- Abx, NE (pressor) and fluids
Neurogenic shock
CO?
Systemic vascular resistance
Rx?
Decreased systemic vascular resistance and CO w/out sympathetic inveration
IV fluids, steroids maybe
Cold and clammy wet skin w/ bradycardia think of? (2)
Hypovolumetric Shock
Cardiogenic Shock
Causes of hypovolumetric shock? (2)
burns
blood loss - trauma
Causes of cardiogenic shock? (7)
MI PE CHF Arrythmia Cardiac tamponode tension pneumo Cardiac contusion
femoral triangle?
Which are in the sheath?
NAVEL
Nerve Artery* Vein* Empty Lymph
Locations of central Lines (3)
How long ?
Complications?
Femoral
- 5-7 days
- can’t really move
Subclavian
- 3-4 weeks
- risk of pnemo
- bad for COPD and lung tumors
Internal jugular
- 3-4 weeks
- may punch the carotid
Swan Ganz usual done through which central line
Right Internal jug
> left Sub clavian (easy loop)
>right sub clavian (hard angle to drop down)
increase of preload has what effect on SV?
Increased SV
NO change in pressures really seen
Increase in Afterload -> what change in SV and ESV
SV decreases while ESV increases
Heart is working harder to meet increased aortic pressure, can’t contract as much
increase in contractility has what change on SV and ESV
Increase in SV and decerease in ESV. more contraction and excretion of the blood
NO real change in pressures so aortic valve still opens fairly normal
Isometric contraction contraction takes place when?
QRS complex occurs and ventricles are contracting increasing pressure, rich before aortic valve opens
S3 is associated with what pathology(4)
Heard when?
Dialated cardiomyopathy CHF Mitral regurgitation L-> R shunt sloshing ing
Heard right after S2 and the heart starts to fill in diastole
S4 is associated w/ what pathology (4)
Heard when
hypertrophic cardiomyopathy
aortic stenosis
chronic hypertension w/ Left ventricular hypertophy
Post MI
A stiff heart
Heard Right before S1 due to initial filling of the heart against a stiff heart wall followed by AV valve closure
a wave
c wave
v wave
Seen in JVD
a- r atrial contraction
c- r. ventricular contraction and bowing in of tricuspid
v- atrial filling against tricuspid valve
Normal splitting is due to?
Hear what?
drop in aortic pressure -> increase venous return and preload in the R ventricle -> delay in pulmonary valve closure vs aortic valve
heard on inspiration
wide splitting due to?
Pathology associated
Due to delay in R ventricle contraction w/ increase fluids and pulmonic valve closes after aortic
Varies with inspiration
pulmonary stenosis or R bundle branch block
Fixed splitting due to ?
Pathology associated?
due to fixed increased blood volume in the R ventricle from a L -> R shunt that is persistent. Increased volume compared to L ventricle delays closure of pulmonic valve vs tricuspid valve
Does not vary w/ inspiration
Atrial septal defect
Paradoxical Splitting
Pathology associated?
Due to L ventricular overfilling and delay in closure of aortic valve compared to pulmonic valve - always pathological,
Aortic stenosis or L Bundle branch block
Benign heart sounds if no pathology(4)
Split S1
Split s2 on inspiration
S3 in a patient <40
Early quiet systolic murmur
Bounding pulses, head bobbing, diastolic murmur
Aortic regurgitation
Hear immediate decrescendo
Diastolic murmurs
Mitral stenosis
Tricuspid stenosis
Aortic regurgitation
Pulmonic Regurgitation
Systolic murmurs
Aortic stenosis
Pulmonic stenosis
tricuspid regurgitation
mitral regurgitation
Inspiration has what effect on heart sounds
louder tricuspid of R heart murmurs
Expiration has what effect on heart sounds
louder mitral of L heart murmurs
Hand grip has what effect of heart sounds
Increased SVR -> increased after load
makes mitral regurgitation louder
Valsava maneuver has what effect on heart sounds
increased intrathoracic pressure -> decreased preload and after load
Quieter murmurs EXCEPT - hypertrophic cardiomyopathy
L side of the sternum diastolic murmur with wide pulse pressure -
aortic regurgitation
Causes of aortic regurgitation (4)
aortic root dilation -> syphilis ->marfans Bicuspid aortic valves - usually stenosis rheumatic fever
Opening snap heard over the apex of the heart in diastole
Can lead to
mitral regurgitation
-enhanced w/ expiration
Left atrial dilation
Cause of mitral stenosis
rheumatic fever
Heart Sounds best heard in L lateral decubitus
mitral stenosis
mitral regurgitation
L Sided S3
L sided S4
Causes of mitral valve regurgitation (5)
rheumatic fever endocaritis ischemic heart disease - ruptured chord tendineae LV dilation mitral valve prolapse
Holosystolic blowing murmur heard loudest at the apex of the heart
made louder w?
Radiates to?
mitral regurgitation
expiration and hand grip/squatting
Axilla
Causes of tricuspid regurgitation (2)
infective endocarditis
rheumatic fever
holosystolic murmur made louder with inspiration radiating to the right sternal border?
