Abdominal Organs and Pain Locations

cecum, appendix, ascending colon, terminal ileum, and right ovary

localized parietal peritoneal signs: percussion tenderness, rebound, found as the disease progresses

Murphy sign: Inspiratory arrest with gently palpation of right upper quadrant owing to increased pain, found in most cases

liver, gallbladder, duodenum, head of pancreas, right kidney and adrenal, hepatic flexure of colon, part of ascending and transverse colon

stomach, spleen, left lobe of liver, body of pancreas, left kidney and adrenal, splenic flexure of colon, part of transverse and descending colon

Part of descending colon
Sigmoid colon
Left ovary and tube
Left ureter
Left spermatic cord

occurs when hollow abdominal organs such as the intestine or biliary tree contract unusually forcefully or are distended or stretched- usually nonspecific and difficult to locate

gnawing, cramping, or aching pain

as the pain progresses, systemic symptoms such as sweating, pallor, nausea, vomiting, and restlessness may follow

liver distention against its capsule from the various causes of hepatitis, including alcoholic hepatitis or biliary pathology

can be suggestive of early acute appendicitis from distention of an inflamed appendix. Gradually changing to parietal pain in the right lower quadrant from inflammation of the adjacent parietal peritoneum

originates from inflammation of the parietal peritoneum called peritonitis, can be localized or diffuse. A steady aching pain that is usually more severe than visceral pain and more precisely localized under the involved structure

typically aggravated by movement or coughing. Patients generally want to lie still

colicky pain- patient to move around frequently trying to find a comfortable position

pain felt in a part of the body other than its actual source

the initial pain becomes more intense and seems to radiate or travel from the initial site. Palpation at the site of referred pain does not result in tenderness.

may be referred to the back, pain from the biliary tree, to the right scapular region, or the right posterior thorax

the epigastric area

body position, association with meals, alcohol, medications, stress, and use of antacids

alarm symptoms: difficulty swallowing, pain with swallowing, recurrent vomiting, evidence of GI bleeding, early satiety, weight loss, anemia, risk factors for gastric cancer, palpable mass, painless jaundice

patients who have uncomplicated GET who fail empirical therapy, age > 55 years old

a metaplastic change in the esophageal lining from normal squamous to columnar epithelium,

diverticulitis

intermittent pain for 12 weeks of the preceding 12 months with relief from defecation, change in frequency of bowel movements, or change in form of stool.

stress incontinence: increased abdominal pressure causing bladder pressure to exceed urethral resistance. There is poor urethral sphincter tone or poor support of bladder neck

urge incontinence: urgency is followed by involuntary leakage due to uncontrolled detrusor contractions that overcome urethral resistance

overflow incontinence: neurologic disorders or anatomic obstruction from pelvic organs or the prostate limit bladder emptying until the bladder becomes overdistended

skin, temperature, color, scars, striae, dilated veins, rashes, umbilicus, contour of the abdomen, symmetry of abdomen, and pulsations

aorta, renal artery, iliac artery, femoral artery

place one hand under back-push deeply with fingertips of other hand in location of liver, as pt deeply inhales, the tip of the liver is sometimes felt

on inspiration, the liver is palpable about 3 cm below the right costal margin in the midclavicular line

mcburney's point, rovsing sign, psoas sign, and the obturator sign

Pushing on LLQ, referred pain in RRQ- indicative of appendicitis

passive extension of the hip leading to RLQ pain (appendicitis)

increased abdominal pain on either techinique is positive and may indicate appendicitis

passive internal rotation of the flexed hip leading to RLQ pain (appendicitis)

Abrupt cessation of inspiration on palpation of gallbladder

a sharp halting in inspiratory effort due to pain from palpation of the gallbladder on examination is a positive murphy sign- positive= acute cholecystitis

epigastric tenderness, rebound tenderness, and localized guarding. Abdominal wall is soft

confined inflammatory process usually in the left lower quadrant involving the sigmoid colon. May have suprapubic or right sided pain. Look for localized peritoneal signs and a tender underlying mass.

intercostal space between 4th and 5th ribs

2nd intercostal

level of the 4th rib

intercostal space between the 7th and 8th ribs as a landmark for thoracentesis with needle insertion immediately superior to the 8th rib

