Cardio - Stuff Missed Flashcards
How do ACE inhibitors cause renal failure?
ACE inhibitors dilate efferent tubules, thus decreasing GFR and renal perfusion.
- For patients who depend on efferent arteriole constriction to maintain renal perfusion (pts with renal artery stenosi), ACE inhibitors can cause ARF
Discuss ACE inhibitors and aldosterone
block release of aldosterone resulting in decreased Na reabsoprtion and increase K retention in distal and collecting tubules
- responsible for hyperkalemia often seen with ACE inhibitor therapy
Cyclooxygenase 2 (COX-2)
- molecular weight of 72kd
- inducible enzyme that is normally undetectable in most tissue except in case of inflammation
“Coffee ground emeisis”
suggests upper GI bleed
- coffee ground color caused by oxidation of heme
- patients may lose a lot of blood and may experence hypvolemic shock
Hypovolemic shock
- when patient loses > 10% of blood volume
- sympathetic NS constricts arteriole and venous beds and stimulate heart
- arteriole constriction - increases total peripheral resistance and maintain organ pressure
- venous constriction - increases blood return to heart to maintain preload
Discuss IV fluid infusions and preload
IV infusions increase intravascular volume by varying degrees of solute composistion
- Preload increase increases mycocardial sarcomere lendgth and increases stroke volume and cardiac outpute
Most common cause of mitral stenosis
Rheumatic dever
Infective endocarditis
- results in larger, more friable vegetations
- destruction of valve leaflet, may cause regurgitation
- embolization of vegetations can cause stroke or septic infarct resulting in brain abscess
Degenerative calcific deposits
develop in mitral valve annulus in women > 60
- found in ppl with myxomatous, floppy mitral valve or elevated left ventricular pressure
Fibrinous pericarditis
- result of prolonged rheumatoid arthritis
- rarely involve the endocardium or heart valves
Reperfusion injury
- when after blood flow is returned to ischemic tissue, cells within damaged tissue die secondary to: - oxygen free radial generation - mitochondrial damage - inflammation
Mechanisms of reperfusion injury
- Oxygen free radical generation by parenchymal cells
- Severe, irreversible mitochondrial damage described as “ mitochondrial permeability transition”
- Inflammation - attracts circulating neutrophils that cause additional injury
- Activation of complement pathway, causing cell injury and further inflammation
Explanation of rise in serum creatinine kinase after thrombus extraction
- Result of reperfusion injury
- When heart, brain, or skeletal muscle are injured, enzyme creatinine kinase leaks across cell membrane and into circulation
Risk factors for intimal tears leading to aortic dissections
- Hypertension
Smoking (risk factor for which vascular diseases)
- ATHEROSCLEROSIS –> aortic aneurysm
2. BUERGER’S DISEASE (Thormboangitis obliterans)
If LAD is occluded by atherosclerotic plauque, what is the preferred vein for grafting?
Left internal mammary artery - preferred vseel
If mutiple coronary arteries/vessels are occluded, what is the preferred vein for grafting?
Great saphenous vein - longest vein in body
Great saphenous vein
- superficial vein that originate on medial side of foot, courses anterior to medial malleolus, and then travels up medial aspect of leg thigh
- drains into femoral vein within femoral triangle, inferior lateral to pubercle triangle
How soon after ischemia do the cardiomyocytes lose contractility?
60 seconds after ischemia
- due to cessation aerobic glycolysis
- ATP decreases rapidly due to high myocardial demand
Myocardial studding
if ischemia lasts less than 30 minues
- restoration of blood leads to REVERSIBLE contractile dysfunction
- contractility returns to normal within days or hours
What happens to cardiomyocytes after more than 30 minutes of ischemia?
IRREVERSIBLE injury
Most reliable indicator of the severity of mitral stenosis
S2 to opening snap interval (A2-OS interval)
- ## the shorter the interval, the more severe the stenosis
Xanthelasmas
- yellowish macules/papules found on medial eyelids
- dermal accumulations of cholesterol and triglucerides
- associated with primary and secondary hyperlipidema or dyslipidemia
- LDL receptor abnormality is most common cause
Normal variant cardiac anomaly in adult patients?