Tricuspid regurgitation
Crescendo decrescndo systolic ejection murmur w/ Ejection Click
Radiates where?
other findings?
aortic stenosis
Carotids
pulsus parvus et tardes - weak pulses
Aortic stenosis can lead to what 3 presenting problems
Syncope
Angina
Dyspnea
Causes of aortic stenosis(5)
bicuspid valve (30-40yrs old) Age related calcification (>60) Rheumatic valve disease unicuspid valve syphylis
Holosystolic harsh murmur that is loudest at the tricuspid?
tricuspid regurgitation
or VSD
Clinical picture key
Late systolic crescendo murmur w/ midsystolic click?
mitral valve prolapse
Phases of ventricular action potential and associated Channels of importance
What phase does myocytes contract
Phase 4 - I K -> polarized
Phase 0 - I Na -> depolarization w/ AP
Phase 1 - slight repolarization w/ Na channels closing and K channels opening
Phase 2 - I Ca channels open -> plateau, K channels still open (*contraction)
Phase 3 - Ca channels close and K channels open -> repolarization
Back to phase 4
Phases of pacemaker action potential
NO PHASE 1 or 2
Phase 4 - I K channels-> polarized w/ I funny channels that slowly depolarize allowing Na to leak in
Phase 0- threshold leads to I Ca channels to create AP
Skip Phase 1 and 2
Phase 3 - K channels open and Ca channels close leading to repolarization
Channels responsible for depolarization in Phase 0 in myocytes vs nodal cells
Myocytes - Na channels
Nodal cells - Ca channels
I funny channels are found where increasing what permeability
Found in nodal cells acting during phase 4 to slowly depolarize the cell by increasing Na permeability
4 Classes of anti arrhythmics and MOA
No Bad boy Keeps Clean
Na channel - phase 0 Beta blocker - Phase IV of Nodes and rate of depolarization (Beta 1 receptive) K channel - phase III Calcium channel (Phase 0 of Nodes)
Class 1A anti arrhythmics
MOA
Side effect as a class?
double quarter pounder
Disopyramide
Procainamide
Quinidine
Na phase 0 blocker -> Increase effective refractory period
increase AP duration (time of contraction of heart)
Torsades de pointes w/ Prolonged QT
Class 1B anti arrhythmic
MOA
mayo lettuce and tomato
mexiletine
lidocatine
tocainide
Na phase 0 blocker -> increase in effective refractory period, most often used ESPECIALLY post MI arrhythmia tacky and digitalis induced
Decrease AP
Rx for wolf parkinson White?
procainamide
Amiodarone
class 1 C anti arrhythmic
MOA
fries please
flecainide
propafenone
Na phase 0 blocker -> increase in effective refractory period, not used too often- NEVER post MI
Last resort for V tachy
No effect on AP
Cinchonism is what and a side effect of what antiarrythmic
HA, Tinnitus, Dizzy
Quinidine
SLE like drug induced antiarrythmic
Procainamide
W/ sulfonamide
Hydralazine,
Isoniazid
Phenytoin
Class II antiarrythmics (5)
MOA
be wary of what
Metoprolol propranolol esmolol atenolol timolol
Decreases nodal (SA and AV) activity by decreasing cAMP (B1 blockade) activity and Ca currents -> slower rate of depolarization of nodal cells
I funny channels not as permeable
Worry of Beta 2 nonselective -> vasospasm in Prinzangina, or those w/ pulmonary disease
Clinical use of beta blockers as antiarrythmics(4)
ventricular tachy
SVT
slowing vent rate during atrial fibrillation or flutter
Class III anti arrhythmic (5)
MOA
Worry of?
Amiodarone* Ibutilide Dofetilide Sotalol* Bretylium
Blocks K channels in myocytes in phase III -> increased effective refractory period
Worry of QT prolongation and torsades
Toxicity w/ Amiodarone - 3 key, are others
pulmonary fibrosis/ cough
hepatoxicity
hyper/hypothryoidsm
- 40% iodine
Check LFTs, PFTs, TFTs
Also skin (blue/grey), corneal deposits, photodermatitis, constipation, bradycardia
Class IV antiarrythmics (2)
MOA
Worry about?
Verapamil and Diltiazem
- nondihydropyridine CCB vs dihydropyridine CCBs(nifedipine, felodipine, Amlodipine)
Affects phase 0 through Ca channel blocking in the nodes lowering the slope and thus increasing effective refractory period
also lowers conduction velocity
Worry about CHF, take off beta blockers if giving
Side effects of adenosine and uses?
Blocked by?
flushing, hypotension, chest pain
used for diagnosing/abolishing SVT
Theophylline (COPD Rx)
Role of K and Mg in arrythmias?
want to keep above 4 for K and >2 in Mg to prevent, especially in a peri MI setting
K depresses ectopic pace maker in hypokalemia
give Mg for torsades
Irregular irregular rhythym?
also characteristic?
atrial fibrilation
No P waves
Biggest Atrial fibrillation concerns?
Guides Rx how?
