Clin Med: Cardio II Flashcards
Takotsubo cardiomyopathy mimics…
MI, but w/o ischemia
Stress cardiomyopathy: Background
Temp heart condition w/ rapid heart muscle weakening following extreme stress
Stress cardiomyopathy: pathophys
Catecholamines released during stress affect the myocardium of the heart
Examples of severe emotional stress
- death of loved one
- divorce
- breakup
- losing job, home, money
Examples of severe physical stress (5)
- severe pain
- running marathon
- asthma attack
- stroke
- surgery
Stress cardiomyopathy is more prevalent in which gender?
female
Stress cardiomyopathy: S/S
- angina
- diaphoresis
- nausea
- vomiting
- dyspnea
- palpitations
- decr BP
Stress cardiomyopathy: Dx
- Hx of stressful, emotional, or physical event
- EKG (ST elevation or T wave inversion)
- Blood test (Troponin & cardiac enzymes typically normal vs MI)
- Coronary angiogram (no obstruction)
- Ventriculography (LV Gram) & Echo (ballooning of LV w/ unusual muscle wall movement)
- Cardiac MRI
Stress cardiomyopathy: Tx
- usually resolves w/ med management
- ACE inhibitors (control BP)
- Beta blockers (regulate HR)
- Diuretics (maintain fluid balance)
- Anti-anxiety meds & stress management techniques
Cardiac muscle contraction is dependent on…
- Na+
- K+
- Ca++
3 general categories of dysrhythmias
- Slow
- Fast
- Other
Sinus bradycardia: Hx
- Syncope
- Dizziness
- Lightheadedness
- Chest pain
- Shortness of breath
- Exercise intolerance
Sinus bradycardia can be normal in which people?
athletes
Rate for Sinus bradycardia
< 60bpm
What can causes Sinus bradycardia?
- hypothermia
- hypothyroidism
- drugs (beta blockers, Ca++ channel blockers)
- myocarditis,
- hypoglycemia
Sinus bradycardia: Hx
- Syncope
- Dizziness
- Lightheadedness
- Chest pain
- SOB
- Exercise intolerance
In pts w/ sinus bradycardia what should you ask about?
- Cardiac history (MI, CHF, valve dz)
- Meds, Toxic exposures
Sinus bradycardia: PE
- Will depend on underlying cause & severity
- Decr LOC
- Cyanosis
- Peripheral edema
- Dyspnea
- Syncope
- Mottled skin
Which pts do we usually see heart blocks in ?
elderly patients
Sinus bradycardia: Dx Labs/imaging
- EKG
- Electrolytes (Na+, K+, Ca++, Mg++)
- Glucose
- Thyroid Function Test
- Toxicology screens
- Troponin
- Others based on probable underlying cause
What is troponin?
cardiac enzyme that is elevated when heart muscle has died due to lack of O2 (MI)
Sinus Bradycardia: Tx
- Treat underlying cause, but do not delay care
- Atropine
- Transcutaneous pacing
- Transvenous pacing
**Expert consult
What is the main med used for Sinus bradycardia?
Atropine
How does atropine work?
binds to & inhibitors muscarinic receptors–> producing wide range of anticholinergic effects–> increases HR
Define a heart block
term for arrhythmia where there is a delay or “block” somewhere along the conduction system
Why do heart blocks occur?
Usually occur as a result of damage to the conduction system (fibrosis, ischemia), but often idiopathic
Where is the signal delayed in a 1st degree AV block?
AV node
What is the PR interval in a 1st degree AV block?
> 200ms
How does the pt usually present w/ 1st degree AV block
asymptomatic & found incidentally
Does a 1st degree AV block require tx?
not usually unless underlying cause (i.e. electrolyte imbalance or due to meds)
Other names for 2nd degree Type I heart block
- Mobitz Type I
- Wenckebach
NOTE
2nd degree: Type I has a consistent P:QRS ratio
2nd degree Type I is often transient, but may occur due to…
- myocardial ischemia
- myocarditis
- cardiac surg
Describe a 2nd degree Type I
Progressive lengthening of the PR interval until a QRS is dropped
When does 2nd degree Type I need tx?
doesn’t need treatment unless symptomatic
2nd degree Mobitz Type I: Tx
Atropine
only if symptomatic
Describe PR interval & QRS complex for 2nd degree Type II heart block.
