The Coronary Arteries
Left & Right coronary arteries arise just distal to the Aortic Valve
Left Main gives rise to LAD & circumflex
LAD: Supplies septum & anterior wall of LV
Circumflex: Supplies lateral (free) wall of LV
RCA: Supplies RV & gives rise to posterior descending a
Coronary artery blood flow
Coronary arteries begin just distal to the Aortic valve
CA BP reflects aortic pressure
CA flow controlled by:
Aortic BP - particularly diastolic BP (Intra myocardial vessels compressed during systole)
Inadequate DBP ? ischemia
Auto-regulation: CA flow ? w
Coronary Heart Disease
CHD is divided into chronic ischemic heart disease & acute coronary syndromes
Ischemia refers to any time that cardiac oxygen demands > supply
Chronic Ischemic Heart Disease has 3 subtypes
stable vs. unstable plaques
Fixed stable plaques ? stable angina
Unstable plaques rupture & form clots ? unstable angina & MI (ACS)
Plaque rupture can be spontaneous but often 2o SNS activity
Plaques are vulnerable to rupture when they have: a large lipid-rich core, inflammation, fe
Acute coronary syndromes
Includes: Q-wave MI (ST elevation), non Q-wave MI (non ST elevation), & unstable angina
Q-wave MI generally from complete coronary artery occlusion
Others generally from incomplete or intermittent occlusion
diagnostic tools
ECG
T wave inversion = ischemia
ST changes = damage
ST depression = subendocardial injury
ST elevation = transmural injury
Q wave = old MI
Changes in leads overlying impacted area
Serum Markers
Necrotic cells release contents into blood
Myoglobin: ?at 1 h
Unstable Angina & Non Q-wave MI
From: Plaque disruption with clot and/or arterial spasm
Pain occurs at rest & is: severe, persistent (>20 min), not relieved by NTG
Called MI if serum markers are ?
Q-wave (ST elevation) MI (The real deal!)
Area of infarct determined by CA that is blocked
symptoms of MI
Abrupt onset of pain
Not revealed by rest & NTG
? more likely to have "discomfort"
Elderly more likely to have SOB
GI symptoms also common
30-50% die from VF in first few hrs
Immediate hospitalization VITAL
Pathologic changes
Extent determined by:
vessel that is occluded
time of occlusion
metabolic needs of tissue
extent of collaterals
Contractility loss almost immediate
Irreversible damage & necrosis in 20-40 min
Reperfusion can reestablish blood flow
Reperfused area "stunned
Management of Acute Coronary Syndromes
Goal: To prevent extension of injury/ necrosis
To prevent sudden cardiac death
Cells may not die if perfusion restored in 20-40 minutes
ER management of acute coronary syndromes
Evaluate for reperfusion, 12 lead ECG
Oxygen optimizes hemoglobin saturation (? Use with normal sat)
ECG 12 lead & monitoring: Watch for ST/ T wave changes & PVCs
Analgesia with MS (IV preferred) relieves pain, ? anxiety
?-blockers ?? myocardial oxygen ne
Fibrinolytic therapy
Dissolve clots
Limit infarct size
Reduce mortality
Best if begun within 90 min of 1st symptoms
PCI - Percutaneous Coronary Intervention
Balloon tip catheter introduced into femoral or brachial artery
Catheter advanced to site of blockage under fluoroscopy
Balloon expanded to dilate stenosis
Acute complications: Thrombosis & vessel dissection
Long-term complications: Restenosis
Stents prev
CABG - Coronary Artery Bypass Graft
Can now be done on or off pump
Graft from aorta to CA distal to blockage
Graft may be venous or arterial
Mammary artery can be used
Recovery from ACS
At 4-7 days infarct is soft & can rupture
Over time (~ 7 wks) necrotic area replaced with granulation tissue ? Fibrous scar
Complications
Heart failure & cardiogenic shock from ? contractility
Dressler's Syndrome: Pericarditis - Hypersensitivity to tissue necrosis
LV aneurysm & rupture from weakened wall
Ventricular septal rupture
Papillary muscle (mitral valve) rupture
Stable angina