Risk of stasis -> clots
< 48 hrs you can have synchronized cardioversion before clot forms
> 48 hrs or unknown need to coat first due to risk of thromboemboli
Rx goals in atrial fibrilation - 3
Anticoag
- heparin of enoxaparin (LMWH) 1st
- Warfarin later
Rate control - especially older
- Beta blockers, digoxin, CCb
Rhythm control - especially younger
- K channel blockers
Risk factors for atrial fibrillation (3)
HTN
CVD
Heart failure
all lead to dilated L atrium and odd conduction patterns
Atrial flutter characterized by what ECG line?
P waves?
sawtooth appearance
a lot of P waves that are regular - > increased HR
1st degree HB characterized by?
infectious cause?
PR interval greater than 200mse (5 little boxes)
Borrelia burgorferi (may cause 3rd degree as well)
2 types of 2nd degree HB and difference?
Rx?
Mobitz type 1/ Wenckebach - progressive lengthening of the PR interval leading to a dropped beat
- none mentioned
Mobitz type II - dropped beats w/out warning usually at regular intervals
- pacemaker,
3rd degree HB characteristic
P waves and RS complexes bear no relation to another,
Bradycardia
maybe narrow QRS but (1/3 are wide)
Wolf parkinson white characteristic ECG tracing?
Due to?
delta wave
due to premature stimulation of the ventricles from an accessory pathway most likely the bundle of Kent
Wolf parkinson white leads to risk of?
RX w?(2)
Risk of SVT w/ re-entry
Amiodarone or procainamide
Paroxysmal SVT tracing?
narrow QRS w. rapid rate
above the node? Re-entry mechanism?
failure of the AV or SA node to generate a beat leads to ?
characterized by? (3)
ventricular escape rhythm
Characterized by
- wide QRS
- no P wave
- bradycardia
Junctional escape rhythm has signal generated by?
Characteristic Tracing? (3)
AV node, SA node is not working
- Narrow QRS
- Bradycardia
- p wave most likely absent
Wide QRS complexes seen w/out P wave at random on a tracing
whys are they called cannon alpha waves?
Preventricular contraction
Usually >0.16s (4 little boxes)
maybe bigeminal or trigeminal in relation to p waves (1:1 or 2:1)
3 or > is potentially ventricular tachycardia
R Atria are contracting against closed tricuspid valve seen in the JVD
Ventricular tachycardia
HR?
Biggest concern?
3 or more successive ventricular complexes w/ widths > 0.16s (4 little boxes), QRS shifted to the left
HR greater than 100 BPM usually
Progression to V fib; defibrilate to prevent before hem dynamic collapse
Shockable rhythms? (2)
V tach
VFib
Drugs at risk for Torsades by prolonging the QT interval?(5)
Abx - Macrolides and choroquine Antipsycholics - Haloperidol and rispiridone Methadone Antiarrythmics - Class IA and III Protease inhibitors
Rx for Torsades de Point?
Push of Magnesium sulfate
Concern w/ torsades de points?
V fib
-essentially it is ventricual tachycardia w/ shifting amplitude
Normal BP in
R ventricle
L Ventricle
25/5
130/12
Barocreptors are located where and what are their respective signals out
Aortic barroreceptor responds to HTN only
-> sends increase signal with high pressure to the medulla via the vagus nerve
Carotid barroreceptor responds to HTN and hypotension. ∆stretch leads to change in firing in the glossopharyngeal nerve to the solitary nucleus of the medulla
Chemoreceptors are located where and respond to what
Chemoreceptors in the aortic arch and carotid artery respond to decrease PaO2, hypercapneia and acidosis
Central chemoreceptors in the brain respond to acidosis and increase CO2 in the CSF (responds to the arterial hypercapneia)
Patient presents w/ hypertension, bradycardia and depressed respiration, what is going on
Cushing reflex. Increased BP to overcome intracranial pressure from a lesion. Bradycardia is a reflex to the HTN
Carotid massage does what
stimulates the glossopharyngeal nerve to increase firing to the solitary nucleus of the medulla to make it perceive HTN an slow down the HR
Organ that receives the most of the systemic blood
Liver
Organ that receives the most systemic blood by weight
kidney
Which organ receives 100% of the CO
Lungs from the R ventricle
Local metabolites that result in vasodilatation of the heart(3)
CO2 - hypoxia
NO - from constituiatve NOS and all its associated factors
adenosine - ATP w/o any phosphates indicates low energy
ANP is released from where ?
What are its actions (2)
From the atrium of the myocytes in response to increase pressure
Results in vascular relaxation and decreased Na absorption (by increasing GFR through efferent arteriole constriction and afferent arteriole dilation) ~counteract aldosterone
How does dihydropyradine CCBs block vasoconstriction?
Drugs like nefedipine block the Ca-Calmodulin complex from forming which normally would: increase myosin light chain kinase activity, phosphrylating myosin and leads to contraction.
The presence of the drug inhibits this
What does does epinephrine on B2 (not alpha1 for this example) and prostaglandin E2 do to result increase vasorelaxation?
B2 and PGE2 act to increase cAMP which blocks myosin light chain kinase from phosphorylating myosin which leads to contration
How does LPS from gram (-) lead to shock and vasodialtion
LPS stimulates inducible NOS chich converts L arginine to NO which activates Guanylyl cyclase which increases cGMP and ultimately activets myosin phosphatase which takes the phosphate off any activated myosin leading to relax ion of the vessel
Sildenafil acts to vasodialate how?