- PR interval consistent
- Intermittent dropped QRS complexes (may be fixed)
2nd degree Type II heart block usually due to…
- ischemia–> damage to the conducting system
- Lyme Dz
3rd degree heart block aka…
complete heart block
3 degree heart block: Tx
- required transcutaneous pacing STAT
- transvenous cardiac pacing
- some will req permanent cardiac pacing
A 3rd degree heart block is…
total block b/t atria & ventricles
3rd degree heart block: S/S
- fatigue
- chest pain
- SOB
- dyspnea
- may be hemodynamically unstable
Describe sinus tachycardia.
regular narrow-complex tachycardia
Describe P wave and QRS complex for Sinus Tachycardia.
- P wave is before every QRS
may be hard to see if fast
Sinus tachycardia: HR
> 100 in adults (peds depends on age)
Sinus Tachycardia: almost always due to…
some underlying issue
Sinus Tach: other common cause (10)
- exercise
- pain
- fever
- hyperthyroidism
- HF
- anemia
- alcohol withdrawal
- drug use
- caffeine
- dehydration
Sinus Tach: Tx
treat underlying issue
AVNRT is a type of…
supraventricular tachycardia
Describe AVNRT
regular, narrow tachycardia
AVNRT Rate
170 - 180
can be as high as 300
AVNRT: S/S
- palpitations**
- lightheadedness
- dyspnea
AVNRT is most common in which gender?
females
AVNRT: Stepwise tx
vagal maneuvers–> adenosine–> BB–> cardioversion
Which “A” drug is used for AVNRT?
adenosine
Atrial flutter: Rate
300 -400
Atrial flutter pattern?
saw tooth pattern w/ narrow QRS
Atrial flutter: S/S
asymptomatic or have palpitations/lightheadedness
Atrial flutter: Tx if stable
rate control w/ diltiazem or verapamil
Atrial flutter: Tx if unstable
anticoagulation & cardioversion
What is Afib & cause?
a common supraventricular tachyarrhythmia caused by uncoordinated atrial activation & associated w/ an irregularly irregular ventricular response
Most common arrhythmia that is considered as irregularly irregular?
Afib
NOTE
Afib is a MAJOR preventable cause of stroke
Define persistent AF
AF that fails to self-terminate w/n 7 days.
- Often req pharmacologic or electrical cardioversion to restore sinus rhythm.
Categories of Afib
- Paroxysmal AF
- Persistent AF
- Long-standing persistent AF
- Permanent AF
Define paroxysmal AF
AF that terminates spontaneously or w/ intervention w/n 7 days of onset. Episodes may recur w/ variable frequency.
Define long-standing persistent AF
AF that has lasted >12mo
NOTE
While a pt who has had persistent AF can have later episodes of paroxysmal AF, AF is generally considered a progressive disease.
Define permanent AF
used to identify ppl w/ persistent Afib where a joint decision by the pt & clinician has been made to no longer pursue a rhythm control strategy.
Describe prevalence of Afib
- 1-2% of gen pop
- 9% is > 65yo
Most common 2ndary causes for AFib
- HTN
- CAD
Afib: pathophys
several reentrant circles in the atria that causes random signals to get through to the ventricles which usually have a normal rate
Afib: Hx-S/S
- usually firstly asymptomatic
S/S
- palpitations
- SOB
- lightheadedness/dizziness
- focal neurological deficit (embolic stroke)**
Afib: PE
- Irregularly irregular HR
- may have evidence of HF
- Evidence of underlying issues (hyperthyroidism, etc)
Afib: Dx labs/imaging
- EKG
- TTE or TEE
- TSH
- Check for suspected underlying conditions
What fraction of pts w/ new onset Afib will spontaneously revert to NSR w/o need for cardioversion?
2/3
New Onset Unstable Afib: Tx
- IV BB (esmolol, propranolol, metoprolol) or CCB (diltiazem or verapamil)
- Heparin
- Electrical cardioversion if severe HTN, pulmonary edema, ischemia*
- Admit
If patient has new onset AFib, what is the first line tx?
electrical cardioversion
New Onset stable Afib: Tx
- Rate control (BB or CCB) IV or PO
- Anticoagulation
- Cardioversion (only after TTE shows no thrombus. If thrombus, anticoagulated for 4 weeks prior to cardioversion)
Chronic Afib: Rate control Tx
- BB or CCB
- Goal- resting heart rate of <80 in symptomatic patients
Chronic Afib: Anticoagulation Tx
- Depends on CHAD score (if >2, anticoag recommended)
- DOAC’s for most pts
When should Warfarin be used in those w/ chronic Afib?
if mechanical heart valve, rheumatic heart disease, can’t tolerate DOAC b/c severe chronic kidney disease
Chronic Afib: Rhythm Tx
If symptoms and/or Afib persist despite rate control: cardioversion and/or ablation
What is happening during PVCs?
ventricular “irritability” causes a beat (or several beats) that originate in the ventricle (ectopic foci)
PVCs are caused by:
- Epi released by the adrenal glands
- Caffeine, amphetamines, cocaine, beta 1 receptor agonists
- Alcohol
- Hyperthyroidism
- Low O2
- Hypokalemia
Do PVCs req tx?
usually SL
PVCs are usually followed by a….
compensatory pause
What is ventricular tachycardia?
a “run” of PVC’s
- wide, monomorphic tachycardia
Variable presentations of VTach
- non-sustained (3-30 in a row) or sustained
- pulse or pulseless
- pts may be stable or cardiac arrest
Which type of VTach can be shocked via defibrillation?
