Cardiology Flashcards
Truncus Arteriosus becomes…
Pathology of TA
Ascending Aorta and Pulmonary Trunk
Transposition of the Great Vessels (failure to spiral), Tetralogy of Fallot (skewed AP septum), Persistent TA (partial AP septum development)
Bulbus Cordis becomes
Smooth part (outflow tract) of L and R Ventricles
Primitive Ventricle Becomes
Trabeculated Ventricles
Primitive Atria become
Trabeculated Atria
Left Horn of Sinus Venosus becomes
Coronary Sinus
Right Horn of Sinus Venosus becomes
Smooth part of RA
Right Common Cardinal Vein and Right Anterior Cardinal Vein become
SVC
What kind of cells forms the aorticopulmonary septum
Neural Crest Cells. Truncal and bulbar ridges spiral and fuse to form AP septum giving rise to the Ascending Aorta and the Pulmonary Trunk
Interventricular Septum Development
- Muscular ventricular septum forms with interventricular foramen
- AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular formane
- Growth of endocardial cushions separate atria from ventricles and contributes to both atrial separation and membranous portion of interventricular septum
Membranous septal defect will lead to
L-R shunt which later reverses to R-L shunt due to onset of PHTN (Eisenmengers syndrome)
Interatrial septum development
- Foramen primum narrows as septum primum grows towards endocardial cushions
- Perforations in septum primum form foramen secundum and FP disappears
- FS maintins R-L as suptum secundum begins to grow
- Septum Secundum contains FO (permanent opening)
- Foramen secundum enlarges and upper part of septum primum degenerates
- Remaining portion of septum primum forms valve of FO
- Septum secundum and septum primum fuse to form atrial septum
- FO closes soon after birth because of increased LA pressure
PFO caused by
Failure of Septum Primum and Septum Secundum to fuse after birth
Fetal erythropoiesis occurs in?
"Young Livers Synthesize Blood" Yolk Sac: weeks 3-10 Liver: week 6 - birth Spleen: 15-30 weeks Bone Marrow: 22 weeks to adulthood
Blood in umbilical vein
PO2
O2 Sat
PO2 = 30mmHg
O2 Sat = 80%
Umbilical arteries O2 Sat?
Low
Fetal Shunts
- Umbilical vein –> ductus venosus –> IVC to bypass liver
- RA –> FO –> LA
- Pulmonary Artery –> Ductus Arteriosus –> Aorta
What happens to fetal circulation when the infant takes its first breath
Decreased resistance in pulmonary vasculature –> increased P in LA –> FO closes
Increased O2 –> decreased prostaglandins –> ductus arteriosus closes
Medication for PDA
Indomethacin closes the PDA
PGE keeps in open
Umbilical vein becomes
Ligamentum teres hepatis contained in the falciform ligament
Umbilical arteries become
Medial umbilical ligaments
Ductus arteriosus becomes
Ligamentum arteriosum
Ductus venosus becomes
Ligamentum venosum
Foramen Ovale becomes
Fossa Ovalis
Allantois becomes
Urachus - median umbilical ligament. The Urachus is part of the allantoic duct between bladder and the umbilicus
Urachal cyst or sinus is a remnant
Notochord becomes
Nucleus pulposus of IV disc
What vessels supplies the SA and AV nodes?
RCA
What percentage of individuals are Right Dominant? Left Dominant? Codominant?
PDA arises from RCA in 85% of individuals
From LCX in 8%
Both in 7%
Most commonly occluded coronary arteries?
LAD > RCA > CFX
Coronary arteries fill during
Diastole
Branches of RCA
Acute Marginal, PDA (80%)
Branches of LCA
CFX, LAD
If LA enlarged
How to diagnose?
Dysphagia (compression of esophagus) + Hoarseness (compression recurrent laryngeal nerve)
Transesophageal Echocardiography
What can transesophageal echocardiography be used to diagnose?
LA Enlargement, Aortic Dissection, Thoracic Aortic Aneurysm
What does LAD supply?
Ant 2/3 of IV septum, anterior papillary muscles, anterior surface of LV
What does LCX supply?
Lateral and Posterior walls of LV
What does PDA supply?
Posterior 1/3 of IV septum and posterior walls of ventricles
Cardiac Output Equation (2)?
CO = SV x HR
Fick Principle
CO = (Rate of O2 consumption)/(arterial O2 - venous O2)
Mean Arterial Pressure Equation? (2)
MAP = CO x TPR MAP = 2/3 Diastole + 1/3 Systole
Pulse Pressure Equation?
What is PP proportional to?
PP = Systolic - Diastolic
PP α SV
Stroke Volume Equation?
EDV - ESV
During exercise, how is CO maintained?
Early?
Late
Early: Increases in HR and SV
Late: HR only, SV plateaus
What happens if HR is too high?
Diastolic filling is incomplete and CO decreases resulting in ventricular tachycardia
What variables affect SV?
SV CAP
Contractility, Afterload, Preload
What decreases Contractility?
BACH
β Blockers (decreased cAMP), Acidosis, Ca Channel Blockers (non-dihydropyridine), Hypoxia/Hypercapnea, Systolic Heart Failure
What Chemicals Increase Contractility?
Catecholamines (increase activity of Ca pump in SR). Digitalis (Increased intracellular Na –> increased intracellular Ca)
SV increases in what states?
Pregnancy, Exercise, Anxiety
Myocardial O2 demands increase with
CARS
Increased Contractility, Afterload, Rate, Size (wall tension)
Preload is equal to?
EDV
Afterload is equal to?
MAP
Proportional to peripheral resistance
What kind of drugs reduce preload?
Venodilators like Nitroglycerin
What kind of drug reduce afterload?
Vasodilators like Hydralazine
Preload increases with
Exercise, Volume, Excitement
Force of contraction proportional to?
Preload
Ejection Fraction Formula Index for? Normal value Decreases in?