Patent foramen ovale (present in 20 - 30% adults
- remains functionally closed, but in situations of increased right atrial pressure may cause right atrial shunt
Endocardial cushion defect
- failure of complete fusion of endocardial cushions in atrioventricular canal
- leads to perisistent AV canal
- associated with Down Syndrome
Persistent truncus arteriosus
- results form incomplete embryonic development of aorticopulmonary septum resulting in single great vesel from heart
- Aorta, Pulm Artery, and coronary vessels
- causes cyanosis and if uncorrected, death within first year of life
Ductus arteriosus
closes by 3rd month of life in response to high PaO2 of blood shunting from left to right through the ductus after birth
- patency beyond 1 year is abnormal
Sotalol
both adrenergic blocking properities class 3 anti-arrhythmic (K+ channel blocking) properties - prolongs both the PR interval and QT interval
STEMI and subsequent Q-wave formation is the result of …
Fully obstructive thrombrus superimposed on ruptured atherosclerotic coronary artery plaqye
Q-wave in V1 - V4 leads. Where is infarct?
Anterior wall (LAD)
Q wave in V1 - V2 leads. Where is infarct?
Anteroseptal (LAD)
Q wave in V4 - V6 leads. Where is infarct?
Anterolateral (LCX)
Q wave in I, AVL leads. Where is infarct?
Lateral wall (LCX)
Q wave in II, III, aVL leads. Where is infarct?
Inferior wall (RCA)
Unstable angina. Describe vasculature.
Caused by obstruction of at least 75% of coronary artery lumen.
Prinzmetal’s angina
- caused by vasospasm
- may occur at sites of coronary atherosclerosis and result in transmural ischemia
Atherosclerotic plaques develop predominantly in which arteries?
- Large elastic arteries (e.g. aorta, carotid, illiac)
- Large/medium sized muscular arteries (e.g. coronary and popliteal arteies)
Order of vessels in which atherosclerotic plaque form.
Abdominal aorta > Coronary arteries > Popliteal arteries > Internal carotid > Circle of Willis
Aortic rupture
- commonly caused by motor vehicle accident
- aortic isthmus (connection between ascending and descending arteries distal to where left subclavian branches off of aorta)
Peak intensity of aortic regurgitation murmur
- occurs after closure of incompetent aortic valve, when the pressure gradient and the left ventricle are at mazium
Aortic Regurgiation murmur
heard best on left sternal border when patient leans forward (bringing valve close to the chest wall) and at end of expiration
Hypetrophic cardiomyopathy
- most common cause of ventricular fibrillation in patients < 30
- most common cause of sudden cardiac death in young athlete
Restrictive cardiomyopathy
- associated with endomyocardial fibriosos, endocardial fibroelastosis, idiopathyic myocardial fibrosis
Stab wound in fourth intercostal space in the midclavicular line hits what structures?
Primarily left lung then if deep enough left ventricle
Stab wound in fourth intercostal space in left sternal border hits what structures?
Primarily right ventricle.
Collagen I
Dermis, bone, tendons, ligaments, dentin, cornea, blood vessels & scar tissue
Dysfunction of collagen I
Osteogenesis imperfecta
Collagen II
cartilage, vitreous humor & nucleus pulposus
Collagen III
Skin, lungs, intestines, blood vessels, bone marrow, lymphatics & granulation tissue
Associated with collagen III
Ehlers-Danlos syndrome
Collagen IV
Basement membrane
Associated with collagen IV
Alport syndrome
Alpha 1 receptors
- Increase IP3
- Peripheral vasoconstriction
- Mydriasis (contraction of pupilary dilator muscle)
- Intestinal and bladder sphincter muscle contraction
Alpha 2 receptors
- DECREASE cAMP
- decrease release of NE and insulin
- decrease lipolysis
- increase platelet aggregation
Beta 1 receptors
- INCREASE cAMP
- increased heart contractility and HR
- increased lipolysis
- increased renin release
Beta 2 receptors
- INCREASE cAMP
- vasodilation
- bronchodilation
- increased HR and contractility
- increased insulin production and aqueous humor production
- ## decreased uterine tone
Norepinpherine
stimulates cardiac B1 receptors which utilize cAMP pathways
Side effect of anthracycline chemo agents (doxirubicin, daunorubicin, epirubicin, idarubicin) on heart
Dilated cardiomyopathy
- these agents form free radical in myocardium
- often presents with symptoms of left and right CHF
Method to prevent dilated cardiomyopathy after doxorubicin administration
Dexrazoxane - iron chelating agent decreases formation of oxygen free radicals
Causes of restrictive cardiomyopathy
- associated with hemochromatosis
- amyloidosis
- sarcoidosis
- radiation therapy
Hypertrophic cardiomyopathy
- associated with mutation of B-myosin heavy chain
Pericardial fibrosis
cardiac surgery
radiation therapy
viral infections
Torsades de pointes
ventricular tachycardia with shifting sinusoidal waves on ECG
- can progress to ventricular fib
- anything that prolongs QT interval can lead to T de P
Tx: magnesium sulfate
Treatment of Torsades de Pointes
Magnesium sulfate
Jervell and Lange-Nielsen syndrome
congenital long QT syndromes due to defects in cardiac sodium and potassium channels
- can present with severe congenital sensorineural defects
Wolf-Parkinson White syndrome
ventricular pre-exciation ndrome
due to accessory conduction pathway from atria to ventricle that bypasses AV node
- ventricles depolarize earlier - leading to DELTA wave
Treatment of Wolf-Parkinson White Syndrome
Procainaomide, Amiodarone
Atrial fibrillation
chaotic and erratic baseline (irregularly irregular) with NO DISCRETE P WAVES in between irregular spaced QRS complexes
- can result in atrial stasis and lead to stroke
Treatment of atrial fibrilliaotn
rate control, anticoagulation, and possible cardioversion
Atrial flutter
rapid succession of identical, back to back atrial depolarization waves
- “sawtooth appearance)
Treatment of atrial flutter
Rx conversion to sinus rhythm: Class IA, IC, or III antiarrhythmics
Rate control: B-blocker or Ca channel blocker
Ventricular fibrillation
completely erratic rhythm with no identifiable waves.
