Cardio Flashcards
What is the microscopic anatomical difference between layers of elastic and muscular arteries?
elastic arteries contain MORE elastic tissue in the tunica media than muscular arteries
What are the location/boundaries of the pericardium?
Lies within the mediastinum; inferior wall of fibrous pericardium attaches to diaphragm
What is the structure of the pericardium?
3 layers (outermost to inner):
- Fibrous pericardium
- Parietal layer of serous pericardium
- Pericardial cavity
- Visceral layer of serous pericardium
What nerve innervates the pericardium?
Phrenic nerve
What is the most posterior part of the heart?
Left atrium
What is the most anterior part of the heart?
Right ventricle
What is the most commonly injured part of the heart in trauma?
Right ventricle
Enlargement of the left atrium can cause what pathologies?
Mitral stenosis; compression of esophagus (dysphagia), compression of L laryngeal nerve causing hoarseness (Ortner syndrome)
Where is the best place to listen to the mitral valve?
5th L ICS MCL (apex)
Where is the best place to listen to the tricuspid valve?
5th L ICS
Where is the best place to listen to the pulmonic valve?
2nd L ICS
Where is the best place to listen to the aortic valve?
2nd R ICS
Where is Erb’s point?
3rd L ICS
What are the murmurs associated with the mitral valve and how do they sound?
Mitral regurgitation (holosystolic)
Mitral valve prolapse - systolic (midsystolic click)
Mitral stenosis (diastolic)
What pathology are associated with the tricuspid valve? For murmurs, know systolic vs diastolic.
Tricuspid regurgitation (holosystolic)
Ventricular septal defect (holosystolic)
Tricuspid stenosis (diastolic)
What pathology are associated with the pulmonic valve? For murmurs, know systolic vs diastolic.
All systolic ejection murmurs
Pulmonic stenosis
Atrial septal defect
Flow murmur
What pathology are associated with the aortic valve? For murmurs, know systolic vs diastolic.
All systolic murmurs
Aortic stenosis
Flow murmur (physiologic murmur)
What pathology are associated with the erb’s point? For murmurs, know systolic vs diastolic.
Aortic regurgitation (diastolic)
Pulmonic regurgitation (diastolic)
Hypertrophic cardiomyopathy (systolic)
At erb’s Point we get High
What pathology are associated with S3?
EARLY diastolic pathology
Mitral regurgitation
HF
Volume overload
Can be normal
What pathology are associated with S4?
LATE diastolic pathology
Hypertrophy
Pressure overload
Extreme HTN
ALWAYS ABNORMAL
S4 Dose Have Pretty Extreme Appetite
What causes the sound you hear for S1?
What part of the heart cycle occurs after S1 and before S2?
Where is it loudest?
Mitral and tricuspid valves closing
Systole
Mitral area
What causes the sound you hear for S2?
What part of the heart cycle occurs after S2 and before the next S1?
Where is it loudest?
Aortic and pulmonic valves closing
Diastole
L upper sternal area
Explain the pathway of conduction throughout the heart
SA node > atria > AV node > IV septum/Bundle of His > L+R bundle branches > purkinje fibers > ventricles
Explain how contraction of the heart is stimulated
Contraction stimulated by conduction system; ion flow across cardiac muscle cells initiates action potent ion and leads to contraction
Then, heart resets and returns to baseline and it all repeats
Where in the heart conduction pathway does the signal slightly delay? Why?
AV node; this is the only place there is no fibrous barrier between atria and ventricles, less gap junctions; allows time for atria to empty blood into ventricles prior to contraction
Control of the conduction pathway!
How does the cardiac conduction pathway begin?
Self excitation of SA node; caused by leaky sodium and calcium ions inward and rising resting membrane potential
How are purkinje fibers able to instantaneously transmit cardiac impulse through ALL of ventricular muscle?
Higher permeability of gap junctions at intercalated discs
What would you call a pacemaker anywhere else besides SA node?
Ectopic pacemaker
Explain the effect parasympathetic stimulation on the heart conduction pathway
Vagal n stimulation at SA/AV nodes > releases Ach at vagal endings, increasing permeability of membrane to K+ ions > increases membrane negativity (hyperpolarization) > tissue less excitable
Decreased SA node rhythm > decreased HR
Decreased excitability of AV junctional fibers b/w atrial muscle and AV node > slows transmission of cardiac impulses to ventricles
Explain the effect sympathetic stimulation on the heart conduction pathway
Sympathetic nerves most concentrated in ventricular muscle
NE released at nerve endings > stimulate beta-1 adrenergic receptors > increases cardiac rhythmicity and conduction > increased rate of SA node > increased rate of conduction and level of excitability throughout heart > increased force of contraction (esp ventricles)
Increased heart force + HR
What does the P wave of the cardiac cycle represent?
Atrial depolarization; followed by atrial contraction
What does the QRS complex of the cardiac cycle represent?
Ventricular depolarization; followed by ventricular contraction
What does the T wave of the cardiac cycle represent?
Ventricular repolarization; slightly before isovolumic relaxation, ventricles remain contracted until end of T wave
What does the R-R interval of the cardiac cycle represent?
Rate of one single cardiac cycle/heartbeat
What does the P-R/P-Q interval of the cardiac cycle represent?
Depolarization of atria to start of ventricle contraction
What does the Q-T interval of the cardiac cycle represent?
Depolarization and repolarization of ventricles
What would inversion of a T wave on an EKG indicate?
Ischemia or recent MI
What would a pathological U wave on an EKG indicate?
Hypokalemia
What does a long QTI predispose pts to? What is it caused by?
Torsades de pointes VTACH (wide QRS) > caused by drugs, low K or Mg, congenital abnormalities
Compare AV node fibers vs sinus nodal fibers
SA node fibers have less negative resting membrane potential, caused by leaky sodium and calcium ions > fast sodium channels blocking from opening due to higher resting membrane potential > slower action potential overall
Where does the myocardial action potential occur?
All cardiac myocytes, except those in SA and AV nodes
Briefly explain overview of myocardial action potential?
