CARDIOLOGY
Presyncope & Syncope(Kruger)
Presyncope- is a premonition of syncope with *NO LOC*
Epidemiology: MC in elderly due to atherosclerosis; pregnant patients due to uterus compress IVC
Pathophys: global decrease in cerebral perfusion, with subsequent lack of nutrient delivery(glucose) to the RAS,
causing LOC
Etiology: hypoglycemia, hyponatremia, hypoxemia, cardiac dysrhythmias, vasovagal, orthostatic hypotn
Types:
Autonomic Reflex Mediated
1.
Vasovagal syncope- incited by noxious stimulus(pain, emotional stress, fear); reclining helps prevent an
attack after onset occurs;
You will have warning symptoms (dizziness, palpitations, tunnel vision, nausea, pale, diaphoretic) *may
last several min.* MUST have prodromal sx to Dx.
2.
Orthostatic syncope- occurs when person assumes upright position, causing blood to shift to lower body
and away from brain. CO decreases and parasympathetic system makes it worse by decreasing further.
Normally sympathetic system would take over.
Sx are onset 2-3 min. after standing up; Caused by diabetic neuropathy, meds, and volume
depletion(dehydration)
3.
Carotid Sinus hypersensitivity- usually occurs in men, elderly, HTN, head and neck malignancies; Assoc.
w/ putting on a tie, use of electric razors, turning head.
Due to stimulation of sensitive carotid; bradycardia will ensue as well as asystole of >3sec or decreased
BP >50mmHg
4.
Situational syncope- response to a specific stimulus such as after eating, micturition, defecation, and
coughing. May be due to increased ICP of intrathoracic pressure.
Cardiac Mediated
Etiology: valvular heart disease, cardiomyopathy, MI, pulmonary HTN, pericardial tamponade, aortic
dissection, Pulmonary embolus
 *Dysrhythmias* are most likely to occur in myocarditis and MI
 Clinical Manif of syncope in dysrhythmias: sudden, prodromal sx, if any, last *<3 seconds*

Syncope from *structural cardiopulmonary disease* often occurs in setting of *physical exertion*

This includes aortic stenosis, hypertrophic cardiomyopathy, and acute pulmonary embolism

Aortic stenosis- radiates to the neck, triad of chest pain, DOE, and syncope; excluded as cause in elderly
Neurological Syncopes
Brainstem ischemia- causes decrease in blood flow to RAS leading to sudden brief episodes of syncope.

Can be due to vertebrobasilar atherosclerotic dz, basilar migraines or steal syndrome.
These are assoc. w/ diplopia, vertigo, dysarthria, dysphagia, ataxia etc.

Subclavian steal syndrome- rare cause of brainstem ischemia, characterized by stenosis of subclavian
artery proximal to the origin of vertebral artery.

s/s: *Exercise of ipsilateral arm causes blood to be shunted*, or stolen, from vertebrobasilar system to
subclavian artery supplying arm muscles. *MC on left*
PE: cold, weakness, paresthesias, decreased pulse volume and BP than other arm, *arm claudication w/
exercise resolves at rest*
Dx: carotid Doppler, angiogram
Tx: stent


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Psychiatric Syncopes
MC dx: anxiety, depression
Other causes: hyperventilation(respiratory acidosis)
Dx (all syncopes:):
 *EKG*
 Holter monitor, CBC
 Cardiac stress test(R/O coronary atherosclerosis caused), CK levels, Echo,
 Carotid Doppler(steal syndrome), EEG(R/O seizure), Carotid sinus massage- R/O carotid sinus
hypersensitivity(CI in CVA, bruits, and MI), head up tilt table test (autonomic dysfx)
Aortic Aneurysm and Dissection (Politi)
Abdominal Aortic Aneurysm
 Most occur b/wn the renal arteries and the iliac bifurcation

