Cardio Flashcards
(101 cards)
1
Q
NYHA Classes of HF
A
I (No symptoms) II (Slight limitation in physical activity - SOB climbing stairs) III (Marked limitation of physical activity - SOB around the house doing chores) IV (Inability to perform activity without significant discomfort)
2
Q
Optimal medical therapy for CHF
A
BB, loop diuretic, aldosterone antagonist
3
Q
Criteria for biventricular pacing in HF patients
A
Must meet all: LVEF less than 35 NYHA II,III,IV LBBB with QRS greater than 150
4
Q
Criteria for ICD
A
Primary prevention - Prior MI and LVEF less than or equal to 30 OR NYHA II/III and LVEF less than or equal to 35. Secondary prevention - Prior VF or unstable VT without reversible cause OR prior sustained VT with underlyng cardiomyopathy
5
Q
What do deep Q waves indicate?
A
Prior MI
6
Q
Pt presents with inferior wall MI 2 weeks following RCA stent placement. What happened?
A
Stent thrombosis is a rare but serious complication typically occuring within 30 days and usually associated with premature cessation of DAPT. Make sure you counsel and aggressively screen for med compliance.
7
Q
Clinical features of Compartments Syndrome
A
Common
- Pain out of proportion to injury
- Pain increasing in passive stretch
- Rapidly increasing and tense swelling
- Paresthesia (early)
Uncommon
- Reduced sensation
- Motor weakness (hrs)
- Paralysis (late)
- Reduced distal pulses
8
Q
Complication of CS
A
Renal failure from anoxic muscle necrosis/rhabdo
Rarely can get DIC from microangiopathic hemolytic anemia
9
Q
Diagnostic tool of choice for CS
A
Direct tissue pressure measurement. Serial measurements are needed even if original pressure is normal. Pressure above 30 is diagnostic or delta pressure (diastolic bp minus compartment pressure) less than 20-30.
Patients with elevated pressure that does not rapidly correct require fasciotomy
Number 1 determinant of prognosis is time to surgery
10
Q
RBC transfusion thresholds
A
Less than 7 - def
7-8 for cardiac surgery, onc patients on treatment, and HF
8-10 for symptomatic anemia, ongoing bleeding, ACS, noncardiac surgery
11
Q
Hemodynamic measurements in shock
A
12
Q
How would cardiac tamponade present with respect to hemodynamic parameters?
A
Rapid accumulation of blood in pericardial space leads to increased RA and RV pressure but there is also characteristic equalization of RA, RV end diastolic, and PCWPs
13
Q
Patient with persistent pain, swelling and accentuated pulsation near access point for recent cardiac cath
A
Likely pseudoaneurysm of R CFA. Happens when bleeding from inadequately sealed arterial puncture site remains confined within the periarterial connective tissue. Leads to contained hematoma that has ongoing communication with the arterial lumen. Diastolic pressure equalizes between artery and confined hematoma resulting In blood flow in and out of the hematoma cavity with systole
Presents as tender, pulsatile mass with a sytolic bruit. Dx is confirmed on US
Small pseudoaneurysms can be treated with US guided compression or thrombin injection into cavity. Largery or rapidly expanding ones are at risk of rupture and need surgical repair.
Main risk factor is inadequate post-procedural compression to achieve hemostasis
Cessation of DAPT is not recommended unless there is life threatening bleed bc of risk of stent thrombosis
14
Q
Femoral AV fistula
A
Presents with localized pain, no mass and a continuous bruit. Sometiems evaluated by lower extremity angio if initial US is nondiagnostic. Angio can also evaluate for femoral artery dissection or thrombosis in a patient with evidence of distal leg ischemia .
15
Q
hematoma after cath
A
Small local hematoma (localized swelling that is non-pulsatile with no bruit) can be managed with symptomatic relief and reassurance.
Obviously large RP bleed is different.
16
Q
WPW pattern plus symptomatic tachyarrythmia
A
WPW Syndrome
WPW pattern triad is short PR, delta wave, wide QRS
17
Q
Acute mitral regurg features
A
Cause
- Ruptured mitral chorda tendinae from MVP, endocarditis, RHD, or trauma
- Papillary muscule rupture due to MI or trauma
Clinical
- Rapid onset pulm edema
- biventricular HF
- hypotension, cardiogenic shock
Physical exam
- Diaphoresis, cool extremities
- JVD, crackles
- Hyperdynamic cardiac impulse
- Apical decrescendo systolic murmur (often absent)
Management
- Bedside echo
- emergent surgery
18
Q
Who is at risk for mitral chorda tendineae rupture?