Depolarization (more positive membrane) > AP plateaus > repolarization (more negative membrane)
Describe phase 0 of the myocardial action potential
Depolarization
Fast Na channels open
Slow Ca channels open
Describe phase 1 of the myocardial action potential
Initial repolarization
Fast Na channels close
Fast K channels open
Slow Ca channels still open
Describe phase 2 of the myocardial action potential
Plateau
Fast K channels close
Slow Ca channels still open, increasing influx balance leaving K more and more
Calcium influx triggers: Ca release from sarcoplasmic reticulum + myocyte contraction via excitation-contraction coupling
Describe phase 3 of the myocardial action potential
Rapid repolarization
Slow Ca channels close
Slow K channels open
Describe phase 4 of the myocardial action potential
Resting membrane potential
High potassium permeability through leaky potassium channels
NaK ATPase and NaCa (Na in Ca out) exchanger at work
Where does the pacemaker action potential occur?
SA and AV nodes
Describe phase 0 of the pacemaker action potential
Opening of Ca channels causes upstroke
fVNaC permanently inactivated > slow conduction velocity used by AV node to prolong transmission from A > V
Describe phase 3 of the pacemaker action potential
Inactivation of Ca channels
Activation of K channels
> K efflux
Describe phase 4 of the pacemaker action potential
Slow spontaneous diastolic depolarization from funny current
Slow/mixed Na/K influx > accounts for automaticity of SA and AV nodes (slope determines HR) > Ach/adenosine will decrease HR, catecholamines will increase HR
What system controls HR and strength?
ANS
What is the basis of regulation of the cardiac cycle?
Intrinsic cardiac pumping regulation in response to changes in volume of blood flowing into the heart
What determines the amount of blood pumped into the heart each minute?
Venous return
What is the Frank-Starling Mechanism?
Ability for the heart to adapt to increasing volumes of blood
More heart muscle is stretched during filling > greater contraction force > greater quantity of blood pumped into aorta
Explain sympathetic stimulation and its role in ANS control of the heart
Increased CO > increases HR and force of contraction > increases volume of blood pumped and ejection pressure
Explain parasympathetic stimulation and its role in ANS control of the heart
Deceased CO >
minor decrease of contraction strength
major decrease of HR
vagal nerve fibers distributed more to atria than ventricles
Explain the effect of potassium ions on heart function
Excess extracellular K > dilated, flaccid heart > slow HR
Excess K could also block conduction of electrical impulse from atria to ventricle
Why?
Decreases resting membrane potential (less neg), decreases intensity of AP, decreased heart muscle contraction
Explain the effect of calcium ions on heart function
Excess intracellular Ca causes opposite effects of potassium
Excess leads to spastic contraction
Why?
Ca initiates the cardiac contractile process
Decreased Ca leads to cardiac weakness like the effects of high K
Where do the coronary arteries lie and where do they supply blood to?
CA and their branches lie in the epicardium and supply blood to the myocardium
During which heart phase do the coronary arteries fill?
Diastole
Describe the branching pattern of the coronary arteries
Aortic root > RCA + LCA
RCA > R marginal
RCA + LCA > PDA
LCA > LAD (widow)
LCA > circumflex > L marginal
What CA supplies blood to the SA node?
RCA
What CA supplies blood to the right ventricle?
RMA
Where does the LAD artery supply blood to?
Anterior 2/3 IV septum, anterior LV
Where does the circumflex artery supply blood to?
LA and posterior walls of LV
Where does the PDA supply blood to?
AV node, posterior 1/3 AV septum
Explain the branching of the aorta below the diaphragm
Inferior phrenic, celiac trunk (foregut), middle suprarenal arteries, renal arteries, SMA (midgut), testicular arteries, IMA (hind gut), lumbar arteries, common iliac arteries
What are the major lower extremity veins?
Anterior tibial, posterior tibial, peroneal veins, lower popliteal fossa, popliteal vein, superficial femoral vein
Explain the anatomy of the femoral and saphenous veins
Deep femoral v is lateral, joins superficial femoral and great saphenous in femoral canal, common femoral vein
In what pathologies would a high pulse pressure be present?
Hyperthyroid, aortic regurgitation, aortic stiffening, OSA, exercise
In what pathologies would a low pulse pressure be present?
Aortic stenosis, cardiogenic shock, cardiac tamponade, HF
What would cause high contractility?
B1R stim, increased intracellular Na/Ca
What would cause low contracility?
B1 blocker, HF, acidosis, hypoxia, NDHPCCB
What medication class would decrease preload?
Venous vasodilator (nitroglycerin, ACEis, ARBs)
What determines the amount cardiac muscles can contract in preload?
End diastolic volume
What determines afterload?
End systolic volume
What blood vessels have the highest total cross sectional area and lowest velocity?
Capillaries
Explain capillary fluid exchange
Cap pressure pushes fluids out, interstitial pressure pushes fluid in
Plasma osmotic and oncotic pressure pulls fluid in, interstitial fluid osmotic pressure pulls fluid out
What are starling forces and what do they determine?
Contraction force is proportional to preload; hearts ability to change contractions and SV in response to venous return. SV increase with increase in amount of blood that fills ventricles (EDV)
Starling forces determine fluid movement through cap membrane
Explain the acute effects of early exercise on the CV system.
CO maintained by increased HR and SV
Explain the adaptive effects of late exercise on the CV system.
CO maintained by HR only (as SV plateaus)
As HR increases > less filling time > decreased CO > diastole is shortened
Explain the function and biochem of atrial natiuretic peptide
Released from atrial myocytes in response to increased blood volume and atrial pressure
Caused vasodilation and decreased Na in the renal/medullary collecting duct
Dilates afferent renal arterioles and constricts efferent arterioles to promote diuresis
Explain the function and biochem of brain natriuretic peptide
Released from ventricular myocytes in response to increased tension
Longer half life than ANP
Used to Dx HF
Explain the function and biochem oF LDL
Transports cholesterol made in the liver to the tissues
Explain the function and biochem of HDL
Scavenges cholesterol from tissues and back to liver for disposal
Explain the unique relationship between the cardiovascular and pulmonary system
Pulmonary vasculature is the only one that vasoconstriction under hypoxia, so the well ventilated areas are perfused
Other areas of the body, hypoxia causes vasodilation
What is pulmonary HTN?
