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Cardiology > Cardio Exam 2 > Flashcards

Cardio Exam 2 Flashcards

1
Q

What is the underlying pathophysiology that results in MI?

A
  • Rupture or erosion of vulnerable plaque. Blood is exposed to inner plaque material and platelets activate, thrombin is generated and thrombi form.
  • Note: vulnerable plaques are often non-obstructive, stenosing vessel by between 40 and 60%. These typically don’t produce abnormal stress test if identified prior to MI
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2
Q

What is ACS?

A
  • Acute coronary syndrome: unstable angina, non-STE MI (caused by non-occlusive platelet rich “white” thrombus) or STE MI (caused by occlusive fibrin rich “red” thrombus.
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3
Q

Which populations present atypically with MI? Symptoms?

A
  • Diabetics, women and elderly.

- Sx: without chest pain, with SOB, nausea, vomiting or fatigue

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4
Q

Treatments for MI

A
  • Immediate reperfusion via
    a. Thrombolytic therapy OR
    b. PCI: percutaneous coronary intervention (cath lab)
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5
Q

STE in the following leads suggest what anatomic area for MI with what culprit artery:

a. V1-4
b. II, III and aVF
c. I, aVL and/or V5, 6

A

a. Anterior: LAD
b. Inferior: RCA (65%), LCX (35%)
c. Lateral: diagonal branches of LAD or obtuse marginal branches of LCX

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6
Q

What are the results if perfusion is not restored in MI?

A
  • Myocardial damage w/shock
  • Reduced EF, early infarct expansion, ventricular remodeling = cardiomyopathy
  • Chronic heart failure
  • Ventricular arrhythmias
  • Sudden death
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7
Q

Describe presentation of inferior STEMI from proximal occlusion leading to right ventricular infarct. What does ECG show? What medication should be avoided in these individuals?

A
  • Hypotension with elevated neck veins and clear lung fields
  • ECG changes in lead V4R?
  • Avoid preload reducers such as NTG. Be cautious with beta-blockers. If hypotensive, try IV fluids.
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8
Q

What does non-STE MI result from? What does ECG show? Can thrombolytics be used in this condition?

A
  • Ruptured/eroded plaque with acute thrombus formation and incomplete obstruction of blood flow. Plaque is platelet rich.
  • ECG: normal or exhibit ST depression, T wave inversion. ST depression doesn’t localize to anatomic territory/culprit artery – just shows subendocardial.
  • Thrombolytics are contraindicated. Not complete obstruction. These exposure more platelets and favor clot formation.
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9
Q

Does normal ECG r/o ACS?

A
  • No. Could be non-STE MI.
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10
Q

Describe medical therapy for STEMI vs NSTEMI?

A
  • All: o2, 325 mg ASA + (P2Y12 inhibitor or GP 2b3a inhibitor), sublingual NTG, anticoag
  • If angina persists, give either: beta-blocker, IV nitro, CCB. Give morphine for analgesia.
    1. STEMI
  • O2 to maintain 92%
  • ASA (+/- P2Y12 inhibitor: some places might prefer to wait until artery IDd)
  • SL NTG (or IV for pain)
  • Anti-ischemic: +/- beta-blocker (metoprolol): if tachy w/HTN or v arrhythmias
  • Anticoagulant (unfractionated heparin of LMWH)
  • Reperfusion via cath lab (w/in 90 minutes) or thrombolytic
  1. NSTEMI
    - O2 to maintain 92%
  • ASA (+/- GP 2b3a inhibitor: if angina refractory)
  • SL NTG (or IV for pain)
  • Anti-ischemic: Beta-blockers
  • Anticoagulant (unfractionated heparin of LMWH)
  • No thrombolytics!
  • Cardiac cath electively in next 24-48 hours.
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11
Q

Describe post MI medical therapy

A
  • ASA for life (81 or 162 mg)
  • P2Y12 inhibitor for a year
  • Beta-blockers
  • ACEi if EF less than 40% class I or less than 50% class II
  • Aldosterone antagonist for HF and EF
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12
Q

Criteria for defining MI

A
  • Symptoms
  • New or presumed new ST segment, T wave changes OR new LBBB
  • Development of pathological Q waves
  • Imaging: evidence of loss of myocardium or regional wall abnormality
  • ID of thrombus
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13
Q

Classification of MI

A
  1. Spontaneous MI caused by primary coronary event: plaque erosion or rupture
  2. MI secondary to increased o2 demand or decreased supply
  3. Sudden unexpected cardiac death
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14
Q

What is the Bezold-Jarisch reflex?

A
  • Sudden bradycardia associated with hypotension, decreased inotropy and coronary vasodilation. Can occur after MI.
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15
Q

Killip risk classification / stratification of MIs

A

Class 1: no rales, no S3 = lowest mortality

Class 2: rales 50%

Class 4: shock = highest mortality

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16
Q

Differential dx for chest pain

A
  1. Cardiac: MI, pericarditis, myocarditis
  2. Pulmonary: PE, pneumonia, asthma, COPD, pleuritis, pneumothorax, mediastinitis
  3. Aortic syndromes: dissection, perforated ulcer, intramural hematoma
  4. Chest wall: costochondritis, MSK
  5. Esophagus: spasm, rupture/perforation, GERD
  6. RUQ pathology
  7. Anxiety
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17
Q

Compare and contrast utility of Trop and CK-MB in MI. When do values peak? When do they return to normal?

A
  • Troponin: rise within 3 hour of acute MI, peak 24-48 hours, remain elevated for up to two weeks (depending on I vs T components)
  • CK-MB: exceeds nml in 4-8 hrs, peak 24 hours, returns to normal in 2-3 days
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18
Q

Absolute contraindications to thrombolytic therapy for MI

A
  • Prior ICH
  • Known cerebral vascular lesion (eg. AV malformation)
  • Known malignant intracranial neoplasm
  • Ischemic stroke within 3 months
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (tendency): excl menses
  • Significant closed head trauma or facial trauma w/in 3 months
  • IC or intraspinal surgery w/in 2 months
  • Severe uncontrolled HTN
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19
Q

Gestational and natal history that can make one suspicious of cardiac issues in neonate

A
  • Infections: rubella, CMV, coxsackievirus B
  • Maternal meds: retinoids, valproate
  • Maternal smoking or etoh intake
  • Maternal conditions such as DM, lupus
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20
Q

Is RR > 60 normal in baby?

A
  • Abnormal in any age
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21
Q

Incidence of congenital heart disease? Recurrence risk?

A
  • About 1% (8-12 out of 1000) = incidence

- Recurrence risk for sibs = ~ 3%

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22
Q

BP changes suggestive of aortic coarctation

A
  • Normal is leg BP >= arm BP

- If arm BP > leg BP: suggestive of coarctation

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23
Q

Correct cuff size in peds patients

A
  • Width of cuff = 125-150% diameter of arm
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24
Q

Splitting of S1 is likely what?

A
  • Systolic ejection click
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25
Q

Where are S1 best heard?

A
  • Apex or LLSB
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26
Q

Grading of heart murmurs

A

1: barely audible
2: soft, but audible
3: moderately loud, no thrill
4: loud with palpable thrill
5: audible with steth 45 degree angle
6: audible with stethoscope off chest

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27
Q

Most heart murmurs are systolic or diastolic?

A
  • Systolic
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28
Q

Causes of systolic ejection murmurs?

A
  • Aortic stenosis
  • Subvalvar or supravalvar aortic stenosis
  • Pulmonary stenosis
  • Branch pulmonary artery stenosis
  • Tetralogy of Fallot
  • Coarctation of the aorta
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29
Q

Causes of systolic regurgitant murmurs?

A
  • VSD
  • AVSD
  • Mitral regurg
  • Tricuspid regurg
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30
Q

Causes of diastolic murmurs?

A
  • Aortic insufficiency
  • Pulmonary insufficiency
  • Mitral stenosis
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31
Q

Causes of continuous murmurs?

A
  • Aortopulmonary or arteriovenous connection: PDA, systemic to PA shunt
  • Disturbed venous flow (venous hum): blood returning from head
  • Disturbed arterial flow
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32
Q

Describe EKG findings in infants and children

A
  • RV dominance in infants therefore RAD and RVH. This is present first 6 months, then adult pattern.
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33
Q

Heart diseases with left-to-right shunt defects

A
  • ASD
  • VSD
  • PDA
  • AVSD
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34
Q

Heart diseases with obstruction to outflow

A
  • Aortic and pulmonary stenosis

- Coarctation of the aorta

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35
Q

With “holes” in the heart, in what direction does blood want to flow? Why?

A
  • From left to right unless there is right-sided obstruction or pulmonary HTN
  • PVR
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36
Q

Atrial septal defect.

a. Prevalence?
b. Most common type?
c. Pathophys?
d. Physical exam findings?
e. EKG and CXR findings?
f. History?
g. Medical management?

A

a. 5-10% of all CHD (congenital heart defects)
b. Secundum type (at site of foramen ovale). Other uncommon: primum (lower closer to AV valves), sinus venosus (closer to SVC)
c. Left-to-right shunt = RA, RV and lung volume overload
d. Soft pulmonary ejection murmur, soft diastolic murmur d/t increased flow across TV, S2 widely split (fixed)
e. EKG: RA enlargement, RAD, possible RVH. CXR: increased pulm vasculature, enlarged hear
f. Usually well tolerated for decades. 3rd/4th decade, leads to pulmonary HTN and atrial arrhythmias
g. Open heart surgery OR ASD (Amplatzer septal occluder) via angiography

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37
Q

Ventricular septal defect

a. Prevalence?
b. Most common type?
c. Pathophys?
d. Physical exam findings?
e. EKG and CXR findings?
f. History?
g. Medical management?