A
Patients with MVP esp when it is related to underlying connective tissue disease (marfan, ED)
Velvety skin with scar formation is supposed to indicate connective tissue disease (esp ED)
19
Q
ED vs Marfans
A
20
Q
Acute rheumatic fever
A
Inflammatory condition following group A strep. Migratory arthritis, carditis or valvulitis, CNS involvement with chorea, erythema marginatum, and subq nodules. Chronic MR is a common sequela of rheumatic fever. acute MR is rare.
21
Q
What is a common side effect of CCBs?
A
Peripheral edema (reported incidence of 25% after 6 months of therapy) likely due to preferential dilation of precapillary vessels (arteriolar dilation) which leads to increased cap hydrostatic pressure and fluid extrav into interstitum
Dihydropyridine CCBs (amlodipine and nifedipine) are potent arteriolar dilators and cause more peripheral edema than non-DHP CCBs (diltiazem and verapamil).
Other side effects of CCBs are HAs, flushing, dizziness.
Renin angiotensin system blockers (ACE or ARB) causes post capillary venodilation and can normalize the increased capillary hydrostatic pressure. Combo of CCBs and ACEs improved risk of peripheral edema compared to CCB alone
22
Q
Side effects of ACE?
A
angioedema
nonpitting swelling of subq or submucosal tissue and most commonly affects lips, tongue, face, and upper airway
Do not cause peripheral or dependent edema
23
Q
Side effects of glyburide
A
Derm side effects (photosensitivity reactions, maculopapular eruptions, purpura, urticaria)
24
Q
Side effects of HCTZ
A
most common are electrolyte imbalances (hyponatremia, hypokalemia), renal failure, hyperuricemia (may precipitate acute gout), and elevated glucose and lipids.
25
Appropriate therapy for secondary prevention of cardiovascular events
Patient with prior MI and CAD
## Footnote
Statin
ASA
ACE or ARB
BB (reduce short term morbidity in patients with recent MI as well as long term mortality if continued)
In addition, patient should undergo further eval for risk stratification (TTE, perfusion stress test, possible cath)
26
Fibrate therapy
Gemfibrozil or fenofibrate
Reduces triglyceride levels in patients with severe hypertriglyceridemia (above 800)
27
Direction of Left to right shunt by oximetry
Find the location of "step-up" in O2 sat.
## Footnote
If it's from IVC/SVC to RA, then the location is atrial. Etiology is ASD, partial anomolous pulm venous drainage, ruptured sinus of valsalva, VSD with tricuspid regurg or coronary fistula to RA
If it's from RA to RV then it's venticular. Etiology is VSD, PDA with pulm regurg, or coronary fistula to RV
If it's from RV to Pulm Artery then it's great vessels. Etiology is PDA or aorto-pulmonary window
28
VSD murmur
Harsh holosytolic murmur with max intensity over Left third and fourth intercostal spaces and a palpable thrill
29
Brachial to femoral pulse delay
Seen in patients with coarctation
30
PDA murmur
Continuous murmur heard at left infraclavicular area. Causes L to R shunting from aorta to main pulm artery
31
TOF
Most common cyanotic congenital heart defect
1) RV outflow obstruction
2) Overriding aorta
3) RVH
4) VSD
32
ASD on auscultation
Fixed splitting of S2
33
Excerise stress testing factors associated with increased risk of adverse cardiovascular events
Clinical
* Poor exercise capacity
* exercise induced angina at low workload
* fall in systolic BP from baseline
* chronotropic incompetence
ECG
* greater than 1mm ST depression (flat or downsloping)
* ST depression at low workload
* ST elevation In leads without Q waves
* Ventricular arrhytmias.
Patients with high risk features likely have atherosclerotic disease and would benefit from revascularization and should undergo cath.