Pulseless VTach
Non sustained VTach: S/S
~ May have w/ lightheadedness or palpitations
- May be asymptomatic & discovered incidentally
How do you evaluate for non sustained VTach?
Look for underlying heart dz
- Hx/Physical
- EKG
- TTE
- Exercise stress testing
- Holter monitor
Non sustained VTach: Tx
asymptomatic & no heart dz: no Tx
symptomatic & no heart dz: rate control (BB) or ablation
asymptomatic or symptomatic WITH heart dz: evaluate & treat underlying dz
Sustained VTach: RFs
- CAD (most common)
- Cardiomyopathies
- Cardiac sarcoidosis
Sustained VTach usually causes…
- cardiac arrest if untreated
may have
- SOB
- chest pain
- palpitations
-syncope
Stable sustained VTach: Tx
Procainamide
not common
Stable, but compromised (hypotension, AMS, chest) sustained VTach: Tx
cardioversion w/ sedation if possible
Sustained VTach leading to cardiac arrest: Tx
- chest compressions
- Defibrillation
–> Epinephrine or Amiodarone
Chronic/recurring sustained VTach: Tx
- treat underlying heart dz
- catheter ablation
- implantable cardioverter defibrillator
Polymorphic ventricular VTach aka…
Torsades de Pointe
Describe Torsades de Pointe.
Shape of contractions from each beat changes as signal begins in different areas of ventricles
Usually a sequalae of Long QT Syndrome
Torsades de Pointe: Tx
- Stop any causative agents
- Fix underlying electrolyte abnormalities
- IV magnesium sulfate***
- Temporary pacing
What is long QT syndrome?
having a QT interval longer than normal
What causes acquired long QT syndrome?
- Drugs (some anti infectives, anti psychotics, anti emetics)
- Electrolyte abnormalities (hypoCa++, hypoMg++, hypoK+)
- Starvation states (anorexia nervosa)
What causes congenital long QT syndrome?
- Genetics
- > in females
- First manifestations is 14 years old
- Should avoid any QT prolonging drugs
- High risk pts may get ICD, & tx chronically w/ BB
Describe VFib.
“bag of worms”
- can lead to sudden cardiac death in mins
- uncoordinated ventricular contraction
- each wave on EKG goes w/ a different part of ventricle contracting
What are the two shockable rhythms?
VFib
Pulseless VTach
VFib usually occurs during a…
MI
What should you do if VFib leads to no pulse?
start CPR immediately
VFib: Tx
- defibrillation
- epi
- amiodarone or lidocaine
CAD refers to
a spectrum of conditions that causes decreased blood flow to the myocardium
What is the spectrum (S/S) of CAD
asymptomatic–> stable angina–> unstable angina–> NSTEMI–> STEMI
Why do symptoms range so widely for CAD?
varying degrees of atherosclerosis (plaque buildup)
NOTE
CAD is most common heart dz
In the US, someone has a MI every 40secs
About how many adults (>/= 20) have CAD?
18.2 million
Every year, how many Americans have a MI?
805,000
CAD: Modifiable RFs
- Tobacco exposure
- Physical inactivity
- Overweight/obesity
- HTN
- Dyslipidemia
- DM
- Metabolic Syndrome
Metabolic Syndrome includes…
HTN + Obesity + DM + dyslipidemia
CAD: Non-modifiable RFs
- FHx (under 55yo) of CAD or HLD
- Sex (M>F)
Atherosclerosis: pathophys
- chronic inflammation disorder of medium & large arteries
- buildup of plaques w/n artery lumen
- inflammatory response to endothelial cell injury
Describe Inflammatory response to endothelial cell injury for atherosclerosis
- Injury due to endothelial stress (HTN, smoking, DM)
- LDL particles leak into the intimal layer, are oxidized
- Immune response (macrophages) leads to inflammation
- Leads to a “fatty streak” in the lumen
- Platelets adhere to the fatty streak & release growth factors
- Leads to development a plaque that can enlarge & rupture
- If rupture, more platelets adhere, forming a thrombus, which can occlude the vessel
Conditions that can accelerate progression of atherosclerosis
- male gender (women after meno)
- FHx
- Primary & 2ndary HLD
- Smoking
- HTN
- DM
- Obesity
- Nephrotic syndrome
- Hypothyroidism
- High Lipoprotein
- Elevated plasma homocysteine
Who has an atypical presentation of Stable angina?
