PANCE Prep- Cardiology COPY Flashcards
In the bradycardia algorithm, if there is a pulse and the pt is unstable (Hypotension, AMS, refractory CP, acute HF, or symptomatic, what do you do?
- Give Atropine (1st line)
- if atropine not effective:
- Epi infusion
- Dopamin infusion
- -Transcutaneous pacing
*there are 3 exceptions to symptomatic/unstable bradycardia
What are the only 2 shockable rhythms using defibrillation (unsynchronized cardioversion)
- Ventricular fibrillation
2. Pulseless VT
In the tachycardia algorithm, what do you do if a person has a pulse but is unstable?
- Unstable tachyarrhythmia
1. Synchronized cardioversion
- if regular, narrow QRS complex, may consider Adenosine
Describe what you check for in the tachycardia algorithm and what you do?
- Check pulse
- if yes, Stable or unstable?
- if unstable–> synchronized cardioversion - if stable, is there a wide QRS 0.12 sec or more?
- If yes (Wide QRS complex tachycardia)–> antiarrhythmic med: amiodarone, lidocaine or procainamide
- If no (narrow QRS complex tachycardia-> vagal maneuvers, adenosine**, BB or CCB
What are the 3 important exceptions to stable tachyarrhythmia rule?
- atrial flutter: BB or CCB 1st line (skip adenosine)
- afib: BB or CCB 1st line (skip adenosine even though Aflutter is often regular and narrow QRS)
- Wolff-Parkinson-White: Procainamide preferred** or amiodarone- avoid use of AV nodal blockers
What med do you usue if you have a regular and narrow QRS tachyarrhythmia?
adenosine
What meds should you avoid in WPW and why?
AV nodal blockers (ABCD)
- Adenosine
- BB
- CCB
- Digoxin
*AV nodal blockade may cause preferential conduction through the fast (preexcitation) pathway–> worsening of the tachyarrhythmia
Describe interpreting an EKG
- Determine rhythm (R-R regular?)
- Rate: (300-150-100-75-60-50) or #r waves in 6 second strip x10
- QRS axis deviation?
- P for every QRS
- PR interval?
- QRS interval?
- LBBB or RBBB?
- RVH or LVH?
- Pathological Q waves: >1 box in depth or height or prolonged QT?
- ST depression or elevation: >1mm
Describe the normal intervals
PR:
QRS:
QT:
Small box:
Big box:
PR: 3-5 small boxes (0.12-0.2sec)
QRS: <3 small boxes (<0.12 sec)
QT: 7.5-11 small boxes (0.3-0.44 sec)
Small box:
Big box:
Describe the sympathetic NS control of the heart
Hormones Epi and NE cause
- increased excitability
- increased force of contraction
- increased SA node discharge rate (increase HR)
*Epi and dobutamine are sympathomimetics (stimulate the SNS)
Describe the parasympathetic NS control of the heart
Hormone acetylcholine (regulated by the vagus nerve) causes:
- decreased excitability
- decreased force of contraction
- decreased SA node discharge rate (decrease HR)
- Vagal stimulation or vagal maneuvers slow down the HR
- Conversely, anticholinergic drugs increase the HR
How do you determine LBBB or RBBB
LBBB:
- Wide QRS >0.12sec
- Broad, slurred/bunny ears bumps R in V5,6
- Deep S wave in V1
- ST elevation in V1-V3
RBBB:
- Wide QRS >0.12sec
- RsR’ in V1, V2
- Wide S wave in V6
Describe the leads involved and artery involved for the area of infarction:
Anterior wall
V1-V4 (V3,4*)–Q waves/ ST elevation
LAD artery or LCA
Describe the leads involved and artery involved for the area of infarction:
Septal
V1 and V2– Q waves/ ST elevation
Proximal LAD
Describe the leads involved and artery involved for the area of infarction:
Lateral wall
I, aVL, V5, V6– Q waves/ ST elevation
Left circumflex artery
Describe the leads involved and artery involved for the area of infarction:
inferior
II, III, aVF– Q waves/ ST elevation
RCA
Describe the leads involved and artery involved for the area of infarction:
Posterior Wall
V1-V2 ST Depression**
RCA or LCX
What is a normal QRS axis
- 30 to +90 degrees
* look at leads I and aVF
Causes of Left axis deviations
- LBBB
- LVH
3 Inferior MI - Elevated diaphragm
- L anterior hemiblock
- WPW
Causes of right axis deviations
- RVH
- Lateral MI
- COPD
- Left posterior hemiblock
in NSR, P waves are positive/upright in leads:___ and neg in leads: ___
Positive P: I, II, aVF
Negative P: aVR
Pathologic causes of bradycardia and what is the 1st line tx
- BB
- CCB
- Digoxin
- carotid massage
- SA node ischemia
- Gram Neg. sepsis
- hypothyroidism
*Anticholinergic Atropine is 1st line (bc excess vagal stimulation is the MC cause of bradycardia)
Heart rate typically ___ during inspiration
Increases in inspiration
decreases in expiration
What is sick sinus syndrome
Brady-tachy syndrome
- Combination of sinus arrest w/ alternating pparoxysms of atrial tachyarrhythmias and bradyarrhythmias
- commonly caused by SA node disease and corrective cardiac surgery
Management of Sick Sinus Syndrome
- Permanent pacemaker if symptomatic (dual chamber pacing usually preferred over ventricular pacing).