Patients without high risk features but with anginal symptoms refractory to several months of optimal medical management should also undergo cath
34
Management of new onset AF
Assess rate vs rythym control
## Footnote
Patients who are hemodynamically unstable get cardioverted emergently
Stable patients will receive medical therapy (BBs, dilt, digoxin) to control ventricular rate. Rate control with medical therapy can often convert back to sinus. Rhythm control (amiodarone) should be considered in patients unable to achieve adequate rate control with recurrent symptomatic episodes (palps, lightheadedness, SOB, angina) or with HF symptoms in setting of underling LV sytolic dysfunction
Regardless of whether or rate or rhythm control is used, patients with AF need to undergo CHADS-VASC score assessment to estimate thromboembolic risk. If 0, then low risk and no further therapy is needed. If 2 or more, patient will need anticoagulation with warfarin or other (dabigatran, rivaroxaban, apixaban). Therapy in patients with a score of 1 is case by case,
35
CHADS-VASC
9 points max
CHF (1)
HTN (1)
Age 75 or up (2)
DM (1)
Stroke/TIA/PE (2)
Vascular disease - prior MI, peripheral artery disease, aortic plaque (1)
Age 65-74 (1)
Sex - female (1)
36
Management of unstable angina/NSTEMI
Patients with ACS should be treated with guideline directed medical therapy
DAPT
Nitrates
BB
Statin
Anticoagularion (unfractionated heparin, LMWH, bivalirudin or fondaparinux)
37
Predictors of major cardiac complications with noncardiac surgery (revised cardiac risk index)
Clinical risk factors
* High risk surgery (vascular)
* History of ischemic heart disease
* HF
* history of stroke
* IDDM
* Prep creatine above 2
Rate of cardiac death, nonfatal cardiac arrest, or nonfatal MI
* No risk factors is 0.4
* 1 (low risk) is 1
* 2 (mod risk) is 2.4
* 3 or more (high) is 5.4
Preop cardiac eval for noncardiac surgery should be done first. Active high risk cardiac conditions (unstable angina or decompensated HF) need to be stabilized prior to surgery. Low risk surgury, patient RCRI less than 1% or patients able to perform more than 4 METS can go to surgery. If not low risk and greater than 1% and cannot perform 4 METs, the nfurther cardiac eval needs prior to surgery (TTE, stress test)
cardiac risk associated with the particular surgery should be considered (separate card)
38
Cardiac risk strat for noncardiac surgical procedures based on surgery type
High risk - Aortic/major vascular, peripheral vascular
Intermediate risk (1-5%) - Carotid endart, Head/neck, intraperitoneal/intrathoracic, ortho, prostate
Low risk (less than 1%) - ambulatory or superficial procedure, endoscopy, breast, cataract
39
What does LCx supply?
Lateral wall LV
40
cardiovascular effects of cocaine intox
Physio
* hypertension, tachycardia
* coronary vasoconstriction
* increased platelet activity and thrombus
clinical
* MI or ischemia
* Aortic dissection
* neuro ischemia or stroke
treatment
* Benzo (first line) and nitro
* BB contraindicated
* CCBs for persistent CP
* Phentolamine (alpha blocker) for persistent HTN
* cath for myocardial ischemia
Unless there is suspicion for dissection, aspirin should be given to patients with cocaine related chest pain. Only give plavix when acs is confirmed (ST changes, elevated trop).
41
Acute pericarditis
Etiology
* Viral or idiopathic
* Autoimmune (SLE)
* Uremia (acute or chronic RF)
* Post MI (Early less than 4d is peri-infarction pericarditis, late is dressler)
Clinical features/dx
* pleuritic CP (better when sitting up) with or without fever
* Pericardial friction rub (highly specific)
* Diffuse ST elevation and PR depression
* Pericardial effusion on TTE
Tx is NSAIDs and colchicine for viral/idiopathic and variable for other etiologies
Tx is high dose ASA for patients with peri-infarction pericarditis. If persistent symptoms, can then add on NSAIDs or colchicine or narcotics
42
Mechanical complications of acute MI
43
Indications for statin therapy in prevention of ASCVD
Secondary prevention
Established ASCVD
* acute ACS
* stable angina
* arterial revascularization (CABG)
* Stroke, TIA, PAD
Age less than or equal to 75: High intensity statin
Age greater than 75: Moderate intensity statin
Primary prevention
LDL at least 190: High intensity statin
Age 40 and up with DM: 10 year ASCVD risk 20% and up get high intensity. Otherwise moderate.