Increased pressure in pulmonary vasculature ONLY; elevated mean pulmonary artery pressure > 20 mmHg at rest
Explain the pathogenesis of pulmonary HTN and what it can lead to
Increased pulmonary vascular resistance > increased right ventricular pressure > increased right ventricular hypertrophy > right HF
What are the different possible causes of pulmonary HTN?
Idiopathic, inherited, drug induced, connective tissue disease
HD/HF (most common)
Lung disease and/or hypoxemia
Chronic thromboembolism
RF for pulmonary HTN
CHF, MI, chronic anemia, COPD/lung disease, chronic thromboembolism, pulmonary arterial HTN (genetic, idiopathic), lung fibrosis
Complications of pulmonary HTN
Arteriosclerosis, medial hypertrophy, intimal fibrous of pulmonary arteries, right HF
Clinical characteristics of pulmonary HTN
PLEXIFORM LESIONS (complex vascular formations originating from remodeled pulmonary arteries, like a spider vein in the lungs)
Fatigue, dyspnea, syncope, peripheral edema, palpitations, chest pain on exertion
Medial hypertrophy of muscular and elastic arteries
What is the most common type of systemic HTN and its causes?
1st degree: multi factorial
Increased CO: increased HR, contractility (exercise, anxiety), increased preload (amount of blood filling heart), decreased afterload
Increased TPR: amount of blood circulating and diameter of BVs
What is the most common cause of second degree systemic HTN?
Renal/renovascular disease
What is seen microscopically in pulmonary HTN?
Smooth muscle proliferation occurs due to decreased apoptosis; genetic connection to BMPR2 gene
RF for systemic HTN
Increased age, obesity, DM, physical inactivity, excess salt, excess alcohol, smoking, fhx
AA > caucasians > Asian
Complications of systemic HTN
CAD, HF, left ventricular hypertrophy, a fib, aortic dissection, aortic aneurysm, stroke, CKD, retinopathy
What defines a hypertensive crisis, hypertensive urgency, and hypertensive emergency?
Crisis: 180/110
Urgency: 180/120+ with NO sx end organ damage
Emergency: 180/120+ with evidence of end organ damage (encephalopathy, stroke, retinal hemorrhage, MI, HF, kidney injury)
Sx of systemic HTN
Commonly asymp
Fundoscopic exam showing hypertensive retinopathy (not required for dx)
What is congestive heart failure?
Cardiac pump dysfunction leads to congestion of the heart, decreased CO, and low perfusion
Types of left sided CHF
Systolic dysfunction: HF with reduced EF, increased EDV, decreased contractility
Diastolic dysfunction: HF with preserved EF, normal EDV, decreased compliance (increased EDP)
Etiology/causes of L CHF
Ischemic HD
HTN
Aortic and mitral valvular diseases
Myocardial disease
Common causes of R CHF
Left HF
Pulmonary HTN
Cor pulmonale - isolated right HF due to pulmonary causes
RF for CHF
Old age, CAD, HTN, DM, valvular heart disease, tobacco, obesity
Complications of L CHF
A fib, stroke/thrombosis, hypoxic encephalopathy, coma, death, right HF
Shared clinical characteristics of both types of CHF
S3 heart sounds, rales, JVD, pitting edema
L CHF clinical characteristics
S3, rales, JVD, pitting edema
pulmonary edema (increased pulmonary venous pressure > pulmonary venous distention and transduction of fluid) > HF CELLS IN LUNGS
Orthopnea (SOB when supine)
Paroxysmal nocturnal dyspnea
Dyspnea, orthopnea, fatigue
R CHF clinical characteristics
S3, rales, JVD, pitting edema
Congestive hepatomegaly (increased central venous pressure > increased resistance to portal flow) > NUTMEG LIVER on cadaver exam
Dyspnea, orthopnea, fatigue
what is angina pectoris?
Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm, no myocyte necrosis
Different types of angina pectoris
Stable angina
Vasospastic/variant
Unstable angina
Stable angina definition
most common
usually secondary to atherosclerosis (>70% occlusion)
triggered by: atherosclerosis, activity, BP, HR
Vasospastic/variant angina definition
occurs at rest secondary to CA spasm
triggered by: cocaine, alcohol, triptans
Unstable angina definition
Thrombosis with incomplete coronary artery occlusion
Triggered by: atherosclerosis, activity, BP, HR
RF for stable and unstable angina
HTN, HLD, tobacco, MI RF
RF for vasospastic/variant angina
Tobacco use
Clinical characteristics of stable angina
Pain on exertion, resolves with rest
No ECG changes
Are troponin levels elevated in any forms of angina?
