CARDIOVASCULAR SYSTEM
CARDIOMYOPATHY
DCM Most common. - Dyspnea on exertion EKG: - Heart failure therapy (ACEi, diuretics).
- Orthopnea - LVH - Abstain from alcohol.
Dilated and impaired contraction of one or both - Lower extremity edema - Left atrial enlargement - Refractory: heart transplant, LVAD.
ventricles. Leads to diastolic and systolic - S3 gallop - Prominent Q waves
dysfunction. Makes it hard to pump blood to the - T wave inversions
body and causes fluid build up in the lungs.
CXR: enlarged cardiac silhouette.
Dilation of LV leads to increased compliance →
leads to LV failure with reduced EF. Echo: best test
- Enlarged LA
Causes: - Decreased LV cavity size
- Idiopathic = MC - LV wall thickness > 15 mm
- Genetic - Family history is common. - Focal septal hypertrophy
- Myocarditis - LV diastolic dysfunction
- Alcohol misuse, cocaine, meth impaired.
- Medications (chemo)
- Viruses (HIV, flu, CMV)
- Postpartum cardiomyopathy ***Athlete’s heart is different:
- Occurs during last month of - Enlarged LV cavity size
pregnancy or during postpartum - NO LA ENLARGEMENT
period. - Sinus brady at rest
- Normal LV diastolic function.
HCM A condition that causes the heart muscle to - Most common cause of sudden ECG: LVH, left atrial enlargement, large - BBs
thicken, making it hard for the heart to pump cardiac death in competitive amplitude QRS complexes, tall R - non-DHP CCBs (more selective for heart!!!) - verapamil, diltiazem.
blood. Often have asymmetric hypertrophy that athletes (ask about FH of sudden waves - Vasodilators!!!
primarily involves the interventricular septum. death!) in leads V1-V2. - Surgery (myomectomy) if severe disease.
- Dyspnea on exertion - Avoid strenuous exercise and dehydration.
Causes reduced compliance of the ventricle, - Chest pain Echo: confirms dx. - Avoid:
impaired diastolic relaxation, and restricted LV - Decreased exercise tolerance - LVH with septal hypertrophy. - Positive inotropes (epinephrine, norepinephrine, dopamine,
filling. - Syncope - LV wall thickness > 15 mm dobutamine)
- Crescendo-decrescendo systolic - Nitrates
Autosomal dominant. ejection murmur at LLSB or apex - - ACEi
increases with valsalva, decreases - These decrease afterload which worsens LV outflow tract
with squatting. obstruction.
- S4 gallop
RCM Least common of the cardiomyopathies. - Right sided heart failure. Echo: Non specific
Walls become stiff but not necessarily thickened. - Dyspnea, fatigue, limited exercise - Impaired diastolic filling Diuretics
capacity, palpitations, syncope. - Preserved systolic function ACE inhibitors
Impaired diastolic function (restrictive filling - CHF symptoms: JVD, Kussmauls, CCBs
and reduced diastolic volume of either or both peripheral edema, rales,
ventricles). hepatomegaly, ascites, S3 and S4 Treat underlying cause!!!
Preserved systolic function. gallops.
- Pulm HTN *do not confuse with constrictive pericarditis, which results from
Causes: - Normal EF scarring and requires anti-inflammatory medications or surgery.
- Infiltrative: amyloidosis, sarcoidosis, - Normal heart size
scleroderma
, - Non Infiltrative: familial, idiopathic
- Hemochromatosis
Stress cardio-
myopathy
ARRHYTHMIAS
Atrial Afib: When multiple areas of atrium are simultaneously depolarizing ECG: Stable:
fibrillation and contraction. This causes them to quiver and beat erratically and - Irregularly irregular rhythm - BBs (metoprolol) or CCBs (diltiazem)
out of sync with the lower chambers. - No discernible p waves - Rhythm control (meds vs synchronized conversion)
- Afib w RVR: rapid HR. - < 48 hrs - cardioversion
Afib w RVR: when lower chambers are involved. The ventricles beat too - > 48 hrs - amiodarone and anticoagulation 21 days prior to
quickly and irregularly, resulting in rapid HR of 100-180 bpm. S/S: cardioversion.
- Asymptomatic
RFs: alcohol, drugs, CAD, congenital heart disease, elderly - Palpitations Unstable (hypotension, hypoperfusion):
- Dizziness, lightheadedness - Emergent synchronized cardioversion.