A

a. 15-20% of CHD (most common)
b. IV septum has two parts. Most common type = perimembranous VSD (below aortic valve on left side of septum and adjacent to septal leaflet of TV on right side). Others = inlet, muscular, outlet.
c. Depending on size, may not have hemodynamic significance. If large, can lead to CHF and pulmonary HTN. Left-to-right shunt. Volume overload here of lungs, LA and LV, not right.
d. If small VSD: well-developed and acyanotic. If large: poor weight gain, CHF, systolic thrill may be present at LLSB. P2 moderately increased with larger VSD. Murmur = systolic regurgitant murmur. Possible diastolic rumble if large. Note: murmur may be absent or soft during first few days of life.
e. Use echo and cath to determine QP/QS ratio, which is pulmonary to systemic blood flow ratio. If nearing 2, significant. EKG: Nml with small, large VSD may show LVH, LAE and LAD. If pulmonary HTN, may see RVH. CXR: cardiomegaly +/-, increased pulmonary vascularity
f. CHF symptoms in large VSDs. Irreversible pulmonary HTN may occur as early as 6-12 months with large VSDs.
g. Tx of CHF with digoxin (give heart kick), diuretics to decrease edema and ACEi to lower SVR and encourage more left shunting. Also high calorie formula for weight gain. Surgery if: growth failure w/o med improvement. Surgery contraindicated if PVR increased d/t long standing condition and Eisenmenger (right to left shunt d/t progression of disease).

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38
Q

What is the most common form of congenital heart disease?

A
  • VSD (15-20% of cases)
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39
Q

Is murmur in ASD flow across defect? In VSD?

A
  • In ASD: not from flow across defect

- In VSD: it is

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40
Q

Compare and contrast murmurs in VSD to stenotic murmurs?

A
  • Murmur in VSD may be absent or soft during first few days of life. Why? PVR to SVR ratio is low. As ratio increases, murmur increases.
  • Stenotic murmurs are always present.
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41
Q

Patent ductus arteriosus

a. Prevalence?
b. Pathophys?
c. Physical exam findings?
d. EKG and CXR findings?
e. History?
f. Medical management?

A

a. 5-10% of CHD

b. L-to-R shunt as PVR

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42
Q

When does ductus arteriosus close?

A
  • First hours of life
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43
Q

LAD in children should lead to suspicion of what?

A
  • VSD or PDA
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44
Q

Atrioventricular septal defect

a. Prevalence?
b. Pathophys?
c. Physical exam findings?
d. EKG and CXR findings?
e. History?
f. Medical management?

A

a. 2% of CHD. With AVSD: 30% have DS. Of pts with DS: 40% have CHD, 40% of those CHDs are AVSD. Know this!
b. Large common communication at center of heart. Associated with PDA and Tet. Ventricular shunt is dominant (left to right as PVR

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45
Q

Pulmonary stenosis

a. Prevalence?
b. Most common type?
c. Pathophys?
d. Physical exam findings?
e. EKG and CXR findings?
f. History?
g. Medical management?

A

a. 8-10% of all CHD
b. Valvar stenosis = most common. Associated with Noonan syndrome (characteristic facies, valvar PS, ASD). Other = subvalvar and supravalvar, which are rare.
c. Higher RV pressure needed to force blood across stenotic valve = RVH and possible TV regurg. R heart failure can lead to hepatomegaly and edema.
d. Systolic thrill possible, systolic ejection click at LUSB, ejection murmur at LUSB. More severe stenosis = longer murmur. Hepatomegaly if CHF develops.
e. EKG: nml in mild cases; RAD, RVH in more severe cases. Critical PS shows LVH d/t relative hypoplasia. CXR: heart size usually normal. Vascularity normal to mildly decreased.
f. Sudden death possible with severe stenosis especially with strenuous activities.
g. Balloon valvuloplasty or surgery.

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46
Q

Aortic stenosis

a. Prevalence?
b. Most common type?
c. Pathophys?
d. Physical exam findings?
e. EKG and CXR findings?
f. History?
g. Medical management?

A

a. 3-6% of all CHD
b. ? common. Valvar, subvalvar and supravalvar.
c. Elevated LV pressure to force blood across stenotic valve = LVH and possible MV regurg. Left-sided heart failure can occur leading to pulmonary edema.
d. Narrow pulse pressure in severe, systolic thrill possible at RUSB, systolic ejection click heard toward apex, ejection murmur at midsternal border.
e. EKG: nml in mild; LVH in severe cases. CXR: heart size usually normal. Severe = cardiomegaly and pulmonary edema.
f. Mild to moderate = asymptomatic. Severe = external chest pain, fatigability and syncope. Critical = CHF.
g. Avoid sustained strenuous activity, anti-congestive meds, balloon valvuloplasty in cath lab, surgery (valvotomy, valve replacement – Ross procedure, myectomy). Ross procedure: pulmonary autograft and placement of pulmonary/aortic homograft between RV and main pulmonary artery.

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47
Q

Coarctation of the Aorta

a. Prevalence?
b. Pathophys?
c. Physical exam findings?
d. EKG and CXR findings?
e. History?
f. Medical management?

A

a. 8 to 10% of all CHD
b. Shelf of ductal tissue located in juxtaductal region of aorta near left subclavian artery. Obstruction to flow distal. LV generates increased pressure to force blood across stenosis. Arm BP higher than leg (pulses). L to R shunting across VSD if present. Obstruction can occur acutely or gradually (collaterals can form).
c. Pale, dyspneic, differential cyanosis, peripheral pulses weak, femoral pulses may be absent, BP different between arm and leg, murmur variable.
d. EKG: RVH younger children, LVH older. CXR: cardiomegaly and pulmonary venous congestion.
e. Poor feeding, dyspnea, poor weight gain. Acute circulatory shock with closure of ductus. Up to 30% develop CHF by 3 months. Renal impairment in late diagnosis.
f. IV prostaglandin to keep duct open. Anti-congestive meds. Balloon angioplasty. Surgery.

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48
Q

Is acrocyanosis a normal newborn finding?

A
  • Yes. There is vasomotor dysregulation for up to 24 months in baby typically. Isolated to hands and feet.
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49
Q

Medical approach to cyanotic infant

A
  1. CXR
  2. ABG
  3. Hyperoxitest: check arterial po2 on RA, place on 100% o2 for 10 mins, recheck arterial po2. Pulmonary cause shows rise in po2. Cardiac right to left shunt demonstrates no significant increase.
  4. Prostaglandin E1 if heart dz suspected. This keeps ductus open.
  5. Call peds cardio
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50
Q

Effect of acidosis on heart?

A
  • Decreases heart contractility
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51
Q

What are the cyanotic heart defects?

A
  • Mnemonic = 5 Ts
  • Truncus arteriosus
  • Transposition of the great arteries
  • Tricuspid atresia
  • Tetralogy of Fallot
  • Total anomalous pulmonary venous return
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52
Q

Transposition of the great arteries.

a. Prevalence
b. Anatomy and pathophysiology
c. History
d. PE
e. EKG, CXR
f. Medical management

A

a. 5% of CHD
b. Aorta arises from RV carrying desaturated blood to body. Pulmonary artery arises from LV carrying oxygenated blood to lungs. Requires defects that permit mixing of these circulations to survive. 50% have small PFO and small PDA. VSD present in 30-40%.
c. Cyanosis from birth, esp full-term males, feeding difficulties. Hypoxia and acidosis will result in death. CHF in first few weeks.
d. Cyanotic, tachypneic w/ no distress (happy tachypneic baby), S2 single and loud, heart murmur only if outflow obstruction. If CHF, hepatomegaly and dyspnea develop.
e. EKG: no specific. RAD and RVH. CXR: mild cardiomegaly with increased vascularity. Egg-shaped heart with narrow mediastinum.
f. Prostaglandin, correct acidosis, o2 for severe hypoxia, balloon atrial septostomy (Rashkind procedure), anti-congestive meds. Surgery = atrial switch, arterial switch.

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53
Q

Tetralogy of Fallot (TOF)

a. Prevalence
b. Anatomy and pathophysiology
c. History
d. PE
e. EKG, CXR
f. Medical management

A

a. 10% of all CHD
b. 4 parts: large VSD, overriding aorta, RVOT obstruction, RVH (secondary to RVOT obstruction). 5th part sometimes seen = atrial shunt. RVOT obstruction limits pulmonary blood flow. R to L shunt across VSD into aorta. Degree of cyanosis depending on degree of RVOT obstruction.
c. Cyanotic at birth, gradually worsens, hypoxic spells (Tet spells, which peak bw 2 and 4 months = sudden onset of rapid, deep breathing, irritability, prolonged crying, increased cyanosis, decreased heart murmur), growth retardation if cyanosis severe.
d. Cyanosis (varying degree), tachypnea, systolic thrill, ejection murmur at mid to LUSB (from RVOT obstruction)
e. EKG: RAD and RVH. CXR: normal heart size, upturned apex from RVH (boot-shaped), decreased pulmonary vascularity
f. Educate parents re: Tet spells, balloon dilatation of RVOT not widely used, palliation with Blalock-Taussing shunt where base of innominate artery is connected to right pulmonary artery, surgical repair

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54
Q

Pathophys of tet spell? Tx?

A
  • Spasm of RVOT = increased R to L shunt across VSD leading to worsening cyanosis and acidosis.
  • Tx: infant in knee-chest position (increase SVR, minimized R to L shunt), o2, morphine, Na bicarb for acidosis
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55
Q

Tricuspid atresia

a. Prevalence
b. Anatomy and pathophysiology
c. History
d. PE
e. EKG, CXR
f. Medical management

A

a. 1-3% of all CHD
b. TV absent, RV hypoplastic. Majority of cases have either pulmonary atresia or stenosis. Small VSD often present. RA blood must cross atrial septum = mixing in LA. Pulmonary blood flow usually limited. Few survive beyond 6 months without surgery.
c. Cyanosis (usually severe) from birth. S2 usually single.
d. Regurgitant murmur of VSD at LLSB. Hepatomegaly if ASD is small.
e. EKG: left superior axis = classic!, LVH and RAE possible. CXR: nml size, decreased vascularity.
f. Prostaglandin, balloon atrial septostomy, surgery with Fontan procedure ultimately: IVC and SVC connected directly to pulmonary arteries.

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56
Q

Truncus arteriosus

a. Prevalence
b. Anatomy and pathophysiology
c. History
d. PE
e. EKG, CXR
f. Medical management

A

a.