No
Clinical characteristics of vasospastic angina
Pain at rest secondary to coronary artery spasm
Transient ST elevation on ECG
Clinical characteristics of chronic ischemic heart disease
Enlarged heavy heart with L ventricular hypertrophy and dilation
Obstructive ordinary atherosclerosis
Scars from healed infarcts
Complications of chronic ischemic heart disease
Leading cause of death worldwide
Progressive CHF leading to heart transplant
Clinical characteristics of unstable angina
Pain on mild extortion or at rest
Possible ST depression/T-wave inversion on ECG
What is chronic ischemic heart disease
Progressive onset of HF over many years due to chronic ischemic myocardial damage
What is myocardial ischemia
Imbalance between supply (perfusion) and demand of heart for oxygenated blood
Etiology of chronic ischemic heart disease
Reduced blood flow to obstructive atherosclerotic lesions in coronary artery, usually preceded by MI
Progression of CAD
Pathogenesis of chronic ischemic heart disease
Long and slow onset w/o sx
Syndrome of ischemic heart disease are late manifestations of coronary atherosclerosis
Appears post infarction due to functional decompensation of hypertrophied non infarcted myocardium
RF of chronic ischemic heart disease
HLD, HTN, MI, tobacco use, alcohol use, sedentary lifestyle, age, SAD diet
What is a myocardial infarction
Death of cardiac muscle due to prolonged severe ischemia
Most common cause of myocardial infarction
Rupture of coronary artery atherosclerotic plaque
Commonly occluded arteries with MIs
LAD > RCA > circumflex
Pathogenesis of MI
Initial event > sudden change in plaque > intraplaque hemorrhage, erosion, ulceration, rupture, fissuring
When exposed to subendothelial collagen and necrotic plaque contents, platelets adhere, become active, release granule contents, and aggregate to form microthrombi
Vasospasm is stimulated by mediators released from platelets
TF activates, activates coagulation pathway, increases bulk of thrombus, occludes complete lumen > leads to ischemia and myocyte death occurring at the location of the anatomical region supplied by artery in question
Biochem of MI
Loss of blood flow > cessation of aerobic metabolism within seconds
Inadequate production of ATP > accumulation of lactic acid
STEMI characteristics
Transmural
Full thickness
ST elevation, pathological Q waves
NSTEMI characteristics
Subendothelial
Subendocardium (inner 1/3)
ST depression
What is seen on microscopy at 0-24 hours, 1-3 days, 3-14 days, and 14+ days post MI
0-24 hrs: wavy fibers, coagulative necrosis, dark eosinophilic stripes
1-3 days: coagulative necrosis, neutrophils showing acute inflammation
3-14 days: macrophages, granulation tissue
14+ days: scar complete
RF for MI
Age, genetics, males, post menopausal women (drop in estrogen), atherosclerosis
Complications of MI
If caught late: necrosis of cardiac myocytes > chronic IHD, CHF, death
DARTH VADER: death, arrhythmia, rupture, tamponade, HF, valve disease, aneurysm, dressers, embolism, recurrence/regurgitation
Complications of MI by time frame (0-24 hours, 1-3 days, 3-14 days, 2+ weeks)
0-24 hours: ventricular arrhythmia, HF, cardiogenic shock
Vinny has constipation for 24 hours
1-3 days: postinfarction fibrinous pericarditis
3-14 days: cardiac tamponade, mitral regurgitation, LV, pseudoaneurysm
2+ weeks: dressier syndrome, HF, arrhythmia, ventricular aneurysm
Clinical characteristics MI
Elevated bio markers (CK-MB, troponins)
Chest/arm/back/neck/jaw pain
Trouble breathing
Lightheadedness
Diaphoresis/cold sweats
N/V
Severe chest pain
Malaise, fatigue
Aortic stenosis - S or D?
S
Aortic regurgitation / insufficiency - S or D?
D
Mitral stenosis - S or D?
D
Mitral insufficiency - S or D?
S
Mitral valve prolapse - S or D?
S
Etiology of aortic stenosis
Age-related calcification, bicuspid aortic valve
RF aortic stenosis
Age, atherosclerosis, bicuspid aortic valve
complications of aortic stenosis
SAD (syncope, angina, DOE), LV pressure is less than aortic pressure during systole
Clinical characteristics aortic stenosis
Cresc-decresc ejection murmur
Pulses parvus et tartus (weak pulse)
Soft S2 and ejection click
Etiology aortic regurgitation
BEAR (bicuspid aortic valve, endocarditis, aortic root dilation, rheumatic fever
Complications aortic regurgitation
L CHF
Clinical characteristics aortic regurgitation
Early diastolic decrescnedo
High, blowing murmur
Wide PP
Pistol shot femoral pulse
Pushing nail bed
Mitral stenosis etiology
Rheumatic fever
Mitral stenosis pathogenesis
L atrial pressure > ventricular pressure
Mitral stenosis complications
Left atrial dilation, pulmonary congestion, a fib, ortner syndrome, hemopytsis, RCHF
Mitral stenosis clinical characteristics
Follows opening snap, delayed rumbling mid-late murmur
Mitral insufficiency etiology
Ischemic heart disease (post MI), MVP, LV dilation, rheumatic fever, infective endocarditis
Mitral insufficiency clinical characteristics and sound
asymptomatic to shortness of breath, fatigue, and inability to exercise may arise (later in disease)
Holosystolic, high pitched blowing murmur
Types of endocarditis
Infective/bacterial
No bacterial thrombotic endocarditis
Etiology infective endocarditis
Infection of endocardial surface of heart, typically involves 1+ heart valves
Bacteria > fungi
Acute: S aureus; large destructive vegetation’s on normal valves; rapid onset
Subacute: strep Viridans; small vegetations on congenitally abnormal or diseased valves; gradual onset
Pathogenesis infective endocarditis
Mitral valve affected more often than aortic
Tricuspid valve associated with IV drug use (Don’t Tri Drugs)
Endothelial injury > formation of vegetation’s consisting of platelets, fibrin, and microbes on heart valves
Non bacterial thrombotic endocarditis etiology
Marantic endocarditis; rare
Vegetations arise on mitral or aortic valve, consists of sterile, platelet-rich thrombi that dislodge easily
RF of infectious endocarditis
Subacute: dental procedure
RF by bacteria;
Prosthetic valves - s epidermis
GI/GU procedure - enterococcus
IV drug use - S aureus, pseudomonas, candida
RF nonbacterial endocarditis
Hypercoagulable state from advanced malignancy (pancreatic adenocarcinoma) or SLE (Libman sacks endocarditis)
Complications of bacterial endocarditis
Leads to valve regurgitation, septic embolism
Complications of nonbacterial endocarditis
Embolism
Clinical characteristics of infectious endocarditis
FROM JANE Fever Roth spots Osler nodes Murmur Jane way lesions Anemia Nail bed hemorrhages Emboli
Vascular phenomena: septic embolism, petechiae, splinter hemorrhages, Jane way lesions
Immune phenomena: immune complex deposition, glomerulonephritis, Osler nodes, Roth spots
Modified duke criteria
Nonbacterial endocarditis clinical characteristics
Asymptomatic