- *if brady alternating with ventricular tachycardia–> permanent pacemaker w/ automatic implantable cardioverter-defibrillator (AICD)
___ is the most helpful in determining the presence of AV conduction blocks
PR interval
Describe 1st, 2nd type 1 and 2, and 3rd degree AV blocks
1st: Fixed, prolonged PRI (>0.2sec) and QRS followed by every P
2nd Type I (Wenckebach): Progressive PRI lengthening then DROPPED QRS
2nd Type II (Mobitz II): Fixed prolonged PRI then DROPPED QRS
3rd: AV dissociation: P waves NOT related to QRS, all P waves NOT followed by QRS = decreased Cardiac output
What is the management of 1st, 2nd type 1 and 2, and 3rd degree AV blocks
1st: none, observe (may progress)
2nd type I (Wenckebach):
- Symptomatic: ATROPINE, epi +/- pacemaker
- Asymptomatic: observe +/- cardiac consult
2nd type II: ATROPINE OR TEMP. PACING, (progression to 3rd degree is common so PPM is definitive tx)
3rd:
- Acute/symptomatic: temporary pacing–> PPM
- Definitive tx: PPM
Describe the appearance of Aflutter and rate
- “saw tooth” waves
2. Rate: 250-350bpm (no P waves but is usually REGULAR)
Management of Atrial flutter
- Stable: Vagal, BB, or CCB
- Unstable: Direct current synchronized cardioversion
- Definitive tx: Radiofrequency ablation
*Anticoagulation use is similar to afib
___ is the most common chronic arrhythmia
atrial fibrillation
*most patients are asymptomatic
Why are people with atrial fibrillation at increase risk for stroke?
The ineffective quivering of the atria may cause thrombi (clots) to form, which can embolize and cause ischemic strokes
7 Etiologies of Afib and gender/race prevalence
- Cardiac disease
- Ischemia
- pulmonary disease
- infection
- cardiomyopathy
- electrolyte/hormone imbalance (hypothyroidism)
- Idiopathic- age, genetics, hemodynamic stress, meds, alcohol
Men> women, white>black
Describe the 4 different types of Afib
- Paroxysmal: self terminating w/in 7 days (usually <24hrs) +/- recurrent
- Persistent: fails to self terminate, lasts >7 days (requires termination via medical or electrical)
- Permanent: persistent AF >1yr (refractory to cardioversion or cardioversion never tried)
- Lone: paroxysmal, persistent or permanent w/o evidence of heart disease
Management of Stable AFib
- Rate control (usually preferred as initial management of symptomatic AF over rhythm control)
- BB: Metoprolol (cautious use in those w/ reactive airway dz**)
- CCB: Diltiazem*, verapamil (non-dihydropyridines)
- Digoxin: +/- use in elderly, **Preferred for rate control in pts w/ hypotension or CHF (not generally used in active patients) - Rhythm control
- Direct current synchronized cardioversion (DCC):
- Pharmacologic: Ibutilide, Flecainide, Sotalol, Amiodarone
- Radiofrequency ablation: PPM, cath-based ablation or surgical MAZE procedure
Direct current (synchronized) cardioversion (DCC) can be done for AFib if:
- AF present >48 hrs OR
- After 3-4 weeks of anticoagulation and a transesophageal echocardiogram (TEE) shows no atrial thrombi OR
- Start IV heparin, cardiovert w/in 24 hrs and anticoagulation for 4 weeks
Management of unstable Afib
Direct current synchronized cardioversion (DCC)
All patients with non-valvular Afib should undergo what two things:
- assessment of the risk of embolization via CHAD2DS2-VASc or CHADS2
* shown to reduce embolic risk by 70% - Determination benefits vs risks of anticoagulation via clinical judgment and discussion w/ patient
Describe the CHA2DS2-VASc Scoring Criteria for afib
- CHF: 1
- HTN: 1
- Age 75 or older: 2
- DM: 1
- S: Stroke, TIA, thrombus hx: 2
- V: Vascular dz (prior MI, aortic plaque, PAD): 1
- A: Age 65-74: 1
- S: Sex: female: 1
-2 or more= moderate to high risk= chronic oral anticoag. recommended
-1= low risk= consider risks/benefits
0= very low risk= no anticoag. needed
Describe the CHADS2 Scoring Criteria for afib
- C: CHF: 1
- H: HTN: 1
- A: Age: 75 or older: 1
- D: DM: 1
- S: Stroke, TIA, thrombus hx: 2
- 2 or more= high risk: Warfarin
- 1= moderate risk: warfarin or ASA
- 0= low risk: non or ASA
Describe types of anticoagulant agents
- Non-vitamin K antagonist oral anticoagulants (NOAC): usually now preferred over warfarin in most cases due to similar or lower rates of major bleedig and less DDI and less drug monitoring
- Dabigatran: direct thrombin inhibitor
- Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors - Warfarin
- Dual Antiplatelet therapy: ASA + clopidogrel (anticoagulant monotherapy is superior to dual antiplatelet therapy)
What are Factor Xa inhibitors?