Increases risk for systemic thromboembolism - Chest pain
- Due to LA enlargement, stasis of blood due to ineffective atrial - Dyspnea
contraction, atrial inflammation, fibrosis. - Pulmonary embolism: Test for hyperthyroidism in patients with Afib.
- Left atrial appendage (LAA) - small saclike structure in LA that - Pleuritic chest pain, acute onset dyspnea,
is susceptible to thrombus formation → can embolize and lead hemoptysis, tachypnea, tachycardia, hypoxemia, ALL PATIENTS NEED ANTICOAGULATION:
to stroke. low grade fever, JVD - Warfarin, apixaban
- Can also cause pulmonary embolism!!! - EKG: S1Q3T3
- CXR: Hampton Hump and Westermark sign CHA2DS2-VASc score to assess risk of stroke and determine if
patient needs anticoagulation:
CHF, HTN, age > 75, DM, stroke hx, sex, vascular disease hx.
- 0: no therapy or aspirin.
- 1: either aspirin or anticoagulation.
- 2+: anticoagulation.
Atrial flutter Stable: Rate control: BBs (metoprolol, esmolol) or nonDHP CCBs
(verapamil, diltiazem)
Atrial
tachycardia
AV block AV block occurs when there is a delay in the conduction of impulses at the AV node, 1st degree: observe if no symptoms.
bundle of His, purkinje fibers, or lower.
2nd degree
S/S: asymptomatic, palpitations, dizziness, lightheadedness, syncope. ● Type 1: often normal variant, sometimes related to increased vagal
tone. Usually requires no treatment.
1st degree: ● Type 2:
● PR > 0.20 -- delay at AV node or bundle of his. ○ Often progresses to complete heart block. Symptomatic
patients need a pacemaker.
2nd degree: ○ Avoid agents that slow conduction through the AV node
● Type 1: Wenckebach (digoxin, BBs, CCBs, adenosine).
○ PR gets progressively longer until a drop. ○ Avoid nitroglycerin. It does not have any affect on the AV
● Type 2: blockage of conduction in the Bundle of His or lower. node but it is a vasodilator and therefore can cause serious
○ PR interval stays the same with a random drop. hypotension and hypoperfusion.
○ QRS is usually wide. ○ If UNSTABLE:
, ■ Dobutamine (beta agonist)
■ Epinephrine (beta agonist)
3rd degree: P and QRS have no correlation - complete AV dissociation.
3rd degree
● Medications: avoid agents that slow conduction through the AV
node.
Bradycardia < 50 bpm - Dizziness, light headed Identify and treat underlying cause.
- Syncope
Commonly seen in acute inferior MI due to increase in vabal tone. - Heart failure If hypotension, shock, AMS, chest discomfort, acute heart failure:
- IV atropine 1 mg bolus → repeat every 3-5 minutes up to 3.0 mg
max.
- If no response…
- Transcutaneous pacing or…
- IV dopamine infusion titrate to patient response or…
- IV epinephrine infusion titrate to patient response
- If no response…
- Consult or transvenous pacing.
If none of the above signs → monitor and observe.
Bundle branch R and R’ (upward bunny ears)
block LBBB: in V4-V6
RBBB: in V1-V3
Idioventricular
rhythm
Junctional
rhythms
Regular narrow Types: Hemodynamic instability → immediate synchronized cardioversion
complex - SVT
tachycardia - Sinus tachycardia Hemodynamic stability:
- Atrial tachycardia 1. Vagal maneuvers
- Atrial flutter 2. Adenosine - 6 mg IV then 12 mg
- AVRT
- AVNRT
WPW Caused by Bundle of Kent (an accessory pathway that prematurely depolarizes a portion Orthodromic: narrow complex: vagal maneuvers, AV nodal blockers
of the ventricles). Basically the depolarization from the SA node cheats and goes (adenosine, BB, CCB)
through this accessory pathway instead of taking the AV node, so the ventricles
become depolarized early. Antidromic: wide complex: procainamide
BYPASS AV NODE BY TAKING BUNDLE OF KENT. Definitive treatment: radiofrequency ablation.
ECG:
- Delta wave (premature depolarization of ventricles)
- Short PR interval <0.20.
- Wide QRS
s/s: may be asymptomatic or have symptoms of tachydysrhythmias
including SOB, palpitations, lightheadedness, syncope, chest pain.