Estimated ASCVD greater than 7.5%: Moderate to high intensity statin
Moderate (atorvastatin 10-20, rosuvastatin 5-10, simvastatin 20-40, pravastatin 40-80, lovastatin 40)
High (atorvastatin 40-80 and rosuvastatin 20-40)
44
Patients with PAD
Reduced ankle-brachial index and claudication
Start on ASA and high intensity statin for secondary prevention of cardiovascular events
Treatment of symptomatic PAD
* Step 1A - risk factor management
* Smoking cessation
* BP and DM control
* Antiplatelet and statin
* Step 1B - supervised exercise therapy
* Step 2 - Cilostazol (preferred over pentoxifylline)
* Step 3 - Revascularization for persistent symptoms (or critical limb ischemia)
* Angioplasty with or without stent
* autogenous or synthetic bypass graft
45
Treatment of choice in patients with inferior wall MI leading to sinus brady
Does this by increased vagal tone triggered by SA node/RV wall ischemia. IV atropine is treatment of choice in patients with hemodynamically significant bradycardia (pulm edema, hypotension) due to inferior wall MI
If no response to atropine then temporary cardiac pacing (epinephrine if NOT from MI)
46
Treatment of DVT/PE
Oral factor 10A inhibition takes 2-4h for onset. No need for overlap or lab monitoring.
Warfarin is a vitamin K antagonist that requires 5-7 days to work. Needs overlap with UFH or LMWH for 5d and requires lab monitoring
Patients are treated for at LEAST 3 months
If patient has underlying malignancy, LMWH is better than factor 10a
47
Developing a PE on hormone therapy for menopause
Stop the hormones. A common alternative is SSRIs (like escitalopram) or SNRIs (venlafaxine). They do improve hot flases somehow
48
Multifocal atrial tachycardia
Etiology
* Exacerbation of COPD
* lytes (low K)
* Catecholamine surge (sepsis)
Clinical - typically asymptomatic. Rapid, irregular pulse. ECG with at least 3 p wave morpholigies and atrial rate greater than 100
Treatment - Correct underlying disturbance. AV nodal blockade (verapamil) if persistent
Usually an eldetly patient. Present with symptoms of the underlying disease.
Elevated atrial rate differentiates this from wandering atrial pacemaker.
49
Berry aneurysms. ED or marfans?
ED
50
Patient with blunt thoracic/abdominal trauma. First test?
FAST
51
Most effective nonpharm measure to decrease BP?
Weight loss in overweight peeps.
1. weight loss - reduction of BMI to less than 25. Leads to 5-20 reduction in SBP per 10kg loss
2. DASH diet - high in fruits and vegetables and low in saturated and total fats - leads to 8-14 point reduction
3. Exercise - 30 mins/day for 5-6 d/w. Leads to 4-9
4. Dietary sodium - less than 3g a day. leads to 2-8
5. Limit alcohol - 2 or less drinks a day in men. 1 in women. leads to 2-4 point reduction.
52
Risk factors for coronary heart disease
CHD risk equivalents
* Noncornary atherosclerotic disease (carotid, peripheral artery, AAA)
* DM
* CKD
CHD established risk factors
* Age (esp over 50 in men and menopause in women)
* Male
* FHx of CAD in first degree relative less than 50 years old in men, 60 in women
* HTN
* dyslipidemia
* Smoking
* Obesity
Note that smoking is not a CHD equivalent therefore having CKD or DM is the highest predictor of CHD/cardiovascular events. More than smoking.
53
Angina classification
Classic - typical location (substernal), quality and duration. Provoked by exercise or emotional stress. Relieved by rest or nitro.
Atypical - 2 of the 3
Nonanginal - less than 2 of the 3
Unstable angina is anginal pain at rest, T wave inversions and normal trop. NSTEMI is same but with elevated trop
54
Management of unstable angina/NSTEMI
1) Risk assessment. Use Thrombolysis in MI risk (TIMI) score (1 point for each)
* Age 65 and up
* 3 or more risk factors for CAD
* known CAD with more than 50% stenosis
* Use of ASA in past 7d
* at least 2 angina episodes within preceding 24h
* Elevated serum trop
* ST segment deviation at least 0.5mm on admission ecg
Low risk (0-2): Stress test prior to hospital discharge
Intermediate risk (3-4) or high risk (5-7): early cath (within 24h).
Hemodynamic instability, HF/new MR, recurrent chest pain, ventricular arrythmia: Immediate cath
55
Bacterial endocarditis ppx
High risk cardiac conditions
* prosthetic heart valve
* previous endocarditis
* structural valve abnormality in transplanted heart
* unrepaired cyanotic congenital heart disease
* repaired congenital heart disease with residual defect
Indicated procedures and appropriate coverage
* Gingival manipulation or respitarory tract incision (tonsillectomy, bronch with biopsy)
* Strep viridans (amoxicillin)
* GU or GI tract procedure in setting of active infection
* Enterococcus coverage (ampicillin or vanc)
* Surgery on infected skin or muscle
* staph coverage (vancomycin)
* Surgical placement of prosthetic cardiac material
* staph coverage (vancomycin)
So you need high risk condition and the above conditions. Even if you have high risk condition and are going for a GI procedure without active GI infection, no ppx is indicated.