What are direct thrombin inhibitors?
Describe their MOA
Factor Xa inhibitors: Rivaroxaban (Xarelto), Apixiban (Eliquis), Edoxaban (Savaysa)–> selectively binds to antithrombin III)
Direct thrombin inhibitors: Dabigatran (Pradaxa)–> binds and inhibits thrombin
What are three contraindications to NOAC? (non-vitamin K antagonist oral anticoagulants)
- Severe chronic kidney disease
- HIV pts on potease inhibitor-based therapy
- on CP450 inducing antiepileptic meds such as carbamazepine, phenytoin
What are common causes of prolonged QT syndrome and common clinical manifestations
congenital or acquired
- Macrolides
- TCA
- electrolyte abnormalities
- recurrent syncope,
- Ventricular arrythymias
- sudden cardiac death
Management of Prolonged QT Syndrome
- DC offending drug and correct electrolyte abnormalities
2. AICD if definitive tx for congenital or recurrent ventricular arrhythmias
What describe rate, rhythm, and EKG appearance for (p)SVT?
- HR >100
- Regular rhythm with narrow QRS
- P waves hard to discern due to rapid rate
Describe the 2 main types of pSVT
- AVNRT: AV nodal reentry tachycardia: 2 pathways both within the AV node (slow and fast) **MC TYPE
- AVRT: AV Reciprocating tachycardia: 1 pathway within the AV node and a second accessory pathway OUTSIDE the AV node ex. WPW and LGL
Describe the conduction patterns that result in Narrow complex tachycardia and wide complex tachycardia
Narrow complex tachy: Orthodromic (95%): Impulse goes down the normal AV node pathway first and returns via the accessory pathway in circles, perpetuating the rhythm
Wide complex tachy: Antidromic (5%): Impulse goes down the accessory pathway first and returns to the atria via the normal pathway (mimics VT)
Management of Stable Narrow Complex SVT vs Stable Wide complex SVT
Narrow Complex SVT:
- Vagal maneuvers (vagus nerve stimulation releases acetylcholine = decrease HR)
- Adenosine 1st line medical tx for SVT (terminates 90% of narrow complex SVT) **may cause bronchospasm for those w/ asthma/COPD
- AV nodal blockers: BB or CCB
Wide Complex SVT:
1. Antiarrhythmics: ex. Amiodarone or Procainamide if WPW
Tx of unstable SVT (wide or narrow complex) and what is the definitive tx of SVT
- direct current synchronized cardioversion
Definitive: Radiofrequency ablation
What rhythm?
- HR <100 and
- 3 or more P wave morphologies
Wandering atrial pacemaker: multiple ectopic atrial foci generated impulses that are conducted to the ventricles
What rhythm?
- HR >100 and
- 3 or more p wave morphologies
Multifocal atrial tachycardia
*same as WAP but HR is >100
Multifocal Atrial Tachycardia (MAT) is commonly associated with ___ and is difficult to tx but usually use: ___
Severe COPD
Tx: CCB (Verapamil) or BB if LV fxn presereved
What 3 EKG findings are associated w/ WPW and what is WPW
- Delta wave (slurred QRS upstroke)
- Wide QRS (>0.12sec)
- Short PRI
*accessory pathway (bundle of Kent) pre-excites the ventricles–> a type of of AVRT
Management of
- Stable WPW
- Unstable WPW
- Definitive management
- Vagal maneuver
- Antiarrhythmics ex. Class IA: Procainamide preferred***, amiodarone, flecainide
- Avoid the use of AV nodal blockers (ABCD) in WPW**
Unstable: direct current synchronized cardioversion
Definitive: radiofrequency ablation
What rhythm?
- Short PRI
- Normal QRS complex
Lown-Ganong-Levine Syndrome (LGL)
*type of AVRT leading to a short PRI) but the accessory pathway (bundle of james) connects to the bundle of HIS so the QRS is narrow in LGL (unlike the wide QRS in WPW)
What Rhythm?
