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Internal Medicine - Emma > Cardiovascular > Flashcards

Cardiovascular Flashcards

0
Q

Describe Sx associated with myocardial ischemia

A

Visceral pain
Dull, aching, tight
Sometimes “burning”
Poorly localized

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1
Q

Signs of pleuritis

A

Increased pain with inspiration and cough

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2
Q

Important life threatening causes of chest pain (3)

A

Myocardial ischemia
Pulmonary embolus
Aortic dissection

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3
Q

Risk factors for CHD (6)

A 
Diabetes mellitus
Smoking
HTN
Dyslipidemia
Fam Hx
Abdominal obesity

Also: age, cocaine use

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4
Q

Pain in pericarditis

A

Pleuritic
Relieved by sitting forward
Can radiate to shoulder/trap due to diaphragmatic irritation

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5
Q

Worrisome features in angina (2)

A

More than 20 min of pain

Pain at rest => UNSTABLE!

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6
Q

Characteristics of aortic dissection (3)

A

Abrupt and Most intense at onset
Tearing pain
Radiates to back

Unequal BP between arms
Use transesophageal ECG to detect at bedside

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7
Q

Chest pain DDx (8)

A

HEART:
Angina => worse with emotion or exercise, relieved by NO/rest, retrosternal pressure like pain
MI
Pericarditis => Sx pleuritic and positional, pericardial rub
Aortic dissection => Sx abrupt, most intense at start, radiates to back

LUNGS:
Pneumothorax => tachypnea, hyperresonant, tracheal deviation
PE => Sx pleurisy and dyspnea

ESOPHAGUS:
Gastrointestinal disease => GERD, esophag spasm

MSK:
MSK => worse on movement/palpation

NEURO:
Neuropathic => VZV

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8
Q

ECG findings - ST depression >1mm

A

Ischemia!

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9
Q

ECG findings - ST elevation

A

Acute MI => only in area of infarction

Perdicarditis => ALL leads involved, may have PR depression

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10
Q

ECG findings - RBBB

A

Right heart strain! => ex. In PE

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11
Q

ECG findings - LBBB

A

Underlying heart disease such as ischemia or HTN

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12
Q

Causes of low CO in cardiogenic shock (3)

A

Right heart failure => pulmonary embolism
Decreased venous filling of heart => tension pneumothorax
Obstruction of outflow => cardiac tamponade

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13
Q

Causes of distributive shock (3)

A

Low SVR resulting from: sepsis, adrenal insufficiency, anaphylaxis

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14
Q

Definition of shock

A

Decreased perfusion and oxygen delivery to body
SBP < 60mmHg
May manifest as organ failure => renal, CNS, lactic acidosis

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15
Q

Pulsus paradoxus is associated with….

A

Cardiac tamponade
Definition: On inspiration, a drop in systemic arterial pressure greater than 10mmHg.
In states in which the ventricle cannot expand outward (e.g. tamponade) or in which the drop in intrathoracic pressure with inspiration is profound (e.g. status asthmaticus), the septal shift is exaggerated and the difference in BP is larger.

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16
Q

Hypovolemic shock: CO, SVR, JVP
Cardiogenic shock
Distributive shock

A

Hypovolemic shock: decrease CO, increase SVR, decrease JVP
Cardiogenic shock: decrease CO, increase SVR, increase JVP
Distributive shock: increase CO, decrease SVR, decrease JVP

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17
Q

Causes of cardiogenic shock (7)

A

MI, cardiomyopathy, tamponade => pump failure
Arrhythmia
Valve failure
Tension pneumothorax, massive PE => Obstructed outflow

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18
Q

Causes of hypovolemic shock (4)

A

Hemorrhage
Diarrhea
Heat stroke
Third spacing

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19
Q

Causes of distributive shock (4)

A

Sepsis
Anaphylaxis
Adrenal crisis
Myxedema coma

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20
Q

Treatment of shock

A

Decreased JVP => hypovolemic OR distributive shock => IV fluids => NS/RL
Anaphylaxis => epinephrine
Adrenal insuff (hyponat, hyperkal, hypogly, abdo pain, eosinophilia, mild hypercal)=> ACTH stim test => IV steroids
Sepsis => blood and urine cultures => empirical ABx
Myxedema => “hypo” syndrome (hypotherm, hypogly, hyponat, hypovent) => TSH/T4 => exogenous thyroid hormone

Increased JVP => cardiogenic shock => CXR (PE, cardiomyopathy, tamponade, pneumothorax) + ECG (PE=> RBBB, MI => ST dep or elevation) + echocardiogram
Pneumothorax => insert chest tube => midclav 2nd intercostal space
Swan-Ganz pulmonary artery catheter => L atrial filling pressure

Rx:
Vasopressors
Dobutamine => beta 1 agonist => increase cardiac contractility
Norepinephrine => alpha and beta 1 => distributive and cardiogenic
Phenylephrine => pure alpha 1 agonist => increase SVR w/o increasing CO