3 lobes

2 lobes

right bronchus is more vertical

a thorough past medical history, complete medication list, and allergy documentation

and investigate social history of tobaccoecreational drug use, occupational and environmental exposures, and travel history

based on the patient's daily activities- how many steps or flights of stairs can the patient climb before pausing for a breathing, how has it affect their life?

acute coronary syndrome

bronchiectasis and lung abscess

anaerobic lung abscess

thick tenacious sputum- mucoid sputum that is translucent, white, or gray

palce your thumbs at about the level of the 10th ribs, with your fingers loosely grasping and parallel to the lateral rib cage. As you position your hands, slide them medially enough to raise a loose fold of skin between your thumbs over the spine. ask the patient to inhale deeply- watch the distance between your thumbs as they move apart during inspiration and feel for the range and symmetry of the rib cage as it expands and contracts

an obstructed bronchus, COPD, pleural effusion, fibrosis, air/pneumothorax, or an infiltrating tumor

use either ball/the bony part of the palm at the base of the fingers or the ulnar surface of your hand to optimize the vibratory sensitivity of the bones in your hand.

Ask the patient to repeat the words "ninety-nine" or "one-one-one".

when fluid or solid tissue replaces air containing lung or occupies the pleural space beneath your percussing fingers

occurs when a complete obstruction is present and there is *no air exchange* in the chest

in pleurisy, pneumonia, and pulmonary embolism

As the pt to say "eee" for about 3-5 seconds. Auscultate the lungs and listen for a change in the character of the sound from that of "E" to "A"

while auscultating, have pt speak in normal voice and say 99 or 123. should be muffled. if sound is louder than expected, bronchophony is present, indicates consolidation

ask the patient to whisper ninety-nine or one-two-three. the whispered voice is normally heard faintly and indistinctly

posterior-interior lung fields

found in the 5th interspace lateral to the midsternal line
at or just medial to left midclavicular line

abrupt deceleration of inflow across the mitral valve

increased left ventricular end diastolic stiffness which decreases compliance

aortic +pulmonic valve is open allowing ejection of blood from the left ventricle into the aorta.

mitral + tricuspid valve is closed preventing blood from regurgitating back into the left atrium

aortic +pulmonic valve is close, preventing regurgitation of blood from the aorta back into the left ventricle.

The mitral +tricuspid valve is open allowing blood to flow from the left atrium into the relaxed left ventricle

A2 and P2 are primarily closures of the aortic and pulmonic valves which fuse into one S2 sound

an earlier mitral and a later tricuspid sound; mitral sound is heard throughout the precordium and loudest at the cardiac apex. The triscupid sound is best heard at the lower left sternal border

right second intercostal space or cardiac apex

left second and third intercostal spaces close to the sternum, but also at higher or lower levels

at or near the lower left sternal border

at and around the cardiac apex

Volume of blood ejected by the heart in one minute:
cardiac output = heart rate x stroke volume

the amount of blood ejected by the heart in any one contraction

refers to the load that stretches the cardiac muscle before contraction. The volume of blood in the right ventricle at the end of diastole constitutes its preload for the next beat

exhalation, dehydration, and pooling of blood in the capillary bed of the venous system

-left ventricular stroke volume
-distensibility of the aorta and the large arteries
-peripheral vascular resistance, particularly at the arteriolar level
-volume of blood in the arterial system

-is the pain related to exertion?
-what kinds of activities bring on the pain?
-how intense is the pain of a scale of 1-10?
-does it radiate into the neck, should, back, or down your arm?
-are they are associated symptoms like shortness of breath, sweating, palpitations, or nausea?
-does it ever wake you up at night
-what do you do to make it better?

anterior chest pain often tearing or ripping and radiating into the back or neck

upper back, neck, or jaw pain; shortness of breath, paroxysmal nocturnal dysnpea, nausea/vomiting, fatigue

obtain an ECG; includes atrial fibrillation which causes an irregularly irregular pulse

does this occur at rest, during exercise, or after exertion?
does it get worse when you lie down?
do you experience any nighttime episodes of sudden dyspnea that awakens you usually 1 or 2 hours after falling asleep, prompting you to sit up and stand up?