Caused by fixed obstruction of coronary artery - usually plaque > 75%
Precipitated by ? Oxygen demands from exercise or emotional stress
Generally relieved within 10 minutes by rest & NTG
Silent MI
MI without angina
Lack of pain may indicate high pain threshold or DM
Vasospastic angina
Spasm of coronary arteries ? angina
Occurs at rest
Associated with life threatening arrhythmias
Angina Classification
Class I: Pain with prolonged exercise
Class II: Slight limitation of normal activity
Class III: Marked limitation of ordinary activity
Class IV: Pain with any physical activity/ at rest
Diagnosis of Chronic Ischemic Heart Disease
R/O non-cardiac pain - Reflux, muscular
Exercise stress test ? ST changes
Holter monitor for vasospastic angina
Treatment of Chronic Ischemic Heart Disease
Goal is to reduce symptoms & prevent MI
Angioplasty (PTCA) or CABG may be needed
Therapeutic Lifestyle changes (TLC)
Anti-platelet drugs
?-blockers ?? cardiac work
Calcium channel blockers dilate arteries
NTG ?? preload & afterload
Infective endocarditis (endocardial and valve disorders)
Infection of endocardium including valves
Most often seen in those with preexisting heart defects, IV drug use, & heart surgery
Usually requires both heart damage & introduction of organism - dental work in person with valve disease
Staph. Aureus: Most co
Rheumatic Heart Disease
Immune response to ?-hemolytic strep infection
Symptoms: Sore throat & swollen glands to start
Carditis ? heart murmur & friction rub
Polyarthritis particularly of large joints
Skin lesions
CNS involvement ? Choreiform movements (jerking)
Dx: Clinical pic
Valvular Heart Disease
Stenotic valves produce resistance to forward blood flow
Incompetent (regurgitate) valves close incompletely ? backflow
Aortic stenosis
? LV pressure work
Aortic valve narrowed ?? resistance to LV ejection
Pressure work of LV ? & SV?
Systolic BP ? but LVP ?
Systolic murmur
Causes: Congenital defect, acquired calcification
Symptoms: Angina, syncope, HF
Mitral stenosis
? LV filling
Mitral valve fails to open fully
Often caused by fused leaflets from RHD
LV fills poorly ?? SV & CO
LA pressure is ?? pulmonary congestion
Mitral regurgitation
? LV volume work
Mitral valve fails to close fully
Retrograde flow into LA during systole ? systolic murmur
Causes: RHD, Chordea tenineae/ papillary muscle rupture
? LAP ?? SV but forward SV?
LV enlarged: Volume work increased
Eventually LV function becom
Aortic regurgitation
? LV volume work
Backflow from aorta ? LV during diastole
SV? but CO to tissues ?
Diastolic pressure ?? ?Coronary art perfusion Pulse pressure widened
LV failure if acute
LV dilates & hypertrophies in chronic
Diagnosis
Echo and auscultation
Rx
Medical management of HF & symptoms, surgical correction
symptoms of mitral stenosis
?CO? Chest pain, weakness, & fatigue
Pulmonary congestion ? SOB, AF, thrombi, Rt side HF
Diastolic murmur
Mitral valve prolapse
One cause of Mitral regurgitation
Causes: Marfan's syn. & other connective tissue diseases
Rx: ?-blockers (relieve symptoms)
Antibiotic prophylaxis (prevent complications)
symptoms of aortic regurgitation
LV failure symptoms (dyspnea)
Angina if DBP too low
Pericardial disease
Double-layered serous membrane: Visceral & parietal pericardium
Visceral adhers to epicardium
Parietal is fibrous & stiff
Pericardial fluid in pericardial space
Acute pericarditis
Inflammation of the pericardium from viral infection, systemic disease
Exudate common with some causes ? scar formation
Symptoms: Chest pain, pericardial friction rub, ECG changes (?ST segments & ?PR intervals)
Rx: Depends on cause - Antibiotics, NSAIDS
I
Pericardial effusion
Accumulation of fluid in the pericardial space: Serous fluid or blood
Develops from: Trauma, inflammation, abnormal Starlings forces
Rx: From NSAIDS to pericardiocentesis depending on size