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57
Q

Total anomalous pulmonary venous return

a. Prevalence
b. Anatomy and pathophysiology
c. History
d. PE
e. EKG, CXR
f. Medical management

A

a. 1% of all CHD
b. Pulmonary veins meet at confluence behind left atrium. They find alternate connection to the right atrium. Most common = supracardiac form drainage. Some of the other vein connections can be obstructed. Condition requires interatrial communication. Complete mixing occurs in right atrium.
c. W/o obstruction: mild cyanosis and CHF. With obstruction: marked cyanosis, respiratory distress with feeding.
d. W/o obstruction: mild cyanosis, signs of CHF, widely split and fixed S2, soft systolic ejection murmur. Most die by one year of age d/t pneumonia. With obstruction: distressed infant with marked cyanosis, loud S2 reflecting pulmonary HTN, pulmonary rales, hepatomegaly (d/t obstruction and backup). Most rarely survive for more than a few weeks.
e. EKG: no specific findings. CXR: w/o: moderate cardiomegaly and increased vascularity. With: normal heart size and pulmonary edema.
f. O2, anti-congestive meds, correct of acidosis, balloon atrial septostomy, surgery.

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58
Q

Normal HR in neonate. RR? SBP?

A
  • HR: 80-180 bpm
  • RR: 30-50 bpm
  • SBP: > 60 mm Hg
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59
Q

Normal HR in 1 week to 2 year old infant. RR? SBP?

A
  • 80-160 bpm
  • 1-6 mo RR: 20-40 bpm
  • 6-24 mo RR: 20-30 bpm
  • 1-12 mo SBP: > 70 mmHg
  • 1-10 yo: > 70 + (2 x years) mmHg
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60
Q

Normal HR in 2 to 10 year old. RR? SBP?

A
  • 75-100 bpm
  • 2-12 yo: 16-24 bpm
  • 1-10 yo: > 70 + (2 x years) mmHg
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61
Q

Normal HR in child > 10 years. RR? SBP?

A
  • 50-100 bpm
  • 2-12 yo: 12-20 bpm
  • > 10 yo: > 90 mmHg
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62
Q

Is BP reliable to assess cardiogenic shock?

A
  • No. It may be the last thing to go.
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63
Q

What is the pathophysiology of shock?

A
  • Inadequate delivery of substrates and o2 to meet needs of tissue. Cells switch to anaerobic metabolism = accumulation of lactic acid. Cell swells, cell membrane breaks down and cell death.
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64
Q

ABCDEs of resuscitation for shock

A
  • Airway
  • Breathing
  • Circulation
  • Draw labs (or give drugs):

o Labs: blood gas, CBC, CMP, blood culture

o Drugs: inotropes, abx, Na bicarb

  • Echo
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65
Q

Discuss case studies from L29

A

Discuss case studies from L29

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66
Q

Symptoms/signs of cardiac decompensation in pediatric patient

A
  • Respiratory distress
  • Tachycardia
  • Poor perfusion
  • These can mimic sepsis
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67
Q

Which heart pathologies are emergencies in pediatric patients?

A
  • Left-sided obstruction*: critical aortic stenosis, critical coarctation of the aorta and hypoplastic left heart syndrome
  • Right-sided obstruction: pulmonary atresia, critical pulmonary stenosis, tricuspid atresia
  • Inadequate mixing: transposition of the great arteries (D-transposition), tricuspid atresia with restrictive ASD, pulmonary atresia with restrictive ASD, HLHS with restrictive ASD
  • Arrhythmias: SVT (incl. WPW), complete heart block
  • Pericardial effusion
  • Pleural effusion
  • Chylothorax
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68
Q

What is hypoplastic left heart?

A
  • Mitral valve is atretic, LV never development, aorta small.
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69
Q

Which heart lesions are PDA dependent for systemic output?

A
  • Left-sided: critical aortic stenosis, critical coarctation of aorta and hypoplastic left-heart syndrome
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70
Q

Signs and symptoms of left-sided obstruction in pediatric patients?

A
  • CHF, shock, oliguria and renal failure, metabolic acidosis

- These occurs after ductus closes

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71
Q

Tx of left-sided heart obstruction in peds patients?

A
  • Maintain PDA via PGE1
  • Inotropic support (dopamine, epinephrine)
  • Correction of metabolic acidosis (IV fluids, Na bicarb)
  • Definitive: interventional (valvuloplasty, angioplasty, surgery, palliation)
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72
Q

Is supplemental o2 helpful in treating pediatric left-sided obstruction case?

A
  • No. o2 acts as pulmonary vasodilator. Since these babies are dependent on elevated pulmonary vascular resistance to drive blood across PDA from right to left. O2 also constricts PDA.
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73
Q

Signs/symptoms of right-sided heart failure in pediatric patients

A
  • Sx surrounding RV obstruction/right-sided heart failure: respiratory issues, hepatosplenomegaly, extremity edema (rare)
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74
Q

Tx of right-sided heart obstruction in pediatric patients

A
  • PGE1 to keep ductus open
  • Possible inotropic support
  • Correct metabolic acidosis
  • O2 if lung dysfunction
  • NO: if ductus open and no other reason for pulmonary blood flow restriction
  • Definitive: valvuloplasty, BT shunt (aorto-pulmonary shunt)
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75
Q

Does o2 have a role in managing right-sided heart obstruction in pediatric patients?

A
  • Low supplement o2 is potentially helpful if lung dysfunction
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76
Q

Symptoms of arrhythmias in children

A
  • Related to CHF, decreased cerebral perfusion and decreased coronary perfusion
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77
Q

Most common arrhythmia in children

A
  • SVT (PAT)
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78
Q

Clinical presentation of SVT in children

A
  • Infants with HR: 220-320. Children with HR: 150-250.

- Usually tolerated for hours if no underlying heart pathology. If underlying disease, then poorly tolerated.

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79
Q

Tx of SVT in pediatric patients

A
  • Increase vagal tone to slow HR via: Valsalva, Gag or application of crushed ice to forehead
  • Adenosine
  • Cardioversion
  • Long-term: beta-blocker, digoxin, CCB, amiodarone, ablation
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80
Q

Causes of complete heart block in children

A
  1. Congenital: secondary to structural heart defects, maternal collagen vascular dz (Lupus)
  2. Acquired: secondary to post-surgical (iatrogenic), inflammatory or infectious diseases
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81
Q

Clinical presentation of complete heart block in children

A
  • Brady
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82
Q

Tx for complete heart block in children

A
  • External pacing

- Implantable pacemaker

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83
Q

What is cardiac tamponade?

A
  • With pericardial effusion, the fibrous pericardium cannot acutely distend. This leads to elevated filling pressure, progressively limited ventricular filling, reduced SV and reduced CO.
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84
Q

Types of cardiac tamponade and causes

A
  1. Non-bloody pericardial effusion: post-pericardiotomy syndrome, cardiac/non-cardiac malignancies, rheumatologic conditions, infections (usually viral)
  2. Hemopericardium: during cardiac cath, early in post-op course, during CV line placement, blunt or penetrating chest trauma
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85
Q

Clinical features of cardiac tamponade

A
  1. Hemodynamic instability
  2. Muffled heart sounds
  3. Possible pericardial friction rub
  4. Large cardiac silhouette on CXR
  5. Echo
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86
Q

Tx for cardiac tamponade

A
  • Pericardiocentesis
  • Correct underlying problem
  • Anti-inflammatory meds
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87
Q

What is chylothorax?

A
  • Lymphatic fluid within the pleural space from the thoracic duct.
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88
Q

Tx of chylothorax

A
  • Pleurocentesis
  • NPO (place on TPN)
  • IV diuretics
  • Octreotide (to tighten up splanchnic bed)
  • Thoracic duct ligation of pleurodesis
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89
Q

What clinical factors contribute to BT shunt obstruction?

A
  • Non-compliance with anti-coagulation
  • Dehydration
  • Poor ventricular function
  • Elevated pulmonary vascular resistance: pneumonia, pleural effusion, pneumothorax
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90
Q

Tx of BT shunt obstruction

A
  • If shunt dependent and patient is hyper-cyanotic with no audible murmur = EMERGENCY! Send to OR or cath lab.
  • Medical options limited: intubate, ventilate, oxygenate, CXR, IV fluid bolus, echo
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91
Q

Presentation of BT shunt obstruction

A
  • Poor feeding, progressive dyspnea, purple
  • PE: cyanotic, clear lungs, no murmur (supposed to hear continuous murmur), incision suggestive of BT shunt surgery (right lateral thoractotomy), good pulses
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92
Q

Describe how BT shunt works

A
  • PVR
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93
Q

What are the complications post-MI?

A
  • Arrhythmia, heart failure, embolic, pericarditis, mechanical features (papillary muscle rupture, VSD, free wall rupture, LV aneurysm formation), cardiogenic shock
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94
Q

Types of arrhythmias associated with acute phase of NSTEMI or STEMI? Which tend to be associated with STEMIs only?

A
  • Ventricular: VBPs, accelerated idioventricular rhythm, vtach, vfib
  • STEMIs only: bradyarrhythmias such as sinus bradycardia and AV block
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95
Q

Tx of PVCs post-MI

A
  • No specific tx, but tx underlying reason for them
  • Correct electrolytes: keep K > 4, Mg > 2
  • Beta-blockers (which you would be using during/after MI anyway right?)
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96
Q

What are the features of accelerated idioventricular rhythm? Why does this occur post MI? When? Tx?

A
  • Called “slow v-tach”
  • V rhythm with rate of 60-100 bpm
  • Why? Enhanced automaticity of Purkinje, which drive a faster rate than sinus node.
  • When? Usually observed shortly after successful perfusion following MI during first 2 days.
  • Tx? Tend to be well tolerated and sometimes a good sign that perfusion has been achieved. Like PVCS: keep electrolytes up and you can use beta-blockers.
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97
Q

Compare and contrast the vtach caused by mycocardial ischemia vs that from scar? Tx?

A
  • Ischemia: causes a polymorphic vtach (QTc may or may not be prolonged, may not have the long-short PVC sequence of torsades)
  • Scar: causes a monomorphic vtach
  • Tx: if hemodynamically unstable, cardiovert. If sustained, use amiodarone (or lidocaine if in acute MI phase).
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98
Q

Which ventricular arrhythmia is associated with an increased risk of sudden cardiac following an MI? In what time frame? Tx?