general appearance and measure bp and hr
estimate the level of jugular venous pressure
auscultate the carotids (bruit) one at a time
palpate the carotid pulse including carotid upstroke and presence of a thrill
inspect the anterior chest wall
palpate the precordium for any heaves, thrills, or palpable heart sounds
palpate and locate the PMI or apical impulse
Palpate for a systolic impulse of the right ventricle, pulmonary artery, and aortic outflow tract areas on the chest wall
Auscultate S1 and S2 in six positions from the base of the apex
Identify physiology and paradoxical splitting of S2
distinguish systolic and diastolic murmurs

Have your patient sit with their head at a 45 degree angle and measure the jugular vein pulsations from the angle of the sternum

auscultating the carotid arteries

presence of absence of a thrill

alternating weak and strong ventricular contractions; indicates severe left ventricular dysfunction

When the BP > 10 mmHg on expiration than on inspiration

heave, thrill, palpable S1 and S2, palpable S3 or S4, apical impulse and PMI, systolic impulse of the RV, pulmonary artery area, aortic outflow area

systolic: falls between S1 and S2
diastolic: falls between S2 and S1

palpating the carotid pulse as you listen can help with timing- murmurs that coincide with the carotid upstroke are systolic

- Innocent
- Physiologic
- Pulmonic stenosis
- Aortic stenosis

begins after S1 and stops before S2. Brief gaps are audible between the murmur and the heart sounds. listen carefully for the gap just before S2, which is more readily detected and if present usually confirms the murmur as midsystolic not pansystolic

mitral regurg
tricuspid regurg
ventricular septal defect

Starts with S1 and stops at S2, without a gap between murmur and heart sounds

mitral valve prolapse

usually starts in mid-or late systole and persists up to S2

Aortic regurgitation
Pulmonic regurgitation
starts immediately after S2 without a discernible gap, then fades into silence before the next S1

reflects turbulant flow across the AV valves

starts a short time after S2. It may fade away or merge into a late diastolic murmur

Starts late in diastole and continues up until S1

PDA or AVMs

begins in systole and extends into all or a part of diastole

grows louder

grows softer

first rises in intensity then falls

has the same intensity throughout

Very faint, heard only after listener has "tuned in"; may not be heard in all positions

softer in volume than S1 and S2, very faint

Quiet, but heard immediately after placing the stethoscope on the chest

moderately loud

loud with palpable thrill

Very loud, with thrill. May be heard when the stethoscope is partly off the chest

Very loud, with thrill. May be heard with stethoscope entirely off the chest

use your palm and hold your fingerpads flat against the chest. Heaves are sustained impulses that rhythmically lift your fingers, usually produced by an enlarged right or left ventricle and occasionally by ventricular aneurysms

press the ball of your hand firmly on the chest to check for a buzzing sensation

palpating for the systolic impulse of the RV

patient must be supine with head elevated to 30 degrees. Ask patient to exhale and briefly stop breathing, then place the tips of your curved fingers in the left third, fourth, and fifth intercostal spaces

pain and/or swelling of legs or arms
cramping in legs on exertion with relief with rest (intermittent claudication)
cold, numbness, pallor or discoloration int he legs; hair loss
abdominal, flank, or back pain

symptomatic limb ischemia
leg pain on exertion and rest and exertional leg pain/carry on

pain with walking or prolonged standing, radiating from the spinal area into the buttocks, thighs, lower legs, or feet

tricuspid stenosis

usually in cornea, anterior chamber- corneal ulcer, uveitis, traumatic hyphema, acute angle closure glaucoma

trauma, bacterial conjunctivitis, scleritis
optic neuritis of multiple sclerosis may be painful and needing immediate referral

Accumulation of blood, mainly RBC's that disperse and layer within the anterior chamber. A severe hymphema obscures entire anterior chamber + will diminish visual acuity severely or completely. Injuries are graded on amount of blood in chamber (Grades I-IV).
S/S:
- Blood in anterior chamber
- Deep, aching pain
- Mild to severe diminished visual acuity
- Increased intraocular pressure

myopia: nearsightedness
hyperopia: farsightedness

exam sclera, palpebral conjunctiva color, vascular pattern, nodules, swelling: yellow sclera= jaundice, local redness= nodular episcleritis

oblique lighting= assess each cornea for opacities

Conductive hearing loss occurs when sound conduction is impeded through the external ear, the middle ear, or both. Sensorineural hearing loss occurs when there is a problem within the cochlea or the neural pathway to the auditory cortex.

usually in cornea, anterior chamber = corneal ulcer, uveitis, traumatic hyphema, acute angle closure glaucoma.