- Regular rhythm
- P waves inverted (negative) if present in leads where they are normally positive (I, II, aVF) or are not seen
- Classical associated w a narrow QRS
AV junctional dysrhythmias
*AV node/junction becomes the dominant pacemaker of the heart
MC rhythm seen w/ digitalis toxicity
AV junctional dysrhythmia
What are the 3 types of AV junctional dysrhythmias
- Junctional rhythm: HR 40-60,
- Accelerated Junctional: HR 60-100
- Junctional tachycardia: HR >100
- Wide, bizarre QRS occurring earlier than expected.
- The T wave is in the opposite direction of the QRS usually
- Associated w a compensatory pause
PVC
*no tx usually needed
Ventricular tachycardia is considered:
3 or more consecutive PVCs at a rate >100bpm
-Sustained VT= lasting 30 or more seconds
___ is a common predisposing condition for VT
Prolonged QT interval
Torsades De Pointes is most commonly due to ___
hypomagnesemia, hypokalemia
Management of the following VTs:
- Stable sustained VT
- Unstable VT w/ a pulse
- Pulseless VT
- Torsades de pointes:
- Stable sustained VT: Antiarrhythmics (amiodarone, lidocaine)
- Unstable VT w/ a pulse: Synchronized cardioversion
- Pulseless VT: defibrillation (unsynchronized cardioversion) + CPR (tx as VF)
- Torsades de pointes: IV magnesium
Management of VF
Unsynchronized cardioversion (defibrillation) + CPR
Management of PEA (pulseless electrical activity) or asystole
- CPR
- Epi
- Checks for “shockable” rhythms every 2 min
Causes of increased jugular pressure Increased JVP + \_\_\_\_ = \_\_\_\_ 1. + Crackles/rales 2. + Normal pulmonary exam 3. + decreased breath sounds
- Crackles/rales: CHF
- Normal pulmonary exam: Pericardial (tamponade or constrictive pericarditis)
- decreased breath sounds: Tension pneumothorax
7 Causes of ST Elevation
- Acute MI
- LVH
- LBBB
- Acute pericarditis
- Early repolarization abnormalities
- Coronary vasospasm/Prinzmetal angina/cocaine
- Brugada syndrome
EKG findings with pericarditis
- Diffuse concave ST elevation in precordial leads (V1-V6)
- PR depression in same leads w/ ST elevation
- in aVR: ST depression and PR elevation
3 EKG signs of LVH w/ LV strain
- ST elevation in right precordial leads (V1-V3)
- Increase voltage
- Asymmetric ST depressions and T wave inversions in the lateral leads (I, aVL, V5, V6)
Describe Brugada Syndrome EKG patterns
- RBBB (often incomplete) in V1-V3
- ST elevation V1-V3 (often downsloping)
- T wave inversion in V1 and V2
- +/- S wave in lateral leads (I, aVL, V5, V6)
Brugada Syndrome is
- MC in ___
- Associated with ___
- Often caused by: ___
- Management includes: ___
- MC in Asian Males
- Associated w/ syncope and sudden cardiac death from ventricular arrhythmias
- Often caused by genetic disorder
- Managed w/ AICD to prevent death from VF
Kussmaul’s sign is an increase rather than the normal decrease in the CVP during inspiration. It is most often caused by
- severe right-sided heart failure;
- constrictive pericarditis or
- right ventricular infarction.
A 25 year-old female presents with a three-day history of chest pain aggravated by coughing and relieved by sitting. She is febrile and a CBC with differential reveals leukocytosis. Which of the following physical exam signs is characteristic of her problem?
Pericardial friction rub- pericarditis
A 22 year-old male received a stab wound in the chest an hour ago. The diagnosis of pericardial tamponade is strongly supported by the presence of
distended neck veins- Cardiac compression will manifest with distended neck veins and cold clammy skin
What test is done to detect ventricular wall dysfunction
Cardiac nuclear scanning
PT-INR is a reflection of the ___ pathway clotting system. Coumadin interferes with Vitamin K synthesis which is needed in the manufacture of factors ___ which are part of that clotting pathway
extrinsic and common
factors II, VII, IX, X
2,7,9,10 (1972- Extrinsic)
What antiarrhythmic drugs can be associated with hyper- or hypothyroidism following long-term use?
amiodarone
What hypertensive emergency drugs has the potential for developing cyanide toxicity?
Sodium nitroprusside metabolization results in cyanide ion production. It can be treated with sodium thiosulfite, which combines with the cyanide ion to form thiocyanate, which is nontoxic
What beta-adrenergic blocking agents has cardioselectivity for primarily blocking beta-1 receptors?