A
  • **
  • Late VT/VF, meaning > 48 HOURS after MI.
  • Tx: immediate defibrillation, amiodarone, beta-blocker, correct electrolytes and r/o recurrent ischemia/re-infarct.
99
Q

Risks associated with sudden cardiac death post-MI? What are the prophylactic measures that can be taken?

A
  • **
  • Late VT/VF, meaning > 48 HOURS after MI
  • EF (ejection fraction)
100
Q

What is the strongest predictor of complications following MI?

A
  • **

- EF = strongest predictor. Also late VT/VF.

101
Q

Causes of sinus bradycardia in / after MI? Sinus node is supplied by what vessels?

A
  • Causes: vessel ischemia, infarction (see below); high PSNS tone usually in IWMI or from Bezold-Jarisch reflex (sudden bradycardia associated with hypotension, decreased inotropy and coronary vasodilation that can occur after MI)
  • Vessels: 55% of time from RCA, 35% from LCX and 10% dually.
102
Q

Types and causes of MIs resulting in AV block. Which requires pacemaker?

A
  1. Inferior MI: at level of AV, high PSNS tone, local accumulation of K/adenosine, AV node ischemia. Usually transient w/o need for pacemaker.
  2. Anterior MI: rarely, below level of AV, usually with extensive infarct of bundle branch, requires pacemaker.
103
Q

Describe types of heart failure during the acute vs post acute phase of MI? Tx?

A

**Know Killip classes

  1. Acute MI phase: 2/2 diastolic function or combination of systolic and diastolic dysfunction. Varies from mild pulmonary congestion (crackles in 50 % lungs = Killip class 3). Why diastolic dysfunction? ATP required to remove calcium, so in ischemia LV becomes stiff and pressure becomes high and is transmitted to lungs leading to pulmonary edema and respiratory failure.
  2. Post acute phase: 2/2 systolic function. Heart not able to pump as strongly as it did before, so EF reduction.
    - Tx for acute phase: vasodilators (esp. NTG) unless hypotensive; if volume overloaded, then diuresis (be careful as many are not and this could make them hypotensive); watch morphine (can respiratory depress them and cause HoTN with high doses); BiPAP (reduce preload and afterload)
    - Tx for post-acute phase: diuretic, ACEi, aldosterone antagonist, wait until compensated to use beta-blocker
104
Q

Cardioembolism is most commonly associated with what type of MI? What are the risk factors? Tx?

A
  • Commonly with AWMI
  • Risks: reduced EF, apical wall motion abnormality, LV aneurysm development
  • Tx: anticoagulation (warfarin)
105
Q

Compare and contrast early vs late presentation of pericarditis following MI? Include tx.

A

**

  1. Early: within 1 week post MI
    - From transmural infarct from local inflammation of pericardium overlying the infarcted area
    - Sx: pleuritic type chest pain (sharp, often localized and positional – worse supine)
    - Friction rub heard, EKG changes
    - Tx: ASA 650 mg q 4-6 hrs. Avoid NSAIDs and steroids – these impair healing and worsen kidney function (esp. NSAIDS). Can use colchicine as adjunct.
  2. Late: 1-8 weeks post MI. Aka Dressler’s syndrome.
    - Autoimmune mechanism where auto abs attack heart.
    - Sx: pericarditis sx + systemic symptoms = malaise, arthralgias, fever, pleural/pericardial effusions, high ESR, CRP
    - Tx: ASA and colchicine. If more than 6 weeks out, can use NSAIDS as MI is healed.
106
Q

Differentiate papillary muscle rupture (acute mitral regurg), VSD, and free wall rupture following MI in terms of: type of MI, risk factors, presentation, PE, dx and tx

A

**Know especially difference b/w VSD and papillary muscle rupture (CAPS)

  1. Papillary muscle rupture (acute mitral regurg)
    - Type of MI: PREDOMINANTLY IWMI leading to primarily posteromedial papillary muscle rupture (mnemonic: PM = night = lights out). Why? Single blood supply by posterior descending artery.
    - Risk factors: older age, females, HTN, first MI, delayed or absent reperfusion
    - Presentation: heart failure, may be of sudden onset with rupture, may be associated with HEMODYNAMIC COLLAPSE, CANNOT TYPICALLY LIE FLAT (LOOSE RULE)
    - PE: NEW HOLOSYTOLIC SYSTOLIC MURMUR* (may or MAY NOT BE LOUD – intensity ≠ severity) that may radiate to LSB; RARELY EXHIBIT THRILL. *murmur can be absent.
    - Dx: echo, LARGE V-WAVES ON WEDGE TRACING
    - Tx: mechanical ventilation, IABP (esp in HoTN), afterload reduction (nitroprusside), surgery is tx of choice (without would result in 90% mortality)
  2. VSD:
    - Types of MI: AWMI, IWMI (EQUALLY)
    - Risk factors: older age, females, HTN, first MI, delayed or absent reperfusion
    - Presentation: chest pain, dyspnea, HoTN, biventricular failure (HEMODYNAMIC COLLAPSE), CAN TYPICALLY LIE FLAT (LOOSE RULE)
    - PE: NEW HARSH HOLOSYSTOLIC MURMUR along LLSB (LOUD) radiating to base, apex and R parasternum; THRILL IN ½ PATIENTS; S3 (volume overload), loud P2 (d/t RV volume) and tricuspid regurg (see P2)
    - Dx: echo, LARGE V-WAVES ON WEDGE TRACING, o2 step-up bw RA and RV
    - Tx: hemodynamic support (IABP, mechanical support, vasodilators), surgical closure (tx of choice), PC closure
  3. Free wall
    - Types of MI: not specified, more common with fibrinolysis following MI vs PCI
    - Risk factors: older age, females, HTN, first MI, delayed or absent reperfusion
    - Presentation:
    a. Acute: sudden hemodynamic collapse, cardiac tamponade, PEA arrest; preceding: transient bradycardia, often restless, nauseating and anxious
    b. Subacute (rupture contained): pericardial pain, hypotension
    - PE: hypotension, pulsus paradoxus, muffled heart sounds, increased JVP
    - Dx: echo
    - Tx: surgical repair (only tx), temporizing measure = pericardiocentesis
107
Q

In a papillary muscle rupture post MI, what are the: types of MI these occur in, risk factors, presentation, PE findings, how is it diagnosed, tx?

A
  1. Papillary muscle rupture (acute mitral regurg)
    - Type of MI: PREDOMINANTLY IWMI leading to primarily posteromedial papillary muscle rupture (mnemonic: PM = night = lights out). Why? Single blood supply by posterior descending artery.
    - Risk factors: older age, females, HTN, first MI, delayed or absent reperfusion
    - Presentation: heart failure, may be of sudden onset with rupture, may be associated with HEMODYNAMIC COLLAPSE, CANNOT TYPICALLY LIE FLAT (LOOSE RULE)
    - PE: NEW HOLOSYTOLIC SYSTOLIC MURMUR* (may or MAY NOT BE LOUD – intensity ≠ severity) that may radiate to LSB; RARELY EXHIBIT THRILL. *murmur can be absent.
    - Dx: echo, LARGE V-WAVES ON WEDGE TRACING
    - Tx: mechanical ventilation, IABP (esp in HoTN), afterload reduction (nitroprusside), surgery is tx of choice (without would result in 90% mortality)
108
Q

In a VSD post MI, what are the: types of MI these occur in, risk factors, presentation, PE findings, how is it diagnosed, tx?

A
  1. VSD:
    - Types of MI: AWMI, IWMI (EQUALLY)
    - Risk factors: older age, females, HTN, first MI, delayed or absent reperfusion
    - Presentation: chest pain, dyspnea, HoTN, biventricular failure (HEMODYNAMIC COLLAPSE), CAN TYPICALLY LIE FLAT (LOOSE RULE)
    - PE: NEW HARSH HOLOSYSTOLIC MURMUR along LLSB (LOUD) radiating to base, apex and R parasternum; THRILL IN ½ PATIENTS; S3 (volume overload), loud P2 (d/t RV volume) and tricuspid regurg (see P2)
    - Dx: echo, LARGE V-WAVES ON WEDGE TRACING, o2 step-up bw RA and RV
    - Tx: hemodynamic support (IABP, mechanical support, vasodilators), surgical closure (tx of choice), PC closure
109
Q

In a free wall rupture post MI, what are the: types of MI these occur in, risk factors, presentation, PE findings, how is it diagnosed, tx?

A
  • Types of MI: not specified, more common with fibrinolysis following MI vs PCI
  • Risk factors: older age, females, HTN, first MI, delayed or absent reperfusion
  • Presentation:
    c. Acute: sudden hemodynamic collapse, cardiac tamponade, PEA arrest; preceding: transient bradycardia, often restless, nauseating and anxious
    d. Subacute (rupture contained): pericardial pain, hypotension
  • PE: hypotension, pulsus paradoxus, muffled heart sounds, increased JVP
  • Dx: echo
  • Tx: surgical repair (only tx), temporizing measure = pericardiocentesis
110
Q

Compare and contrast true vs pseudo LV aneurysm

A
  • True: all three layers of heart present, wide necked bulge, no damage to wall, will often times be clot present in area, don’t tend to rupture and doesn’t require surgery
  • Pseudo: tear of endocardium and myocardium with pericardium intact and containing aneurysm, narrow neck (neck narrower than width of sac), high risk of rupture and requires surgery
111
Q

What is cardiogenic shock? What are the criteria? What is pathophysiology? How is this diagnosed? Tx?

A
  • Shock (state of inadequate o2/energy delivery to maintain metabolic needs) secondary to impaired cardiac function w/reduced CO.
  • Criteria: cardiac index 18 mmHg
  • Pathophys: Systolic dysfunction = decrease CO & HoTN = decrease systemic and coronary perfusion = compensatory vasoconstriction and decreased coronary perfusion = ischemia. Diastolic dysfunction = increased LVEDP = pulmonary congestion = hypoxemia = ischemia.
  • Dx: echo, PA cath
  • Tx: revascularization of heart, vasodilators (NTG, nitroprusside), inotropes (dobutamine, milirinone), vasopressors (dopamine, NE), mechanical support (IABP, pVAD, ECMO). Pharmacologic agents depend on systolic BP.
112
Q

Define shock

A
  • State wherein the CV system cannot maintain adequate cellular perfusion resulting in cell dysfunction then tissue dysfunction which eventually is irreversible and leads to death.
113
Q

Types of shock? What can each result from?