Cardiac tamponade
A life-threatening complication of pericardial effusion
Causes: Surgery, trauma, cardiac rupture from MI
Sudden ? in pericardial fluid ?? pericardial pressures & ? venous return
Patient in shock: ?HR, ?BP & CO, jugular veins distended
Pulsus paradoxus: LV
Genetic cardiomyopathy
Hypertophic Cardiomyopathy
Excessive hypertrophy most notable in septum
Causes outflow obstruction ? symptoms like aortic stenosis
Seen in children & young adults - Familial pattern
Can ? sudden cardiac death
Autosomal dominant disorder: Mutations of card
Mixed Genetic & Non-Genetic Cardiomyopathies
Dilated Cardiomyopathy
Ventricles dilated ? walls thinned ? pump poorly
Etiology: Infection, toxins (ETOH), autoimmune, genetics
Symptoms: Heart failure ? ?EF, PVCs, dyspnea, weakness
Rx: Relieve HF symptoms - Digoxin, diuretics, vasodilators
Acquired Cardiomyopathy: Myocarditis
Inflammation of heart muscle ? necrossis
Usually viral: Coxsackievirus or HIV
Mechanisms of necrosis:
Direct cell destruction by infection
Toxins released by infectious agent
Autoimmune - molecular mimicry
Symptoms: From none ? heart failure & death
May f
Acquired Cardiomyopathy: Peripartum Cardiomyopathy
Develops late in pregnancy or in months after delivery
Produces systolic heart failure
Causes: ?? infection, immune response, genetic
May resolve spontaneously but not always
Fetal circulation
Physiology: PO2 low (30-35 mm Hg), CO high, Hgb has high O2 affinity
umbilical arteries
Take off from femorals
Carry low oxygen blood to placenta
umbilical vein
Carries high oxygen blood from placenta to fetus
Flows into liver
Ductus venousus
Bypasses hepatic tissue
Joins IVC (brings high oxygen blood)
Mixing reduces oxygen sat
Foramen ovale
Opening from right to left atrium
Allows blood to bypass lungs: Closes at birth
Ductus arteriosus
Opening from PA to aorta
Allows blood to bypass lungs: Closes at birth
Congenital Cardiac Defects:
Shunting: direction determined by pressure (resistance)
Movement of blood between pulmonary & systemic circulations
L ? R shunt defects
From LA to RA, from LV to RV, from aorta to PA
Atrial and ventricular septal defect, PDA
Produce little cyanosis
R ? L shunt defects
Flow from RV to LV thru VSD when pulmonary valve resistance high
Tetrology of Fallot
Transposition of great vessels
Produce cyanosis
?PA blood flow ?
PA hypertension
diagnosis and treatment of congenital cardiac defects
Ultrasound & fetal echoes after 16 wks
Rx: Supportive medical care & surgery
PDA
Blood flows from Aorta to PA
Effects: Rt HF & pulmonary edema
Rx: Indomethacin inhibits prostaglandin synthesis or Surgery
ASD/VSD
Blood flows from LV to RV or LA to RA
Effects: Right heart failure & pulmonary edema
Pulmonary hypertension in VSD
Rx: spontaneous or catheter closure
Tetralogy of Fallot
VSD, Pulmonary stenosis, Overriding Aorta (over VSD), RV hypertrophy
Blood flows from RV to LV ? Aorta receives blood from both RV & LV
Blue baby
Rx: Surgical correction
Transposition of great vessels
Aorta from RV & PA from LV
Needs some communication between circuits for life (PDA or septal defect)
Rx: prostaglandin keeps PDA open ? Surgical correction necessary
Coarctation of the aorta
Narrowing of aorta
BP in arms > legs
Rx: balloon angioplasty or open surgery
Functional single ventricle anatomy (rt)
May be single rt or single lt ventricle
Here we have single right ventricle with hypoplastic left ventricle
RV supplies lungs & systemic circulation (via PDA)
Palliative surgery but no full correction possible
Kawasaki Disease: acute vasculitis which may involve coronary arteries
? Immune in origin - Most common acquired heart disease of young children
S&S: Conjunctivitis, fever, rash, swelling of hands & feet, swollen cervical lymph nodes
Cardiac Involvement: CA aneurysms
Rx: Gamma globulin & ASA