Optic neuritis of multiple sclerosis may be painful = immediate referral

exam sclera & palpebral conjunctiva color, vascular pattern, nodules, swelling: yellow sclera = jaundice, local redness = nodular episcleritis

oblique lighting, note opacities

= w oblique lighting = assess each cornea for opacities

markings clearly defined? Shine light directly from temporal side

inspect each iris, markings clearly defined. Shine light directly from temporal side = crescentric shadow medial side
Iris bows abnormally far forward = very narrow angle w cornea, light casts a crescentric shadow medial side (see pp. 235 Bates). This angle increases acute narrow-angle glaucoma (sudden increase in IOP d/t aqueous humor blockage).

, normal = fairly flat w relatively open angle w cornea therefore no shadow. Narrow angle = increases narrow -angle glaucoma risk (increase in IOP w aqueous humor blocked).

normal spatial relation between iris & cornea = fully lit iris

difference in pupillary diameter 0.4mm> = no
pathologic etiology, ~35% healthy people rarely >1.0mm;
benign if = in dim & bright light w brisk constriction to light.
Assess direct reaction & consensual reaction; if impaired test near reaction in dimright light 1 eye 1 at a time = hold finger 10 cm from pt.'s eye, pt looks alternately at finger & into distance directly behind it.

Proptosis = abnormal protrusion of eyeballs (rim of sclera visible) = hyperthyroidism & characteristic stare on frontal gaze. Unilateral = orbital tumor, retrobulbar hemorrhage from trauma

Convergence = normal, eyes follow object within 5-8cm of nose; poor in hyperthyroidism

mydriatic eye drops = head injury & coma & any suspicion of narrow-angle glaucoma

= suggests lens opacity e.g. cataract, vitreous, artificial eye, possibly detached retina, retinoblastoma in children

inspect fovea & surrounding macula. Pt looks directly in light
macular degeneration = central vision loss in older
adults; dry atrophic = more common, less severe, wet
exudative, neovascular.

Drusen = cellular debris. Hard, sharply defined or soft & confluent w altered pigmentation.

Vitreous floaters = dark specks or strands
Between fundus & lens.

Cataracts = densities on lens

ETIOLOGY
¡Bacterial:
§Staphylococcus aureus
§Streptococcus pneumoniae
§Haemophilus influenzae
§Gonococcal:
▪Ophthalmic emergency
§Chlamydia:
▪Transmission occurs via autoinoculation from genital secretions. Often occurs in newborns

¡Viral:
§Adenovirus most common
§Epidemic keratoconjunctivitis (EKC) is caused by adenovirus subtypes.
§Frequently associated with upper respiratory infections or exposure to someone with a red eye
§Most commonly referred to as "pink eye"
§Herpes simplex virus (HSV)
§Recurrent ocular infection occurs in 25% patients within 2 yr.
§Use of steroids is contraindicated:
▪Allergic
§Frequent history of allergy, atopy, nasal symptoms
§Contact related
§May be due to chemical irritation, hypersensitivity from preservatives, medications, shampoo, chlorine, dust, smoke
§Pseudomonas commonly implicated organism:
May be found in patients using saliva to clean contact lenses

SIGNS AND SYMPTOMS
¡General:
§Red eye (conjunctival irritation)
§Gritty, foreign body sensation
§Sensation of eyes burning
§Discharge
§Eyelid sticking (worse upon awakening)
§Conjunctival edema (chemosis) and eyelid edema Itchy eyes
§Increased tearing
¡ Bacterial:
§Mucopurulent or purulent discharge
¡Gonococcal:
§Hyperacute, copious purulent discharge:
§Discharge starts 12 hr after inoculation.
§Severe chemosis
§Eyelid swelling
§Preauricular lymphadenopathy typically absent
§ Invades intact conjunctiva and cornea within 24 hr and causes ulcerations, scarring, and perforations leading to blindness