A
  • Cardiogenic (myocardium lost or severely depression = reduced CO / LVEF): AMI, dilated cardiomyopathy, valvular etiology (acute MR, endocarditis), arrhythmia
  • Hypovolemic (reduced circulating BV = reduced CO): hemorrhage (trauma, GI), severe burns, vomiting, diarrhea
  • Distributive (profound peripheral vasodilation w/normal or high CO * tank is too large for heart to fill up): most common = sepsis; others: drug OD, anaphylaxis, neurogenic etc.
114
Q

What is the general clinical presentation of shock?

A
  • Very low systolic BP (
115
Q

What is the most important indicator of overall prognosis in cardiogenic shock?

A
  • LV function. This is true in any heart disease.
116
Q

What are the multiorgan consequences of shock?

A
  • Acidemia (depresses cardiac function)
  • Myocardial dysfunction
  • ARDS
  • ATN: acute tubular necrosis
  • Hepatic injury (shock liver)
  • Intestinal ischemia/injury
  • CNS: Post-anoxic encephalopathy, death
117
Q

What are the general tx strategies in shock?

A
  1. Most important: ICU (cardiac monitors, two IVs, fluids, meds), o2 w/ventilatory support, ABGs
  2. Meds = vasopressors, inotropes and abx as needed
118
Q

43 yo female underwent removal of left great toe for S. Aureus osteomyelitis. In PACU she developed: BP 60/0, HR 140, RR 28. What steps must be taken to stabilize this patient?

A
  • Fluid resuscitate (IV wide open x 2)
  • Supplement o2 prn
  • Obtain blood cultures and sensitivities (blood / urine)
  • Call specialist
  • Labs: ABG, electrolytes, BUN/Cr, Hg/Hct
  • Monitor rhythm
  • 12-lead ECG to see if cardiogenic
  • Determine shock syndrome and choose further mgmt. based of type
119
Q

67 yo man presents to ED with severe CP. Began two hours ago. Can only answer questions with groan. Wife gives history: DM x 21 years, a previous smoker (none in > 10 years), overweight. Nothing similar in past. Vitals: BP 64/0, HR 48, RR 28. What steps must be taken to stabilize the patient? If it is determined to be cardiogenic shock, what is the treatment?

A
  • ICU: fluid resuscitate (IV wide open x 2)
  • Supplement o2 prn
  • Obtain blood cultures and sensitivities (blood/urine)
  • Monitor cardiac rhythm
  • 12-lead ECG to determine if cardiogenic
  • Labs: trop and CK-MB, ABG, electrolytes, Hg/Hct
  • If cardiogenic:
  • Balance fluids, cath lab or thrombolysis, beta-blocker, don’t treat bradycardia yet as it demands too much o2, dopamine (pressor)
120
Q

Define HTN

A
  • Confusing and depends on what governing body/scientific group one relies on
  • Per JNC7: >= 140 / >= 90. Normal = 60 years old:
121
Q

Most common comorbidities for HTN

A
  • IHD, HF, Afib, CVA

- For every 20 mmHg increase in SBP, risk for MI, HF, stroke and kidney dz doubles

122
Q

What is the lifetime risk of developing HTN in 55 yo normotensive individuals?

A
  • 90%

- Why? Vessel wall does not change with each ventricular ejection. Lots of collage in vessel wall vs elastin.

123
Q

Pathogenesis behind obesity-related HTN

A
  1. Visceral obesity leads to
    a. Increase in leptin and POMC = SNS activation = RAAS activation = increase BP
    b. Activation of RAAS = increase BP
    c. Direct renal compression = increase Na reabsorption = increase BP
    d. Development of metabolic disorders such as insulin resistance, glucose intolerance, dyslipidemia, inflammation and lipotoxicity = increase BP
124
Q

Describe pathogenesis of end-organ damage with HTN

A
  1. Vasculopathy: endothelial dysfunction, remodelling, generalized atherosclerosis and stenosis, aortic aneurysm
  2. Heart disease: LVH, afib, coronary microangiopathy, CHD, MI, HF
  3. Cerebrovascular damage: acute HTNsive encephalopathy, CVA, IC hemorrhage, lacunar infarction (deep penetrating artery CVA), vascular dementia, retinopathy
  4. Nephropathy: albuminuria, proteinuria, chronic renal insufficiency, renal failure
    - Pathogenesis underlying these processes = hemodynamic load, SNS, catecholamines, ATII, aldosterone, inflammation etc.
125
Q

Compare and contrast secondary with primary (essential) HTN in terms of prevalence and pathogenic mechanisms

A
  1. Primary (essential) HTN: interplay between environment, behavior, physiology and genes. Factors such as stress, high salt intake, inactivity and obesity, drug and etoh abuse are important.
    a. Central factors: augmented SNS discharge, aberrant responses to peripheral signals (such as blunted baroreflex, enhanced chemoreflex)
    b. Vascular dysfunction: exaggerated response to vasoconstrictors, depressed response to vasodilator, remodelling
    c. Renal dysfunction: Na and water handling defects
  2. Secondary HTN: CKD, renovascular dz (fibromuscular dysplasia, arteriosclerosis), other (pheo, coarctation of aorta, primary aldosteronism, Cushing, OSA). When initial onslaught is treated, you typically get rid of HTN.
126
Q

Review the mechanisms of BP regulation

A
  1. Neural mechanism:
    - Low BP = increase SNS = increase renin release (activation of RAAS, see below) & increase TPR (vasoconstriction)
  2. Volume control
    - Low BP = decrease in renal blood pressure = increase renin release = activation of RAAS = increase TPR + increase aldosterone = increase Na and h2o = increase ECF volume
127
Q

Pathogenesis of obstructive sleep apnea

A
  • Nocturnal hypoxia/hypercapnia = chemoreceptor stimulation = activation of cardiopulmonary excitatory ctrs = increase SNS / decrease PSNS outflow = increase ventilation and increase HR = decrease CO2 and increase o2
128
Q

How is secondary HTN treated

A
  1. Renovascular HTN
  2. Renal parenchymal dz: replace kidney
  3. Coarctation of the aorta: surgery
  4. Cushing’s and pheochromocytoma: excise tumor
  5. OSA: open airway
129
Q

Tx strategies for HTN

A
  • Lifestyle modifications: weight reduction (greatest impact – 5-20 mmHg/10 kg ), DASH eating plan, dietary sodium restriction, physical activity, moderate etoh consumption
  • Pharmacologic agents: aldosterone antagonists, angiotensin receptor blockers, beta blockers, renin inhibitors, ACEi. See Hoff’s lecture.
  • Device-based therapy: baroceptor/carotid sinus implant stimulator (= activation of cardioinhibitory centers = decrease SNS and increase PSNS outflow = vasodilation and decrease HR = decrease CO and TPR = decrease BP)
130
Q

What is the most common reason for visits for a physician and for the use of rx drugs in the US?

A
  • SAH (systemic arterial HTN)
131
Q

Is the risk of CHD (coronary heart disease) higher in women or men with HTN?

A
  • Women (3 x), men (2x)
132
Q

Which populations is HTN prevalent in?

A
  • Black men, black women and white men

- Also elderly

133
Q

Define borderline HTN

A
  • Borderline: BP only occasionally exceeds normal
134
Q

Define HTNsive encephalopathy

A
  • This is a HTNsive emergency (life-threatening) w/SSX of cerebral edema d/t severe/sudden rise in BP. Includes: confusion, stupor, somnolence and coma.
135
Q

Define HTNsive emergency

A
  • DBP generally >= 120 mmHg
  • Life-threatening presenting with focal or generalized sx of acute, ongoing target-organ damage: CNS/retina, cardiac etc.
136
Q

Define malignant HTN

A
  • Former term, now known as hypertensive grades III and IV and severe BP elevation
137
Q

How is systemic BP measured?

A
  • Indirect: BP cuff

- Direct: via intra-arterial catheter

138
Q

Pitfalls in BP determination?

A
  • Narrow or too-loose cuff with overestimate BP
  • Several readings necessary
  • Caffeine, smoking, adrenergic stimulants (eg. Nasal sprays)
139
Q

What target organs are affected by HTN?

A
  • Kidney, CNS and heart (most common form, IHD)
140
Q

Grades of HTNsive retinopathy

A

**

  • Keith-Wagener-Barker (KWP) classification system
  • Grade 1: arteriolar narrowing (reddish appearance like copper wires, shinier than other arterioles)
  • Grade 2: AV nicking
  • Grade 3: hemorrhages and exudates (scars)
  • Grade 4: papilledema (swelling of nerve head)
  • Note: features are additive. Eg. Grade 2 will have AV nicking and arteriolar narrowing.
141
Q

What are the CNS consequences of HTN?

A
  • Decreasing cognitive function
  • TIA
  • CVA (hemorrhagic or thromboembolic)
142
Q

What is the leading cause of end-stage renal disease in the US?

A
  • SAH
143
Q

Renal consequences of HTN?

A
  • Albuminuria
  • Nephrosclerosis = loss of renal concentrating ability = renal failure and uremia (high levels of urea that can lead to toxemia)
144
Q

What are the heart consequences of HTN?

A
  • Early: increase LV mass = los of diastolic function d/t poor filling
  • Chronic: LVH = eventual LV dilation and failure with eventual death
145
Q

Presenting sx of HTN

A
  • Most often asymptomatic
  • Related to CNS: HA, dizzy, blurred vision, somnolence, confusion, stupor, coma, CVA, TIA
  • Related to CV: CP, DOE, palpitations, impotence, epistaxis
  • Related to renal: hematuria
146
Q

Risk factors for HTN

A
  • Cigarette smoking, obesity, dyslipidemia, DM, age (> 55 men, > 65 women), sedentary lifestyle, family hx of CV dz (men
147
Q

What organ system must never be omitted when performing PE for HTN?