The Coronary Arteries
Left & Right coronary arteries arise just distal to the Aortic Valve
Left Main gives rise to LAD & circumflex
LAD: Supplies septum & anterior wall of LV
Circumflex: Supplies lateral (free) wall of LV
RCA: Supplies RV & gives rise to posterior descending a
Coronary artery blood flow
Coronary arteries begin just distal to the Aortic valve
CA BP reflects aortic pressure
CA flow controlled by:
Aortic BP - particularly diastolic BP (Intra myocardial vessels compressed during systole)
Inadequate DBP ? ischemia
Auto-regulation: CA flow ? w
Coronary Heart Disease
CHD is divided into chronic ischemic heart disease & acute coronary syndromes
Ischemia refers to any time that cardiac oxygen demands > supply
Chronic Ischemic Heart Disease has 3 subtypes
stable vs. unstable plaques
Fixed stable plaques ? stable angina
Unstable plaques rupture & form clots ? unstable angina & MI (ACS)
Plaque rupture can be spontaneous but often 2o SNS activity
Plaques are vulnerable to rupture when they have: a large lipid-rich core, inflammation, fe
Acute coronary syndromes
Includes: Q-wave MI (ST elevation), non Q-wave MI (non ST elevation), & unstable angina
Q-wave MI generally from complete coronary artery occlusion
Others generally from incomplete or intermittent occlusion
diagnostic tools
ECG
T wave inversion = ischemia
ST changes = damage
ST depression = subendocardial injury
ST elevation = transmural injury
Q wave = old MI
Changes in leads overlying impacted area
Serum Markers
Necrotic cells release contents into blood
Myoglobin: ?at 1 h
Unstable Angina & Non Q-wave MI
From: Plaque disruption with clot and/or arterial spasm
Pain occurs at rest & is: severe, persistent (>20 min), not relieved by NTG
Called MI if serum markers are ?
Q-wave (ST elevation) MI (The real deal!)
Area of infarct determined by CA that is blocked
symptoms of MI
Abrupt onset of pain
Not revealed by rest & NTG
? more likely to have "discomfort"
Elderly more likely to have SOB
GI symptoms also common
30-50% die from VF in first few hrs
Immediate hospitalization VITAL
Pathologic changes
Extent determined by:
vessel that is occluded
time of occlusion
metabolic needs of tissue
extent of collaterals
Contractility loss almost immediate
Irreversible damage & necrosis in 20-40 min
Reperfusion can reestablish blood flow
Reperfused area "stunned
Management of Acute Coronary Syndromes
Goal: To prevent extension of injury/ necrosis
To prevent sudden cardiac death
Cells may not die if perfusion restored in 20-40 minutes
ER management of acute coronary syndromes
Evaluate for reperfusion, 12 lead ECG
Oxygen optimizes hemoglobin saturation (? Use with normal sat)
ECG 12 lead & monitoring: Watch for ST/ T wave changes & PVCs
Analgesia with MS (IV preferred) relieves pain, ? anxiety
?-blockers ?? myocardial oxygen ne
Fibrinolytic therapy
Dissolve clots
Limit infarct size
Reduce mortality
Best if begun within 90 min of 1st symptoms
PCI - Percutaneous Coronary Intervention
Balloon tip catheter introduced into femoral or brachial artery
Catheter advanced to site of blockage under fluoroscopy
Balloon expanded to dilate stenosis
Acute complications: Thrombosis & vessel dissection
Long-term complications: Restenosis
Stents prev
CABG - Coronary Artery Bypass Graft
Can now be done on or off pump
Graft from aorta to CA distal to blockage
Graft may be venous or arterial
Mammary artery can be used
Recovery from ACS
At 4-7 days infarct is soft & can rupture
Over time (~ 7 wks) necrotic area replaced with granulation tissue ? Fibrous scar
Complications
Heart failure & cardiogenic shock from ? contractility
Dressler's Syndrome: Pericarditis - Hypersensitivity to tissue necrosis
LV aneurysm & rupture from weakened wall
Ventricular septal rupture
Papillary muscle (mitral valve) rupture
Stable angina