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21
Q

Three stages of atherosclerotic plaque formation

A
  1. Endothelial dysfunction => fatty streak= smooth muscle cells in intima and accumulation of lipid
  2. LDL enters endothelium => oxidized => macrophages come and recruit fibroblasts and other inflamm cells
  3. Smooth muscle + CT + lipids incorporated into plaque => fibrous cap formation => narrow artery lumen

Plaques can rupture and lead to thrombosis

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22
Q

Characteristics of unstable angina

A
  • angina that occurs AT REST

- significant change in the pattern of existing chronic angina

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23
Q

Symptoms to look for in atypical angina

A

Jaw pain
Dyspnea

=> think diabetes

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24
Q

Other PE findings of atherosclerosis (7)

A 
Arteriovenous nicking
Copper wire changes in retinal vaculature
Third heart sound
Fourth heart sound
Arterial bruits
Diminished peripheral pulses 
Xanthomas
25
Q

S4

A

It occurs just after atrial contraction and immediately before the systolic S1
caused by the atria contracting forcefully in an effort to overcome an abnormally stiff (decreased compliance of ischemic myocardium) or hypertrophic ventricle

26
Q

S3

A

occurs soon after the normal two “lub-dub” heart sounds (S1 and S2). The S3 is associated with heart failure.

27
Q

Reasons for stopping an exercise stress test (used to Dx CHD)

A 
Mod/severe chest pain
Dyspnea
Dizziness
>2mm ST segment depression => test = positive of ST segment depression >1mm
Fall in SBP >10mmHg
Sustained ventricular tachycardia
28
Q

Causes of false positive ST depression on exercise stress test (4)

A

LBBB
LVH
WPW syndrome
Digoxin

29
Q

Tools to Dx CHD (5)

A
  1. Exercise stress test (look at ECG for ST depression >1mm)
  2. Radiolabeled tracers such as sestamibi to determine regional myocardial perfusion
  3. Pharmacological stress test with selective vasodilators such as dipyridamole, adenosine => blood shunted away from atherosclerotic vessels
  4. Dobutamine stress echocardiography to look for wall motion abnormalities
  5. Coronary angiography => GOLD STANDARD
30
Q

Treatment of stable angina (ABCDEs)

A

A: aspirin, ACE inhibitors, antianginals (Beta blockers, calcium channel blockers, Nitro)
B: beta-blockers and BP control
C: cholesterol and smoking cessation, CABG (if severe), coronary stents (percutaneous coronary intervention)
D: diet and diabetes control
E: education and exercise

31
Q

Side effects of beta blockers (4)

A

Fatigue
Impotence
Bradycardia
Worsening of CHF

32
Q

When to consider CABG over medical management of CHD

A

Left main disease OR LAD + proximal left circumflex
Three vessel disease w/ reduced EF
Severe proximal LAD stenosis
Survivors of sudden cardiac death/ V.tach/fib

33
Q

Complete occlusion of the coronary artery often results in ……. (ECG)

A

STEMI!
Leads to necrosis of the myocardium
May occur throughout entire thickness => pathological Q waves

34
Q

Mechanisms that compromise coronary blood flow/oxygen supply (8)

A

Atherosclerotic plaque rupture
Demand ischemia => tachycardia, hypotension, severe hypoxia
Coronary artery dissection
Coronary vasospasm => drugs, Prinzmetal angina
In situ thrombus formation => hypercoagulable
Coronary embolism
Vasculitis => Kawasaki
CO poisoning

35
Q

Complications leading to death from AMI (5)

A 
Arrhythmias => heart block, V.tach/fib
Heart failure => cardiogenic shock
Ventricular rupture => usually within 3-5 days
Ventricular septal defects
Mitral papillary rupture
Reinfarction (>1 month later)
36
Q

Prognostic factors for UA or NSTEMI (7)

A 
TIMI risk score (/7)
Age >65
At least 3 risk factors for CAD
Known CAD with at least 50% stenosis
ST segment changes
At least 2 episodes of angina in past 24 hrs
Aspirin use in past week
Elevated CPK-MB or troponin
37
Q

Tx of a patient with possible MI

A
  1. Rapid clinical assessment => vitals, Hx, P/E, 12 lead ECG
  2. Give OXYGEN
  3. Give 162-325mg ASPIRIN
  4. Give SL NITROGLYCERIN (0.4mg every 5 min x 3) => beware hypotension
  5. Consider IV morphine for pain and pain-related sympathetic drive
  6. Give IV beta blockers to control HR and relieve myocardial demand
  7. Treat with a statin, oral ACE inhibitors,
38
Q

Thrombolytic therapy agents

A

Streptokinase
Alteplase
Tenecteplase
Reteplase

39
Q

Absolute contraindications for thrombolysis (6)

A 
Previous intracranial hemorrhage
Significant closed head injury within past 3 mo
Stroke within 1 yr
Intracranial malignant neoplasms
Aortic dissection
Active bleeding

Relative contraindications include: uncontrolled HTN, distant Hx stroke, recent trauma/surgery, pregnancy, current use of anticoagulants

40
Q

STEMI vs. NSTEMI

A

STEMI = full thickness damage to myocardium, complete occlusion of major coronary artery, complications are more common

NSTEMI = partial thickness, complete occlusion of minor artery or partial occlusion of major artery, milder elevations in troponin and CPK-MB compared to STEMI, may see T wave inversions on ECG, thrombolytic Tx is harmful (i.e. NO streptokinase)

41
Q

Major risk factors for congestive heart failure (5)

A 
Coronary heart disease
Hypertension
Diabetes
Valvular heart disease
Cardiomyopathy => amyloid, drug-related, idiopathic
42
Q

BP is determined by SVR and CO. CO is in turn determined by _________, _________, and ____________.