Metoprolol
Describe the mechanisms of the following classes of antiarrhythmic drugs:
- Class I:
- Class II:
- Class III:
- Class IV:
- Class I: Na+ channel blockade
- Class II: Beta-adrenergic receptor blockade, BB
- Class III: K+ channel blockers
- Class IV: Ca channel blockade, CCB
What is the EKG manifestation of cardiac end-organ damage due to hypertension?
LVH
Periodic measurements of blood pressure should be part of routine preventive health assessments beginning at the age of __
3 years.
____ is characterized by a medium- pitched, mid-systolic murmur that decreases with squatting and increases with straining.
Hypertrophic cardiomyopathy
EKG Pattern:
- (incomplete) RBBB in V1-V3
- ST elevation V1-V3 (often downsloping)
- T wave inversion in V1 and V2
- +/- S wave in lateral leads (I, aVL, V5, V6)
Brugada syndrome
How do vagal maneuvers and carotid massage decrease HR in tachycarrhythmias?
baroreceptors sense increase carotid artery pressure–> reflexive decrease in HR
What is the equation for cardiac output
CO= SV X HR
What is pulsus paradoxus and when is it seen?
> 10mmHg decline in SB with inspiration (palpable peripheral pulses disappear w/ inspiration)
EX: Cardiac tamponade and tension pneumothorax
Cautious use w/ IV nitro and morphine with what types of MIs and why?
R-sided (inferior and posterior MIs)
-Bc right side is more dependent on preload and SV to maintain CO and nitro and morphine decreases preload
Describe how BP is controlled
Renin-Angiotensin-Aldosterone System
-low BP–> renin release by kidneys–> renin+ angiotensinogen= angiotensin I–> cleaved by ACE from lungs= angiotensin II–> increases BP
Angiotensin II Effects:
- increase aldosterone= increase Na retention (K+ and H+ secretion)
- Increase ADH= H20 retention
- Vasoconstriction= increase BP
- Increase sympathetic tone= increase BP
SE of ACE inhibitors and why
- can cause hyperkalemia bc they inhibit aldosterone which typically increases K+ excretion
- Cough or angioedema bc they potentiate other vasodilators (ex. bradykinin)
*ARBs (angiotensin II receptor blockers) block the receptor for AGII but don’t cause angioedema or cough
7 Risk factors for CAD
- DM (worst)
- Cig smoking (most important modifiable)
- Hyperlipidemia
- HTN
- Age (M >45, F>55)
- FHX 1st degree relative
- Men
Describe the pathophysiology of atherosclerosis
- Fatty streak formation: lipid deposition in WBC–> smooth muscle proliferation (forms streaks)
- LDL enters endothelium in the fatty streaks and LDL becomes oxidized which attracts other WBCs
- proliferating smooth muscle cells and CT makes “fibrous cap” and arterial lumen narrowing +/- calcification (stabilized plaque)
Arterial lumen is typically ____% narrowed when a patient becomes symptomatic to myocardial ischemia w/ exertion and ____% narrowed when symptomatic at rest
70% or more narrowed w/ exertion
> 90% at rest
What is angina pectoris
substernal CP usually brought on by exertion (inadequate tissue perfusion due to decrease coronary blood supply and increased demand)
Describe common features of cardiac CP in stable angina
substernal, poorly localized, exertional, radiates to arm, teeth, lower jaw, back, typically UNDER 30 min, relieved w/ nitro or rest
**diaphoresis, numbess, N/V, fatigue
Resting EKG is normal in __% of patients with stable angina
50%
When is PTCA indicated for management of angina
1-2 vessel disease in nondiabetics NOT involving Left main CA and in whom LV fxn is normal/near normal
*restenosis is prevented with stents w/ drug-eluting properties
Indications for CABG
- Left main coronary artery stenosis
- Symptomatic or critical stenotic 3-vessel disease (>70% stenosis), 2 vessel disease in DM
- Decreased LV EF <40%
What is the pharmacologic management of stable (chronic) angina
(and their MOA)
- PRN Nitrates (increases O2 supply, reduces coronary spasm, and decreases demand by decreased preload venodilation)
- BB (increase O2 supply by prolonging coronary artery filling times/diastolic time, and decreased O2 demand) **1st line
- Statin
- ASA (prevents platelet activation/aggregation by inhibiting cyclooxygenase–> decreased thromboxane A2 and inhibit prostaglandins)
Typical Regimen: ASA + SL nitro PRN + BB + statin
**CCB if BB can’t be used or in prinzmetal angina: increase O2 supply and prevents ischemia induced coronary vasospasm
4 SE of Nitrates
And 3 contraindications to nitrates
- HA
- flushing
- hypotension
- tachyphylaxis after 24 hrs
CI: SBP <90, RV infarction, Use of sildenafil and other PDE-5 inhibitors
What medication is the 1st line drug for chronic management in stable (chronic) angina
Beta blockers - reduces mortality, symptoms and prevents ischemic occurrences)
What BB are cardioselective (B1) and what ones are nonselective?