Why is adding a nitrate a bad idea on top of this?
Sildenafil blocks the enzyme cGMP phosphodiesterase that degrades cGMP. Thus there is more cGMP around to encourage myosin phosphatase to be active and take off the phosphate on myosin and relax
Nitrate induces guanylyl cyclase to make more cGMP and thus have even more cGMP around
bradykinin, ACh, alpha 1 agonists, histamine, serotonin an dshear stress all act to vasodialate vessels how
Act on endothelial cells to increase intracellular Ca. This works on constitutive NOS system to convert L arginine to NO and citrulline. The NO diffuses to nearby smooth muscle to induce guanylyl cyclase to creaste more cGMP -> increases myosin phosphatase which takes the phosphate off activated myosin -> relaxation
Values describing hypertension and prehypertension
HTN >140/90
Pre HTN >120/80
Most common cause of HTN
Essential HTN
Most common cause of 2ry HTN
Other causes?(6)
Renal disease and Renal artery stenosis
-Hypokalemia, ab bruits, increase creatinine/BUN
Pheochromo Cushing Drugs Hyperthyroid Sleep Apnea hyperaldosereone (Conns)
Complications of HTN (6)
Arteriosclerosis L Ventrical hypertrophy CHF Stroke -hemorragic and ischemic retinopathy aortic dissection
Risk factors for HTN
Age Obesity Race Back>white>asian DM Smokine
Hypertensive urgency?
BP > 180/120 w/o signs of end organ damage
Becomes an emergency w/ end organ damage
L ventriculae hypertrophy complications
A stiff heart (S4)
lack of myocardial perfusion w/ thickening (MI risk)
Decreased CO with less room for filling
Risks for aortic dissection(3)
HTN
Cystic medial necrosis (Marfans)
bicuspid valve
CXR of aortic dissection
mediastinal widening
CT shows false lumen between tunica intima and media
Differnece between type A and type B atherscerosis and management techniques
Type A involves the arch and the ascending aorta
-medical emergency w/ surgical intervention
Type B involves the aorta distal to the branches- often use a beta blocker to Rx
antihypertensive that causes 1st dose orthostatic hypertension
Alpha 1 antagonists
ototoxic anti HTN - especially w/ aminoglycosides
Loop dieuretics
Hypertrichosis as a SFx for anti -HTN
minoxidil
Hair gain
Cynaide toxicity concern w/ this anti-HTN
Nitroprusside, used in malignant HTN
Bradycardia an asthma exacerbation concern w/ this anti-HTN
beta blockers
Reflex tachycardia ant -HTN
Any thing that vasodialates
- ACE, Hydralazine, Nitro, CCBs
Cough is seen as a side effect w. this anti-HTN due to?
Ace inhibitors
Due to increase in bradikinin(not broken down)
Anti HTN drug to avoid with sulfa allergy
Thiazides and Loop dieuretics
Possible concern w/ angioedema w this anti-HTN (2)
ACE inhibitors
ARBs
Hypercalcemia as a concernw/ hypocalemia if used as a dieuretic
Thiazide
Loops lose Ca
What antihypertensives benefit heart failure patients (4)
ARBs
ACE inhibitors
Aldosterone antagonists
Beta blockers - carvediol, metoprolol, bisoprolol
Loops are only symptomatic
Which antihypertenisves are safe in pregnancy (4)
HTN mothers love Nifedipine
Hydralazine*
Methyldopa
Lobetelol
Nifedipine
NO ACE
Avoid this Anti HTN in gout
Thiazide -> hyperuricemia
Anti HTN to avoid in renal artery stenosis-
Why?
ACE inhibitors/ARBs
due to renal insufficiency from dilation of the efferent arterial leading to a drop in GFR
Drug of choice in lowering HTN w/ DM
Ace inhibitors/ARBs
First line Rx for essential HTN
Thiazide dieuretics
Maybe anACE
Drug of choice for malignant HTN
Risk?