Caused by fixed obstruction of coronary artery - usually plaque > 75%
Precipitated by ? Oxygen demands from exercise or emotional stress
Generally relieved within 10 minutes by rest & NTG
Silent MI
MI without angina
Lack of pain may indicate high pain threshold or DM
Vasospastic angina
Spasm of coronary arteries ? angina
Occurs at rest
Associated with life threatening arrhythmias
Angina Classification
Class I: Pain with prolonged exercise
Class II: Slight limitation of normal activity
Class III: Marked limitation of ordinary activity
Class IV: Pain with any physical activity/ at rest
Diagnosis of Chronic Ischemic Heart Disease
R/O non-cardiac pain - Reflux, muscular
Exercise stress test ? ST changes
Holter monitor for vasospastic angina
Treatment of Chronic Ischemic Heart Disease
Goal is to reduce symptoms & prevent MI
Angioplasty (PTCA) or CABG may be needed
Therapeutic Lifestyle changes (TLC)
Anti-platelet drugs
?-blockers ?? cardiac work
Calcium channel blockers dilate arteries
NTG ?? preload & afterload
Infective endocarditis (endocardial and valve disorders)
Infection of endocardium including valves
Most often seen in those with preexisting heart defects, IV drug use, & heart surgery
Usually requires both heart damage & introduction of organism - dental work in person with valve disease
Staph. Aureus: Most co
Rheumatic Heart Disease
Immune response to ?-hemolytic strep infection
Symptoms: Sore throat & swollen glands to start
Carditis ? heart murmur & friction rub
Polyarthritis particularly of large joints
Skin lesions
CNS involvement ? Choreiform movements (jerking)
Dx: Clinical pic
Valvular Heart Disease
Stenotic valves produce resistance to forward blood flow
Incompetent (regurgitate) valves close incompletely ? backflow
Aortic stenosis
? LV pressure work
Aortic valve narrowed ?? resistance to LV ejection
Pressure work of LV ? & SV?
Systolic BP ? but LVP ?
Systolic murmur
Causes: Congenital defect, acquired calcification
Symptoms: Angina, syncope, HF
Mitral stenosis
? LV filling
Mitral valve fails to open fully
Often caused by fused leaflets from RHD
LV fills poorly ?? SV & CO
LA pressure is ?? pulmonary congestion
Mitral regurgitation
? LV volume work
Mitral valve fails to close fully
Retrograde flow into LA during systole ? systolic murmur
Causes: RHD, Chordea tenineae/ papillary muscle rupture
? LAP ?? SV but forward SV?
LV enlarged: Volume work increased
Eventually LV function becom
Aortic regurgitation
? LV volume work
Backflow from aorta ? LV during diastole
SV? but CO to tissues ?
Diastolic pressure ?? ?Coronary art perfusion Pulse pressure widened
LV failure if acute
LV dilates & hypertrophies in chronic
Diagnosis
Echo and auscultation
Rx
Medical management of HF & symptoms, surgical correction
symptoms of mitral stenosis
?CO? Chest pain, weakness, & fatigue
Pulmonary congestion ? SOB, AF, thrombi, Rt side HF
Diastolic murmur
Mitral valve prolapse
One cause of Mitral regurgitation
Causes: Marfan's syn. & other connective tissue diseases
Rx: ?-blockers (relieve symptoms)
Antibiotic prophylaxis (prevent complications)
symptoms of aortic regurgitation
LV failure symptoms (dyspnea)
Angina if DBP too low
Pericardial disease
Double-layered serous membrane: Visceral & parietal pericardium
Visceral adhers to epicardium
Parietal is fibrous & stiff
Pericardial fluid in pericardial space
Acute pericarditis
Inflammation of the pericardium from viral infection, systemic disease
Exudate common with some causes ? scar formation
Symptoms: Chest pain, pericardial friction rub, ECG changes (?ST segments & ?PR intervals)
Rx: Depends on cause - Antibiotics, NSAIDS
I
Pericardial effusion
Accumulation of fluid in the pericardial space: Serous fluid or blood
Develops from: Trauma, inflammation, abnormal Starlings forces
Rx: From NSAIDS to pericardiocentesis depending on size