Etiology: atherosclerosis, HTN, trauma, smoking, vasculitis

s/s:
o
o
Asymptomatic usually, sense of fullness, pain could be present at hypogastrium, lower back
pulsatile mass on physical exam
o
Near rupture could give signs such as sudden onset of severe pain in lower back, or lower
abdomen, radiating to the groin, buttocks, or legs;


o
*Grey Turner’s sign- ecchymosis on back;
*Cullen’s sign- ecchymosis around umbilicus
If rupture does occur: *Triad- abdominal pain, hypotension, and palpable pulsatile mass*,
could be w/ or w/o syncope, cardiovascular collapse, N/V

Dx: U/S (gold standard), CT scan also useful, abdominal radiographs

Tx:
o
o
Unruptured- if aneurysm is >5cm in diameter or symptomatic, *surgical resection* w/
synthetic graft placement is recommended.
Ruptured- *emergency laparotomy*
Aortic Dissection
 Risk Factors: HTN, trauma, Marfan’s, bicuspid aortic valve, coarctation of aorta
 Stanford Classification:
o Type A(proximal): involves ascending aorta
o

Type B(distal): limited to descending aorta
Clinical Manif:
o Severe, tearing, *ripping*, stabbing pain, either in the anterior(A) or back of the chest(B)
o
Diaphoresis, most are hypertensive but could be hypotensive
o
Pulse or BP asymmetry b/wn limbs, aortic regurgitation(esp. in A)

Dx: CXR- widened mediastinum(>8mm in AP view), transesophageal echocardiogram,
o *aortic angiography(best test)*

Tx: IV beta blockers, IV nitroprusside if HTN emergency(Type B); Type A usually with surgery
Coarctation of Aorta
 Narrowing or stricture of aorta usually at *left subclavian artery near ligamentum arteriosum*, leading to
obstruction b/wn the proximal and distal aorta, causing increase LV afterload.

s/s:
o
o
o
o
*HTN in upper extremities with hypotension in lower extremities*
Well developed upper body with underdeveloped lower body
Midsystolic murmur heard best over the back
HA, cold extremities, claudication upon exercise, and leg fatigue

Dx: EKG shows LV hypertrophy
CXR- notching of the ribs, *Figure 3* appearance

Tx: surgical decompression, or percutaneous balloon aortoplasty in certain cases
Infective Endocarditis and Pericarditis(Politi)
Infective Endocarditis
 Infx usually involving the cusps of the valves

Acute endocarditis- *MCC staph aureus*, occurs on *healthy heart valve*; fatal in <6wks

Subacute endocarditis- caused by staph viridians and enterococcus, occurs in *damaged valves*, takes
much longer for it to be fatal

Etiology: coagulase (-) streptococci MC in prosthetic valve endocarditis


Risk Factors: rheumatic, congenital, or valvular heart dz, prosthetic heart valve, IV drug abusers
s/s:
o Fever, chills, weakness, dyspnea, anorexia

o
new onset of heart murmur(mitral>aortic in non-IVDA) (tricuspid in IVDA)
o
*Osler’s nodes(small tender nodules on the finger and toe pads), Janeway lesions(small
peripheral hemorrhages on palms and soles; Roth’s spots(retinal hemorrhages)
Dx: Duke’s criteria- must have 2 major criteria, 1 major and 3 minor criteria, OR 5 minor criteria to dx;
o Major criteria: sustained bacteremia, endocardial involvement(using echocardiogram)
o

Tx: Empiric therapy w/ penicillin or vancomycin or ceftriaxone + gentamicin; prophylaxis-amox
Acute Pericarditis
 Etiology:
o
o
o

o
chest pain(not always present): severe and *pleuritic* that radiates to trapezius ridge and neck;
 pain worsens by lying supine, coughing, swallowing, and deep inspiration; it is
*relieved by leaning forward*
*pericardial friction rub(PFR), *Fever w/ non productive cough;
Dx:
o


Idiopathic(post viral after recent flu), Collagen vascular dz(SLE, rheumatoid arthritis)
Viral(echo, coxsackie virus, HIV, hep A+B)
Bacterial(Tb), Acute MI(first 24 hrs),
After MI(*Dressler’s Syndrome)* Tx for Dressler: aspirin
s/s:
o