Nitroprusside, short acting, titrated IV
Risk of cyanide poisoning
Why does creatine increase and serum potassium level increase w/ an ACE inhibitor
Less angiotension II means less constriction of the efferent arteriole of the glomeruli and as a result there will be less GFR and filtration of creatinine
K increases due to the blocking of angiotension II increasing aldosterone secretion from the adrenal cortex
DO NOT GIVE W/ BILATERAL RENAL STENOSIS
ARBS and ACE inhibitors share what big concern of S FX
Angioedema
Most common locations of athersclerotic plaque and associated complications (4)
Abdominal aorta; AAA
Coronary Arteries; CAD and MI
Popliteal Artery; PAD and Claudication
Carotids; Stroke and TIA
ST segment elevation only during brief episodes of chest pain
prinzmetal angina
CAD risk factors (5)
>45 family history high LDL Smoking HTN
Patient is able to point to their chest pain with one finger is most likely due to
muscularskeletal
Chestwall tenderness on palpation
muscular skeletal
Rapid onset of sharp chest pain in a 20 something and SOB
Spontaneous pneumo
Chest pain that occurs after heavy meals and improved by antiacis
GERD or could be esophageal spasm
Deadly causes of chest pain (5)
MI
aortic dissection
Unstable angina
tension pneumothorax
PE
Arteriosclerosis
vs atherosclerosis
Arteriosclerosis is general term for hardening of the arteries
Athersclerosis is fibrous plaques and atheromas in the intima of the arteries
-it is a type of arteriosclerosis
Monckeberg
Type of athersclerosis where the tunica media calcifies and hardens
especially the radial and ulnar nerve in the elderly
benign
Does NOT obstruct blood flow
Arteriolosclerosis
hyaline thickening go the small arteries
-seen in HTN and DM
Atherosclerosis pathophysiology(8)
Risk factors of smoking, HTN, DM and dyslipidemia -> inflammation
Endothelia dysfunction
- > macrophage and LDL accumulation
- > foam cell formation
- > fatty streaks
- > smooth cell migration (PDGF and FGF)
- > proliferation and EC matrix depostion
- > fibrous plaques
- > complex atheromas in the intima
Abdominal aneurism complications(4)
Pathophys?
nutrient and waste diffusion compromised due to thickened vessel -> necrosis and weakness
Pulsating mass
rupture
embolize
obstruct branch vessel
impinge on adjacent structure
AAA are more common in (2)
due to athersclerosis
seen in smokers and men >50
When do you repair a AAA
athersclerotic plaque -> problems w/ diffusion of waste and nutrients -> wall necrosis and weakness
US serially q 6 months until > 5cm then repair
3 types of Angina and causes
Stable - predictable in onset, usually due to atherscerosis. may see ST depression w/ exertion
Unstable -rupture of thrombosis w/ incomplete artery occlusion, ∆ in pattern and maybe increasing severity in pain
Prinzmetal - more often younger patients w/ coronary vasospasm, transient pain at REST w/ ST elevations seen
Rx for prinzmetal angina
Give dihydropradine CCBs like
- Verapamil
- Diltiazem
Chronic ischemic heart disease is/?
progressive onset of CHF over yrs due to chronic ischemic myocardial damage; patchy fibrosis replacing cardiac muscle -> decreaes contractility
Right dominant circulation means what?
the SA nodal branch feeding the SA node is coming off the posterior descding /interventricular artery (PDA) which is coming off the R coronary artery
Coronary arteries fill when?
during diastole,
the aortic valve closes and the blood falls back into the sinuses right above the valve
Left atrial heart enlargement can have what 2 extra cardiomanifestations?
Dysphagia - impinging the esophagus
Hoarseness- impinging the R recurrent laryngeal nerve
Branches off the Right and Left Coronary artery
2 and 2
Right coronary artery (RCA)
- Right marginal artery (R atrium)
- Posterior descending/interventricular artery (PDA)
Left coronary artery (LCA)
- Left anterior descending artery (LAD)
- Left Circumflex coronary artery (LCX)
- —may sometimes have the PAD off it (20%)
coronary artery most commonly affected in an MI
LAD - left anterior descending
supplies anterioe 2/3 of the inter ventricular septum
What part of the heart is most posterior?
Anterior?
Posterior is the L atrium
- sitting on the posterior wall
Anterior is the R Ventricle
2 cholesterol lowering drugs that may cause RUQ pain?
Cholesterol Gallstones
Fibrates (gemfibrizil, clofibrate, bezafibrate, fenofibrate)
Bile acid resins (cholestryramine, colestipol, colesevelam)
drugs good for lowering tryglycerides (2)
preventing what complication?
Omega 3
Fibrates (gemfibrozil and clofibrate
pancreatitis
Prevent the most adverse complication of niacin by doing what>
giving ASA or NSAIDs 30 min prior
also have skin rashes and itching
hyperuricemi and hyperglycemia
Combination of drugs given to help w/ CAD?(2)
goal of treatment
Beta blockers (lowers after load) -NOT pindolol, acebutolol - (partial beta agonist)
Nitrates(lowers preload)
Maybe throw in an ACE
Goal of treatment is to reduce myocardial oxygen demand
Factors looked at when trying to lower oxygen demand of heart in angina pectoris(5)
preload, contractility, BP (afterload), ejection time, HR
Thus the beta blockers and nitrates
Also CCBs, ACE inhibiters
Myocardial infarction ECG changes in
Acute Hours Day 1-2 Days Weeks
Acute - ST elevation
Hrs - ST elevation w/ R decreasing and Q appearing
Days 1-2 - T wave inverts and Q deepens
Days - ST normal; T inverted
Weeks: ST normal, T normal Q wave persists
Indication on ECG of an MI weeks later
persisitent Q wave
one block wide or 1/3 the height of the qrs
ECG changes w/ MI (4)
ST segment elevation at least 1mm in 2 contiguous leads
T wave inversion
New LBBB
New Q waves that are > 1 block wide or 1/3 the height of the QRS
most common lethal complication post MI
Arrhythmia
0-4 hrs after a MI see what?
a lot of nothing.