Mitral valve prolapse etiology
Rheumatic fever, chordae rupture, myxomatous degeneration (primary or secondary due to connective tissue disease)
Mitral valve prolapse complications
Typically benign, can predispose to infective endocarditis
Mitral valve prolapse clinical characteristics
Late crescendo murmur with midsystolic click occurring after carotid pulse
Rheumatic heart disease definition
Immune mediated (type II hypersensitivity)
Antibodies react to M protein, cross-react with self-antigens (often myosin)
Rheumatic heart disease etiology
Pharyngeal infection with group A B-hemolytic strep
Not direct effect of bacteria
Pathogenesis rheumatic heart disease
Affects heart disease mitral > aortic > tricuspid (MAT)
Complications rheumatic heart disease
Early valvular regurgitation
Late valvular stenosis
Clinical characteristics rheumatic heart disease
Aschoff bodies: granuloma with giant cells
Anitschkow cells: enlarged macrophages with ovoid, wavy, rod-like nucleus
J<3NES (major criteria):
Joint (migratory arthritis)
<3 carditis
Nodules in skin (subcutaneous)
Erythema marginatum (evansecent rash with ring margin)
Sydenham chorea (involuntary irregular movements of limbs/face)
Carcinoid heart disease definition
Cardiac manifestation of systemic syndrome caused by carcinoid tumors (occurs in 50% of people)
Carcinoid heart disease etiology
Involves endocardium and valves of right heart
Cardiac lesions: firm, plaque like endocardial fibrous thickening inside tricuspid and pulmonary valves (contain smooth muscle cells and collagen fibers)
Carcinoid heart disease complications
Tricuspid insufficiency then pulmonary valve insufficiency
Carcinoid heart disease clinical characteristics
Flushing of skin, cramps, N/V, diarrhea
Types of cardiomyopathies
Dilated, Hypertrophic, Restrictive
Dilated cardiomyopathy etiology
Most common, dilation of cardiac chambers (ventricles)
Idiopathic, genetic, drugs, infxn, ischemia, systemic
Hypertropic cardiomyopathy etiology
Second most common; enlargement of cardiac muscle surrounding ventricles
Familial, autosomal dominant, chronic HTN, friedrich ataxia
Restrictive cardiomyopathy etiology
Known as infiltrative, decreased ventricular compliance
PLEASe Help: P: postradiation fibrosis L: Loeffler endocarditis E: endocardial fibroelastosis (kids) A: amyloidosis Se: sarcoidosis Help: hemochromatosis
Dilated cardiomyopathy complications
Systolic dysfunction
Clot formation
Hypertrophic cardiomyopathy complications
Diastolic dysfunction
Sudden death in young athletes
Arrhythmias
Restrictive cardiomyopathy complications
Diastolic dysfunction
Dilated cardiomyopathy clinical characteristics
CHF, S3, systolic regurgitation murmur, dilated heart on echo
BALLOON APPEARANCE OF HEART ON CXR, ECCENTRIC HYPERTROPHY IN VENTRICLE, sarcomeres added in series
Hypertrophied cardiomyopathy clinical characteristics
S4, systolic murmur, mitral regurgitation, dyspnea, syncope
VENTRICULAR CONCENTRIC HYPERTROPHY, MUSCLE TISSUE ENLARGED, sarcomeres added in parallel
Restrictive cardiomyopathy clinical characteristics
Low voltage ECG
MUSCLE LESS COMPLIANT, LESS CONTRACTILE
Myocarditis etiology
Inflammation of myocardium > global enlargement of heart and dilation of all chambers
Viral: coxsackie A and B virus
Parasitic; trypanosoma cruzi, toxoplasma gondii
Bacterial: borrelia burgdorferi, myoplasma pnemoniae, diphtheriae
Toxins: CO, black widow venom
Rheumatic fever
Drugs (cocaine)
Autoimmune disease
Complications of myocarditis
SCD (Major cause in adults >40)
Arrhythmias, heart block, dilated cardiomyopathy, CHF, mural thrombus with systemic emboli
Myocarditis clinical characteristics
Dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever)
If viral in etiology: lymphocytic infiltrate with focal necrosis
Pericarditis definition
Inflammation of pericardium, fluid accumulates around heart
Pericarditis etiology
Primary and secondary
SCCARR IIN pericardium
Surgery Connective tissue disorder CV events Autoimmune Radiation Renal failure Idiopathic (most common) Infection (coxsackie B) Neoplasm
Pericarditis complications
Pericardial effusion
Pericarditis clinical characteristics
Sharp pain, WORSE BY INSPIRATION, BETTER SITTING UP AND LEANING FORWARD
Friction rub
Diffuse ST elevation or depression
Patent ductus arteriosis definition
Ductus arteriosis failes to close after birth; allows blood to flow back to lungs
Patent ductus arteriosis etiology
Fetal period: normal (R to L) shunt
Neonatal period: decreased vascular resistance, shunt becomes L to R
Leads to RVH and/or LVH and HF
Patent ductus arteriosis complications
Late cyanosis in lower extremities
Patent ductus arteriosis clinical characteristics
No symptoms or cyanosis, fatigue, tachycardia
Continuous machine-like murmur
PDA is normal in utero, and normally closes after birth
Tetralogy of fallot etiology
Anterosuperior displacement of infundibular septum
Most common cause of early childhood cyanosis
Tetralogy of fallot complications
Pulmonary stenosis forces R to L flow across VSD > RVH
Tetralogy of fallot clinical characteristics
Pulmonary infundibular stenosis
RVH - boot heaped heart on xray
Overriding aorta
VSD
“Tet spells” often caused by crying, fever, exercise
Aneurysm definition
Dilation of aorta
Types of aneurysm
Abdominal aortic
Thoracic aortci
Abdominal aortic aneurysm pathogenesis
Transmural (all 3 layers)
Inflammation and extracellular matrix degradation
Abdominal aortic aneurysm RF
Tobacco, age, males, Fhx
thoracic aortic aneurysm pathogenesis
Aortic root dilation due to high pressure could lead to aortic valve regurgitation
Thoracic aortic aneurysm RF
HTN, bicuspid aortic valve, connective tissue disease (Marfan), tertiary syphilis
Abdominal aortic aneurysm Complications
Aortic dissection
thoracic aortic aneurysm
Aortic dissection
Abdominal aortic aneurysm clinical characteristics
Abdominal/back pain as sign of leaking, dissection, imminent rupture
Palpable pulsatilla abdominal mass
Abdominal aortic aneurysm clinical characteristics
Abdominal/back pain as sign of leaking, dissection, imminent rupture
Aortic dissection definition
Longitudinal intimal tear forming a false lumen
Types of aortic dissection
Stanford type A: proximal, ascending aorta
Stanford type B: distal, descending aorta, below L subclavian artery
Aortic dissection RF
HTN, bicuspid aortic valve, inherited CT disorders (Marfan syndrome)
Aortic dissection complications
Organ ischemia, aortic rupture, death
Aortic regurgitation, cardiac tamponade
Aortic dissection clinical characteristics
Tearing, sudden-onset chest pain radiating to back
Unequal BP in arms
CXR: mediastinal widening
Arteriosclerosis definition
Hardening of arteries, arterial wall thickening, loss of elasticity
How dose Arteriosclerosis affect blood vessels and which ones?