Selective (B1): Metoprolol and Atenolol
Nonselective: Propranolol, Nadolol
What medication is indicated for prinzmetal angina?
CCB
nondihydropyridines: Diltiazem or verapamil (long acing)
Who are most likely to suffer from a “Silent or atypical MI”. what are usually the presenting sxs?
- women
- Elderly
- Diabetics
- obese
sx: abdominal pain, jaw pain, dyspnea w/o CP
STEMI is defined as:
ST elevations 1mm or more in 2 or more anatomically contiguous leads +/- reciprocal changes in opposite leads
**New LBBB is considered STEMI equivalent
Cardiac markers for MI include:
-Standard is usually __ sets every ___
-describe when these markers appear, peak and return to baseline
- Troponin- most sensitive and specific**
-appear 4-8hr
-peaks: 12-24hr
-Returns to baseline: 7-10 days - CK/CK-MB
-appear 4-6hr
-peaks: 12-24hr
-Returns to baseline: 3-4days - Myoglobin
-appear 4-8 hr
-peaks: 12-24 hr
returns to baseline 1 day
*3 sets q8hrs
Management of unstable angina or NSTEMI
1). MONA= chewable ASA, NTG, oxygen (at least 4L) +
obtain cardiac markers and EKG
**morphine ONLY if NTG not relieving pain or pt on PDE5 inhibitor
2) . If EKG shows ST depressions and/or T wave inversions: know its UA or NSTEMI
3) . - cardiac enzymes = UA, + cardiac enzymes = NSTEMI
4) .Start Antithrombotic therapy: HEPARIN (LMWH or UFH)
* *consider plavix (ADP inhibitors) or GP IIb/IIIa inhibitors
5) . Then consider adjunctive anti-ischemic
* **BB
6). assess TIMI risk score (estimates mortality for these pts)
Compare the MOA of
- Unfractionated heparin:
- LMWH (enoxaparin):
- Fondaparinux:
Heparin (UFHLMWH): inhibits thrombin by activating antithrombin III and inhibits factor Xa
- (LMWH more specific to Factor Xa than UFH)
-Fondaparinux: direct factor Xa inhibitors (binds to and enhances antithrombin)- no direct effects on thrombin
Management of STEMI
1) . MONA: morphine, oxygen, nitro, ASA (NO NTG or MORPHINE IN INFERIOR/POST MI) + EKG and cardiac enzymes
* *Morphine only given if pain not relieved by NTG or pt on PDE5 inhibitor
2). EKG shows ST elevation
3) . Give Antithrombotics: Heparin (LMWH or UFH)
* *consider plavix or GP IIb/IIIa
4). Consider adjunctive therapy: BB
5) . REPERFUSION (most important) w/in 12 hrs of sxs onset (PCI or thrombolytics w/ rTPA)
* *DOOR TO PCI <90 mins, DOOR TO FIBRINOLYTICS , 30 mins
6). long term: ACEIs (slows the progression of CHF by decreasing ventricular remodeling)
PCI is best w/in ___ hours of sx onset
3 hours (esp c/n 90min)
- Door to thrombolyics: w/in 30 min
- Door to PCI: w/in 90 mins (+/- 30min)
Management of Cocaine-induced MI
CCB = treatment of choice
+ ASA, NTG, O2, Heparin, anxiolytics
*AVOID BB bc of unopposed alpha vasoconstriction/vasospasm
What is Dressler Syndrome
- post MI pericarditis
- fever
- pulmonary infiltrates
What is variant (prinzmetal) angina and how is it diagnosed?
sxs such as rest angina due to coronary artery spasm w/ transient ST elevations (usually w/o MI)
- CP usually nonexertional, often at rest
- DX: EKG +/- transient ST elevations
- angiography vasospasm w/ IV Ergonovine administration
Sx and ST elevations resolve w/ CCB or nitro
What is the drug of choice to tx variant (prinzmetal) angina?
CCB* and nitro PRN
NO BB
What is cocaine induced CP/MI?
coronary artery vasospasm due to cocaine/s activation of sympathetic nervous system and alpha-1 receptors causing vasoconstriction of arteries
***MI can occur if vasoconstriction is prolonged
Most common cause of CHF
CAD
What is the chief adverse effect of thiazide diuretics?
-hypokalemia**
Also causes
-hyponatremia
-retention of Ca++
___ is classically described in children as a continuous machinery-type murmur that is widely transmitted across the precordium.
Patent ductus arteriosus
___ leads to enlargement of the left atrium, which is the major predisposing risk factor for the development of atrial fibrillation.