56
Antithrombotic therapy in patients with mechanical heart valves
Aspirin
* 75-100mg/d (in addition to warfarin) in all patients with aortic valve replacement or mitral valve replacement
* 75-325mg/d in patients who cannot take warfarin
Warfarin goal INR 2-3
* Aortic valve replacement if no risk factors (Afib, severe LV dysfunction like less than 30%, prior thromboembolism, presence of hypercoagulable state) are present
Warfarin goal INR 2.5-3.5
* Mitral valve replacement
* aortic valve replacement with risk factors
* in the first 3 months after aortic valve replacement (weak rec)
57
Bicuspid aortic valve
Etiology
* Affects 1% of pop
* usually male
* present in 30% of patients with Turner Syndrome
* AD with incomplete penetrance or sporadic
Diagnosis - screen echo for patient and first degree relatives
Complications
* endocarditis
* severe regurgitation or stenosis
* aortic root or ascending aortic dilationn
Management
* Follow up echo q1-2 years
* balloon valvuloplasty or surgery (valve and ascending aorta replacement)
Most common congenital heart disease in adults
58
Most common cause of mitral stenosis
Rheumatic heart disease
symptoms present 10-20 years after initial rheumatic fever.
SOB, orthopnea, PND
loud first heart sound with mid diastolic rumble heard best at apex
59
Trastuzumab-associated cardiotoxicity
mab that targets HER2-positive tumors. Can cause a decline in LVEF which is usually asymptomatic but may lead to over clinical HF. Incidence of cardiac toxicity is about 5% alone and 25% when combined with anthracycline (doxorubicin) and cyclophosphamide.
In most cases, it's reversible and there is recovery of cardiac function after ending treatment.
In contrast, chronic anthracycline associated cardiac toxicity may not be reversible due to scarring from cumulative dosing.
Trastuzumab cardiac toxicity responds well to normal HF therapy (BB and ACE)
60
left atrial myxoma
Look for young person with arterial occlusion and signs of mitral valve obstruction (apical diastolic murmur, tumor plop), worsening HF, and new onset AFib
Most common primary cardiac tumor. Often flick off emboli and lead to arterial occlusion in otherwise healthy patients.
61
TCA overdose
CNS - AMS, seizures, resp depression
CV - sinus tachy, hypotension, prolonged PR/QRS/QT, arrhythmias (VTach, VFib)
AntiCh - dry mouth, blurred vision, dilated pupils, urinary retention, flushing, hyperthermia
Management - supportive care and therapy
* supplemetal O2, intubation
* IV fluids
* activated charcoal for patients within 2h of ingestion
* IV sodium bicarb for QRS widening or ventricular arrhythmias
TCAs act at His-Purkinje tissue
Sodium bicarb is most effective agent for management of cardiotoxic effects. Increases serum pH and extracellular Na. This modifies TCAs to their neutral (nonionized) form making them less available to bind rapid sodium chanels.
Patients who are refractory to sodium bicarb may respond to adjuvant Mg or Lidocaine
62
Warfarin interactions
Increased Warfarin effect (high INR)
* Metronidazole, quinolones (mess up intestinal flora)
* Azoles, amiodarone (CYP2C9 inhibitition)
* Acetaminophen (less vitamin k recycling)
Decreased effect (low INR)
* Rifampin, phenytoin, st johns wort (induce CYP)
* OCPs (increase coag factors)
* Green leafy vegetables (increase vit K ingestion)
INR independent interaction
* NSAIDs, plavix (inhibit platelets0
* Ginkgo (increased bleeding)
When starting amiodarone is started, it is recommended to reduce warfarin by 25-50%
63
When is BNP worthless?
BNP less than 100 is often helpful in ruling out HF, but obesity lowers BNP making it unreliable
64
STEMI cath time
90 minutes
65
Clinical features of acute decompensated heart failure
Presentation
* Acute SOB, orthopnea, PND
* HTN common, hypotension suggests severe disease
* Diffuse crackles with possible wheezes (cardiac asthma)
* Accessory muscle use, tachycardia, tachypnea
* possible S3, JVD, peripheral edema
Treatment
Normal or elevated BP with adequate end organ perfusion
* supplemental O2
* IV loop diuretics
* consider IV vasodilator (nitro)
Hypotension or signs of shock
* supplemental O2
* IV loop as appropriate
* IV vasopressor (norepinephrine)
Sudden increase in PCWP (along with LA and LV filling pressures) leads to fluid in pulm interstitial and alveolar spaces
BB are recommened in long term treatment but NOT in acute.