Fatal arrhythmia without immediate CPR and defibrillation
1st degree AV block
PR interval is prolonged (> 200 msec)
- Assymptomatic
2nd degree AV block: Mobitz type I
Progressive lengthening of PR interval until a beat is dropped (P wave is not followed by QRS complex)
- Usually assymptomatic
2nd degree AV block: Mobitz type II
- dropped beats that are not preceded by change in length of PR interval
- Abrupt nonconducted P waves result in pathological condition
- Often found as 2:1 block, where there are 2 or more P waves to 1 QRS complex
- May progress to 3rd degree heart block
- Treated with pacemaker
3rd degree AV block (complete)
- Atria and ventricles beat independently of each other.
- Both P waves and QRS complexes are present, though P waves have no relation to each other
- Atrial rate are faster than ventricular rate
- Usually treated with pacemaker
- Lyme disease can result in 3rd degree AV block
ANP
released from atrial myocytes in response to increased blood volume and atrial pressure
- causes vascular relaxation and decreased NA reabsorption at collecting tubules
- constricts EFFERENT renal arterioles and relaxes AFFERENT renal arterioles (cGMP mediated)
- promotes diuresis and “ escape form aldosterone”
Metabolites mediating vasodilation in heart
CO2, adenosine, NO
Metabolites mediating vasodilation in brain
CO2
Pulmonary hypertension
- taking appetite suppressants for > 3 months can lead to Pulmonary HTN
Cerebral berry aneurysms
associated with AKPD and Ehlers Danlos syndrome
- risk factors are hypertension and smoking
Medial calcinosis
calcific deposits in muscular arteries in ppl > 50 y.o
- femoral, tibial, radial, and ulnar arteries are typically affected
- visible by radiography and palpable
- assymptomatic and DO NOT NARROW vessel lumen
Aortic dilation
result of HTN, aging, and/or aortic stenosis
- can result from atherosclerosis,, cystic medial degeneration, aortitis
Left atrial enlargement
can cause left recurrent laryngeal impingement
- can result in dysphagia
- can result in left vocal cord paresis and hoarseness
Ortner syndrome
mitral stenosis that leads to left atrial enlargement that result in impingement on left recurrent nerve
Drug efficacy
maximum pharmacodynamic effect achievable by drug
Potency
refers to dose of drug required to produce given effect.
Drugs that bind to receptors will higher affinity or better able to gain access to target tissue will have greater portency (lower ED50)
Most common causes of lightening related death
Fatal cardiac arrhythmias and respiratory failure
Lichtenberg figures
cutaneous red marks in fern-leaf pattern
- seen with lightening injury
Claudication
- intermittent muscle pani caused by exercise and relieved by brief period of rest
- result of atherosclerosis of larger arteries
- stenotic atheromas (lipid filled intimal plaques)
Hyaline arteriosclerosis
homogenous deposition of hyaline material in initima and media of small arteries and arterioles
Hyperplastic arteriosclerosis
results from malignant hypertension
- seen in diastolic pressures > 120 mm Hg
- leads to onion-like concentric thickening of arteriolar walls due to SMC
Valsava maneuver in auscultation
decreases venous return reduce left ventricular volume and blood pressure
- MS and MVP become MORE audible
- Aortic stenosis becomes less audible
S3
low frequency sound
results from left systolic failure - chamer remains dilated
- listen best on left lateral ducubitus position
Signs of irreversible injury in heart
Appearance of vacuoles and phospholipids densities in mitochondria
- implies permanent inability to generate ATP
Progressive exertional dyspnea in heavy smoker
Think: COPD!