Minor criteria: predisposing condition(abnormal valve), fever, vascular phenomena(pulmonary
emboli, ICH, Janeway lesions), immune phenomena(Osler’s nodes and Roth’s spots), positive
blood cultures, positive echocardiogram
EKG- shows ST elevation, and *PR depression*(specific for this dz), then ST will return to
normal, T wave will invert, T wave will return to normal
Tx: self limited, NSAIDs are mainstay
Cx: pericardial effusion, cardiac tamponade
Constrictive Pericarditis
o Characterized by *fibrous scarring of the pericardium*, this will restrict diastolic filling
o Clinical Manif:
o Initial are secondary to venous pressure elevation: edema, ascites, hepatic congestion
o Late manif. due to elevation of left sided intracardiac pressures: cough, dyspnea, orthopnea
o JVD, *Kussmaul’s sign*(JVD fails to decrease after inspiration), edema, pericardial knock
o Dx: EKG- t wave flattening or inversion and left atrial abnorm., Echo, CT, MRI, Cardiac
catheter*(shows rapid y descent or a “square root sign”)*
o Tx: resection of pericardium(significant mortality rate)
Pericardial Effusion
o Any cause of acute pericarditis that leads to exudative fluid into pericardial space
o Clinical Manif: muffled heart sounds, soft PMI, dullness at lung base, PFR(may not be present)
o Dx: *Echo(procedure of choice)*, pericardial fluid analysis- may clarify the cause of effusion
Pericardial Tamponade
o *Rate of fluid accumulation is important NOT the amount*
o Pathophys: pericardial effusion that impairs diastolic filling of the heart leading to decr. CO
o Etiology: penetrating trauma to the thorax, iatrogenic(central line), pericarditis, Post MI
o Clinical Manif:
o *Beck’s Triad: JVD, hypotension, muffled heart sounds*, pulsus paradoxus
o Dx: *Echo*
Tx: pericardiocentesis( if hemodynamically unstable), if renal failure(dialysis)
Coronary Heart Disease, MI (Politi)
Etiology: Atherosclerosis
Stable(Classic) Angina
 Risk Factors: DM, HTN, Hyperlipidemia, smoking, elevated homocysteine levels

s/s:
o
o
Chest pain or substernal pressure sensation lasts <10-15 min brought on by *exertion*
Relieved w/ rest and nitroglycerin

Dx: Stress EKG- ST segment depression,
o Stress Echo(both tests if positive go for *cardiac catheterization w/ coronary angiography*)

Tx: beta blockers, aspirin, nitrates, NDP calcium channel blockers(2nd line when nitrates/beta don’t
work)
Unstable Angina (Acute Coronary Syndrome)
 s/s:
o Chest pain that is new onset, accelerating and occurs at rest
o can lead to an MI

Dx: EKG at rest- ST depression, T wave inversion

Tx: MONitrates(first line), Aspirin, beta blockers(first line), LMW heparin, glycoprotein inhibit.,
cardiac catheterization/revascularization
Variant(Prinzmetal’s Angina)
 Involves coronary vasospasm that is usually accompanied by a fixed atherosclerotic lesion, but can occur
in normal coronary arteries
 Episodes of angina *occur at rest* and are assoc. w/ ventricular dysrhythmias

Dx: EKG- ST elevation during chest pain, representing transmural ischem., *coronary angiography*

Tx: Nitrates/calcium channel blockers
Myocardial Infarction
 s/s:
o Chest pain that is substernal and crushing pain(+ Levine’s sign)
o Radiates to the neck, jaw, arms, or back, commonly left side
o epigastric discomfort
o Dyspnea, diaphoresis, N/V, syncope, weakness/fatigue