Only have an increase risk of arrhythmia and changes on the ECG
4-12 hrs later in an MI see
Grossly
Microscopically (2)
Risks(1)
gross- dark mottling
Micro
- coagulative necrosis
- hemorrhage, edema, NO inflam yet
Risk of Arrhythmia
12-24 hrs later in an MI see
Grossly
Microscopically(3)
Risks?(1)
goss- dark mottling (still)
Micro
- coag necrosis -> release of necrotic cell content into the blood (cardiac enzymes)
- Contraction bands from reprofusion injury
- PMN infiltration begins
arrhythmia
1 day 3 days later in an MI see?
Grossly
Microscopically (3)
Risks (2)
gross - hyperemia* (redness of the infarct) on top of the dark mottling
Micro
- extensive coag necrosis
- Acute inflammation
- PMN migration
Arrhythmia fibrinous pericarditis (especially transmural)
3-14 days after an MI see?
Grossly
Microscopically(2)
Risks?(3)
gross- yellow tan w/ hyperemic border (softens) ~ bruise
micro
- macrophage** infiltration
- Granulation tissue w/ remodeing
Risk of Free wall rupture -> cardiac tamponade
papillary muscle rupture -> murmur
ventral wall aneurism
Weeks after an MI see?
Grossly
Microscopically(3)
Risks?(3)
Grey scar tissue seen
microscopically
- contracted scar complete
- hypocellularity
- increased collagen
Risk of
Dresslers syndrome - autoimmune pericarditis
Ventricular aneurism
CHF
Both of the last 2 have to due w/ lack of myocytes and inefficient pumping
3 Cardiac enzymes and timeline of them being seen in serum
Cardiac troponin I seen w/in 4 hrs - stays elevated for 7-10 days
CK-MB - in cardiac and skeleton muscle, stays elevated only for 48 hrs (good for MI on top of another) -
CPK is another, any muscle damage
May also see myoglobin
What cardiac enzyme would be good to check to see if a patient had 2 MIs w/in a week of each other
CK-MB stays elevated for only 48 hrs
CK-MB may also be helpful in blunt trauma to the chest to asses cardiac contusion
ratio CK-MB : total creatine Kinase
2 types of MIs and how do they differ
Transmural MI
- ST elevation and Q waves
- Affects the entire wall
Subendocardial MI
- ST depression
- only the subendocardial wall, <50% of the wall
- -times of hypoperfusion
What sort of ECG changes would you see with an anterior wall MI
Artery affected?
Leads V1-V3, maybe V4 and V5 - ST changes
LAD
What sort of ECG changes would you see with a lateral anterior wall MI
Artery Affected?
Leads aVL, V5 and V6 - ST changes
LCX
What sort of ECG changes would you with an inferior wall MI; Posterior wall MI
Leads II, III and aVF; ST Changes
- Change in r precordial EKG and V4 if posterior wall
-RCA infarct
Cardiac complications post MI (7)
Arrhythmia- V tach most common cause of mortality
LV failure and pulmonary edema
Cardiogenic shock
Structural integrity compompromised
- Papillary muscle -> mitral regurg
- Free ventral wall rupture -> cardiac tampanode
- interventicualr wall rupture -> VSD
Ventricular anuerism -> mural thrombosis
-> stasis -> emboli risk and stroke
Post infarct pericarditis (1-3 after)
Dressler’s syndrome - Autoimmune rxn weeks after
Patient a couple days after an MI has a murmur. What can be the cause? (2)
Papilalry muscle tear-> mitral regurb
Interventricular rupture -> VSD
Muffeled heart sounds w/ hypotension and a JVD right after an MI
be concerned of cardiac tamponode where the free wall ruptured
Rx for every acute MI (10)
ABCs MONA -Morphine -O2 if hyperemic -Nitrates -ASA Beta blockers (if no HF or asthma) Statins Antiplatelet- Clopidogril or ticagrelor Anticoag - Heparin or enoxaparin K > 4 and Mg >2
If having a STEMI what are your reprofusion options after initial management
Cath lab
or if less than 2 hrs fibrinolytics
If having a NSTEMI what are your reprofusion options after initial management?
Just the Cath lab, no fibrinolytics
Patient is having symptoms of CAD, hap acceded is is arteries
75%
Fibrinolytic therapy timeline for
Stroke?
MI?
Stroke - 3Hrs
MI - 2hrs
Drugs for post MI patient(6)
ASA +/or clopidogril Beta blocker* ACE* ARBs K sparing diuretics Statins*
Stars reduce mortality
Most common cardiomyopathy?
Causes?
Dialated
Chronic alcoholism chronic myocardial ischemia wet beriberi Cox B myocarditis Chagas Doxorubacin Cocain use hemachormaosis (also restricted but less)
Symptoms of dilated cardiomyopathy (3)
Systolic dysfunction due to large heart
S3
Enlarged heart on CXR
Apical impulse displaced laterally
Most common cause of hypertrophic cardiomyopathy
General pathophys
hereditary in a Auto Dom (b mysoin heavy chain mutation)
Intraventricular thickening due to disorganized tangled hypertrophied myocardium being made leads to an outlet obstruction with the mitral valves being closer to the heart wall
Systolic murmur heard as a result
Most common cause of sudden death in young athletes
Hypertophied cardiomyopathy
Auto dom inheritied. Thick inter ventricular heart wall leads to outlet obstruction. Hypovolumia in a game leads to decrease pre lead which is necessary to keep the valve open.