Dilation of RV and increased central venous pressure
Right heart failure
- interstitial fluid pressure rises due to increae in net plasma filtration
- as interstitial fluid pressure increases, lymphatic drainage does to prevent intestitial edema
- Edema occurs when lymphatics can’t compensate
Sudden cardiac death
cardiac arrest that begins within 1 hours od event and proves fatal
- mostly due to coronary artery disease
- acute plaque change leads to acute MI which leads to letal arrythmias
Most common cause od death in MI patients
Cardiac arrhythmias
Phase 0 of cardiomyocytes vs. Phase 0 of Purkinje cells
Phase 0 of cardiomyocytes (pacemaker cells) have Ca influx
Phase 0 of Purkinje cells is due to influx of Na
Turner’s Syndrome
Triad: “streak ovaries, amenorrhea, and infertility
- most associated with coarctation of aorta, webbed neck, low posterior hairline, and short stature
Kawasaki’s disease
vasculitis of medium sized arteries that presents with persistent fever, bilateral conjunctivitis, cervical lymphadenopathy and mucocutaneous involvemet
-
Most common cause of dilated coronary arteries
Elevated right-sided heart pressure (anything that cause right atrial dilation) secondary to pulmonary artery hypertension
** coronary arteries not seen on ECG in healthy inviduals
Normal splitting
inspiration leads to drop in intrathoracic pressure and increase in venous return.
- more blood in RV and longer ejection time
- DELAYED CLOSURE OF PULMONIC VALVE
Wide splitting
- Seen in conditions that delay RV emptying (e.g. pulmonic stensois, right bundle blokc0
- Delay in RV emptying causes delayed pulmonic sound (REGARDLESS OF BREATH_
Fixed splitting
Seen in ASD. ASD –> left to right shunt –> RA and RV volumes –> increased flow through pulmonic valve such that regardless of breath, pulmonic valve is GREATLY delayed
Paradoxical splitting
seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block)
- Normal order of valve closure is reversed (pulmonic valve closes before aortic balbe)
- on inspiration, P2 cloes later and moves closer to AP
Congenital heart defects associated with Down’s syndrome
endocardial cushion defects
Common genetic cause of Down syndrome
- caused by maternal meiotic nondisjunction
Fenoldopam
D1 receptor agonist
- causes arteriolar dilation and natiuresis leading to decreased SVR and BP reduction
- only IV agent that improves renal perfusion
Esmolol
short acting B-blocker
- decreases heart rate, contractility, and cardiac output
- used in post operative hypertension
Nicardipine
Ca channel blocker that works by blocking Ca in vascular smooth mucle
Signs of acute pericarditis
- sharp and pleuritic pain
- decreases when patient sits up and leand forward
- canbe caused by myocardial infarction, rheumatic fever, or uremia or infection
- Pericardial friction rub is most striking sign
Kussmaul’s sign
paradoxical increase in JVP during inspiration
- found in chronic constrictive pericarditis, severe RHF, tricuspid stenoisis and RARELY cardiac tamponade
Pulsus paradoxus
drop in systolic blood pressure of > 10 mm Hg or more during inspiration
- exaggeration of response during inspiration
Prostacyclin
produced by vacular endothelial cell
- when secreted vasodilates
- inhibits platelet aggregation
- increases vascular permeability
- opposes THROMBOXANE
Hageman Factor
synthesized by liver and is activated by collagen exposed to damaged vascular Basement Membrane
Kallikrein
converts kininogen to bradykinin. Bradykinin is normally degraded by ACE and is responsible for cough seen in bradykinin
Unilateral renal stenosis
cause of secondary hyperension
- caused by atheromatous plaque in renal artery
- occurs more in patients in males and increases with age
- ischemic kidney secretes high levels of renin to cause HTN
- ischemic kidney atrophies
Irregularly irregular tachyarrhythmias
Atrial fibrillation (absent P waves)
Torsades de Pointes
- heart beat is fast, but rhythm is regular
Dofetillide
Class 3 antiarrhythmic agen blocks potassium efflux
- prolongs phase 3 of myocyte action potential
Potassium-sparing diuretics act where?