Dx:
o
EKG: ST elevation or non ST elevation, T wave inversion, Q waves(specific) and are seen late,
o
o
CK-MB(increases w/in 4-8 hrs and returns to normal in 48-72 hrs);
Troponin I(increases w/in 3-5 hrs and return to normal 5-14 days; peak at 24-48 hrs, must
get every 8hrs for 24 hrs
o
STEMI: transmural which involves entire thickness of wall and tend to be larger
o
NSTEMI: subendocardial which involves inner 1/3 to 1/2 of wall; tend to be smaller and
similar to unstable angina
Tx: MONA,
o beta blockers, ACE Inhibitors, Heparin(all pts w/ MI), Enoxaparin preferred(lmwh),
revascularization
Thrombolytic Contraindications
CVA/head trauma in past 3 months
Major surgery in past 14 days
History of intracranial bleeds
GI or GU hemorrhage w/in past 21 days
Seizure with onset of stroke
Glucose <50 or >200
BP >185/110
Heparin in past 48 hrs
Platelets <100,000
Diagnostic Imaging for Cardiac patients(Politi)
PET scan: used to determine if there is adequate blood flow to the heart; assess the amount of damage to the heart
after a heart attack and to evaluate the effectiveness of your treatment plan.
 Used for pts unable to exercise on treadmill or stationary cycle. *Rubidium used as contrast*
Non-Cardiac Surgery in Cardiac Patient(Beysolow)
 Unstable angina pt. should avoid elective surgery unless for bypass grafting same with MI
 Most innocent heart murmurs are apical(mitral) and never associated w/ palpable thrill; *no such thing
as an innocent diastolic murmur*

Valsalva maneuver should normally not change the pitch or character of an innocent murmur
Dripps-American Surgical Classification is the MC used assessment chart for risk vs benefit analysis
1. Healthy patient
2. Mild to moderate systemic disturbance
3. severe systemic disturbance
4. life threatening disturbance
5. Not expected to survive; w/ or w/o surgery



Score of < 25 on the cardiac risk scale, w/ all factors considered minimal surgical risk.
Score > 25 implies there is high surgical risk.
Score >26 suggests risk of fatal coronary event

All patients with a history of cardiac disease are required to have a preoperative evaluation of cardiac fx

*Pulmonary surgical procedures the goal is to leave the patient postoperatively with an FEV1 of at least
800ml-1L; pt with less than this should be considered inoperable and should not be taken off ventilator*
After surgery in cardiac patient two considerations must be taken:
1. Catecholamine surge- response to pain and anxiety; increase HR & contractility
2. Person has suppression of fibrinolytic system
Men w/ DM have 2x the risk of cardiovascular mortality; Women w/ DM have 4x risk
Congestive Heart Failure (Podd)
Etiology: Ischemia(MCC), MI, HTN, dilated, hypertrophic cardiomyopathy, aortic sten/regur, mitral regu
Systolic Heart Failure: *MC*

Inability of ventricles to pump blood out of ventricles causing an *increase in preload(EDV) and
afterload*, a decrease in CO and stroke volume causing a *decrease in ejection fraction*
(EFˇ=SVˇ/EDVˆ)

3 compensatory mechanisms to prevent decreased SV include: Frank Starling Principle, Ventricular
dilation and myocardial hypertrophy, and Renin Angiotensin aldosterone system.

Frank Starling’s fails because increased preload causes too much stretching of fibers

Too much dilation and hypertrophy will cause the cells to need more oxygen, and will be less efficient in
pumping

The RAAS system will cause an increase in afterload and preload due to constriction
Diastolic Heart Failure:
 Inability of ventricles to relax having a preserved contractility, thus having a decrease in EDV(preload),
afterload, and CO and stroke volume. Because of this a *normal or increased ejection fraction*
(EF=SVˇ/EDVˇ)
Left Ventricular Failure
 Mostly systolic dysfx in nature

S/S: *DOE*, paroxysmal dyspnea, orthopnea(lying makes it worse), productive cough, chest pain,
tachycardia, cyanosis of skin, diaphoresis, cold extrem., rales, crackles, pleural effusion

Pulmonary edema could ensue eventually and indicates decompensated CHF due to fluid build up
Right Ventricular Failure


Diastolic dysfx in nature; leading cause is left sided heart failure so may have same S/S
Other etiologies: hypertrophic/restrictive cardiomyopathy, cor pulmonale
S/S:
o
o
o
*Weight gain*, Bipedal edema, dyspnea/SOB, HTN, *JVD*, hepatojugular reflex, *ascites*,
S4 sound
caput medusae(engorged paraumbilical veins)
Dx (L & R heart failure):
o *Echocardiogram*- best test and tells you the EF, wall thickness etc.,
o
o
o
CXR: bat winged appearance for pulmonary edema, Kerley B Lines
EKG: S wave in V1 and an R in V5 will be >35 mm
Right heart(Swan Ganz)/left heart catheterization
Tx: BADD- Beta blockers (carvedilol, metoprolol), ACE inhibitors, Loop diuretics (furosemide), Digoxin
Shocks (Kruger)
1.
Hypovolemic shock