A

Preload, contractility and afterload

43
Q

Frank Starling law of the heart

A

As preload is increased, the stroke work or contractility (inotropy) of the heart is also increased.

The relationship between increasing preload and CO, in a heart with decreased contractility/ejection fraction….i.e. Post MI etc.

44
Q

Causes of high output heart failure (rare)

A

Hyperthyroidism
beri beri => thiamine deficiency
Arteriovenous malformation

=> increased metabolic demands!

45
Q

DDx dyspnea + dilated cardiomyopathy (7)

A 
Post MI
HTN
Valvular
Toxic (Rx, cocaine etc)
Viral (coxsackie!!)
Hemochromatosis
Hypothyroidism
46
Q

Tx acute pulmonary edema in CHF

A

LMNO
Lasix (decrease preload)
Morphine (venodiltor and anxiolytic)
Nitroglycerin (arterial and venous dilator AND coronary vasodilator)
Oxygen (decrease pulmonary vasoconstriction)

47
Q

Tx CHF caused by systolic dysfunction

A 
ACE inhibitors
ARBs 
Beta blockers
Diuretics
Fluid and salt restriction
Cardiac glycosides (ex. Digoxin)
Inotrope infusions
Ventricular assist devices
48
Q

Causes of absent P waves

A

Failure of SA node to fire => sinus arrest => Sick Sinus Syndrome
Failure of SA node to excite atria => sinus exit block

Also atrial fibrillation => no organized atrial activity

49
Q

Difference between first, second and third degree AV block

A

Both cause a prolongation of the PR interval (>200msec)

First degree: generally no Sx or significant bradycardia
Second degree: leads to a blocked beat => QRS fails to follow a P wave
Third: COMPLETE heart block, no relationship between P waves and QRS complex (variable PR interval), P waves fail to conduct to ventricles => slower pacemaker takes over

50
Q

Difference between Type 1 and Type 2 second degree AV blocks

A

Type 1 Wenkebach => PR intervals progressively lengthen until a P wave fails to conduct (i.e. A P wave that is NOT followed by a QRS), AV nodal disease

Type 2 => dropped beat occurs suddenly, infranodal disease, higher risk of progressing to complete heart block

51
Q

Indications for permanent pacemaker (3)

A

Complete heart block w Sx
Sinus node dysfunction w Sx
Bifasicular block with intermittent type 2 second degree AV block
Type 2 second degree AV block after an MI

52
Q

Approach to tachycardia

A

Look at HR => >100
Look at QRS complex => wide (supraventricular OR ventricular) or narrow (always supraventricular)?
Narrow? => regular or irregular
look at P waves => Present? Absent? Sawtooth? P waves before QRS?
Wide? => look at morphology => variable vs. uniform

53
Q

Tx for hemodynamically stable SVT (i.e. How to block the AV node)(5)

A 
Vagal maneuvers (valsalva/ carotid sinus massage)
Adenosine
Beta blockers
Calcium channel blockers
Digoxin
54
Q

Three main Tx concerns in Atrial Fibrillation

A

Rate control
Rhythm control
Anticoagulation

55
Q

Causes of prolonged QT interval (4)

A

Medications => type 1A and III antiarrhythmics, phenothiazines, tricyclic antidepressants
Electrolyte disorders => hypokalemia, hypomagnesemia, hypocalcemia
Congential
Ischemia

56
Q

Major causes of secondary HTN (10)

A 
Renovascular disease 
Intrinsic kidney disease 
Primary aldosteronism
Pheochromocytoma
Cushing syndrome
Hyper AND hypoyroidism
Obstructive sleep apnea
Coarctation of the aorta 
Drugs (ex. OCP, alcohol)
57
Q

The 7 “Ps” of pheochromocytoma

A 
Pounding headache
Perspiration
Palpitations
Pallor
Pyrexia
Pressure (BP) elevations
Postural Sx

Usually lasting 10-60min

58
Q

Signs of target organ damage in HTN

A 
LV heave
S4 
Edema (pulmonary and peripheral)
Carotid bruits
Neurological deficits
Diminished pulses
Aneurysms
Arteriovenous nicking, papilledema, hemorrhages
Renal bruits
59
Q

The six Ps of acute peripheral arterial occlusion

A 
Pulselessness
Pallor
Poikilothermia (temperature varies with ambient temp)
Pain
Paralysis
Paresthesias

Internal Medicine - Emma (5 decks)

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