A
  • Funduscopic exam
148
Q

What are the non-drug therapies for managing HTN?

A
  1. DASH: veg, fruit, whole grains, low-fat dairy, poultry, fish, legumes, non-tropical veg oils, nuts, low refined sugar and red meats
  2. Na restriction
149
Q

What levels of BP should you initiate drug management of HTN based on age, race/ethnicity and associated diagnoses?

A
  • Per JNC VIII: 140/90 in =60 age group, goal 150/90

- SPRINT: SBP

150
Q

Drug classes recommended by JNC VIII in treated SAH, particularly drugs of choice and alternative drugs that may be added or substituted.

A
  • Drugs of choice = thiazide diuretics
  • Alternative: CCBs, ACEis, ARBs
  • Beta-blockers not included in JNC VIII recommendations owing to RCT evidence showing no superiority to other drug classes or showing detriment to ARB (single RCT though). SPRINT group used beta-blockers.
151
Q

Initial HTN meds for non-black population including DM

A
  • Thiazide diuretic or CCB/ACEi/ARB
152
Q

Initial HTN meds for black population including DM

A
  • Thiazide diuretic or CCB
153
Q

Initial HTN meds for > 18 yo with CKD (regardless of DM)

A
  • ACEi or ARB to improve kidney outcomes
154
Q

What is peripheral arterial disease?

A
  • Clinical disorder in which there is stenosis or occlusion in the aorta or arteries of the limbs.
155
Q

Which groups is PAD (peripheral arterial disease) highest in?

A
  • > Age 70 group

- M > F

156
Q

Etiologies of PAD

A
  • Atherosclerosis, thrombosis, embolism, vasculitis, fibromuscular dysplasia, cystic adventitial disease, trauma
157
Q

What are the risk factors for atherosclerosis? What are the biggest risk factors?

A
  • Tobacco and DM = biggest

- HTN, advanced age, dyslipidemia

158
Q

Symptoms of PAD

A
  • Most commonly = intermittent claudication = cramping in calf, thigh, buttock exacerbated by walking, palliated with rest.
  • Severe dz: hair loss, thickened nails, smooth/shiny skin, reduced skin temp, pallor or cyanosis. Ulcers or gangrene may develop. Pain while at rest.
  • In over ½ patients, felt to be asymptomatic
159
Q

In which vessels is PAD more common?

A
  • Femoral and popliteal (80-90%)
160
Q

What simple test with high degree of sensitivity and specificity can be used to determine PAD? Results?

A
  • ABI: Ankle/Brachial index
  • Normal: ankle and brachial BPs same/similar if not slightly higher in ankles. If brachial > ankle, that is indication of stenosis.
  • > 1 = normal

-

161
Q

In patient’s with PAD, what are most deaths from?

A
  • ACS. Worse prognosis in DM and smokers.
162
Q

What are tx options for PAD?

A
  • Tx HLP, HTN, DM

- Exercise, foot care, smoking cessation!!!, angioplasty, surgery

163
Q

Which PAD patients require referral to IR or vascular surgeon?

A
  • Pain at rest (severe), non-healing lower extremity ulcers w/low ABIs, severe/debilitating claudication
164
Q

What are the 2 principal causes of acute arterial occlusion?

A
  • Embolism (travelling clot)

- Thrombus in situ (stationary clot)

165
Q

Most common sources of emboli?

A
  • Heart (afib, ACS, heart valves, atrial myxoma/growths, endocarditis), aorta (aneurysms) and large arteries (bifurcations)
166
Q

Reasons for thrombi in situ formation

A
  • At atherosclerotic lesions (most frequently)
  • In bypass grafts
  • Polycythemia vera
  • Hypercoagulable states
167
Q

Fibromuscular dysplasia.
a. What is it?

b. Typical presentation
c. Tx

A

**

a. Hyperplastic conditional affecting medium-sized and small renal arteries.
b. Predominantly in females, often diagnosed during workup for secondary HTN, usually involves renal arteries (other times: carotid, iliac and subclavian)
c. PTA (percutaneous transluminal angioplasty) and surgical reconstruction

168
Q 
Thromboangiitis obliterans (aka Buerger’s dz)
a.	What is it?

b. Typical presentation
c. Tx

A
  • *
    a. Inflammatory dz of the small and medium sized arteries and veins of extremities

b. Young person, often man, directly related to smoking (chain smokers), presents with Raynaud’s phenomenon, ulcers and pain typically.
c. Tx = immediate termination of smoking critical!

169
Q

Atheroembolism.
a. What is it?

b. Typical presentation?
c. Tx

A

a. Subset of acute arterial occlusion. These are multiple small deposits of fibrin, platelets and cholesterol debris embolizing downstream of occlusion.
b. Patient was in cardiac cath lab and have thrombus “vacuumed” up. Was fine after procedure, but on rounds see areas is ischemia throughout the body with acute pain/tenderness at sites.
c. No good tx options

170
Q

What is Raynaud’s?

A
  • Attacks of pallor and cyanosis of digits in response to cold or emotion. Disease when primary, but syndrome when secondary to another dz / cause.
  • Onset 20-40s, F>M
171
Q

What is Livedo Reticularis? Primary vs Secondary?

A
  • Localized areas on extremities develop a reddish/blue net-like (rete) appearance (mottling).
  • Primary: benign + / - ulcerations, F > M, onset 3rd decade
  • Secondary: atheroembolism, SLE, cryoglobulinemia etc.
172
Q

What puts patients at risk for venous thrombosis (ie. risk factors for DVT)?

A

**

  • Virchow’s Triad
  • Stasis, vascular damage and hypercoagulability
  • Other risks: pregnancy (1 month post-partum), ACS, CHF, E, hypercoagulability, neoplasms, surgery (esp hip, knee and pelvis), obesity
173
Q

What is thromboembolism or thrombophlebitis?

A
  • Thrombi within superficial or deep vein and accompanying inflammatory response
174
Q

Are thrombi more common in venous or arterial side?

A
  • Venous
175
Q

Signs, sx and diagnosis of DVT?

A
  • Sx: pain, swelling, redness of LE, pain worsened w/ activity, fever
  • Signs: edema, increased girth of extremity, erythema, cyanosis, tenderness along vessel, palpable cord, unilateral leg swelling, warmth, Homan’s sign = increased resistance/pain with force plantarflexion (per Hilgerson, virtually never +ve)
  • Dx: d-dimers, dopper US (duplex), ascending contrast venography (Gold Std!), +/- MRI, impedance plethysmography
176
Q 
Acute PE (pulmonary embolus)
a.	Risks

b. Clinical findings

A

a. Surgery/injury, sedentary/immobility, BCPs, tobacco, cancer, HTN, infections, prior history, prolonged anesthesia, burns, heme problems, hypercoagulable state, E
b. Tachypnea, course or diminished lung sounds, chest pain/pleurisy, hemoptysis

177
Q

What is the most common finding of the CXR of a patient with a known PE?

A
  • Normal
178
Q

If there are findings seen on CXR for PE, they are?

A
  • Hampton’s hump (wedge sign)? He didn’t explain what this what, so I don’t think high yield.
179
Q

How are PEs diagnosed? Tx?

A
  • Pulmonary angiography!!, H&P, EKG, d-dimer, VQ, CXR, ABG, CT
  • Tx: heparin, coumadin, thrombolytics (+/-), filter, surgical embolectomy
180
Q

What is chronic venous insufficiency? Sx? PE findings? Tx?

A
  • May result from DVT and / or valvular incompetence where blood pools in venous system
  • Sx: dull ache, worse with prolonged standing, resolving with leg elevation
  • PE: increased leg circumference, edema, superficial varicose veins, erythema, dermatitis, hyperpigmentation, also cellulitis
  • Tx: rare surgical intervention
181
Q

Common causes of mitral regurgitation

A
  • Consider the anatomical features of the mitral valve. Overall, causes = Rheumatic dz, infective endocarditis, collagen-vascular disease, cardiomyopathy, IHD, mitral valve prolapse
    1. Leaflets
  • Rheumatic heart disease = shortening, thickening, deformity of MV cusps
  • Infective endocarditis = perforation, retraction of cusp or growth of vegetation on cusp
    2. Annulus
  • Dilated cardiomyopathy diseases
  • Calcification from rheumatic heart disease, or idiopathic
    3. Chordae tendinae
  • Various pathologies can lead to chordae tendinae lengthen and rupture = MVP, infective endocarditis, trauma
    4. Papillary muscles
  • Ischemia = rupture
182
Q

Pathophysiology of mitral regurgitation in terms of flow, pressure, hemodynamics

A
  • Afterload is lowered as LV can eject blood two ways
  • LV has to do less work, excess volume maintained in LA and pulmonary circulation
  • Blood going wrong way and must come back to LV and cause LV overload eventually leading to diastolic overload and failure (takes up to 20 years before decompensation)
183
Q

Clinical history, PE findings and prognosis of mitral regurgitation

A
  • Hx: primary sx = dyspnea (exertional at first, later PND or orthopnea), other = afib (palpitations), hemoptysis, systemic emboli, angina pectoris, RV failure
  • PE: carotid artery pulses (sharp in severe) d/t higher SV, apical impulse (displaced left and down d/t LV dilation), occasional late-systolic LA thrust palpable left parasternal. S2 widely split because of early A2 closure. S3 common d/t LV volume excess. If RV, then tricuspid murmur. S4 if pulmonary HTN. Murmur: holosystolic loudest at apex (heard at back).
  • Prognosis: takes up to 20 years before decompensation. See pathophys.
184
Q

Treatment of mitral regurgitation

A
  1. Meds
    - Tx LV failure through afterload reduction, which decreases regurg volume. Drug of choice = ACEi. In acute, use nitroprusside. If HoTN, use dobutamine in conjunction.
    - Digitalis may improve inotropism.
  2. Surgery
    - Valve repair, valve replacement (don’t less often)
185
Q

Common causes of mitral stenosis

A
  • 99% of cases from rheumatic fever: 2/3rd female, 25% have MS only, 40% have mixed MS/MR
186
Q

Pathophysiology of mitral stenosis in terms of flow, pressure, hemodynamics

A
  • Forms? Most common = commissural
  • Obstruction to LV inflow = creation of pressure gradient across valve
  • Normal MV opening = 4-6 cm2, mild MS = 2 cm2, critical = 1 cm2 or less
187
Q

What conditions mimic mitral stenosis?