2.
Cardiogenic Shock


3.
↓ CO w/ normal ECF volume, ↓ coronary artery perfusion
MC in post-MI pt (w/ >40% of LV muscle function loss)
o Myocardial stunning- post-MI tissue that responds to drugs& can potentially restore itself (or
cause cardiogenic shock)
o Hibernating Myocardium- compensatory response that reduces myocardial O2 demand due to
persistent ischemia, revascularization can lead to restoration (w/o restoration  cardiogenic
shock)
Obstructive Shock
 ↓ CO due to impedance of circulation
1.
2.
3.
4.
4.
Etiology: External blood loss (decreased venous return), internal (rupture of abdominal aortic aneurism),
fluid loss (V,D…)
Class I (0-15% - 750 mL blood loss)- ↓ pulse pressure, slight tachycardia
Class II (15-30% - 750-1500 mL)- ↓ pulse pressure, tachycardia mottle skin
Class III (30-40%- 1500-2000 mL)- ↓ SBP (<100), AMS
Class IV (>40% - >2000mL)- ↓ SBP (<70), life threatening
Pericardial Temponade- ↓ ventricular filling due to increased intrapericardial pressure, Beck’s Triad,
pulsus paradoxus.
Tension Pneumothorax- air in pleural space  mediastinal shift ↓ preload
Pulmonary Embolism- embolus originating from venous circulation
Aortic Dissection- “dissection” of aortic layers (ripping/tearing chest pain radiating to back)
Distributive Shock (“special”)