Mitral stenosis
__ and __ are the most common drugs that may cause a lupus-like eruption.
Procainamide and hydralazine
Which electrolyte abnormality is associated with an increase in the risk for digoxin toxicity?
hypokalemia
*Decreased concentration of potassium results in the increased activity of cardiac glycosides by increasing tissue binding and decreasing renal excretion of digoxin. Potassium loss is the only significant electrolyte abnormality that significantly affects digoxin metabolism.
___ is characterized by a holosystolic murmur at the lower left sternal border.
Ventricular septal defect
___ is characterized by a systolic thrill at the left sternal border with a systolic ejection murmur that may or may not have an associated systolic click.
Tetralogy of Fallot
__ is associated with a systolic ejection click or a short systolic murmur at the left sternal border.
Coarctation of the aorta
An electrocardiogram (ECG) shows a sinus rhythm with varying T wave heights, axis changes every other beat and a wandering baseline. Which of the following is most likely the diagnosis?
Pericardial effusion
- electrical alternans`
Who is most at risk for developing primary HTN
Black non-Hispanic adults have the highest risk of hypertension.
What is the optimal INR for a patient with a mechanical mitral valve prosthesis on warfarin (Coumadin)?
2.5-3.5
Coronary artery perfusion occurs primarily during __
diastole
Pulmonary capillary wedge pressure indirectly measures which of the following?
left atrial filling pressure
Causes of left sided heart failure
- CAD **
- HTN**
- Valvular dz
- cardiomyopathies
Causes of Right sided heart failure
- Left sided heart failure**
- Pulmonary dz** (COPD, PHTN)
- Mitral stenosis
What is the difference btwn systolic and diastolic HF
Systolic: decreased EF +/- S3 gallop. (MC form)
Diastolic: normal EF +/- S4 gallop = forced atrial contraction into a stiff ventricle (associated w/ normal cardiac size)
Causes of systolic HF
- Post MI
- dilated cardiomyopathy
- myocarditis
Causes of diastolic HF
- HTN
- LVH
- Elderly
- Valvular dz
- cardiomyopathies
- Constrictive pericarditis
Compare and contrast diastolic and systolic HF
Diastolic: NORMAL/increased EF, THICK ventriular walls, SMALL LV chamber, +S4
(thick and stiff)
Systolic: DECREASED EF, THIN venticular walls, DILATED LV chamber, S3
Describe the NY Heart Association Functional Class of Heart Failure
Class I: No sx or physical limitations
Class II: Mild sx (dyspnea or angina), slight limitation
Class III: sx w/ limitation w/ activity, comfortable at rest
Class IV: sx at rest w/ severe limitations
Describe the pathophysiology of heart failure
Initial insult leads to **Increased Afterload, increased preload and/or decreased contractility (heart tries to compensate for a short term)
Compensation includes:
1. SNS activation
2. Myocyte hypertrophy/remodeling
3. RAAS activation: fluid overload, ventricular remodeling/hypertrophy===> CHF
Clinical Manifestations of Left sided HF
- *Increase pulmonary venous pressure from fluid backing up into the lungs
1. Dyspnea (MC SX)
2. Pulmonary congestions (rales, rhonchi)
3. Pink frothy sputum w/ nonproductive cough
4. HTN
5. Cheyne-Stokes breathing (deepr faster w/ gradual decrease and peroids of apnea)
6. S3 (SHF) or S4 (DHF)
7. Increased adrenergic activation (dusky, pale, diaphoresis)
MC cause of transudative pleural effusions
CHF (left sided)
Clinical manifestations of right sided HF
- *Increase systemic venous pressure–> signs of systemic fluid retention
1. Peripheral edema
2. Increased JVP/jugular venous distention
3. GI/Hepatic congestion- hepatosplenomegaly, anorexia
How do you diagnose HF
- Echo** (measures LV function and EF)
- CXR: esp. for congestive HF
- Increased BNP: ventricles release BNP during volume overload
What is the most important determinant of prognosis for HF
EF
What is a normal and abnormal EF
Normal: 55-60%
EF less than 35%: increased mortality, Needs a cardioverter defibrillator in place to reduce mortality
What is the initial management of HF
- ACEI (1st line in HF) + diuretic (for sx)
- Add BB
- Add Hydralazine + NTG
- Digoxin (add earlier if Afib)
*ACEI>BB best 2 drugs for decreased mortality
Lifestyle changes to help manage HF
- Salt restriction <2g/d
- Fluid restriction <2L/d
- exercise
- smoking cessation
HF meds to decrease afterload
- vasodilators
1. ACEI
2. ARBs
3. BB
4. Hydralazine + Nitrates combo
SE of ACEI
- hypotension
- Renal insufficiency
- hyperkalemia
- cough and angioedema (due to increased bradykinin)
*CI in pregnancy
HF meds that decrease preload
- Diuretics
- HCTZ
- Metolazone
What are loop diuretics