EF = SV/EDV
Index for ventricular contractility
Normally ≥ 55%
Decreases in Systolic HF
Pressure formula
P = Q x R
Resistance formula (2)
R = P/Q = (8 x viscosity x length)/π(r^4)
Viscosity depends on…
Increases with…
Hct
Increases with Polycythemia, Hyperproteinemic state (multiple myeloma), Hereditary spherocytosis
Viscosity decreases with
Anemia
Most of the total peripheral resistance due to
Arterioles
S1
Loudest at
Mitral and Tricuspid valves close
Loudest in Mitral area
S2
Loudest at
Aortic and Pulmonary valves close
Loudest at L sternal border
S3 When Associated with Sign of Normal in
In early diastole Associated with increased filling pressures MR, CHF Sign of dilated ventricles Normal in Pregnants and Children
S4
When
Caused by
Associated with
Atrial Kick in late diastole
Caused by high atrial pressure
Associated with ventricular hypertrophy
JVP wave
a: atrial contraction
c: RV contraction (tricuspid valve bulges into atrium)
x: atrial relaxation
v: RA filling
y: blood flow from RA to RV
Normal Splitting Physiology
S1 - A2-P2
Inspiration –> drop in intrathoracic pressure –> increased venous return to RV –> increased RV SV –> increased RV ejection time –> delayed closure of pulmonic valve
Inspiration also leads to increased capacity of pulmonary circulation which also delays P closing
Wide Splitting
Pathology
Seen in conditions with
Due to delayed RV emptying
Pulmonic stenosis, R bundle branch block
Fixed Splitting
Seen in
Pathophysiology
ASD. L-R shunt –> ⇑ RA and RV volumes –> ⇑ flow through pulmonic valves such that regardless of breath, valve closure greatly delayed
Paradoxical Splitting
PathoPhys
Seen in what conditions
Seen in conditions that delay LV emptying (Aortic Stenosis, Left Bundle Branch Block).
Reversal of A2 and P2
What can be heard in aortic area?
Systolic murmors: AS, Flow Murmur, Aortic Valve Sclerosis.
What can be heard over Left Sternal Border
Diastolic murmurs: AR, PR
Systolic murmurs: HOCM
What can be heard in Pulmonic Area?
Systolic ejection murmur: Pulmonic stenosis, Flow murmur from ASD or PDA.
What can be heard in the tricuspid area?
Pansystolic murmurs: Tricuspid Regurg, VSD
Diastolic murmurs: Tricuspid stenosis, ASD
What can be heard over Mitral area?
Systolic: MR
Diastolic: MS
ASD
Early presentation
PathoPhys
Later presentation
“Drs press forward”
Diastolic rumble and pulmonary flow murmur
Blood flow across ASD does not cause the murmur because there is no pressure gradient
The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery
Where is the best place to hear a PDA?
What does it sound like?
Due to
Left infraclavicular region. Continuous machine like murmur. Loudest at S2
Often due to congenital rubella or prematurity
Bedside Maneuver: Inspiration
Increased intensity of R heart sounds
Bedside Maneuver: Expiration
Increased intensity of L heart sounds
Bedside Maneuver: Hand Grip
What does it do physiologically
⇑systemic vascualr resistance.
⇑ intensity of MR, AR, VSD, MVP
⇓ intensity of AS, HOCM
Bedside Maneuver: Valsala
What does it do physiologically
⇓ venous return
Bedside Maneuver: Valsala
⇑ MVP and HOCM
Bedside Maneuver: Rapid Squatting
What does it do physiologically?
⇑ venous return, ⇑ preload, ⇑ afterload (if prolonged)
⇓ MVP and HOCM
Sound of MR Loudest at? Radiates? Enhanced by? Often due to?
Holosystolic high pitched blowing murmur.
Loudest at apex and radiates towards axilla
Enhanced by maneuvers that ↑ TPR (squatting, hand grip) and ↑ LA return (expiration)
Most often due to Ischemic heart disease, MVP, LV dilation, RF, infective endocarditis
Sound of TR Loudest at? Radiates? Enhanced by? Often due to?
Holosystolic high pitched blowing murmur.
Loudest at tricuspid area and radiates to R sternal border
Enhanced by maneuvers ↑ RA return (inspiration)
Most often due to RV dilation, RF, infective endocarditis
Aortic Stenosis Sound and Radiation Pressures Presentation Caused by
Crescendo-decrescendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets) that radiates towards carotids and loudest at heart base
P in LV > P in Aorta
“SAD” –> Syncope, Angina, Dyspnea
Pulsus Parvus et Tardus
Age related calcification or bicuspid valve
VSD
Sound
Location
Maneuvers
Holosystolic, harsh sounding murmur loudest at tricuspid area and ↑ by handgrip (increased afterload)
MVP Sound Location? When? Predisposes pts to Caused by Enhanced by
Late systolic crescendo murmur with midsystolic click (from sudden tensing of chordae tendineae)
Best heard over apex during S2
Predisposes to infective endocarditis
Caused by myxomatous degeneration, RF, chordae rupture.
Enhanced by maneuvers that ↓ venous return (standing, valsala)
Most frequent valvular lesion
MVP
Aortic Regurgitation Sound Presentation Due to Affected by
Immediate high pitched blowing diastolic decrescendo murmur.
Wide pulse pressure, bounding pulse, head bobbing.
Due to aortic root dilation, bicuspid endocarditis, RF.
↓ by vasodilators
↑ by hand grip
Mitral Stenosis Sound Pressures Due to Can lead to Enhanced by
Delayed rumble in late diastole with opening snap (abrupt halting of leaflets due to fusion)
P in LA (measured by PCWP) > P in LV
Due to RF and can lead to LA dilation
Enhanced by maneuvers that ↑ LA return (expiration)
Ventricular AP also occurs in
Bundles of His and Purkinje fibers
Phases of Ventricular AP
0: INa
1: Na channels inactivated, K channels open
2: Plateau. Ca channels open
3: Repolarization. K channels open. Ca channels close
4: Resting Potential. High K permeability
Ca enters cardiac myocytes by
Ca induced Ca release
Pacemaker AP Phases
0: Ca mediated upstroke
2: no plateau
3: Inactivation of Ca channels, Opening of K
4: Slow diastolic depolarization because of Na funny channels
What affects Slope of Phase 4 in pacemaker cells?