A
  • Left atrial myxoma
  • Left atrial ball-valve thrombus
  • Infective endocarditis with large vegetations
  • Cor triatriatum (congenital)
188
Q

Clinical history, PE findings and prognosis of mitral stenosis

A
  • Hx of rheumatic fever in distant past
  • Sx: embolization may be first symptom of MS event when valvular stenosis is mild (Why? Virchow’s triad). 50% of cases = cerebral infarct (CVA). Other = endocarditis, chest pain, hemoptysis.
  • PE: mitral facies (purple-pink cheeks in severe MS owing to low output and vasoconstriction), apical impulse inconspicuous to absent, occasionally thrill in LLD. Auscultation: S1 commonly loud (pathognomonic!), opening snap heard best at apex (d/t sudden deceleration and tensing of cusps), S4 with pulmonary HTN. Murmur: diastolic murmur, Graham-Steell murmur (dilated pulmonary artery d/t pulmonary HTN severe), tricuspid murmur if RV dilated. Echo: Hockey-stick sign.
  • *Temperate climates there is up to 20 year latency after RF before symptomatic MS. Progresses more rapidly in tropics, subtropics, Alaskan Inuit and Polynesias. India – critical MS often found in children.
189
Q

Treatment of mitral stenosis

A
  1. Meds: prophylaxis against infective endocarditis and beta-hemolytic strep. Anticoagulate if afib. Also cardiovert afib to NSR. If not possible, slow ventricular rate to improve CO w/BB, CCBs, digitalis.
  2. Surgery: valve surgery
  3. Other: avoid strenuous activities with severe MS, women shouldn’t become pregnant, maintain sinus rhythm (get out of afib), reduce salt/water
190
Q

In what populations is afib most prevalent?

A
  • 65-85 yo group

- M>F

191
Q

What is the most common sustained arrhythmia in the USA?

A
  • Afib
192
Q

What are the etiologies of afib? Pathogenesis?

A
  • Etiologies: HTN, rheumatic heart disease, valvular heart disease, MI (CAD), alcoholism, thyroid dz, stroke, anticancer tx
  • Afib often precipitated by a supraventricular premature, foci often near pulmonary veins, multiple wavelets propagate, some more organized than others, result = loss of atrial addition to SV (about 25% loss). Afib begets Afib meaning that refractory period of atrial tissue shortens in this condition.
193
Q

How is atrial fibrillation classified?

A

**

  • Paroxysmal afib: episodes may last 1-7 days (usually 7 days, called “paroxysmal” when recurrent after reversion?
  • Permanent afib: lasts > 1 year, cardioversion either failed or not attempted
  • Lone afib: no overt CV pathology, asymptomatic, comprises 10-15% of all afib. Note, extremely low risk of CVA compared to other classes above.
194
Q

How does atrial fibrillation present (sx and PE) and how it is diagnosed?

A
  • Sx: palpitations, sx of heart failure such as SOB, PND etc.
  • PE: irregularly irregular pulse!, variable intensity S1, heart murmur (MR or MS), pulmonary rales/rhonchi, portahepatic edema, peripheral edema
  • Diagnosis:
    1. EKG: irregular irregularlity, no P waves, fibrillatory (“f”) waves, note: ventricular response > 100 = rapid; response
195
Q

What are the ECG manifestation of atrial fibrillation? Differentiate from atrial flutter.

A
  • Afib: irregularly irregular, no P waves, small f waves at rate of 450-600/min
  • Aflutter: regular, larger F waves at rate of 300/min, commonly with 2:1 AV conduction (meaning if atrium at 300 bpm, then ventricle at 150 bpm)
196
Q

When is anticoagulation indicated for atrial fibrillation?

A
  • This is NB because Afib increases risk of CVA in men and women by 2.4 and 3.0 respectively when compared to general population.
  • Recommended for either rate or rhythm control
  • Provide at least three weeks prior to, during and at least four weeks after cardioversion if Afib duration is > 48 hours.
  • Not indicated if: under 60 yo and with lone Afib
  • Note: rivaroxaban (Xarelto, the factor Xa inhibitor) is non-inferior to warfarin for prevention of CVA or embolism.
197
Q

Who with afib is at increased risk for CVA?

A
  • Age > 65, HTN, rheumatic heart dz, previous CVA/TIA, DM, CHF
198
Q

What therapies are available for atrial fibrillation?

A
  • General tx strategies target either rhythm control (get into NSR) or rate control (maintain acceptable ventricular rate)
  • AFFIRM study came out showed rhythm vs rate control showed no survival advantage between two groups, CVA risk similar
  • Preferred method = rate control unless symptoms persist with this method or if it doesn’t work
  • DC conversion to NSR needed if current MI, evidence of hypoperfusion, severe HF symptoms, pre-excitation is present. When you cardiovert (electrical preferred to drug tx). Requires pre-anticoagulation tx to decrease risk of thromboembolism.
  • Only 30-35% remain in NSR after conversion, so then rate control becomes goal. Goal of 80-110.
  • Must anticoagulate patients regardless of rate or rhythm control strategy unless under 60 or with lone Afib.
  • Other therapies: ablation of AV node + pacer, DDD-R (dual chamber), other = maze procedure, atrial defibrillator.
199
Q

60 yo male evaluated for CP of 4 months duration. Described as sharp, located in left chest with no radiation of associated symptoms. Occurs with walking 1-2 blocks and resolves with rest. Occasionally, the pain improves with continued walking or occurs during the evening hours. He has HTN. FMHx does not include CV dz in any first-degree relatives. His only medication is amlodipine. On PE, he is afebrile, BP 130/80, pulse 72, RR 12. BMI is 28. No carotid bruits are present, and a normal S1 and S2 with no murmurs are heard. Lung fields are clear, and distal pulses are normal. ECG is NSR and non-ischemic without hypertrophy or arrhythmias. Which of the following is the most appropriate diagnostic test to perform next?

a. Adenosine nuclear perfusion stress test
b. Coronary angiography
c. Echo
d. Exercise treadmill stress test

A
  • Answer = D
200
Q

72 yo male undergoes a preoperative eval prior to left hip replacement surgery. He describes intermittent sharp left-sided chest discomfort that spontaneously occurs at rest and after physical activity, occasionally radiating toward right side of chest. These sx have been present for 1-2 years. The sx have been stable and have not been associated with dyspnea, palpitations, or syncope. Medical hx is remarkable for COPD and osteoarthritis. He used to smoke, but quit 10 years ago. Meds are albuterol and ipratropium bromide. On PE, he is afebrile, BP 118/60, pulse 80 and regular. No JVD. Heart sounds distant, with regular S1 and S2; no murmurs are heard. Breath sounds are distant. No pedal edema noted. Baseline ECG shows sinus rhythm with non-specific ST-T wave changes in lateral leads. Which of the following is most appropriate diagnostic test for perform next?

a. Coronary angiography
b. Dobutamine stress echo
c. Exercise echo stress testing
d. Vasodilator myocardial perfusion single-photon emission CT (SPECT)
e. No further testing

A
  • Answer = B given hx of COPD and ipratropium use.
201
Q

How to classify chest pain?

A
  1. Location
  2. Exertion
  3. Relieved with rest or NTG
    - 3 elements = typical CP
    - 2 elements = atypical
    - 1 or less = non-cardiac
202
Q

Purpose of developing a pre-test probability of MI before sending for additional tests/therapies

A
  • Bayes theorem says that a diagnostic test is its best when pretest probability is 50% +. Want to use a test to increase the number of true positives.
  • Eg. 32 yo F with non-anginal chest pain has a 2% chance of having ACS vs 68 yo M with typical chest pain has 94% chance of having ACS.
  • How we can use this information to demonstrate need for doing tests? 35 yo F with non-cardiac chest pain. Would you stress test? Probably not. What are you going to do if the stress test is positive? Will you believe it and cath patient? Probably not. Other hand: 68 yo M with DM, HTN and high cholesterol with typical CP. Should patient be stressed? Probably not. What are you going to do with a negative test? 94% chance of ACS. If negative, you probably wouldn’t believe and send the patient to cath lab anyhow.
203
Q

What is the gold standard for determining ischemic heart disease?

A
  • Treadmill EKG: 1st line choice for those capable of exercise and without EKG abnormalities who have intermediate pre-test probability of low pretest probability of IHD who require testing.
204
Q

Which patient is best suited for treadmill EKG?

A
  • Used in patients with intermediate probability of stable IHD.
  • Can exercise
  • Have interpretable EKG
205
Q

What patient is best suited for exercise echo?

A
  • Pt with SIHD who are able to exercise, but have uninterpretable EKG not d/t LBBB or ventricular pacing.
  • Pt with SIHD who are able to exercise, and have an interpretable EKG
206
Q

What is the target HR for treadmill EKG?

A
  • 85% of (220-age)
207
Q

With treadmill EKGs, does location of ST changes correspond to territory of ischemia? What EKG changes are positive?

A
  • No
  • Positive = horizontal ST depression or downsloping ST depression; STE. Negative or equivocal = J point only depression and upsloping ST depression respectively.
208
Q

Which patients should the chemical heart stress test be done on?

A
  • Immobile patients: unable to exercise
209
Q

What chemical should be used in chemical heart stress test?

A
  • Dobutamine if no arrhythmias

- Vasodilator stress test: adenosine, regadenoson and dipyridamole if no AV nodal block or bronchospastic disease

210
Q

If a patient can exercise and has no baseline EKG changes, what stress test should they get?

A
  • Treadmill EKG
211
Q

If a patient can exercise, but has baseline EKG changes, what stress test should they get?

A
  • Stress echo
212
Q

If a patient cannot exercise, and has no baseline EKG changes, what stress test should they get? What if they have a hx of ventricular arrhythmias? Hx of COPD?

A
  • Pharmacologic stress test
  • If hx of ventricular arrhythmias, use vasodilator (adenosine, regadenoson, dipyridamole)
  • If hx of COPD, use dobutamine.
213
Q

What are the heart stress testing modalities? Describe in terms of which are most sensitive and specific?