In collecting tubule
Acetazolamide
- blocks carbonic anhydrase thus block reabsorption of HCO3
- works in proximal tubules
Micro changes after MI: 0-4 hrs
minimal change (normal)
Micro changes after MI: 4 -12 hrs
early coagulation necrosis, edema, hemorrhage
WAVY FIBERS
Micro changes after MI: 12 -24 hrs
coagulation necrosis and marginal contraction band
Miro changes after MI: 1 - 5 days
coagulation necrosis and neutrophilic infiltrate
Micro changes after MI: 5 - 10 days
macrophage phagocytosis of dead cells
- greatest risk of ventricular rupture
Micro changes after MI: 10 to 14 days
granulation tissue and neovascularization
Micro changes after MI: 2 weeks to 2 months
Collagen deposition/Scar formation
Most common cause of aortic stenosis
caused by bicuspid aortic valve
AV shunts
- can be congenital or acquied
- can increase preload and decrease afterload by routing blood directlt from arerioal system
- result in high output cardiac failure
Temporal (Giant cell) arteritis
characterized granulomatous inflammation of media
- most common form of vasculitis
- usually elderly woman complaining of headaches and risk of blindness
- responds well to glucocorticoid therapy
Drugs used for MRSA infections
- Vancomycin
- Daptomycin
- Linezolid
Vancomycin
- blocks glycopeptide polymerization by binding to tightly to D-alanyl-D-alanine
Side effects: Red man syndrome (mediated by histamine); Nephrotoxicity
Daptomycin
- depolarization of cell membrane
Side effects: myopathy and CPK elevation; inactivated by pulmonary surfactant
Linezolid
inhibits bacterial protein synthesis by binding to 50 S unit
- Side effects: cause thrombocytopenia, optic neuritis, high risk for serotonin syndrome
Specific sign of left sided heart failure
Orthopnea
Specific sign of RHF
Bilateral lower extremity edema and congestive hepatomegaly
Myocardial hibernation
- repetitive ischemia of cardiomycoctes or persistent hypoperfusion of mycocytes that result in loss of fxn
- can be reversed with reperfusion
Intensity of AS murmur is determined by abnormal pressure gradient between LV and Aorta during systole
True
Paroxysmal supraventricular tachycardia
- occurs in young people without real heart hx
- sudden onset of palpitations and may resolve spontaneously
Adenosine
- used to treat paroxysmal supraventricular tachycardia
- rapidly cleared and half-life of 10 secons
- commonly causes flushing, bronchospasms (chest burning), and high grade block
- used for chemical stress test
Verapamil
Class IV antiarrhythmic
- most cardioselective of all Ca channel blcoker
- assocciated with constipation and gingerval hyperplasia
Amiodarone
Class III antiarrhythmic and overdose or toxicity with lidocaine most commonly causes neurologic symptoms
Pathogenesis of atherosclerotic plaques
release of PDGF by locally adherent platelets, endothelial cells, and macrophages, promotes migrations of SMCs from media into intimas
Phenoxybenzamine
non-selective irreversible a1 and a2 adrenergic antagonist that reduces number of receptors available
Aschoff bodies
myocardial granulomas
- associated with rheumatic carditis
- contain plump macrophages with abundant cytoplasm and central round to ovoid nuclei with central ribbons of chromatin (Anitschow cells)
Hypertrophic cardiomyopathy
due to abnormal systolic anterior motion of anterior leaflet of MV toward hypertrophied interventricular septum
Strep viridans
- produce dextrans from glucose that aid organisms colonize dental enamel and heart surfaces
- can cause subacute bacterial endocarditis in patients with already existing cardial defects after dental manipulation
Fibrous initimal thickening with endocardial plaques limited to right heart
Carcinoid syndrome
- endocardial fibrosis due to serotonin levels and 5-hydroxyindoleacteic acid
Carcinoid syndrome symptoms
episodes of skin flushing, abdominal cramping, vomiting, and diarrhea
- severity of symptoms correlates with serotinin levels and urinary excretion of serotinin metabolite, 5-HYDROXYINDOLEACETIC ACID
Adult (post-ductal ) type of congenital aortic coarctation
- signs of hypertension in arterial tree proximal to coractation
- hypoperfusion in lower extremities
- results in dilated intercostal artries
Post-ductal congenital aortic coarctation
Triad:
- upper body hypertension (headaches, dizziness)
- Diminished lower extremity pulses (difficulity walking)
- Enlarged intercostal artery collaterals
Nitrates + Phosphodiesterase (PDE) inhibitors used for erectile dysfunction and pulmonary hypertension
- causes PROFOUND systemic hypotension
- both classes of drugs (nitrates + PDE inhibitors) increase cGMP - which causes smooth muscle dilation
Wolf-Parkinson White Syndrome triad
- SHORTENED PR- interval
- DELTA wave at start of QRS complex
- widened QRS interval
- pre-exciation syndrome associated with re-entry circuit
- associated with PSVT