Findings in asymmetric conncentric hypertrophy of the the heart (4)
S4
increased ejection fraction (less filling, easier to empty)
Systolic murmur
Increased apical impulse
Rx for hypertrophy of the heart(2)
Want to slow the heart down and allow it to fill
Beta blockers
Ca channel blockers - Verapamil
What sort of murmur is hear in hypertrophy of the heart and what maneuvers can change the quality of the murmur
Systolic murmur
- valvsava makes it quieter due to decreased preload and less LV outflow (opposite of others)
- squating reduces after load and thus makes the murmur quieter
Major causes of restrictive heart disease(5)
LEASH
Lofflers syndome - eosinophilic infiltrate and endocardial fibrosis
Encocardial fibroelastosis-thick fibroelastic tissue in endocardium of kids
Amyloidosis - MOST common
Sarcoidois
Hemochromatosis(more dilated)
Lowfflers syndrome
Form of restrictive endocarditis
w/ eosinophilic infiltrate and endocardial fibrosis
Culture negative endocarditis causes (5)
HACEK
Hamopholis Actinobacillus Cardiobacertum Eikenella Kingella
Myocarditis is most commonly due to
Coxsackie B
-generalized inflammation of the myocardium
See diffuse interstitial infiltrate w/ myocyte necrosis on histology
Causal agent
myocarditis w/ Coxsackie B most likely
Diagnosis of infective endocarditis
Dukes criteria
New murmur
Echo - transesophageal
positive blood cultures (2/3)
Also
-fever, emboli, immune problems
Oslers nodes vs Janeway lesions
Osler nodes are painful emboli found on the tips of the fingers
Janeway lesions are more on the plans and soles and painless
Also have roth spots
4 most common causes of infectious endocarditis
Staph aureus - acute
viridans step - sub acute
Enteroccci - Rx resistant
Staph epidermidis - prosthetic valves
2 forms of non infectious endocarditis
Liedman sacks
-SLE
Both sides to the valve affected
Marantic endocarditis
- METS
- platelet fibrin aggregates in pts w/ hypercoagable states
Complications of endocarditis - long term(4)
chordae rupture
glomerulonephritis
supperlative pericaditis
emboli - brain, spleen, kidneys
Most common cause of constrictive pericarditis in the US
Lepus
TB worldwide
Kassmaul Sign
What is it?
MOA
Diseases
It is presence of JVD on inspiration
Due to Decreased capacity of R ventricle to fill
Primary due to constrictive pericarditis
Pulsus paradox
What is it?
MOA
Diseases associated
it is decreased systemic BP by at least 10mmHg upon inspiration
Due to insufficient L ventricile filling due to over expansion of the R ventricle w decreased intrathoracic pressure
Associated w/ cardiac tampanode and disease requiring increased straining of breath -asthma, etc…
major criteria for rheumatic fever
JONES
J- Joints - polymigratory heart - pancarditis N - nodules - Sub Q, painless E -erythema margininatum S - Sydnea Chorea
4 non superlative diseases associated w/ Strep Pyrongenes
Scarlet Fever - toxin mediated
Rheumatic fever - Type II Hypersens
post strep glumerulolnephritis - Type III hypersens
Strep Toxic shock syndrome - post skin infection mainly, can be sore throat too
Aschoff bodies
granulomas w/ giant cells seen in rheumatic fever
Anischkows bodies
activated histiocytes seen in rheumatic fever (owl eye appearance)
Specialty cells seen in rheumatic fever (2)
Aschoff bodies - granulomas w/ giant cells
Anischkow bodies - activated histiocytes
Which valve is affected most in rheumatic fever and what is the presentation early and late
Mitral valve
Early you have regurgitation
Late- stenosis
Presentation of pericarditis(3)
sharp peuritic pain that is more painful with inspiration, less leaning forward
Friction rub
ECG changes DIFFUSE ST elevation
Categories of pericarditis etiology (4)
Fibrinous
- Dresslers
- uremia
- radiation
- RA
Serous
- viral
- SLE
- Rheumatic fever
Superlative
-Pneumococcus and strep, TB
Cancer METs
Kassmaul sign and sharp peurtic chest pain w/ a creatinine of 5
Fibrinous pericarditis
Pathophys of cardiac tampanode
What are the findings in a cardiac tampanode(5)
compression of the heart by fluid -> lower CO and equilibrium of diastolic pressure in all 4 chambers
hypotension increase in JVD distant heart sounds increase HR pulsless paridoxis
ECG shows electrical alternans
Dx?
Cardiac tamponade
The QRS complex alternates in intensity of size
most common primary cardiac tumor in adults?
in kids?
Left atrium myxoma
Rhabdomyoma
associated w/ tuberous sclerosis -> astrocytoma and angiomyolipoma
Most common tumor of the heart
METS
4 disorders associated w/ Reynolds phenomenon
Mixed connective tissue disease
Bruegers
CREST scleroderma
SLE
Most common childhood systemic vascultis?