Affects small arteries and arterioles
Hyaline: thickening of vessel walls secondary to plasma protein leak into endothelium in essential HTN ad DM
Hyperplastic: onion skinning in severe HTN with proliferation of smooth muscle cells
Atherosclerosis definition
Form of arteriosclerosis
Build up of cholesterol plaques in tunica intima
Elastic arteries and medium/large size muscular arteries
Atherosclerosis Etiology
Location: A copy cat named Willis: abdominal aorta > coronary artery > popliteal artery > carotid artery > circle of Willis
Inflammation > endothelial cell dysfunction > macrophage and LDL accumulation > foam cell formation > fatty streaks > smooth muscle cell migration > proliferation and ECM deposition > fibrous plaque > complex atheromas > calcification
Atherosclerosis complication
Atherosclerosis of CA (CAD) is #1 killer of M +F in US
CAD, MI
Atherosclerosis RF
HTN, tobacco, HLD, DM
Age, males, postmenopausal status, Fhx
Atherosclerosis clinical characteristics
Angina, claudication, asymptomatic
Familial hypercholesterolemia definition
Receptor disease from mutation in gene encoding for LDL
Familial hypercholesterolemia Pathophysiology
Loss of feedback > increased cholesterol levels
Premature atherosclerosis
Increased risk of MI
Familial hypercholesterolemia RF
Fhx
Familial hypercholesterolemia Complications
MI, CAD
Familial hypercholesterolemia clinical characteristics
Very high LDL at young age
Nodules or raised bumps on skin, tendons, eyelids
White ring around cornea
Medications do not work for LDL
Giant cell (temporal) arteritis etiology
Focal granulomatous inflammation
Increased ESR, IL-6 levels correlate with disease activity
Affects branches of carotid artery
Giant cell (temporal) arteritis RF
Females, over 50, polymyalgia rheumatica
Giant cell (temporal) arteritis complications
Irreversible blindness due to anterior ischemic optic neuropathy
Giant cell (temporal) arteritis clinical characteristics
UL HD, temporal artery tenderness, jaw claudication
Peripheral arterial disease (PAD) definition
Insufficient tissue perfusion due to narrowing or occlusion of aorta or peripheral branches
Peripheral arterial disease (PAD) Etiology
Narrow arteries reduce blood flow to arms/legs
Buildup of fatty, cholesterol-containing deposits on artery walls (atherosclerosis), reduces blood flow through arteries
Peripheral arterial disease (PAD) RF
Fhx, HTN, HLD, age, obesity, CAD
Peripheral arterial disease (PAD) Complications
Critical limb ischemia, stroke, MI
Peripheral arterial disease (PAD) clinical characteristics
Coldness in LE or foot LE numbness Weakness Loss of peripheral pulses Cramping Skin color change Sores that wont heal ED Hair loss
Pulmonary embolism definition
Obstruction of pulmonary artery or one of its branches by thrombus
Pulmonary embolism Etiology
Affected alveoli are ventilated but not perfused (V/Q mismatch)
Pulmonary embolism RF
THROMBOSIS T: trauma, travel, thrombophilia H: hypercoagulable state, hormone replacement R: rec drugs/IV drugs O: old age M: malignancy B: birth control pills/patches O: obesity, obstetrical (pregnancy- 6 wk postpartum) S: surgery I: immobilization, iatrogenic (CVC) S: serious illness
Pulmonary embolism Complications
Sudden death due to clot preventing blood from filling LV
Hypotension, shock, recurrent thromboembolism, pulmonary infarction, RHF
Pulmonary embolism Clinical characteristics
Sudden onset dyspnea, pleuritic chest pain, cough, hemoptysis, tachyon ear, tachycardia, syncope, hypoxemia, respiratory alkalosis, sx of DVT,
Wells criteria for PE
ECG: R heart strain - S wave in 1, Q wave in 3, inverted T wave in 3
Raynaud phenomenon definition
Color changes of skin due to decreased blood flow
Raynaud phenomenon Etiology
Decreased blood flow to skin due to arteriolar (small vessel) vasospasm in response to cold or stress
Primary: idiopathic
Secondary: mixed connective tissue disease, SLE, CREST syndrome
Raynaud phenomenon complications
Secondary: Digital ulceration
Raynaud phenomenon clinical characteristics
Color change from white (ischemia) to blue (hypoxia) to red (reperfusion)
Most often to fingers/toes
Thromboangitis Obliterans / Buerger disease definition
segmental, thrombosis, acute and chronic inflammation of medium sized and small arteries (tibial and radial)
Thromboangitis Obliterans / Buerger disease Etiology
Direct endothelial cell toxicity by tobacco or immune response to the same agents
Thromboangitis Obliterans / Buerger disease RF
Heavy cigarette smokers before age of 35
Thromboangitis Obliterans / Buerger disease Complications
Vascular insufficiency
Thromboangitis Obliterans / Buerger disease Clinical characteristics
Superficial nodular phlebitis, severe pain at rest, chronic ulceration of toes, fingers, feet
Deep vein thrombosis definition
Blood clot within a deep vein (proximal LE veins - iliac, femoral, popliteal)
DVT etiology
Virchow triad (SHE) Status - post op, long drive/flight Hypercoagulability - defect in coagulation cascade proteins, OCPs, pregnancy Endothelial damage - exposed collagen triggers clotting cascade
DVT RF
Obesity, contraceptives, pregnancy, fhx, previous venous thromboembolism, HRT