CARDIOMYOPATHY
DCM Most common. - Dyspnea on exertion EKG: - Heart failure therapy (ACEi, diuretics).
- Orthopnea - LVH - Abstain from alcohol.
Dilated and impaired contraction of one or both - Lower extremity edema - Left atrial enlargement - Refractory: heart transplant, LVAD.
ventricles. Leads to diastolic and systolic - S3 gallop - Prominent Q waves
dysfunction. Makes it hard to pump blood to the - T wave inversions
body and causes fluid build up in the lungs.
CXR: enlarged cardiac silhouette.
Dilation of LV leads to increased compliance →
leads to LV failure with reduced EF. Echo: best test
- Enlarged LA
Causes: - Decreased LV cavity size
- Idiopathic = MC - LV wall thickness > 15 mm
- Genetic - Family history is common. - Focal septal hypertrophy
- Myocarditis - LV diastolic dysfunction
- Alcohol misuse, cocaine, meth impaired.
- Medications (chemo)
- Viruses (HIV, flu, CMV)
- Postpartum cardiomyopathy ***Athlete’s heart is different:
- Occurs during last month of - Enlarged LV cavity size
pregnancy or during postpartum - NO LA ENLARGEMENT
period. - Sinus brady at rest
- Normal LV diastolic function.
HCM A condition that causes the heart muscle to - Most common cause of sudden ECG: LVH, left atrial enlargement, large - BBs
thicken, making it hard for the heart to pump cardiac death in competitive amplitude QRS complexes, tall R - non-DHP CCBs (more selective for heart!!!) - verapamil, diltiazem.
blood. Often have asymmetric hypertrophy that athletes (ask about FH of sudden waves - Vasodilators!!!
primarily involves the interventricular septum. death!) in leads V1-V2. - Surgery (myomectomy) if severe disease.
- Dyspnea on exertion - Avoid strenuous exercise and dehydration.
Causes reduced compliance of the ventricle, - Chest pain Echo: confirms dx. - Avoid:
impaired diastolic relaxation, and restricted LV - Decreased exercise tolerance - LVH with septal hypertrophy. - Positive inotropes (epinephrine, norepinephrine, dopamine,
filling. - Syncope - LV wall thickness > 15 mm dobutamine)
- Crescendo-decrescendo systolic - Nitrates
Autosomal dominant. ejection murmur at LLSB or apex - - ACEi
increases with valsalva, decreases - These decrease afterload which worsens LV outflow tract
with squatting. obstruction.
- S4 gallop
RCM Least common of the cardiomyopathies. - Right sided heart failure. Echo: Non specific
Walls become stiff but not necessarily thickened. - Dyspnea, fatigue, limited exercise - Impaired diastolic filling Diuretics
capacity, palpitations, syncope. - Preserved systolic function ACE inhibitors
Impaired diastolic function (restrictive filling - CHF symptoms: JVD, Kussmauls, CCBs
and reduced diastolic volume of either or both peripheral edema, rales,
ventricles). hepatomegaly, ascites, S3 and S4 Treat underlying cause!!!
Preserved systolic function. gallops.
- Pulm HTN *do not confuse with constrictive pericarditis, which results from
Causes: - Normal EF scarring and requires anti-inflammatory medications or surgery.
- Infiltrative: amyloidosis, sarcoidosis, - Normal heart size
scleroderma
, - Non Infiltrative: familial, idiopathic
- Hemochromatosis
Stress cardio-
myopathy
ARRHYTHMIAS
Atrial Afib: When multiple areas of atrium are simultaneously depolarizing ECG: Stable:
fibrillation and contraction. This causes them to quiver and beat erratically and - Irregularly irregular rhythm - BBs (metoprolol) or CCBs (diltiazem)
out of sync with the lower chambers. - No discernible p waves - Rhythm control (meds vs synchronized conversion)
- Afib w RVR: rapid HR. - < 48 hrs - cardioversion
Afib w RVR: when lower chambers are involved. The ventricles beat too - > 48 hrs - amiodarone and anticoagulation 21 days prior to
quickly and irregularly, resulting in rapid HR of 100-180 bpm. S/S: cardioversion.
- Asymptomatic
RFs: alcohol, drugs, CAD, congenital heart disease, elderly - Palpitations Unstable (hypotension, hypoperfusion):
- Dizziness, lightheadedness - Emergent synchronized cardioversion.