ACh and Adenosine –> ↓ Slope –> ↓ HR
Catecholamines –> ↑ Slope –> ↑ HR
P wave on EKG
Atrial depolarization
Speed of conduction of parts of heart
Purkinje > atra > ventricles > AV node
Speed of conduction of pacemaker cells
SA > AV > Bundle of His/Purkinje/Ventricles
PR interval represents
Normal value
Conduction delay through AV node
Normally < 200 msec
QRS Complex represents
Normally
Ventricular depolarization
Normally < 120 msec
QT interval represents
Mechanical contraction of the ventricles
T wave represents
Inversion may indicate
Ventricular repolarization
T wave inversion may indicate recent MI
ST segment
Isoelectric
Ventricles Depolarize
U Wave causes
HypoK, Bradycardia
Conduction pathway in heart
SA –> Atria –> AV –> Common Bundle –> Bundle Branches –> Purkinje Fibers –> Ventricles
Atrioventricular delay?
Allows for?
100 msec delay allows for ventricular filling
V Tach
Can progress to
What predisposes towards it
Treatment
Can progress to Vfib
Long QT interval predisposes towards it
Treatment is Magnesium Sulfate
Congenital Long QT syndrome
Defect in
Can present as
Defect in cardiac Na or K channels
Can present with congenitcal sensorineural deafness (Jervell and Lang Nielsen Syndrome)
Afib
ECG
Can lead to
Treatment
Irregularly irregular with no discrete P wave between irregularly spaced QRS
Can result in atrial stasis which leads to stroke
Treatment: anticoagulants, β Blockers, cardioversion, Ca Channel Blockers, Digoxin
Atrial Flutter
EKG
Treatment
Back to back P waves (sawtooth)
IA, IC, II, III, IV
V fib
EKG
Treatment
Erratic rhythm with no identifiable waves
Fatal without CPR and Defib
1st Degree AV Block
PR interval prolonged (>200 msec)
Asymptomatic
2nd Degree AV Block
Mobitz Type I
Wenckenbach
Progressive lengthening of PR interval until a beat is dropped
Usually asymptomatic
2nd Degree AV Block
Mobitz Type II
Treatment
Risk
Extra P waves
Treat with pacemaker
Can progress to 3rd degree black
3rd Degree AV Block
Treat with
Can be caused by
A and V beat independently
Treat with pacemaker
Can be caused by Lyme Disease
ANP
Released by
In response to
Leads to
Released by atrial myocytes in response to ↑ vol and atrial pressure.
Leads to vascular relaxation and ↓ Na reabsorption in medullary collecting tubule.
Constricts EA and dilates AA (via cGMP)
Aortic arch receptors
Transmit via … to … responds to …
Transmit via Vagus nerve to NTS in medulla and respond to ↑ BP only
Carotid Sinus
Transmits via … to … and responds to …
Transmits via glossopharyngeal nerve to NTS and responds to any change in BP
Baroreceptors
Course of signals
↓ BP –> ↓ stretch –> ↓ afferent baroreceptor firing –> ↑ efferent sympathetic firing and ↓ efferent parasympathetic firing –> vasoconstriction, ↑ HR, ↑ contractility, ↑ BP
Carotid Massage
↑ pressure on carotid artery –> increase stretch –> ↑ afferent firing –> ↓ HR
Cushings Rxn
Presentation
PathoPhys
HTN, Bradycardia, Respiratory Depression
↑ ICP constricts arterioles –> cerebral ischemia –> reflex HTN –> ↑ stretch –> Reflex baroreceptor induced bradycardia
Peripheral Chemoreceptors
Carotid and Aortic bodies stimulated by ↓ PO2 (< 60mmHg), ↑ PCO2, and ↓ pH
Central Chemoreceptors
Stimulated by change in pH and PCO2 of brain interstitial fluid
Do not directly respond to PO2
Organ with largest share of systemic CO
Liver
Organ with highest blood flow per gram of tissue
Kidney
Organ with largest O2 extraction
Heart
~80%. ↑ O2 demand must be met with ↑ blood flow
Pressures in the Heart
RA: less than 5 RV: 5-25 PA: 25-10 LA: less than 12 LV: 130-10 Aorta: 130-90
Approximation of P in LA
Measured with…
PCWP measured with Swan-Ganz catheter
Autoregulation of blood flow to heat mediated by
Local metabolites - CO2, Adenosine, NO
Autoregulation of blood flow to Brain mediated by
Local metabolites - CO2, pH
Autoregulation of blood flow to Kidneys mediated by
Myogenic and tubuloglomerular feedback
Autoregulation of blood flow to Lungs mediated by
Hypoxia vasoconstriction
Autoregulation of blood flow to Skeletal Muscle mediated by
Local metabolites - lactate, adenosine, K
Autoregulation of blood flow to Skin mediated by
Sympathetic stimulation for temperature control
Starling Equation
J = K[(Pc-Pi)-(πc-πi)]
Edema from Heart Failure in terms of Starling Equation
↑ Pc pushes fluid out of capillaries
Edema from ↓ plasma proteins in terms of Starling Equation
↓ πc
Edema from ↑ capillary permeability in terms of Starling Equation
What causes a change in capillary permeability?
↑ K
Toxins, Infections, Burns
Edema from ↑ interstitial fluid colloid osmotic pressure in terms of Starling Equation
Caused by
πi
Caused by lymphatic blockage
Blue Baby
PathoPhys
Causes
R-L shunt Tetralogy of Fallot (most common) Transposition of the great vessels Persistent Truncus arteriosus (with PDA) Tricuspid atresia Total Anomalous Pulmonary Venous Return
What usually accompanies a persistent truncus arteriosus?
PDA
What accompanies TAPVR?