Presentation(4)
Henoch schonelin Purpura
Palpable purpura on the butt/legs
Arthralgia (knee)
GI - ab pain, melan
Renal Disease -> Bergers/IgA glomerulonephritis
Vascultitis associated w/ IgA deposition in many areas in =cluding the kidney
Hencoh Schonlein
Most common in kids
History of asthma and has necrotizing vasculitis w/ eosinophilia
Lab marker?
Churg Strauss
maybe a pANCA
Vasculitis associated w/ cANCA
Granulomatosis w/ polyangitis
- Wegeners
Vasculitis associated w/ pANCA
microscopic polyangiitis
Churg Straus sometimes
Churg Strauss presentation(3)
asthma/sinusitus
palable puprua
peripheral neuropathy (foot drop)
also can involve the heart, GI and kidneys -> pauci-immune glomerulonephritis
pANCA
Triad of Wegeners?
Focal necrotising vasculitis
necrotizing granulomas in the lung and upper airway
necrotizing glomerulonephritis
small vessel vasculitis commonly involving the lung, kidneys and skin w/ paucu glomerulonephritis and papable purport
lab test?
Microscopic polyangiitis
pANCA
Microscopic polyangiitis presentation(3)
small vessel vasculitis commonly involving the
lung,
kidneys
skin w/ pauci glomerulonephritis and papable purport
pANCA
3 symptoms of unilateral HA, jaw claudication and irreversible blindness risk
Disease affects branches of what artery?
A lab you could run ?
Giant cell/temporal arteritis
Affects branches of the carotid artery
ESR to r/o if NOT the case
vasculitis associated w/ polymylagia rheumatica
- dosas of pain and joint stiffness (proximally)
Giant cell/temporal arteritis
Vasculitis is found in a young asian female?
Also known as?
Takayasu
pulses disease
granulomatous thickening of the aortic arch and proximal great vessels
Affects which population mainly?
takayasu’s pulseless disease
asian females <40yrs
also have fever, night sweats, arthritis, myalgias and skin nodules
Patient w/ HBV is at increased risk of this vasculitis
Preferentially attacks which vessels (2)
Polyarteritis nodosa (PAN_
attacks renal and visceral vessels(sparing the lung)
Polyarteritis nodosa presentation
Young adult that is HBV positive(30%0
transmural inflammation of the medium arteries sparing the lungs preferring the renal and visceral arteries
PAN lab test?
no ANCA
Kawasacki vaculitis symptoms
CRASH
Conjunctivitis Rash - diffuse Adenopathy Strawberry tounge Hands and soles - desquamitating
Also fever
Kawasakis most concering complication
coronary artery spasm -> MI or thrombosis
Rx for Kawasacki disease(2)
Age group affected?
< 4 yrs, usually asian
IV immunoglobin to have negative feedback on the deranged immune system
Aspirin - thrombosis risk
Intermittent claudication that may lead to gangrene and autoamputation of the digits?
also superficial nodular phlebitis
Buergers Syndrome
-associated w/ Reynalds
Due to smoking
Rx - stop smoking
Strawberry hemangioma
benign capillary tumor found in infants,
regresses spontaneously around 5-8yrs
cherry hemangioma
benign capillary hemangioma in the elderly, red, around the size of a mole
Do not regress
Pyogenic granuloma
associated w?(2)
Found
Polypoid capillary hemangioma
Associated w/ trauma and pregnancy
Found on luis and gums and can ulcerate and bleed
Cystic hyproma
Associated w?
cavernous lymphangioma of the neck
associated w/ Turners Syndrome
Red vascular tumors(3)
Strawberry hemangioma
Cherry hemangioma
Pyogenic hemangioma
Glomus Tumor
location?
Benign painful red/blue tumor under the fingernails
Arises from smooth muscle cells
Bacillary angiomatosis
benign capillary papule due to Bartonella henselae infection
Mistaken for karposi’s often
Karposi’s sarcoma is often mistaken w/
Bacilliary angiomatosis
-Bartonella henslae infection
also higher prevalence in HIV
Angiosarcoma
Due to?
Location?
rare blood vessel malignancy
- due to radiation exposure
Usually in the head, neck and breast
Lymphangiosarcoma
Due to?
Location
lymphatic malignancy associated w/ persistent lymphedema
arms can be affected post radical mysectomy and nicking the lymph ducts
Karposi sarcoma
3 etiologies
Indolent - Older men and mediterranian descent
Endemic - Sub saharra
HHV8 - HIV
Karposi sarcoma
Location
endothelial malignant most commonly on the skin but also the mouth, GI and respiratory tract
Sturge Weber disease
Sign
Path
Congenital vascualr disorder that affects capillaries
Port wine stain w/ ophthalmic distribution on the face indicates an ipsilateral lelomeningeal angiomatosis (intracranial Arterial-ventrical malformation)
also siezures and glaucoma
Nevus flames seen over a patients eye
be concerned of what congenital disease and ultimately what complication
Sturge Weber disease
worry of leptomeningeal angiomatosis - and intracerebral AVM
also have seizures and early glaucoma