DM pts & women
Stable angina: Hx
- chest pain w/ activity & relieved by rest
- tightness, squeezing, burning, “gas,” indigestion
- Pain behind or slightly to left of midsternum w/ poss. radiation to the left shoulder, upper arm, jaw, back
- > 30 minutes duration
- Pain relieved w/ nitroglycerin and/or rest
Stable angina: Physical
- elevated BP
- signs of underlying dz/RFs for cardiac ischemia
- Diaphoresis
Stable Angina Pectoris
Primarily a clinical diagnosis
What should the workup include for stable angina?
- Labs: look for underlying issues (lipids, kidney disease)
- EKG will be normal at rest
- EKG may show ST segment changes during activity
- Pts w/ low probability of CAD -> noninvasive stress test
- For pts w/ high probability CAD -> cardiac cath
Stable angina: Anti anginal therapy
- Acute: short acting nitrates (nitroglycerin)
- Prevent: Beta blockers
- If >70% stenosis in 1 vessel, coronary artery revascularization
How to prevent dz progression of stable angina?
- Anti platelet therapy (ASA–> aspirin or clopidogrel if allergic)
- Lipid lowering therapy
- ACEI/ARB if diabetic or CKD (chronic kidney dz)
When should you follow up w/ stable angina?
6-12 months, sooner if symptoms change
What is unstable angina?
pain during activity & at rest
Unstable angina is usually due to…
a ruptured plaque meaning less room for blood flow leading to areas of myocardium ischemia
Unstable angina has a high risk of progressing to a
MI
NOTE
Unstable angina is not distinguishable from NSTEMI until cardiac enzymes are obtained
Unstable Angina: Hx
- Chest pain at rest or does not improve w/ rest
- Pain described similarly to stable angina
Unstable Angina: Physical
- Levine sign
- VS variable
Workup for Unstable Angina
- EKG (poss ST segment changes)
- Cardiac enzymes (NEGATIVE) x2
- If stable, may be observed for 24-48 hours, then stress test
- If unstable (or high risk), may have immediate cardiac cath w/ PCI
Acute Unstable Angina: Tx
- ASA (aspirin)
- Antiplatelet therapy (P2Y12 Inhibitor) (Plavix)
- Anticoagulation
–>heparin (if invasive therapy)
–> LMWH (if noninvasive therapy) - Cardiology consult
- Likely cardiac cath w or w/o PCI
(percutaneous coronary intervention)
Ongoing Unstable Angina: Tx
- ASA
- Antiplatelet therapy
- Nitroglycerin
- BB & ACEI
- Lipid reduction
- Glucose control
NSTEMI stands for
Non-ST Elevation Myocardial Infarction
Describe a NSTEMI
Unstable Angina w/ elevated cardiac enzymes
NO ST elevations on EKG (will likely have ST segment depression)
NSTEMI: Tx
Consult cardiology
- Treated like STEMI (not quite the same urgency)
- PCI is preferred tx
What is a STEMI?
ST elevation MI
STEMI: median age
68 years
STEMI: gender prevelance
male>female
STEMI: RFs
- prior MI
- CAD
- Cocaine uses
STEMI: Pathophys
STEMI: Hx Typical
- pain starts in retrosternal area & may radiate to 1 or both arms, neck, or jaw
- occurs at rest or w/ minimal exertion
- ≥ 10 mins in duration
- may be new-onset angina or angina w/ incr intensity
- unrelieved w/n < 5 minutes of rest or nitroglycerin
STEMI: Hx Atypical
- arm
- shoulder
- back
- neck
- jaw
- epigastric
seen in women, DM & every elderly pts
STEMI: Hx anginal equivalents
- new-onset or incr exertional dyspnea (most common)
- nausea
- vomiting
- diaphoresis
- abdominal pain
- syncope
- unexplained fatigue
STEMI: Physical
~ bradycardia or tachycardia
- JVD indicates right atrial HTN
- Soft heart sounds indicate left ventricular dysfunction
- S4 common
- Mitral regurg due to papillary muscle dysfunction
- Cyanosis
- Decr peripheral pulses
STEMI: Dx labs/imaging
- EKG (w/n 10 mins of pt arrival)
–>Repeat @ 15min intervals if non-dx - Cardiac biomarkers
–>Troponin (preferably high sensitivity) - Other tests (to aid in evaluation and treatment)
–> CXR
–> Echo
–> PT/PTT/INR
–> BNP
STEMI: Tx
- PCI w/n 90 mins of arrival if available
- PCI w/n 120 mins of arrival if transfer needed
- If PCI unavailable w/n 120 mins, pharmacologic reperfusion (fibrinolysis) w/ plans for PCI ASAP
What should be given to any patent presenting w/ chest chain & could be having a heart attack?