Inherited thrombophlebitis:
Factor V Leiden mutation
Protein C deficiency
Protein S deficiency
DVT complication
PE
DVT clinical characteristics
Leg swelling, pain, warmth, redness
Unilateral pitting edema in leg
D-dimer: rule OUT DVT
Wells criteria for DVT
Varicose veins etiology
Prolonged increased intraluminal pressure and loss of vessel wall support
Superficial veins of LE
Varicose veins RF
Obesity, FHx, females
Varicose veins complications
Increased venous pressure, venous stasis, pedal edema, stasis dermatitis, ulcerations
Varicose veins definition
Abnormally dilated, tortuous veins
Vasculitis definition
Vessel wall inflammation
Large vessel Vasculitis Etiology
aorta and large branches to extremities, head, neck
giant cell (temporal arteritis
Takayasu arteritis: granulomatous inflammation occurring in pts under 50
Types of Vasculitis
Large vessel, medium vessel, small vessel
Medium vessel Vasculitis etiology
Main visceral arteries and branches
Kawasaki disease: arteritis with mucocutaneous lymph node syndrome, in children. Coronary arteries involved with aneurysm or thrombosis
Small vessel Vasculitis etiology
Arterioles, venues, capillaries, small arteries
Westerns granulomatosis: granulomatous inflammation involving respiratory tract and necrotizing vasculitis affecting small vessles
Churg-Strauss syndrome: same as wegeners but associated with asthma and blood eosinophilia
Microscopic polyangitis: necrotizing small vessel vasculitis with few or no immune deposits
Viral myocarditis etiology
Adenovirus, coxsackie B, parvovirus B19, HIV, HHV-6
Viral myocarditis clinical characteristics
Lymphocytes infiltrate with focal necrosis is highly indicative
The truncus arteriosis gives rise to…
Asc aorta + pulmonary trunk
Bulbus cordis gives rise to…
Outflow tract of LV and RV
Primitive ventricle/aorta gives rise to…
Trabeculated part f R + L ventricles/aorta
L horn of sinus venosus gives rise to…
Coronary sinus
R horn of sinus venosus gives rise to…
Smooth part of R atrium (sinus venarum)
When does the foremen ovale close? What causes this closure?
Immediately after birth, due to increased LA pressure
Breath > decreased pulm vasc resistance > increased LA pressure > fossa oval is > increase in O2 > decrease in PGEs > closure of ductus arteriosus
What is patent foramen ovale
Failure of septum primum and secundum to fuse after birth
What eventually develops into the arterial system?
Aortic arch derivatives
1st aortic arch derivative
Maxillary arteries - branch of ext carotid
1st arch is max
2nd aortic arch derivative
Stapedial and hyoid arteries
second stapedial
3rd aortic arch derivative
Common carotid artery and proximal part of internal carotid artery
4th aortic arch derivative
Aortic arch and proximal right subclavian artery
6th aortic arch derivative
Proximal part of pulmonary arteries and ductus arteriosus (left)
Endocardial cushion gives rise to…
Atrial septum, membranous IV septum, AV + semilunar valves
R common cardinal + R anterior cardinal vein gives rise to…
SCV
Posterior, subcardinal + supracardinal veins give rise to…
IVC
Primitive pulm vein gives rise to…
Smooth part of LA
What are the three roles of the lymphatic system
Returns interstitial fluid from tissues back to heart
Helps large molecules like hormones and lipids enter the blood
Helps with immune surveillance
When does interstitial fluid become lymph?
Once in the lymphatic vessels
Where is all of the collected lymph dumped?
Veins
When do the one way mini valves of lymphatic capillary walls open?
When pressure in interstitial space is greater than pressure in lymphatic capillary, endothelial mini valves open
Lymph vessel flow
Capillaries > bigger vessels > trunks > ducts
What “pushes” lymph through the lymphatic system?
Smooth muscle in the lymph vessels react to pulsing of nearby arteries, then the squeezing of skeletal muscles exerts external pressure to keep lymph moving and reaching a lymphatic trunk
What are the lymphatic trunks? What are they named after?
The lymphatic trunks are named after the regions of the body they drain the lymph into:
Two lumbar trunks Two bronchomediastinal trunks Two subclavian trunks Two jugular trunks One interstitial trunk
what places does lymph go from the trunks?
Either the right thoracic duct (collects from right arm and right side of head and chest)
OR
Thoracic duct, much bigger (collects from rest of body)
Where does the right lymphatic duct dump lymph into?
The junction of the right jugular vein and right subclavian vein
Where does the thoracic duct dump lymph into?
The junction of the left jugular vein and left subclavian vein
Same junction as right duct but on L side of body
Why do lymph ducts dump into the junction of jugular and subclavian veins?
Because the pressure is very low, easier for lymph to flow in
What are lymph nodes in the intestinal wall called?
Peyer’s patches
What types of cells detect pathogen in lymph nodes?
Dendritic cells
Pathway of infection in lymph
Lymphatic capillary > vessel > node: sensed by dendritic cell and presented to B cells to make antibodies
Circulating T cells look for pathogens tagged with antibodies
What are the three MAIN groups of lymph nodes?