Increases risk for systemic thromboembolism - Chest pain
- Due to LA enlargement, stasis of blood due to ineffective atrial - Dyspnea
contraction, atrial inflammation, fibrosis. - Pulmonary embolism: Test for hyperthyroidism in patients with Afib.
- Left atrial appendage (LAA) - small saclike structure in LA that - Pleuritic chest pain, acute onset dyspnea,
is susceptible to thrombus formation → can embolize and lead hemoptysis, tachypnea, tachycardia, hypoxemia, ALL PATIENTS NEED ANTICOAGULATION:
to stroke. low grade fever, JVD - Warfarin, apixaban
- Can also cause pulmonary embolism!!! - EKG: S1Q3T3
- CXR: Hampton Hump and Westermark sign CHA2DS2-VASc score to assess risk of stroke and determine if
patient needs anticoagulation:
CHF, HTN, age > 75, DM, stroke hx, sex, vascular disease hx.
- 0: no therapy or aspirin.
- 1: either aspirin or anticoagulation.
- 2+: anticoagulation.
Atrial flutter Stable: Rate control: BBs (metoprolol, esmolol) or nonDHP CCBs
(verapamil, diltiazem)
Atrial
tachycardia
AV block AV block occurs when there is a delay in the conduction of impulses at the AV node, 1st degree: observe if no symptoms.
bundle of His, purkinje fibers, or lower.
2nd degree
S/S: asymptomatic, palpitations, dizziness, lightheadedness, syncope. ● Type 1: often normal variant, sometimes related to increased vagal
tone. Usually requires no treatment.
1st degree: ● Type 2:
● PR > 0.20 -- delay at AV node or bundle of his. ○ Often progresses to complete heart block. Symptomatic
patients need a pacemaker.
2nd degree: ○ Avoid agents that slow conduction through the AV node
● Type 1: Wenckebach (digoxin, BBs, CCBs, adenosine).
○ PR gets progressively longer until a drop. ○ Avoid nitroglycerin. It does not have any affect on the AV
● Type 2: blockage of conduction in the Bundle of His or lower. node but it is a vasodilator and therefore can cause serious
○ PR interval stays the same with a random drop. hypotension and hypoperfusion.
○ QRS is usually wide. ○ If UNSTABLE:
, ■ Dobutamine (beta agonist)
■ Epinephrine (beta agonist)
3rd degree: P and QRS have no correlation - complete AV dissociation.
3rd degree
● Medications: avoid agents that slow conduction through the AV
node.
Bradycardia < 50 bpm - Dizziness, light headed Identify and treat underlying cause.
- Syncope
Commonly seen in acute inferior MI due to increase in vabal tone. - Heart failure If hypotension, shock, AMS, chest discomfort, acute heart failure:
- IV atropine 1 mg bolus → repeat every 3-5 minutes up to 3.0 mg
max.
- If no response…
- Transcutaneous pacing or…
- IV dopamine infusion titrate to patient response or…
- IV epinephrine infusion titrate to patient response
- If no response…
- Consult or transvenous pacing.
If none of the above signs → monitor and observe.
Bundle branch R and R’ (upward bunny ears)
block LBBB: in V4-V6
RBBB: in V1-V3
Idioventricular
rhythm
Junctional
rhythms
Regular narrow Types: Hemodynamic instability → immediate synchronized cardioversion
complex - SVT
tachycardia - Sinus tachycardia Hemodynamic stability:
- Atrial tachycardia 1. Vagal maneuvers
- Atrial flutter 2. Adenosine - 6 mg IV then 12 mg
- AVRT
- AVNRT
WPW Caused by Bundle of Kent (an accessory pathway that prematurely depolarizes a portion Orthodromic: narrow complex: vagal maneuvers, AV nodal blockers
of the ventricles). Basically the depolarization from the SA node cheats and goes (adenosine, BB, CCB)
through this accessory pathway instead of taking the AV node, so the ventricles
become depolarized early. Antidromic: wide complex: procainamide
BYPASS AV NODE BY TAKING BUNDLE OF KENT. Definitive treatment: radiofrequency ablation.
ECG:
- Delta wave (premature depolarization of ventricles)
- Short PR interval <0.20.
- Wide QRS
s/s: may be asymptomatic or have symptoms of tachydysrhythmias
including SOB, palpitations, lightheadedness, syncope, chest pain.