ASD and sometimes PDA to allow for R-L shunt to maintain CO
Blue Kids
PathoPhys
Causes
Frequency of causes
L-R shunt
VSD > ASD > PDA
Eisenmengers Syndrome
PathyPhys
Presents as
Uncorrected VSD, ASD, PDA causes compensatory pulmonary vascular hypertrophy –> PHTN
As pulmonary resistance ↑, the shunt reverses and becomes R-L
Presents as Cyanosis, Clubbing, Polycythemia
Tetralogy of Fallot Caused by Characteristics Shunting? XR Treatment
Caused by anterosuperior displacement of infundibular septum
PROV
Pul stenosis, RVH, Overriding Aorta (overrides VSD), VSD
R-L shunting –> cyanosis
Boot-shaped heart on XR
Surgery
What do pts with ToF do to relieve symptoms
Squatting –> ↓ blood flow to legs –> ↑ Resistance –> ↓ R-L shunt across VSD
Transposition of the Great Vessels
Only compatible with life if there is a
Due to
Treatment
Only compatible with life if there is a VSD, PDA, or PFO
Due to failure of the aorticopulmonary septum to spiral
Surgery
Coarctation of the aorta
Results in
Aortic Regurgitation
Coarctation of the aorta: Infantile Type
Location of stenosis?
Associated with?
On physical exam remember to check…
Stenosis proximal to ductus arteriosus
Associated with Turners Syndrome
Check femoral pulses
Coarctation of the aorta: Adult Type
Location of stenosis?
Associated with?
On physical exam remember to check…
Stenosis distal to ligamentum arteriosum
Associated with bicuspid aortic valve
On Physical Exam: Notching of the ribs due to collateral circulation, HTN in upper extremities, Weak pulses in lower extremities
Presentation of uncorrected PDA
Cyanosis in the lower extremities (differential cyanosis)
Consequences of PDA on the heart?
L-R shunt –> RVH and/or LVH and failure
Cardiac defect associated with 22q11 syndrome (DiGeorge syndrome)
Truncus arteriosus and ToF
Cardiac defect associated with Down Syndrome
ASD, VSD, AVSD (endocardial cushion defect)
Cardiac defect associated with Congenital Rubella?
Septal defects, PDA, Pulmonary artery stenosis
Cardiac defect associated with Turners Syndrome
Preductal coarctation of the aorta
Cardiac defect associated with Marfan’s Syndrome
Aortic insufficiency and dissection (late)
Cardiac defect associated with diabetic mother
Transposition of the great vessels
TAPVR pathophys?
Pulmonary veins drain into R heart
Definition of HTN?
> 140/90
Risk factors for HTN
Age, diabetes, obesity, smoking, genetics
Risk of HTN in different races?
Black > White > Asian
Primary vs Secondary HTN
90% primary. 10% Secondary
Primary HTN
Related to ↑ CO and TPR
Secondary HTN usually caused by
Renal disease
Malignant HTN definition and prognosis
> 180/120 and rapidly progressing
HTN predisposes pts to
Aterosclerosis, LVH, Stroke, CHF, Renal Failure, Retinopathy, Aortic Dissection
Atheroma definition
Lipid plaques in blood vessel walls
Xanthomas definition. Where are they found?
Plaques or nodules composed of lipid laden histiocytes in the skin. Found on eyelids (xanthelasma), tendons (Tendinous Xanthomas) (esp Achilles tendon)
Corneal arcus definition.
Sign of?
Lipid deposits in cornea.
Nonspecific (arcus senilis)
Monckeberg PathoPhys Usually affects Problem? Layers involved?
Calcification of media of arteries. Especially radial or ulnar. Usually benign and does not obstruct blood flow. Only involves media, not intima
Arteriolosclerosis
Types
Where is each type present?
Hyaline: Thickening of small arteries seen in essential HTN and DM
Hyperplastic: “onion skinning” seen in MHTN
Atherosclerosis
Definition
What kind of arteries
Where in the artery?
Fibrous plaques and atheromas for in the intima of elastic arteries and large/medium muscular arteries.
Modifiable risk factors of Atherosclerosis
Smoking, HTN, Hyperlipidemia, Diabetes
Non-modifiable risk factors for Atherosclerosis
Age, Male, Postmenopausal women, family history
Progression of Atherosclerosis
Endothelial cell dysfunction –> macs and LDL accumulation –> Foam cells –> Fatty streaks –> SM migration (PDGF and FGF), proliferation, and ECM deposition –> Fibrous plaque
Complications of Atherosclerosis
Aneurysm, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
Common locations of Atherosclerosis
Abdominal Aorta > coronary arteries > Popliteal arteries > carotid arteries
Atherosclerosis presentation
angina, claudication, but may be asymptomatic
Abdominal Aortic Aneurysm
Classic pt?
Atherosclerosis in Male smoker >50 with HTN
Thoracic Aortic Aneurysm associations
HTN, Marfan’s (Cystic Medial Necrosis), and Tertiary Syphilis
Aortic Dissection Definition Associations Presentation CXR Can result in...
Longitudinal tear forms false lumen
Associated with HTN, Bicuspid Aortic Valve, Cystic Medial Necrosis, Connective Tissue Disorder (i.e. Marfan’s)
Presents with tearing chest pain radiating to the back
CXR shows mediastinal widening with false lumen larger than true lumen
Can result in pericardial tamponade, aortic rupture
How narrow must the coronary artery be to produce angina?
> 75% but this does not produce myocyte necrosis
Stable Angina
Definition
Mostly due to
EKG
Retrosternal chest pain with exertion
Mostly secondary to atherosclerosis
ST depression on ECK
Prinzmetals Angina
Due to
EKG
Secondary to coronary artery vasospasms
ST elevation on EKG
Unstable Angina
Definition
Caused by
EKG
Worsening chest pain at rest or with minimal exertion. Caused by thrombosis with incomplete coronary artery occlusion. ST depression on ECK
Coronary Steal Syndrome
Vasodilators aggravate ischemia by shunting blood from affected area to region of higher perfusion
Myocardial infarction
Definition
Most often due to…
ECK
Complete occulsion of coronary artery producing myocyte necrosis.