66
severe AS
soft, single second heart sound
parvus et tardus (delayed and diminished carotid pulse)
Loud and late peaking systolic murmur
67
What should be performed in patients with acute decompensated CHF of unclear etiology?
echo
68
recommended therapy for WPW Syndrome
Catheter ablation of accessory pathway
69
Approach to adult cardiac arrest
Start CPR, give O2, and attach monitor/defibrillator
If VF/pulseless VT: Shock. Then CPR, airway,IV accesses, epi every 3-5min. Pulse/rhythm check every 2 mins. Repeat.
If PEA/systole: Not shockable. Just go to the CPR,IV,epi with pulse checks to see if maybe now it's shockable.
Keep repeating until ROSC.
Note. Amiodarone is given after 3rd shock .
70
Reversible causes of asystole/PEA
5Hs and 5Ts
## Footnote
Hypovolemia
Hypoxia
Hydrogen ions (acidosis)
HypoK or hyperK
Hypothermia
Tension PTX
Tamponade
Toxins (benzo, narcotics)
Thrombosis (PE or cardiac)
Trauma
71
Vasovagal (neurocardiogenic) syncope
Clinical presentation
* Inciting event (stress, prolonged standing)
* Prodrome (pallor, nausea, diaphoresis) - these symptoms can persist for a brief period following the episode
* Consciousness regained rapidly (less than a min)
Diagnosis
* Mainly clinical
* upright tilt table testing in uncertain cases
Treatment
* Reassurance
* Avoidance of triggers
* Counterpressure techniques for recurrent episodes
Palpitations prior to syncope suggests cardiogenic due to arrhythmias
72
Coarctation
RUE HTN
lower extremity claudication
murmur
Commonly associated with Turners, but most commonly sporadic and affects males.
weak/delayed distal pulses
CXR with rib notching from collateral vessels and a figure 3 sign at site of aortic narrowing. Echo confirms diagnosis.
73
PDA closure in newborn with coarctation
Can lead to HF causing hepatomegaly due to hepatic congestion. However, coarct needs to be severe. If presenting in later childhood it is usually mild and not associated with HF
74
Pulsus paradoxus
large decline in BP (more than 10 mmHg) during inspiration that occurs with cardiac tamponade (CP, SOB, hypotension, JVD, muffled heart sounds)
75
Preferred antiarrythmic therapy in patients with AFib
No CAD or structural heart disease: Flecainide, propafenone
LVH: Dronedarone, amiodarone
CAD without HF: Sotalol, Dronedarone
HF: Amiodarone, Dofetilide
Recurrent AF symptoms refractory to meds: RF ablation
76
Anomalous aortic origin of a coronary artery
In patients under 35, SCD is usually due to underlying structural heart disease with ventricular tachyarrhythmia as most common terminal event
High risk types are among most common causes of SCD in young athletes.
1) L main coronary artery coming from R aortic sinus
2) R main coronary artery coming from L arotic sinus
These lead to sharp curvature and make it less able to tolerate high flow. And they pass between aorta and PA making them prone to external compression during exercise. Echo and ECG may be nondiagnostic. CTA/cardiac MR is diagnostic test of choice.
77
Perioperative medication management
BB - withdrawal can cause HTN - continue during surgery
Alpha2agonists (clonidine) - withdrawal can cause HTN - continue during surgery
CCBs - may lead to slightly higher bleeding risk - continue during surgery
ACE - possible hypotension
* continue during surgery for patients with HF
* Hold night before for other patients
Diuretics - possible hypovolemia and hypotension - continue up to day of surgery and hold that morning
Statins - slight risk of myopathy - continue during surgery
Raloxifene (SERMs) should be stopped 4 weeks prior to surgery associated with mod to high risk of clot (knee replacement)
78
Statins and muscle injury
Statin therapy can potentiate muscle injury and elevation of CK levels following prolonged and vigorous exercise. Most such patients can be restarted on statin once CK levels normalize.
Patients with symptomatic myopathy (not from an attributable cause) from statin use should d/c therapy. In asymptomatic patients, CK levels more than 10 times upper limit of normal range is considered indication for d/c.