Cardiac tamponade
A life-threatening complication of pericardial effusion
Causes: Surgery, trauma, cardiac rupture from MI
Sudden ? in pericardial fluid ?? pericardial pressures & ? venous return
Patient in shock: ?HR, ?BP & CO, jugular veins distended
Pulsus paradoxus: LV
Genetic cardiomyopathy
Hypertophic Cardiomyopathy
Excessive hypertrophy most notable in septum
Causes outflow obstruction ? symptoms like aortic stenosis
Seen in children & young adults - Familial pattern
Can ? sudden cardiac death
Autosomal dominant disorder: Mutations of card
Mixed Genetic & Non-Genetic Cardiomyopathies
Dilated Cardiomyopathy
Ventricles dilated ? walls thinned ? pump poorly
Etiology: Infection, toxins (ETOH), autoimmune, genetics
Symptoms: Heart failure ? ?EF, PVCs, dyspnea, weakness
Rx: Relieve HF symptoms - Digoxin, diuretics, vasodilators
Acquired Cardiomyopathy: Myocarditis
Inflammation of heart muscle ? necrossis
Usually viral: Coxsackievirus or HIV
Mechanisms of necrosis:
Direct cell destruction by infection
Toxins released by infectious agent
Autoimmune - molecular mimicry
Symptoms: From none ? heart failure & death
May f
Acquired Cardiomyopathy: Peripartum Cardiomyopathy
Develops late in pregnancy or in months after delivery
Produces systolic heart failure
Causes: ?? infection, immune response, genetic
May resolve spontaneously but not always
Fetal circulation
Physiology: PO2 low (30-35 mm Hg), CO high, Hgb has high O2 affinity
umbilical arteries
Take off from femorals
Carry low oxygen blood to placenta
umbilical vein
Carries high oxygen blood from placenta to fetus
Flows into liver
Ductus venousus
Bypasses hepatic tissue
Joins IVC (brings high oxygen blood)
Mixing reduces oxygen sat
Foramen ovale
Opening from right to left atrium
Allows blood to bypass lungs: Closes at birth
Ductus arteriosus
Opening from PA to aorta
Allows blood to bypass lungs: Closes at birth
Congenital Cardiac Defects:
Shunting: direction determined by pressure (resistance)
Movement of blood between pulmonary & systemic circulations
L ? R shunt defects
From LA to RA, from LV to RV, from aorta to PA
Atrial and ventricular septal defect, PDA
Produce little cyanosis
R ? L shunt defects
Flow from RV to LV thru VSD when pulmonary valve resistance high
Tetrology of Fallot
Transposition of great vessels
Produce cyanosis
?PA blood flow ?
PA hypertension
diagnosis and treatment of congenital cardiac defects
Ultrasound & fetal echoes after 16 wks
Rx: Supportive medical care & surgery
PDA
Blood flows from Aorta to PA
Effects: Rt HF & pulmonary edema
Rx: Indomethacin inhibits prostaglandin synthesis or Surgery
ASD/VSD
Blood flows from LV to RV or LA to RA
Effects: Right heart failure & pulmonary edema
Pulmonary hypertension in VSD
Rx: spontaneous or catheter closure
Tetralogy of Fallot
VSD, Pulmonary stenosis, Overriding Aorta (over VSD), RV hypertrophy
Blood flows from RV to LV ? Aorta receives blood from both RV & LV
Blue baby
Rx: Surgical correction
Transposition of great vessels
Aorta from RV & PA from LV
Needs some communication between circuits for life (PDA or septal defect)
Rx: prostaglandin keeps PDA open ? Surgical correction necessary
Coarctation of the aorta
Narrowing of aorta
BP in arms > legs
Rx: balloon angioplasty or open surgery
Functional single ventricle anatomy (rt)
May be single rt or single lt ventricle
Here we have single right ventricle with hypoplastic left ventricle
RV supplies lungs & systemic circulation (via PDA)
Palliative surgery but no full correction possible
Kawasaki Disease: acute vasculitis which may involve coronary arteries
? Immune in origin - Most common acquired heart disease of young children
S&S: Conjunctivitis, fever, rash, swelling of hands & feet, swollen cervical lymph nodes
Cardiac Involvement: CA aneurysms
Rx: Gamma globulin & ASA