Most often due to thrombosis
ST depression progressing to ST elevation
ST depression means
Subendocardial wall damage
ST elevation means
Transumarl wall damage
Sudden Cardiac Death
Definition
Most commonly due to
Associated with
Death from cardiac cause within 1 hour of symptom onset
Most commonly due to lethal arrhythmia (Vfib)
Associated with CAD
Chronic Ischemic Heart Disease
Definition
Progresses to
Chronic ischemic myocardial damage. Progresses to CHF
MI presentation
Diaphoresis, naseau, vomiting, retrosternal pain, pain in left arm and/or jaw, dyspnea, fatigue
0-4 hours after MI
Gross
LM
Risk
Gross: none
LM: none
Risk: Arrhythmias, CHF exacerbation, shock
4-12 hours after MI
Gross
LM
Risk
Gross: Dark mottling. Pale with tetrazolium stain
LM: Early coagulative necrosis, edema, hemorrhave, wavy fibers
Risk: Arrhythmias
12-24 hours after MI
Gross
LM
Risk
Gross: Dark mottling. Pale with tetrazolium stain
LM: Contraction bands from reperfusion injury, Release of necrotic cell contents into blood, Beginning of neutrophil migration
Risk: Arrhythmias
1-3 days after MI
Gross
LM
Risk
Gross: hyperemia
LM: Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation. Neutrophil migration
Risk: Fibrinous pericarditis
2-14 days after MI
Gross
LM
Risk
Gross: Hyperemic border with centrally yellow-brown softening (maximally yellow at day 10)
LM: Macs. Granulation tissue at margins
Risk: Free wall rupture –> tamponade, Papillary muscle rupture, Aneurysm, IV septal rupture
2-Several weeks after MI
Gross
Risk
Gross: Gray-white tissue
Dresslers syndrome
Diagnosis of MI
EKG and blood tests
EKG is gold standard in the first 6 hours. Troponin I rises after 4 hours and is elevated for 7-10 days (specific). CKMB predominantly found in myocardium but also skeletal muscle. Useful in diagnosing reinfarction because returns to normal after 48 hours
Transmural infarct: EKG
ST elevation. Pathological Q wave
Subendocardial infarcts
EKG
Necrosis?
ST depression. Necrosis of <50% of ventricle wall
EKG diagnosis of Anterior wall infarct based on leads showing Q waves?
“SAL”
Anteroseptal: V1-V2 (LAD)
Anterior: V1-V4 (LAD
Anterolateral: V4-V6 (LCX)
EKG diagnosis of Lateral or Inferior wall infarct based on leads showing Q waves?
“Love Is Incredible. Nothing Like It”
Lateral: I, aVL (LCX)
Inferior: II, III, aVF
Dresslers Syndrome
PathoPhys
Autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI
Causes of Dilated Cardiomyopathies
Most common cause = idiopathic (>50%)
“A Bold, Devout Christian Crusader Charged Petrified Hindus”
Alcohol, wet Beriberi, Doxorubicin, Chagas, Coxackie B, Cocaine, Postpartum, Hemochromatosis
Dilated Cardiomyopathy Common? Sound, US, CXR What kind of hypertrophy? What kind of dysfunction? Treatment
Most common cardiomyopathy (90%)
S3, US = dilated heart, CXR = balloon
Eccentric hypertrophy w/ sarcomeres added in series –> systolic dysfunction?
Treat w/ Na restriction, ACEI, diuretics, digoxin, transplant
HOCM: PathoPhys
Genetics
Association
Hypertrophied IV septum is too close to mitral valve and obstructs aortic outflow
60-70% are caused by autosomal dominant mutation in β myosin heavy chain –> disorganized, tangled myocardial fibers
Associated with Friedreich’s Ataxia
HOCM
Classic Pt
Size, Sound, Murmur, Impulses
Treatment
Cause of death in young athletes
Normal sized heart, S4, Systolic murmur, apical impulses
Treat with II or nonDHP IV
HOCM
Hypertrophy
Kind of dysfunction?
May produce?
Concentric hypertrophy with sarcomeres added in parallel
Diastolic dysfunction ensues
May produce syncopal episodes.
Causes of Restrictive Cardiomyopathies
“A SHELF”
Amyloidosis, Sarcoidosis, Hemochromatosis, Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffers Syndrome (endomyocardial fibrosis with eosinophils), Fibrosis (post radiation)
What kind of dysfunction ensues in restrictive cardiomyopathies?
diastolic
Treatment for CHF
Mortality reducers?
Symptom relief?
Both?
Mortality reducers: ACEI, II (except in acute decompensated HF), ATII antagonists, Spironolactone
Symptom relief: Thiazide and Loop Diuretics
Both: Hydralazine and Nitrates
CHF presentation
Dyspnea, fatigue, edema, rales
What produces Cardiac Dilation?
Greater EDV
Why do Pts experience dyspnea on exertion
Failure of CO to Increase
Results of LHF?
Pul Edema: transudation of fluid into alveoli. Hemosiderin laden Macs in lung
Paroxysmal Nocturnal Dyspnea and Orthopnea: Increased venous return –> pulmonary vascular congestion
Results of RHF?
Hepatomegaly (nutmeg liver), Peripheral edema, JVD
Bacterial Endocarditis Presentation
“FROM JANE”
Fever, Roth Spots, Osler’s Nodes, Murmur, Janeway Lesions, Anemia, Nail-bed hemorrhages, Emboli
Roth Spots
Round, white spots on retina surrounded by hemorrhage
Osler’s Nodes
Tender raised lesions on finger and toe pads caused by IC deposition
Janeway Lesions
Small, painless, erythematous lesions on palm or sole. Hemorrhagic
Complications of Bacterial Endocarditis
Chordae rupture, Glomerulonephritis, Suppurative pericarditis, emboli
Site of infection in Bacterial endocarditis?
Usually Mitral Valve
Tricuspid in IV drug users
Main Causes of Bacterial Endocarditis
Acute: S aureus (large vegetations on normal valve)
Subacute: S. viridans (small vegetations on abnormal or diseased valve)
Common after dental procedures
Organisms Causing Tricuspid Bacterial Endocarditis
S aureus, Pseudomonas, Candida
Causes of non bacterial endocarditis
Malignancy, Hypercoagulable state, SLE
Bacterial endocarditis in colon cancer caused by
S bovis
Bacterial endocarditis with a prosthetic valve caused by…
S epidermidis
Rheumatic Fever Presentation
“FEVERSS”
Fever, Erythema marginatum, Valve damage, ESR ↑, Red-Hot Joints (migratory polyarthritis), Subcutaneous nodules, St. Vitus dance (Sydenham’s Chorea)
RF Organisms causing it Valves affected Early vs Late Type of Disease?