79
Most common congenital heart defect in Downs
Endocardial cushion defect (dx with echo)
Other things are duodenal atresia, hirschsprung, atlanto-axial instability and hypothyroidism.
Also at risk for acute leukemia later in life. Also ADHD, autism, depressive disorder, seizure disorder, Alzheimer
80
Patient has suspected ACS but ECG and trop are normal
Keep and observe with serial ECG and trop
81
How soon after MI can you resume sexual activity?
Moderate walking corresponds to sexual activity in turms of METs
If low risk for developing cardiovascular complications, can resume sex soon like in 1-4 weeks
High risk need referral for advising. These are refractory angina, NYHA IV, significant arrthymias, severe valvular disease
Intermediate risk gets stress test
82
Cyanide accumulation and toxicity
Skin - flushing, cyanosis (later)
CNS - HA, AMS, seziure, coma
CV - arrhythmias
Resp - Tachypnea followed by resp depression, pulm edema
GI - abdominal pain, n/v
Renal - metabolic acidosis (from lactic acidosis), renal failure
Nitroprusside is used in management of hypertensive emergency. Side effect is Cyanide tox (esp if you have CKD), so make sure you have low infusion rate (less than 2 mcgs per kg per min) and closely monitor. treat with stopping and sodium thiosulfate .
Goal of hypertensive emergency is to rapidly lower diastolic pressure to 100-105 over 2-6 hrs with total drop in BP being no more than 25% of initial value.
83
Cardiac tamponade
Etiology
* aortic aneurysm or post MI
* malignancy or radiation
* infection (viral, TB)
* connective tissue disease (SLE)
* cardiovascular surgery
Clinical signs
* beck triad: hypotension, JVD, low heart sounds
* pulsus paradoxus
Dx
* ECG with low voltage QRS, electrical alternans
* CXR with enlarged cardiac silhouette, clear lungs
* echo with RA and RV collapse, plethora of IVC
84
cardiogenic syncope
Aortic stenosis or HCM
* Exertional syncope
* systolic murmur on exam
Ventricular tachycardia
* no preceding symptoms
* cardiomyopathy or previous MI
SSS
* preceding fatigue or dizziness
* sinus pauses on ecg
Advanced av block
* bifascicular block or long PR interval on ecg
* dropped qrs complexes on ecg
Torsades
* no preceding symptoms
* meds that prolong QT
* hypoK or hypoMg
These patients should all be admitted to the hospital for tele monitoring and echo. Treatment with some combo of phatm therapy (amiodarone), ablation or ICD is likely indicated
85
Infnat of diabetic mother complications
Maternal hyperglycemia
First trimester
* congenital heart disease
* neural tube defects
* small L colon syndrome
* spontaneous abortion
Second/third trimester
* fetal hyperglycemia and hyperinsulinemia
* polycythemia (more metabolic demand leading to fetal hypoxemia leading to more erythopoiesis)
* organomegaly
* neonatal hypoglycemia
* brachial plexopathy, clavicle fracture, perinatal asphyxia (big baby being born)
* hypertrophic cardiomyopathy (increased glycogen stores lead to glycogen deposition in interventricular septum)
Most babies recover from cardiomyopathy without surgery, even if they have symptoms
86
Most common cause of sudden death due to steering wheel injury
Aortic injury from rapid deceleration causing shearing force along aortic arch
87
Peripartum cardiomyopathy
Risk factors
* maternal age over 30
* multiple gestation
* preeclampsia, eclampsia
Clinical
* LVEF less than 45
* onset at 36w to 5 months postpartum
* no other cause of HF
Management
* deliver based on maternal hemodynamic stability
* standard systolic failure regimen
* thromboembolism prophylaxis
Recurrence risk
* LVEF less than 20 at diagnosis
* Persistent LV dysfunction
After delivery, some patients will have spontaneous resolution of ventricular dysfunction and can discontinue their med regimen. However, there is a risk of recurrence in patients who LV was super messed up at disgnosis (as above) or in patients who have PPCM.