¡Chlamydia:
¡Lacrimation
¡Mucopurulent discharge
¡With or without photophobia
¡Concomitant genital infection (>50%)
¡Transmission occurs via autoinoculation from genital secretions
¡Viral—general:
¡Preauricular adenopathy
¡Viral syndrome:
¡Watery, mucous discharge, lacrimation
¡Gritty feeling or foreign body sensation in eye
¡Spreads to other eye in 24-48 hr
¡Pinpoint subconjunctival hemorrhages:
¡EKC:
§Conjunctival hyperemia
§Chemosis Corneal infiltrates
§Decreased vision
¡Contact related:
§ Acute symptoms result of corneal ulceration
§Normal visual acuity and intraocular pressures

¡
¡
¡
¡
¡HSV:
§Acute follicular conjunctival reaction
§Skin lesions or vesicles along eyelid margin or periocular skin
§ Corneal involvement—dendritic lesion
¡ Herpes zoster virus (HZV):
§Associated with pain or paresthesia of the skin
§ Rash or vesicles involving the distribution of cranial nerve V1
§Dendritic characters on cornea
§Rarely vesicles or ulcers form on the conjunctiva.
¡Allergic: Hallmark:
§ Itching Red conjunctiva
§Watery discharge
§ Papillary hypertrophy
§Frequent history of allergy, atopy, nasal symptoms

¡Onset of inflammation
¡Environmental or work-related exposure Ill contacts
¡Sexual activity, discharge, rash
¡Use of over-the-counter medicines or cosmetics
¡Systemic diseases
¡Careful physical exam including slit-lamp exam including fluorescein staining

¡Bacteriologic studies:
§Not indicated in routine cases
§Indications:
▪Ophthalmia neonatorum (except chemical)
▪Suspected gonococcal ophthalmia
▪Compromised host
▪Signs and symptoms of systemic disease
▪Refractory to treatment within 48-72 hr (with good compliance)
§Positive Gram stain for gram-negative intracellular diplococci:
▪Sufficient to initiate systemic and topical treatment for gonococcal disease
§Rapid plasma reagent (RPR):
For suspected cases of sexually transmitted disease

¡Be sure to disinfect slit lamp and chair used for patients to avoid contamination.
¡Conjunctivitis is extremely contagious.
¡Viral conjunctivitis contagious for up to 2 wk.
¡EKC is especially contagious.
§Extreme caution should be taken when using corticosteroids, as they may worsen an underlying HSV infection.

SIGNS AND SYMPTOMS
¡Severe ocular pain
¡Gritty (scratchy) discomfort
¡Tearing
¡Blepharospasm
¡Foreign body sensation
¡Photophobia (particularly if secondary traumatic iritis present)
¡Conjunctival injection
¡Diminished or blurred vision
¡Headache

¡If indicated, evaluate for other life-threatening injuries with attention to the primary survey.
¡Complete eye exam:
§Focus is to evaluate for evidence of penetrating injury and/or infection
§Gross visual inspection Visual acuity
§Penlight exam to evaluate for conjunctival injection, the pupil shapeeactivity, and for any evidence of corneal infiltrate or opacity
§Evert upper lids to check for retained foreign body
§Slit-lamp exam to evaluate for anterior chamber reaction, infiltrate, corneal laceration, and penetrating trauma
§Fluorescein dye to identify size and location of corneal epithelium defect

¡Always diligently evaluate for penetrating trauma to the globe.
¡
¡Always diligently evaluate for evidence of infection.
¡
¡Do not discharge the patient with any topical anesthetic.
¡
¡It is felt to be toxic to the epithelium and retards healing, although a recent small study indicated it might be safe to discharge with dilute proparacaine.
¡
¡Do not use a mydriatic agent on a patient with a history of glaucoma.
¡
¡Do not recommend return to contact use until followed up and cleared by ophthalmology.

¡Nonproliferative retinopathy (NPDR) consists of a variable display of nerve-fiber layer infarcts (cotton-wool spots), intraretinal hemorrhages, and hard exudates, and microvascular abnormalities (including microaneurysms, occluded vessels, and dilated or tortuous vessels) primarily in the macula and posterior retina
¡Visual loss in nonproliferative retinopathy is primarily through the development of macular edema (ME)
¡NPDR can be further classified into mild, moderate, severe and very severe categories
§This stratification primarily impacts the risk of progression to proliferative retinopathy, which influences follow up intervals and treatment strategies. Whereas the one-year risks of progression to proliferative retinopathy for mild and moderate nonproliferative retinopathy are 5 and 15 percent, respectively, the severe and very severe categories have respective one year risks of 52 and 75 percent