- furosemide
- bumetanide
- torsemide
What type of diuretic is most effective tx for sx for mild-moderate CHF
loop diuretics
SE of loop diuretics
- volume depletion
- hypOkalemia
- hypOcalcemia
- hypOnatremia
- HYPERglycemia
- HYPERuricemia
SE of potassium sparing diuretics
- HYPERkalemia
2. gynecomastia w/ spironolactone
___ diuretic is associated w/ decreased mortality and added in severe CHF
spironolactone
Positive inotropes HF meds
(sympathomimetics)
- Digoxin
- Dobutamine
- Dopamine
When is digoxin indicated
HF with Afib
*decrease hospitalizations and sx but NO mortality benefit w/ digoxin**
What meds decrease mortality in HF
- ACEI
- ARBs
- BB
- Nitrates + hydralazine
- spironolactone
___ meds are not generally sued in systolic HF
CCB
what is congestive heart failure
acute decompensated HF w/ worsening of baseline sx, pulmonary congestion
CXR findings of CHF
- Cephalization of vessels
- Kerley B lines (short linear markings at lung periphery)
- Peribronchial cuffing
- Cardiomegaly
- Perihilar congestion
*Management of acute pulmonary edema/CHF
“LMNOP”
- Lasix (removes fluid and relieves sx)
- Morphine (decreases preload and heart strain)
- Nitrates (venodilator that reduces preload and afterload)
- Oxygen
- Position (upright to decrease venous return)
What is the use of echocardiogram in pericardititis
used to assess for complications of acute pericarditis (effusion or tamponade)
Tx of pericardial effusion
- Observe if small and no evidence of tamponade
- tx underlying cause
- +/- pericardiocentesis if tamponade or large effusion
What is pulsus paradoxus
exaggerated>10mmHg decrease in systolic BP w/ inspiration and pulses decrease w/ inspiration
What is constrictive pericarditis
Thickened, fibrotic, calcified pericardium (from chronic pericarditits and inflammation) that restricts ventricular diastolic filling-> increases venous pressure and decreases stroke volume = decreased CO
Clinical manifestations of constrictive pericardititis
- Dyspnea (MC SX)
- Right sided HF sx (increased JVD, peripheral edema)
- Kussmaul’s sign* (increased JVD during inspiration)
- pericardial knock*- high pitched 3rd heart sound due to sudden cessation of ventricular filling
Management of constrictive pericarditits
pericardiectomy is definitive tx*
-diuretics may be used for symptomatic control
how to diagnose stable angina
clinical + testing
ECG: initial test of choice (normal in 50%, ST depression is classic finding)
stress testing: most important noninvasive test (stress ECG, stress echo, perfusion imaging)
coronary angiography is definitive (location and extent of CAD)
Stress ECG: indications, positive findings, limitations
indications: useful only if baseline EKG is normal
findings: ECG changes (ST depressions, T wave inversions) or reproduction of sxs
Limitations: does not locate the area of ischemia
stress ECHO: indications, how to perform, contraindications
indications: can be used if baseline EKG is abnormal, gives info based on location and extent of ischemia
can be done with exercise or positive inotrope med (dopamine or dobutamine)
contraindications to meds: severe LV outflow obstruction (aortic stenosis), ventricular arrhythmia, recent MI (1-3d), severe systemic HTN
myocardial perfusion imaging: indications , how to perform, contraindications
uses thallium or technetium for imaging
indications: useful if baseline ECG is abnormal, gives info regarding location and extent of ischemia
can be done with exercise or vasodilator med (adenosine or dipyridamole)
contraindications to meds: bronchospastic disease, hypotension, AV blocks
three indications to perform coronary cath
1) . confirm/exclude CAD in pts with CAD sxs
2) . confirm/exclude CAD in pts with negative noninvasive testing for CAD
3) . patients who may possibly need revascularization
when is aspirin used for primary prevention of atherosclerotic CV disease?
select patients aged 40-70 who are not at an increased risk of bleeding
difference between stable and unstable angina
UNSTABLE if:
1) . first occurrence of angina
2) . increase in anginal intensity (no longer relieved by rest or NTG)
3) . increase in frequency
what is triad of RV infarction?
increased JVP + clear lungs + positive Kussmaul sign (inc JVP with inspiration)
**inferior MI
what are q waves a sign of?
INFARCTED tissue
*whereas ST depression or T wave inversions are signs of ischemia
what is the ECG progression of a STEMI?
1) . hyperacute T waves
2) . ST elevations
3) . q waves
how to treat pts who onset of chest pain sxs began over 12 hrs ago OR low TIMI without current chest pain
ASA (+/- Plavix for 9 months), statin, BB, ACEI, NTG PRN