Therefore, regardless of PPCM resolution, patients are evaluated with serial echo for a few years. Those with recurrent or persistent LV dysfunction are advised to avoid pregnancy
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Marfan and sports
Screening echo first to look for aortic root disease
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Valve replacement in aortic stenosis
Severe AS
* Aortic jet velocity over 4 OR
* mean transvalvular pressure gradient of 40 and up
* valve area usually 1 or under but not required
Indications for replacement: Severe AS plus at least one of the following
* Onset of symptoms (angina, syncope)
* LVEF less than 50
* Undergoing other cardiac surgery (CABG)
AVR is associated with increased survival in patients with symptomatic severe AS
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constrictive pericarditis
common complication of CABG. Most patients are asymptomatic from small effusions. But continued pericardial inflammation occuring over months may lead to devleopment of thickened fibrous pericardium and constrictive pericarditis
Important cause of R heart failure. They will have peripheral edema, asciate and hepatic congestion with hepatomegaly which can progress to cardiac cirrhosis. pericardial calcs on cxr
Treatment involves supportive care (anti inflammatory agents) or pericardectomy for refractory cases
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cardiac amyloidosis
suspect in patients with unexplained chf (predominantly diastolic), low voltage on ecg, and echo showing increased ventricular wall thickness with normal LV cavity dimensions (esp in patients with HTN)
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long term amiodarone toxicity
thyroid dysfunction
hepatotoxicity
cardiac bradyarrhythmias
chronic interstitial pneumonitis
neuro (ataxia, peripheral neuropathy)
blue-gray skin
visual disturbances
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Patient with immediately-threatened extremity
Severe pain, delayed cap refill, absent arterial doppler, sensory/motor deficits
At risk for irreversible myonecrosis within 4-6h and should have anticoagulation and emergency surgical revascularization
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sympotmatic lower extremity varicose veins
initially with conservative measures like leg elevations, weight reduction and compression stockings
Surgical ligation is used for large symptomatic veins with ulcers, bleeding or recurrent thrombophlebitis
extrernal lasers used to treat particular veins and/or telangectasias. Not varicose veins
Injection sclerotherapy with/without anesthesia used in patients with small symptomatic veins that have failed at least 3-6 months of conservative treatment
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aortic dissection
intravenous BBs are preferred initial therapy (esmolol) to reduce HR and BP and reduce LV contractility in patients with acute AD. Sodium nitroprusside should be used only in addition to BB if systolic BP remains above 100-120 after adequate BB
Emergent surgical repair for ascending dissection
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Digoxin toxicity
nausea, vomiting, anorexia, fatigue, confusion ,visual disturbances, cardiac abnormalities. Verapamil inhibits renal tubular secretion of digoxin and will raise serum levels.
Other meds that can do this:
quinidine
amiodarone
spironolactone
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AAA
Most commonly affects infrarenal aorta (more than 3cm)
Risks
* Smoking, smoking, smoking
* male
* older
* white
* FHx
* atherosclerosis
Screening - abdominal US in men age 65-75 who have EVER smoked
Symptoms
* mostly ASx
* may have abdominal, back or flank pain
* lower limb ischemia and/or thromboembolism
* rupture often presents with abdominal distention and shock
Management
* Smoking cessation is number 1!!!
* aspirin and statin
* elective repair recommended for
* large (at least 5.5cm)
* rapidly enlarging (at least 0.5cm in 6 months)
* AAA associated with peripheral artery disease or aneurysm
Follow up imaging - medium (4-4.5): US every 6-12months. smaller. US every 2-3 years.
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RV MI
hypotension, shock, JVD but clear lungs
Avoid nitrates
Give fluids (need preload)
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Clinical features of pulm HTN
Type 1 - pulmonary arterial hypertension (idiopathic)
Type 2 - left sided heart disease
Type 3 - chronic lung disease (COPD, ILD)
Type 4 - chronic thromboembolic disease
Type 5 - other (sarcoid)
Symptoms - SOB, weakness, exertional angina, syncope, abdominal distention/pain
Signs - L parasternal lift, RV heave, loud P2, right sided S3. pansystolic murmur of tricuspid regurg. JVD, ascites, peripheral edema, hepatomegaly.
Echo should be done to allow for measurement of pulm arterial pressure and should be the initial diagnostic evaluation in patients with suspected pHTN
Endothelin receptor antagonists (bosentan, ambrisentan) show delayed progression of idiopathic pHTN in symptomatic patients
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do you need to screen for bicuspid aortic valve?
YES. screen first degree relatives with echo
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Indications for implantable cardioverter-defribrilator placement in hypertrophic cardiomyopathy
Primary prevention
* family history of SCD
* syncope (recurrent and/or associated with exertion
* nonsustained VT on Holter
* Hypotensive BP response to exercise
* extreme LVH (more than 3 cm maximum septal wall thickness)
Secondary prevention
* survivors of cardiac arrest
* sustained spontaneous ventricular arrythmias