A
  • Nuclear (myocardial perfusion imaging) = (looking for) hypoperfusion = high specificity / sensitivity (85 and 90% respectively)
  • Echo = systolic dysfunction (88% and 90% for sensitivity and specificity)
  • Stress test (70-77% sensitivity and specificity)
214
Q

When should exercise EKG stress test be terminated?

A
  • Patients desire, STE > 1mm, drop in SBP > 10 mmHg (paradoxical), moderate-severe angina, syncope, dizziness, signs of poor perfusion, sustained VT
215
Q

Side effects of dobutamine stress test?

A
  • Arrhythmias, hypotension, CP and dyspnea
216
Q

Contraindications to dobutamine stress test?

A
  • Unstable angina
  • Recent MI
  • SBP 200
  • Hx of ventricular tachyarrhythmias
  • Severe AS
  • HOCM
  • Large aortic aneurysm of dissection
217
Q

Contraindications to vasodilator stress test?

A
  • Severe asthma, COPD (relative for regadenoson)

- SBP

218
Q

What are the side effects of vasodilator stress test? Antidote?

A
  • SE: flushing, HA, nausea, hypotension, bradyarrhythmia, bronchospasm, transient AV block
  • Antidote: aminophylline
219
Q

What type of stress testing should be done in SIHD (stable ischemic heart disease) patients?

A
  1. Able to exercise with uninterpretable EKG:
    - Class I: exercise echo or MPI
    - Class IIa: pharm stress
    - Class IIb: coronary angiography
  2. Unable to exercise
    - Class I: pharm stress echo or MPI
    - Class IIa: pharm stress
    - Class IIb: coronary angiography
    * Bottom line: if someone with history of IHD, must increase sensitivity and specificity from just EKG. Myocardial perfusion imaging increases sensitivity in hx of CAD.
220
Q

59 yo male presents to office for evaluation of CP. He indicates to you that his CP is substernal, radiating down left arm with nausea and diaphoresis. He can reproduce these sx when he walks up stairs to his 2nd floor, yet resting can help sx reside. You examine him and do not notice any abnormal findings. You alertly order and EKG which demonstrates sinus arrhythmia but otherwise no gross abnormalities.
Which of the following would be the most specific of the stress tests?
a. Exercise treadmill EKG
b. Regadenosine MP scan
c. Dobutamine stress echo
d. Dobutamine myocardial perfusion scan

A
  • Answer = C. MPI are sensitive, but not specific.
221
Q

Which of the following statements about the prognostic value of stress echo is correct?

a. LVEF is not important if the peak wall motion score index is increased
b. Development of wall motion abnormalities at low HR does not have prognostic implications
c. Assessment of myocardial viability has no prognostic value
d. Event rate of a patient with intermediate pretest probability of CAD and a negative stress echo is

A
  • Answer = D
222
Q

72 yo female with recurrent angina to your office. Her PMH includes CAD, DM II, HTN, HL, Vtach, CHF necessitating a pacemaker and defib. She is a former smoker and unfortunately is on home o2 too. She wants to come off a lot of her medicines. She currently is stable and her PE is remarkable for crackles at the lung bases with end respiratory wheezing, JVP to the angle of the jaw, positive S3, 2+/4 bilateral lower extremity edema. EKG was remarkable for a dual AV paced rhythm, no ST-T wave abnormalities. What would be the most appropriate stress test?

a. Exercise treadmill EKG
b. Dobutamine stress echo
c. Regadenosine MP scan
d. Dobutamine MP scan
e. Coronary angiogram

A
  • Answer = C. Cannot use dobutamine d/t vtach hx. She is exercise intolerant. It is true that lung dz is a relative contraindication for regadenosine.
223
Q

21 yo male student evaluated for a murmur heard during an athletic participation physical exam. He is asymptomatic. His medical and family hx is unremarkable and he takes no medications. On PE, pt is afebrile, BP 118/76, HR 68, RR 14. BMI is 18. He wears corrective lenses for myopia. Mild thoracic scoliosis is noted. He has long, thin fingers and a mild pectus excavatum deformity. His height is 188 cm (6 2) and arm span is 200 cm from fingertip to fingertip. On cardiac auscultation, a soft early diastolic decrescendo murmur is heard and is best heard along LLSB during expiration with patient seated and leaning forward slightly. A transthoracic echo demonstrates dilatation of the aortic root of 6.2 cm. Which of the following is the most appropriate tx?

a. Admit to hospital, begin metoprolol
b. Begin oral losartan and metoprolol
c. Plan urgent surgery
d. Repeat echo in 6 months

A
  • Answer = C d/t size
224
Q

86 yo male is evaluated in hospital for progressive weakness of 1 month’s duration. His PMHx include HTN, IL, COPD, CHF (NYHA class III, LVEF 30%). 2 months ago, he received a drug eluding sten in the LAD following an acute anterior MI. He used home o2. He has unintentionally lost 9.1 kg in 6 months. His meds are lisinopril, carvedilol, atorvastatin, aspirin, clopidrogel, and furosemide. On PE, the patient appears ill and frail. He is afebrile, BP 138/80, pulse 68 and regular and respiratory rate is 16. BMI is 17. JVD is present. Crackles are heard in lower quarter of both lung fields and an S3 gallop is present. The abdomen is scaphoid, a pulsatile mass is palpable above the umbilicus, and a soft bruit is present in the same location. Rectal exam is normal.
Which of the following is the most appropriate next test to evaluate this patient’s abdominal mass?
a. Abdominal US
b. CT of abdomen with contrast
c. MRA
d. No diagnostic testing

A
  • Answer = D. Why?
225
Q

Are aneurysms symptomatic or asymptomatic?

A
  • Most are asymptomatic, often incidental
226
Q

What imaging modalities can be used to assess for aneurysms?

A
  • CT, MRI, US (most sensitive/specific)
227
Q

What are the most sensitive symptoms for aortic dissection?

A
  • Severe, sudden onset chest pain. No pain is unlikely dissection.
228
Q

Definition of aortic aneurysm vs dissection

A
  • Aneurysym: bulging/enlargement of aorta

- Dissection: tear in intima of aorta allows access of blood into media and formation of true and false lumens.

229
Q

PE findings of aortic aneurysm

A
  • Check BP and pulses bilaterally
  • Aortic regurg murmur (aneurysm is bulging and sending pressure back through valve)
  • Cardiac tamponade (hypotension, JVD, clear lungs)
  • Signs of heart failure
  • Neurologic deficit
  • Pulsatile abdominal mass
  • Abdominal bruit
230
Q

What feature on CXR could be suggestive of aneurysm?

A
  • Wide mediastinum. Not very specific test.
231
Q

Risk factors for AAA (abdominal aortic aneurysm)

A
  • Atherosclerosis, smoking, male, advanced age, dyslipidemia, family hx, infectious (mycotic aneurysm)
  • Marfans, EDanlos, Loeys-Dietz
232
Q

Classic triad for AAA rupture

A
  • Pain (depending on where lesion is), hypotension, pulsatile abdominal mass
233
Q

Treatment of AAA

A
  • Smoking cessation, lipid control, BP control (dP/dT: pressure/time), ASA, beta-blockers, ACEi
  • Surgery: GRAS criteria = Growth (rapid expansion > 0.5 cm in 6 months), Rupture, Absolute size (> = 5.5 cm in males, 5.0 cm in females), Symptoms
  • Note: AAA of 4 to 5.4 cm requires imaging q 6-12 months
234
Q

Screening recommendations for AAA per USPSTF

A
  • Grade B. One-time screening for AAA for US in men ages 65 to 75 who have every smoked.
235
Q

Are TAA or AAA more common? Which parts of aorta are TAAs more common?

A
  • AAA
  • TAA in > 50, M>F
  • Ascending aorta d/t highest pressure w/o friction.
236
Q

Treatment for TAA

A
  • BP control: dP/dT

- HR

237
Q

What is the recommended size threshold for elective TAA repair in asymptomatic patients?

A
  1. Ascending:
    a. Non-syndromic: >= 5.5 cm or rapid growth >0.5 cm / year
    b. Genetic disorders: >= 5.0 cm and even at 4-5 cm in some cases
  2. Aortic arch: >= 5.5 cm
  3. Descending: >= 5.5-6 cm
238
Q

Genetic risk factors for acute aortic syndromes (dissection, aneurysm)

A
  • Marfan, Ehlers-Danlos, bicuspid valve, coarctation, Loeys-Dietz
239
Q

Classifications of aortic dissection? What is the treatment for each?

A
  • Stanford type A = ascending aorta = surgical emergency

- Stanford type B = descending aorta = medical management vs endovascular treatment

240
Q

What lab test is a good rule out test for aortic dissection?

A
  • D-dimer
241
Q

Treatment for aortic dissection?

A
  • Meds: beta-blockers preferred

- Surgery

242
Q

Describe follow up instructions for aortic dissection patients

A
  • BP
243
Q

24 yo male presents with acute sudden onset of chest pain with radiation to his back. His past medical hx is relatively unremarkable but he does have a history of cocaine use. His PE reveals an uncomfortable man with BP 200/110 in left and 180/94 in right arm with unequal pulses. His lungs are clear to auscultation bilaterally and he has no other neurologic deficits. An EKG reveals sinus tachy without any other abnormalities.
Which is next best step in mgmt. of this patient?
a. Emergent surgery
b. CTA
c. Beta-blockers to lower BP
d. Endovascular repair
e. B&C

A
  • E
244
Q

55 yo female presents to office for annual surveillance. She carries a hx of a bicuspid aortic valve and has been seeing you for annual CTAs to monitor size of her aorta. She is currently asymptomatic. Her aorta was measured at 47 mm this year. It was previously 41 mm last year. What is the next best mgmt. for this patient?

a. Medical therapy focusing on BP and lipid control
b. Use another modality to image more accurately
c. Surgical intervention
d. Monitor size in 3 months
e. Monitor size in 1 year

A
  • Answer = C. Growth of 0.6 cm in 1 year. Per guidelines: 0.5 cm in 6 months is criteria for surgery.

Cardiology (2 decks)

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