MONA
- morphine
- O2 (some pts)
- Nitroglycerin
- Aspirin (chewable 325mg)
Ongoing treatment after STEMI
- ASA (aspirin)
- Antiplatelet therapy (Plavix)
- Nitroglycerin
- BB & ACEI
- Lipid reduction
- Glucose control
- Evaluate EF w/ echo
- Stress test–> look for residual ischemia
Prinzmetal angina aka
Vasospastic angina
What is Prinzmetal Angina?
Chest pain that occurs at rest & is associated w/ transient ST segment elevation
Prinzmetal Angina is caused by…
- focal spasm of the coronary artery
- Unclear pathophysiology
Prinzmetal Angina is usually seen in…
younger pts w/ fewer RFs
Prinzmetal Angina: Dx
Coronary angiography
(acetylcholine given to provoke spasm)
Prinzmetal Angina: Tx
nitrates & CCB
How long does Prinzmetal Angina usually last before it resolves?
6 months
What two scoring methods are used for chest pain?
TIMI & Heart score
What does the TIMI score do?
estimates mortality for pts w/ unstable angina & STEMI
What does the heart score do?
6wk risk of having a major cardiac event (used on every pt)
Two types of lipids in the blood?
- cholesterol
- triglycerides
What does cholesterol do in the body?
backbone of a lot of hormones
What does triglyceride do in the body?
transfer energy from food s into the cells
Lipids are carried throughout the body on…
lipoproteins
What are the density classifications of lipids?
- HDL
- LDL
- Very low-density lipoprotein
Higher LDL means what related to CAD
higher risk of CAD
Higher HDL means what related to CAD?
lower risk of CAD
Higher levels of VLDL means what related to CAD?
higher risk of CAD
What are the functions of cholesterol?
- Cell membrane structure
- Precursor to steroid hormones, bile acids, & Vit D
What do triglycerides do?
store fat for energy
What are lipid disorders?
Disorders of lipoprotein metabolism
- clinical disorders associated w/ abnormal levels of total, HDL, & LDL cholesterol, as well as triglycerides
What is dyslipidemia?
Used for lipid values that are associated w/ dz or incr risk of dz & for which lipid-altering therapy might be of value.
What is hyperlipidemia?
Elevation of serum total, LDL cholesterol or triglyceride.
High cholesterol affects what percentage of adults in the US?
35%
RFs for Lipid disorders?
- FHx
- Type II DM
- older age
- male
- overweight or obesity
Lipid Disorders:
AHA/ACC screening
- repeat every 5 years if no RFs
- more often w/ RFs (1-2 yrs)
Lipid Disorders: AAP screening
Age 9-11 yo
Age 2-9 if high risk
–> immediate family have had MIs or have been dx w/ blocked arteries or stroke, at age </=55yo in men, or </= 65yo in women
–> immediate family have total blood cholesterol levels of >/= 240
–> Those whose family health background is not known
Lipid disorders: Hx
- Usually asymptomatic
- Ask about:
–> FHx
–> Activity levels
–> Medication use (progestins, steroids can incr)
–> Diet
Lipid disorders: PE
- Usually unremarkable
- May develop xanthomas if extremely high triglycerides
Lipid disorders: Dx/Labs
Lipid profile (FASTING)
- HDL
- LDL
- Triglycerides
- VLDL
People who would benefit form statin therapy?
- Pts w/ any form of clinical ASCVD
All patients w/ elevated lipids should be counseled on…
lifestyle changes
Lipid disorders: Medications
- Statins (atorvastatin, etc.)
- Ezetimibe
- Bempedoic
Hypertriglyceridemia: serum triglycerides above 150mg/dL would benefit from what meds?
- Statins
- Fibrates
STUDY SLIDE 10 in Cardio III
10 mins
What is familial hypercholesterolemia?
an inherited disorder of low-density lipoprotein cholesterol metabolism
What things can suggest familial hypocholesteremia?
- FHx
- Early onset (<50)
- Extreme hypocholesteremia
What should be done in children: have measurable atherosclerosis by age 12..
- begin meds around age 8
- expert consult (pediatric Cardiologist)