Bad autoregulation of vessel tone  irregular distribution of blood
↑ pulse, ↓ DBP, warm extremities w/ good capillary refill
a.
Septic Shock- MCC, systemic infx w/ endotoxins and cytokines in blood  ↓ ECF, ↓CO cool
extremities
Anaphylactic Rxn- results in urticaria, hypotension, bronchospasm, angioedema. MCC: PNCs, foods
Neurogenic shock- pt. w/ hx of neck injury  ↓ sympathetic neural vasoconstriction
 vasodilation w/ hypotension & bradycardia, blood in extremities, inability to conserve heat
(shiver)
 Tx: Trendelenburg (pt supine, leg elevation), atropine
Metabolic & Endocrine- compensated or decompensated
b.
c.
d.
Dx (all shocks): *Invasive Hemodynamic monitoring (CO, arterial & venous pressures)
Tx (all shocks):
 ↑ O2 delivery (SaO2 >95%), avoid excessive (+) pressure ventilation (↓ CO)
 fluid (2 bore IV lines of isotonic crystalloid, if doesn’t work  blood transfusion
 Steroids- Neurogenic shock
 ↑ tissue perfusion (vasopressors)
o Dopamine- at >10 mcg/kg/min, septic shock
o Dobutamine- given if SBP>80mmHg (not too low)
o NE- if SBP < 70mmHg, septic shock.
o Epinephrine- last option, ↑CO, ↑O2 demand
Peripheral Vascular Diseases (Podd)
Acute Arterial Occlusion
 Embolic or thrombotic
s/s:
 P’s (pain, pallow, polar, paresthesia, paralysis, pulse)
 Cuanosis, necrosis
Dx: angiography
Tx: tissue plasminogen activator, heparin, cold avoidance
Cx: amputation (if not treated within 30 days)
Peripheral Arterial Occlusive Dz (PAD)
 Chronic, atherosclerotic artery that can narrow extensively or trap a traveling thrombus
 Hx: smoking, CAD, CVD, DM, age
s/s:
 *intermittent claudication (reproducible discomfort w/ exercise, such as paresthesias, weakness, tingling,
<10mins)
 lower extremity hair loss (1st sign)
 diminished pulse(s) (depends on artery, if tibial a., then popliteal pulse present)
Dx: US, ABI (anckle-brachial index), arteriography (GOLD)
Tx: walk (until pain), plavix, phosphodiesterase inhibitors, lower legs at night
Thromboangitis Obliterans (Buerger’s Dz)
 segmental & inflammatory thrombotic process of small arteries of arms & legs, diminished distal pulses
(ulnar, radial)
s/s: “CRISP G”, *no calcifications
 Claudication (tingling, paresthesias)
 Reynaud’s phenomenon
 Idiopathic
 Segmental thrombophlebitis (red & tender nodule on saphenous vein)
 Pain @ rest
 Gangrene
Tx: antiplatlet tx, no smoking.
Deep Venous Thrombosis (DVT)
 Clotting of blood in deep veins of an extremity (calf, thign) thrombus formationembolus (w/o tx)
 Virchow’s Triad (causes): venous stasis (no muscle movement), endothelial injury, hypercoaguble state
s/s: asymptomatic (50%), unilateral lower extremity edema, *Homan’s sign
Dx: US
Varicose Veins
 valvelar weakeness causes dilated superficial veins at lower extremities (long saphenous vein)
 Primary: dilation of vein wall due to weakness
 Secondary: venous insufficiency, venous HTN
s/s: dilated, tortuous veins/ telangectasias, edema
Dx: US
Tx: stockings, surgery (if persistent pain), leg elevation
Superficial Thrombophlebitis
 Inflammation of superficial vein (saphenous) due to a blood clot
s/s: pain (local), erythema (linear induration)
Tx: NSAIDs, ambulation, surgery.
Chronic Venous Insufficiency
 Inability of lower extremity veins to push blood toward heart, causing venous HTN, edema (unilateral
@ ankle) & inflammation
s/s: unilateral ankle & calf edema, stasis dermatitis (hemosiderin deposition), painless skin ulcers
Dx: US, venous pressure studies
Tx: leg elevation, aspirin, surgery.
Myocarditis
 Inflammation of myocardiumrapid destruction of cardiac cells & necrosis
 MCC: coxsackie B (adenovirus). HIV pts
s/s: prodrome (w/ low fever), tachycardia, sharp-stabbing chest pain, leukocytosis,
 Syncopy (poor prognosis, risk of sudden cardiac death, high grade AV block)
Dx: *EKG: ST elevation w/o reciprocal depression (depresses in MI)
 *Endomyocardial Bx: molecular mimicry, inflammatory infiltrates (lymphocytes, macrophages)
Tx: “ABCDD” (ACE-I, BB, CCB, Diuretics, digitalis)
Cardiomyopathies- dz’s that affect the heart muscle itself & not a result of HTN, congenital or acquired vulvar,
coronary or pericardial abnormalities
Dilated Cardiomyopathy
 dilation of all heart chambers, ↓ ejection
 Alcoholics, pt w/ hypophosphatemia
s/s:
 *stretched ventricles produce problems during systole  abnormal CO @ rest due to ↓ ejection fraction
 generalized fatigue
Dx: EKG (bi-ventricular enlargement)
Tx: ACE-I, BB (long term), transplant
Hypertrophic Cardiomyopathy
 genetic hypertrophy/thickening of ventricular septum (and atrial)
 “young pt who played a sport”
s/s: problems w/ diastole (enlarged interventricular septum), dyspnea
Dx: mitral regurgitation, murmur ↑ w/ valsalva
 Echo: thick interventricular septum
Tx: Abx’s (prophylaxis), BB, CCB, cardiac defibrillators, ↓ physical activity.
Restrictive Cardiomyopathy
 Atrium filled w/ infiltrates  ↑ effort by atrium to fill the ventricle  *atriomegaly  ↑ atrial &
venous pressures  backing up pf blood in periphery  peripheral edema, *edema at liver
(hepatojugular edema), *presence of S3 (fluid hitting fluid) & S4.
Dx:
 CXR: enlarged atria. Echo: normal ventricular cavity w/ larger wall. *Needle bx.
Tx: surgery (resection of fibrosis), vasodilators & dgitalis don’t work.