GAS (β hemolytic strep)
mitral > aortic»_space;> tricuspid
Early MR, late MS
Type II Hypersensitivity Rxn with Abs against bacterial M protein
RF
Histology
Blood titers
Aschoff Bodies (granuloma with giant cells), Antischkow cells (activated histiocytes), Elevated ASO
Acute Pericarditis
Presentation
PE findings
EKG
Sharp pleuritic pain relieved by sitting up and leaning forward.
Friction rub
Widespread ST elevation and/or PR depression
Fibrinous Pericarditis
Causes
Findings
Dressler’s, Uremia, Radiation
Loud Friction Rub
Causes of Serous Pericarditis
Viral (often resolves spontaneously), noninfectious inflammatory disease (SLE, RA)
Causes of SuppurativePurulent Pericarditis
Bacterial infection (Pneumococcus Streptococcus) Rare now with antibiotics
Cardiac Tamponade
What happens to diastolic pressures?
HR? Sounds? BP? PE findings?
Diastolic pressures equalize in all 4 chambers. HR↑, Distant heart sounds, hypotension and Pulsus Paradoxus, JVD
Pulsus Paradoxus
Definition
Seen in what diseases?
↓ in systolic P by >10mmHg during inspiration
Seen in pericarditis, tamponade, asthma, obstructive sleep apnea, croup
Syphilitic Hearth Disease
Causative agent
MoA
Risk for
Tertiary Syphilis disrupts vasa vasorum of the aorta and vessel wall atrophys and dilates.
Risk for aortic aneurysm (ascending and arch) and aortic insufficiency (dilation of aorta and valve ring)
In Syphilitic Hearth Disease, what happens to the aortic root and ascending aortic arch? How does the aorta appear?
Calcification
Tree bark appearance
Cardiac Myxoma Common? Usually described as Location Present with
Most common primary cardiac tumor in adults. “ball valve” obstruction of LA presents with multiple syncopal episodes
Rhabdomyomas
Common?
Associated with?
Most common primary cardiac tumor in children. Associated with Tuberous Sclerosis
Most common cardiac tumor?
Metastatic (melanoma, lymphoma)
Kussmaul’s Sign
Definition
Seen in
↑ in JVP during inspiration because negative intrathoracic pressure not transmitted to the heart
Constrictive Pericarditis, Restrictive Cardiomyopathy, RA or RV tumors, Cardiac Tamponade
Raynaud's Phenomenon PathoPhys Location Disease Syndrome Presentation
↓ blood flow to skin due to arteriolar constriction in response to cold or stress
Fingers and toes
Disease if primary (idiopathic)
Syndrome if secondary to connective tissue disease, SLE, CREST
Cyanosis of fingertips and toes
Temporal Giant Cell Arteritis Kind of vasculitis? Classic Pt Presentation Risk of Associated with Affects which vessels? Histo Blood Treatment
Large vessel
Old female with unilateral temporal headache and jaw claudication
Risk of blindness due to ophthalmic artery occlusion
Associated with Polymyalgia Rheumatica
Branches of Carotid artery.Focal Granulomatous inflammation, ↑ESR, Treat with corticosteroids
Takayasu's Arteritis Kind of vasculitis? Classic Pt Presentation Affects which vessels? Histo Blood Treatment
“FAN My Skin On Wed”
Large vessel
Asian female < 40 with weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
Granulomatous thickening of aortic arch and proximal great vessels, ↑ESR
Treat with corticosteroids
Polyarteritis Nodosa Kind of vasculitis? Classic Pt Presentation Affects which vessels? Histo What mediates the disease? Ages of lesions? Arteriogram Treatment
“Scalded My Right Hand on the PAN”
Medium vessels
Young Adult with HepB with fever, wt loss, malaise, headache, abdominal pain, melena, HTN, Neuro dysfunction (wrist drop), Cutaneous eruptions, renal damage
Renal and Visceral vessels
Transmural inflammation with fibrinoid necrosis
IC mediated
Typically of different ages
Arteriogram shows many aneurysms and constrictions
Corticosteroid and cyclophosphamide
Kawasaki Disease Kind of vasculitis? Classic Pt Presentation Affects which vessels? Risk of Treatment
Medium vessels
“FEAR ME”
Asian child < 4 with Fever, conjunctival infection (Eye), cervical lymphAdenitis, desquamating Rash, Mouth and Extremity erythema
Coronary vessels
Risk of coronary aneurysm –> MI, Rupture
Treat with IV Igs and Aspirin
Buerger’s Disease (Thromboangiitis Obliterans)
Kind of vasculitis?
Classic Pt Presentation
Treatment
Medium vessels
“SCRAPS”
Male < 40 with Segmenting Thrombosing vasculitis, Claudication (may lead to gangrene and auto-amputation), Raynaud’s, Smoker, Painful, Superficial Nodular Phlebitis
Treat with smoking cessation
Microscopic Polyangiitis Kind of vasculitis? Histo Organs involved w/ manifestation? Blood Treatment
Small vessels Necrotizing vasculitis w/ No Granulomas Lungs, Kidney (Pauci Immune Glomerulonephritis), and Skin (Palpable Purpura) P-ANCA Cyclophosphamide and Corticosteroids
Wegener's Granulomatosis (Granulomatosis with Polyangiitis) Kind of vasculitis? Presentation Histo Blood CXR Treatment
Small vessels Upper Respiratory Tract: Perforated nasal septum, sinusitis, otitis media, mastoiditis Lower RT: Hemoptysis, Cough, Dyspnea Renal: Hematuria, RBC Casts Focal Necrotizing vasculitis + Necrotizing granulomas in the lung and upper airway + Necrotizing glomerulonephritis c-ANCA Large Nodular Densities Cyclophosphamide and corticosteroids
Churg Strauss Syndrome Kind of vasculitis? Classic Presentation But can also affect Histo Blood
Small vessels
“BEAN SAP? No, Go to Hell”
Blood Eosinophils, Asthma, Neuropathy (food/wrist drop), Sinusitis, Allergies, Palpable Purpura, glomeruloNephritis (pauci immune), GI, Heart
Granulomatous, necrotizing vasculitis w/ eosinophilia
p-ANCA + ↑ IgE
Henoch-Schonlein Purpura Kind of vasculitis? Most common vasculitis in... Classic Presentation Disease Mediated by Associated with Age of lesions?