Inguinal
Axillary
Cervical
What group of lymph nodes drained abdominal wall below umbilicus, lower extremities, and genitalia
Inguinal
What group of lymph nodes drains the posterior pharynx, tonsils, thyroid, and throat?
Anterior cervical
What group of lymph nodes drains the scalp, neck, thorax, cervical, and axillary lymph nodes?
Posterior cervical
What group of lymph nodes drains the Mediastinum, lungs, esophagus, and abdomen
Supraclavicular via thoracic duct
What group of lymph nodes drains the Majority of the breast?
Axillary
What are the great arteries of the heart that carry blood away from the heart?
Aorta + pulmonary arteries
Describe the flow of blood to and from the heart, including when it is oxygenated and not.
LV pumps oxygenated blood > aorta > rest of body > deoxygenated loop comes back via RA > RV > to lungs via pulmonary artery > LA > LV
What are the lymphaitc organs?
Diffuse lymphoid tissue, nodes/peyers patches, Thymus, spleen, tonsils
Lymphatic function of tonsils
Form ring of lymphoid tissue around throat, trap pathogens from food eaten and air inhaled
Lymphatic function of thymus
Development of T cells, making sure T cells that react to normal antigens are destroyed
Active neonatal and preadolescent then slowly atrophies and is replaced by fat after puberty
Lymphatic function and location of spleen
L side of body below diaphragm, abovestomach
White pulp: antibodies generated by B cells, antibody coated bacteria filtered out
Red pulp: old and defective blood cells are destroyed, keeps RBC and platelets available
What is the major relationship between the cardio and pulmonary systems?
They work together to circulate blood and oxygen throughout the body.
What are the starling forces that affect lymph?
Govern passive exchange of water between capillary microcirculation and interstitial fluid
Determine directionality of net water movement between two compartments and the rate at which water exchange occurs
The direction of water exchange is determined by combo of relative hydrostatic and oncotic pressure of these two compartments, rate is governed by permeability of capillary itself
What is the most common etiology of metastatic disease?
Lung tumors
What is pericardial effusion?
Any fluid above normal 30-50mL found in pericardial space
Pericardial effusion etiology
Typically due to hydrostatic or oncotic forces
What is a hemopericardium? What causes it and what can it lead to?
Blood in pericardial sac
MI with rupture, traumatic perforation
Cases cardiac tamponade, death may occur
Complications pleural effusion
Cardiac tamponade (fluid compresses heart, decreased CO)
Pleural effusion clinical characteristics
Alternans on ECG, QRS alternating due to moving around in fluid
CXR-water bottle appearance
Echo- heart dancing in pericardium
Bicuspid aortic valve etiology
Usually R + L coronary cusps are fused (common)
Bicuspid aortic valve definition
2 instead of 3 lobes
Complications bicuspid aortic valve
Ascending aortic aneurysm
Bicuspid aortic valve clinical characteristics
Aortic stenosis and aortic regurgitation
Systolic ejection click just after S1
Patent ductus arteriosis (PDA) RF
Prematurity
Rubella
What is the most common septal congenital defect?
Interventricular septal defects
Interventricular septal defects Complications
Increased risk of endocarditis
Interventricular septal defects clinical characteristics
Asymptomatic holosystolic murmur
CHF
What is the tetralogy in tetralogy of fallot
VSD
Pulmonic stenosis
RVH
Dextroposed aorta overriding VSD
What are the four types of shock?
Hypovolemic, cardiogenic, obstructive, distributive
What are causes of hypovolemic shock?
Hemorrhage, dehydration, burns
What are causes of cardiogenic shock?
Acute MI, HF, valvular dysfunction, arrhythmia
What are causes of obstructive shock?
Cardiac tamponade, PE, tension pneumothorax
What are causes of distributive shock?
Sepsis, anaphylaxis, CNS injury
What are sx of hypovolemic shock?
Cold, clammy skin
What are sx of cardiogenic shock?
Cold, clammy skin
What are sx of obstructive shock?
Cold, clammy skin
What are sx of distributive shock?
Warm, dry skin
What are hemangiomas?
Common vascular birthmarks made of extra blood vessels in the skin, benign
What is kaposi sarcoma?
Endothelial malignancy most commonly affecting skin, mouth, GI tract, respiratory tract
Metastatic, dangerous
HHV-8, HIV
RF kaposi sarcoma?
Old Eastern European males, AIDS, organ transplant, lindau von hipple disease (cavernous type)
complications kaposi sarcoma
Pericardial effusion
Cardiac tamponade
kaposi sarcoma clinical characteristics
Purple/black papules that may scale
What is Chagas’ disease?
Parasite (trypanosoma cruzi)
“Kissing bug”
What is the leading cause of infectious myocarditis worldwide?
Chagas’ disease
RF Chagas’ disease
Central American, Mexico, southern US (rare)
Complications Chagas’ disease
Dilated cardiomyopathy, HF, reduced EF, arrhythmias, heart block
Cardiac arrest
Enlarged esophagus
Enlarged colon
Chagas’ disease clinical characteristics
Swelling at bite sitefever Fatigue Rash Body aches Headache
What is the etiology of Lyme disease?
Borrelia burgdorferi
Deer tick bite
RF Lyme disease
NE US
Lyme disease complications
AV block Carditis Bell’s palsy Migratory myalgia Encephalopathy Chronic arthritis
Lyme disease clinical characteristics
Erythema migrans rash - bullseye rash
Flu like sx
Rocky Mountain spotted fever etiology
Rickettsia rickettsii
Tick vector
Rocky Mountain spotted fever clinical characteristics
Headache, fever, rash (vasculitis)
Rash starts at wrists and ankles and spreads to trunk, palms, soles
What are the three types of viral hemorrhagic fever?
Yellow fever, dengue fever, filoviruses
Yellow fever (viral hemorrhagic fever) clinical characteristics
High fever, black vomitus, jaundice
May see councilman bodies on liver biopsy
a deficiency B1 can lead to what
B1 deficiency (wet beriberi) can lead to high output cardiac failure (dilated cardiomyopathy)