¡ Proliferative diabetic retinopathy (PDR) is marked by the presence of neovascularization arising from the disc and/or retinal vessels, consequences of this neovascularization, including preretinal and vitreous hemorrhage, subsequent fibrosis, and traction retinal detachment. PDR may develop in the setting of prior or coexisting severe nonproliferative changes, or may arise without substantial nonproliferative retinopathy.
¡Visual loss in PDR may occur acutely if bleeding from the abnormal vessels into the vitreous blocks the light path to the retina; however, the blood is often reabsorbed and vision clears spontaneously. More permanent loss of vision may occur through retinal detachment, ischemia of the macula, or combinations of these factors.

Subjective findings
¡Symptoms that may be present
§Flashing lights in peripheral visual fields
§Blurred vision
§"Cobwebs"
§Black spots
§Sudden loss of vision

SIGNS AND SYMPTOMS
¡Flashes of light
¡Floaters
¡Curtain-like vision loss
¡Peripheral/central vision loss or other visual field defects
¡Asymptomatic

History
¡Symptoms onset, course, description:
§May progress over hours or weeks
§Dark curtain or veil
§Usually begins peripherally
¡Associated symptoms: Flashing lights, floaters, painless
¡Ophthalmologic history: Baseline eyesight, myopia, surgery, eye disease, trauma
Systemic disease

Physical-Exam
¡Visual acuity, visual fields by confrontation—prior to dilation:
§May have normal visual acuity if macula spared Detachment is on opposite side of field defect
¡
¡May have afferent pupillary defect
¡
¡May have loss of red reflex
¡
¡Fundoscopy:
§Pale, opaque, wrinkled retina
§Cannot rule out detachment on fundoscopy alone
¡
¡Slit-lamp exam:
§Anterior vitreous pigment granules ("tobacco dust") suggest retinal tear.

Diagnostic Procedures/Surgery
¡Intraocular pressure (IOP) measurement: IOP usually lower in the affected eye
¡Dilating pupil with short-acting mydriatic carries very low risk of acute angle-closure glaucoma.

§Open angle: Painless and gradual loss of vision
§Closed angle: Painful loss of vision with fixed midsized pupil

¡Primary open-angle glaucoma:
§Gradual reduction in peripheral vision or night blindness
§Typically bilateral
§Painless
¡Primary angle-closure glaucoma:
§Severe deep eye pain and ipsilateral headache often associated with nausea and vomiting
§Decrease in visual acuity often described as visual clouding with halos surrounding light sources
§Associated abdominal pain, which may misdirect diagnosis
Concurrent exposure to dimly lit environment such as movie theater

¡Primary open-angle glaucoma:
§Decreased visual acuity
¡Primary angle-closure glaucoma:
§Decreased visual acuity
§Pupil is mid-dilated and nonreactive.
§Corneal edema with hazy appearance
§Conjunctival injection, ciliary flush
§Firm globe to palpation

¡Peripheral vertigo:
§Often, severe symptoms Intermittent episodes lasting seconds to minutes, occasionally hours
§Horizontal or horizontal-torsional nystagmus (also positional, fatigues, and suppressed by fixation)
§Normal neurologic exam
§Sometimes associated hearing loss or tinnitus
¡Central vertigo:
§Usually mild continuous symptoms
§All varieties of nystagmus (horizontal, vertical, rotatory)
§No positional association
§Presence of neurologic findings most of the time

Peripheral
¡Acute peripheral vestibulopathy (APV):
§Vestibular neuritis (most common):
▪Single acute attack continuous rotational vertigo
▪Constant for several days
▪Present even when still
▪No hearing deficits
▪Highest incidence in 3rd-5th decade
§Acute labyrinthitis:
▪Similar to vestibular neuritis but:
▪Associated with hearing deficit
▪May be viral (common), serous, acute suppurative, toxic, or chronic
¡
¡Benign paroxysmal positional vertigo (BPPV):
§Most common cause recurrent vertigo
§Posterior canal, 85-95% of BPPV cases
§Lateral semicircular less common
§Probable cause is loose particles (otoliths) in semicircular canals
§Can be secondary to other entities including trauma and APV
Ototoxic drugs:
§Aminoglycosides
§Antimalarials
§Erythromycin
§Furosemide
¡Ménière disease:
§Episodic vertigo, hearing loss, and tinnitus
¡Acoustic neuroma:
§Tumor of Schwann cells enveloping the 8th cranial nerve (CN VIII) Develops into central cause Progressive unilateral hearing deficits and tinnitus May also involve CN V, VII, or X
¡Trauma:
§Rupture of tympanic membrane, round window, labyrinthine concussion, or development of perilymphatic fistula can all have severe symptoms.
¡Otitis media and serous otitis with effusion
Foreign body in ear canal