Small vessels Most common vasculitis in children "NAPA" Child following URI with Nephropathy, Abdominal pain (melena), Purpura, Arthralgia Mediated by IgA complex deposition Associated with IgA nephropathy Multiple lesions of same age
Essential HTN therapy
ACEI, ARB, Diuretics, IV
When are II contraindicated?
Cardiogenic shock and must be used with caution in decompensated CHF
Treatment for Diabetes Mellitus?
ACEI, ARB, Diuretics, II, α blockers, IV
Ca Channel Blockers Names MoA Used to treat Tox
Verapamil, Diltiazem, Nifedipine, Amlodipine
–/ Voltage gated L-type Ca channel in plasma membrane
Used to treat HTN, Angina, Arrhythmias (not N), Prinzmetals Angina, Raynaud’s
Cardiac depression, AV block, Peripheral edema, Flushing, Dizziness, Constipation
Hydralazine MoA Used to treat First line therapy for Coadministration Tox Contraindicated in
↑cGMP –> Smooth Muscle relaxation. Vasodilates arterioles > veins –> ↓ afterload
Used to treat HTN, CHF
First line therapy for HTN in pregnancy with methyldopa
Coadministered with II to –/ reflex tachycardia
Compensatory tachycardia, fluid retention, nausea, headache, angina, Lupus.
Contraindicated in Angina/CAD
Treatment for MHTN
Nitroprusside (short acting) –> Release of NO –> ↑cGMP –> Smooth Muscle relaxation. Can cause cyanide poisoning
Fenoldopam = D1 agonist –> coronary, peripheral, renal, and splanchnic vasodilation. ↓ BP and ↑ Natriuresis
Nitric Oxide (NO) Releasing Drugs Names MoA Use Tox
Nitroglycerin, Isosorbide, Dinitrate
NO –> ↑cGMP –> Smooth Muscle relaxation. Dilates veins > arteries –> ↓ preload
Used to treat angina and Pul Edema
Reflex tachycardia, Hypotension, Flushing, Headache, Monday disease (industrial exposure)
Goal of Antianginal therapy
Reduce O2 demand of myocardium
Reduces Contractility, Afterload, Rate, Size (wall tension = Preload)
Nitrates as Antianginal EDV BP Contractility HR Ejection time MVO2
EDV ↓ BP ↓ Contractility ↑ (response) HR ↑ (response) Ejection time ↓ (response) MVO2 ↓
II as Antianginal EDV BP Contractility HR Ejection time MVO2
EDV ↑ BP ↓ Contractility ↓ HR: ↓ Ejection time: ↑ MVO2: ↓
Nitrates + II as Antianginal EDV BP Contractility HR Ejection time MVO2
EDV: No change or ↓ BP: ↓ Contractility: NC HR: ↓ Ejection time: NC MVO2: ↓↓
Which IV are similar to Nitrates?
Which IV are similar to II?
Nitrates: Nifedipine
II: Verapamil
Partial β blockers contraindicated in angina
Pindolol, Acebutolol
Strawberry Hemangioma Benign or malignant? What kind of vessels? Time and frequency Course
Benign capillary hemangioma of infancy
Appears in first few weeks of life
1/200 births
Grows rapidly and regresses spontaneously at ages 5-8
Cherry Hemangioma Benign or malignant? What kind of vessels? Time and frequency Course
Benign capillary hemangioma of the elderly
Does not regress
Frequency increase with age
Cystic Hygroma
What kind of growth?
Where on body?
Associated with?
Cavernous lymphangioma of the neck. Associated with Turners Syndrome
Pyogenic Granuloma
What kind of tumor?
What can it do?
Associations?
Polyploid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy
Glomus Tumor Benign or malignant Painful or not? Color? Location? Arises from?
Benign, painful, red-blue, tumor of fingernails. Arises from modified smooth muscle cells of glomus body
Bacillary Angiomatosis Benign or malignant Which vessels? Location? What kind of Pts? Cause? Frequently confused with
Benign capillary skin papules found in AIDS pts. Caused by Bartonella henselae infection. Frequently mistaken for Kaposi Sarcoma
Angiosarcoma Frequency? Kind of malignancy? Location on body? Associated with what kind of pts? Prognosis?
Rare blood vessel malignancy typically occuring in head, neck and breast areas. Associated with pts recieving radiation therapy (breast cancer, Hodgkin’s lymphoma).
Very aggressive and difficult to resect due to delayed diagnosis
Lymphangiosarcoma
What kind of malignancy?
Associated with?
Lymphatic malignancy associated with persistent lymphedema (post-radical masectomy)
Kaposi Sarcoma What kind of malignancy Location on body Associated with Frequently mistaken for...
Endothelial malignancy found on skin, mouth, GI tract, respiratory tract. Associated with HHV8 and HIV. Frequently mistaken for bacillary angiomatosis
Sturge Weber Disease
What kind of disease?
Vessels affected?
Manifestation?
Congenital
Capillary sized blood vessels
Port-Wine stain (nevus flammeus) on face, Ipsilateral leptomeningeal angiomatosis (intracerebral arteriovenous malformation), Seizures, early onset Glaucoma
HMG CoA Reductase Inhibitors (Statins) LDL HDL Tri MoA Tox
LDL ↓↓↓ HDL ↑ Tri ↓ MoA --/ conversion of HMG-CoA to mevalonate (a cholesterol precursor) Hepatotoxic (↑LFTs), Rhabdomyolysis
Niacin (Vit B3) LDL HDL Tri MoA Tox
LDL ↓↓
HDL ↑↑
Tri ↓
MoA Inhibits lipolysis in adipose tissue. Reduced hepatic VLDL secretion
Red, flushed face (↓ by aspirin). Hyperglycemia (acanthosis nigricans), Hyperuricemia (exacerbates gout)
Bile Acid Resins Names LDL HDL Tri MoA Tox
Cholestyramine, Colestipol, Colesevelam
LDL: ↓↓
HDL: Slightly ↑
Tri: Slightly ↑
Prevents intestinal reabsorption of bile acids forcing liver to use cholesterol to make Bile
Bad taste, GI discomfort, ↓ absorption of soluble vitamins, Cholesterol Gallstones
Cholesterol Absorption Blockers Names LDL HDL Tri MoA Tox
Ezetimibe LDL: ↓↓ HDL: - Tri: - MoA: Prevents cholesterol reabsorption in small intestine brush border Rare ↑ in LFTs, Diarrhea
Fibrates Names LDL HDL Tri MoA Tox
Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate
LDL ↓
HDL ↑
Tri ↓↓↓
Upregulate LPL –> ↑ TG clearance
Myositis, hepatotoxic (↑ LFTs), cholesterol gallstones
Cardiac Glycosides Names Bioavailability Protein bound? T1/2 Excretion
Digoxin 75% bioavailability 20-40% protein bound T1/2 40h Urinary excretion
Digoxin
MoA
Use
–/ Na/K ATPase. ↑ Na –/ Na/Ca exchanger –> ↑ Ca –> ↑ contractility
–> Vagus Nerve –> ↓ HR
Used to treat CHF (↑ contractility), Afib (↓ conduction at AV node, depression at SA node)
Digoxin
Tox
EKG
Factors predisposing to toxicity
Cholinergic –> nausea, vomiting, diarrhea, blurry yellow vision
AV block, Hyperkalemia,
↑ PR, ↓QT ST scooping, T wave inversion, arrhythmias
Predisposition: renal failure (↓ excretion), Hypokalemia (permissive binding of Na/K pump), Quinidine (↓ clearance. displaces digoxin from tissue binding sites)
Digoxin OD antidote
Slowly normalize K, Lidocaine, Cardiac Pacer, Anti Digoxin Fab Fragment, Mg
Class I antiarrhythmics What kind of molecules What do they do? Dependence? Toxicity is aggravated by...
Local anesthetics
↓ conduction in depolarized cells. ↓ slope of phase 0. ↑ threshold for firing in abnormal pacemaker cells
Are state dependent (selective depress frequently depolarized tissues)
Hyperkalemia ↑ toxicity
Class IA antiarrhythmics Name Action on AP? Action on EKG? Regions of heart? Especially useful in treating
Procainamide, Disopyramide, Quinidine ↑ AP duration. ↑ effective refractory period ↑ QT Affect both Atria and Ventricles Reentrant and Ectopic SVT and Vtach
Class IA antiarrhythmics
Toxicity
Thrombocytopenia, torsades de pointes
Q –> cinchonism (headache + tinnitus)
P –> SLE
D–> heart failure
Class IB antiarrhythmics Names Affect on AP? Preferentially affects Useful in Tox
Lidocaine, Mexiletine, Tocainide, (Phenytoin)
↓ AP duration
Preferentially affects ischemic or depolarize Purkinje and ventricular tissue
Useful in acute ventricular (Is Best Post MI) + digitalis induced arrhythmias.
Local anesthetic, CNS↑↓, CV depression
Class IC antiarrhythmics Name Affect on AP? Useful in Usually only used as Affect on AV node Toxicity Contraindicated
Flecainide, Propafenone
No affect on AP duration
Useful in Vtach that progresses to Vfib + intractable SVT
Usually used only as a last resort for refractory tachyarrhythmias
Prolongs refractory period in AV node
Tox: Proarrhythmic
Contraindicated Post MI and structural heart disease
Class II antiarrhythmics Names MoA Affect on AP Area particularly sensitive? Use
Metoprolol, propanolol, esmolol (very short acting), atenolol, timolol
Decrease SA and AV nodal activity by ↓ cAMP –> ↓ Ca currents
Decreases phase 4 slope in pacemaker cells
AV node particularly sensitive (↑ PR interval)
VTach, SVT, Slows ventricular rate during Afib + Aflutter
Class II antiarrhythmics
Tox
BBC Loses Viewers in Houston
Bradycardia (AV block, CHF), Bronchoconstriction (aggravates asthma), Claudication, CNS effects (sedation), Lipids (metoprolol), Vivid dreams, Hypoglycemia masked
Propanolol can exacerbate
Vasospasms in Prinzmetal’s angina
Beta Blocker OD treatment
Glucagon
Class III antiarrhythmics Names MoA Effect on AP Used when EKG effects
"AIDS" Amiodarone, Ibutilide, Dofetilide, Sotalol --/ K channels ↑AP duration, ↑ERP, Used when other antiarrhythmics fail ↑QT interval
Class III
Toxicity
Sotolol: TdP, excessive β Block
Ibutilide: TdP,
Amiodarone: Pul Fibrosis, Hepatotoxic, Hypo/HyperThyroidism
Amiodarone Toxicity
Real Classification
Pul Fibrosis, Hepatotoxic, Hypo/HyperThyroidism (40% I by weight), Corneal deposits, Skin deposits (blue/gray) –> photodermatitis, neurological effects, constipation, AV affects (bradycardia, heart block, CHF)
Affects lipid membranes so has I, II, III, and IV activity
Class IV antiarrhythmics Names Affects on AP Used to Tox
Verapamil, Diltiazem
↓ conduction velocity, ↑ERP, ↑PR
Used to prevent nodal arrhythmias (SVT)
Constipation, Flushing, Edema, CV (CHF, AV block, Sinus node depression
Adenosine MoA Drug of choice for Speed Toxicity Affects blocked by
↑K out of cells –> hyperpolarization and ↓ Ca current.
Drug of choice for SVT (diagnosis and treatment)
Very short acting (15 sec)
Flushing, hypotension, angina
Blocked by caffeine and theophylline
Mg used to treat
TdP and Digoxin toxicity
Names of β1 selective β Blockers
Start with A-N
Names of non-selective β Blockers (β1 and β2)
Start with O-Z
Breathing in a pt with CHF
Cheyne Stokes Breathing