¡Vertebrobasilar artery insufficiency:
§Disturbances may be transient or exacerbated by movement of the neck.
¡Cerebellar infarction
¡Cerebellar hemorrhage:
§Neurosurgical emergency
§Sudden onset of headache, vertigo, vomiting, and ataxia
§Visual paralysis to affected side
§Ipsilateral CN VI paralysis
¡Brainstem hypertensive encephalopathy
¡Trauma:
§Vertiginous symptoms common after whiplash injury
§Postconcussive syndrome or damage to labyrinth or CN VIII secondary to basilar skull fracture
§Vertebral artery injury has been seen after chiropractic manipulation.
¡Hypoglycemia

¡Hypertension is a medical condition in which blood pressure is higher than 140/90 mmHg in two separate occasions.
¡Hypertensive urgency- blood pressure of 220/120 mmHg or higher without any end organ damage.
¡Hypertensive emergency - blood pressure of 220/120 mmHg or higher with end organ damage.
¡Hypertensive encephalopathy - blood pressure of 240/140 mmHg or higher with neurologic symptoms.

Specific signs of left-sided heart failure include:
§Cardiomegaly
§S3 gallop
§S4
§Crackles (rales) in the lungs
§Dullness to percussion of the lungs
¡
Specific signs of right-sided heart failure include:
§Jugular venous distension (JVD)
§Liver congestion and hepatomegaly
§Ascites
§Peripheral edema
§Right ventricular heaves
§Nocturia

venous doppler ultrasound

most accurate test is venography

D-DIMER

¡ROS Intermittent claudication, muscular cramping with exercise; quickly relieved by rest. Pain in buttocks and thighs suggests aortoiliac disease; calf muscle pain implies femoral or popliteal artery disease. More advanced arteriosclerotic obstruction results in pain at rest; painful ulcers of the feet (sometimes painless in diabetics) may result.
¡
¡Physical Examination Decreased peripheral pulses (ankle:brachial index <1.0; <0.5 with severe ischemia), blanching of affected limb with elevation, dependent rubor. Ischemic ulcers or gangrene of toes may be present.
¡

§Occur when an ectopic focus in the atria fires before the next sinus node impulse. P waves usually look different (i.e., either smaller or peaked).
§Rate usually "resets" itself, resulting in one premature beat followed by a normal series of beats in sinus rhythm.

§No discernible P waves; fibrillatory waves are noted instead.
§PR interval is not measurable (wavy baseline).
§QRS complex is regularly irregular.
§Atrial rate is commonly 300 to 400 bpm or greater.
§Ventricular rate is usually 100 to 160 bpm or greater. B.
§Etiology.
▪Congestive heart failure
▪Hypoxemia
▪Valvular disease
▪Hyperthyroidism
¡Clinical manifestations.
§Patient may be asymptomatic.
§Patient may report palpitations
§Decreased cardiac output leads to hypotension and loss of consciousness.

§Sawtooth appearance of flutter waves (F waves), especially if the rhythm strip is turned upside down
§PR interval is not measurable.
§Atrial rate ranges from 240 to 360 bpm.
§QRS complex is usually normal.
§Etiology.
▪Congestive heart failure
▪Hypoxemia
▪Valvular disease
▪Hyperthyroidism
§Clinical manifestations.
▪Decreased cardiac output
▪Hypotension
▪Loss of consciousness
▪Treatment: same as for atrial fibrillation

§Because the beat originates in the atrioventricular (AV) node, usually, no P waves precede QRS complexes.
§Occasionally, P waves are retrograde conducted, resulting in a downward deflection before or after the QRS complex.
§Rate is usually 40 to 60 bpm (i.e., the intrinsic AV node rate).
§Accelerated junctional rhythms have the same criteria, but rates range from 60 to 100 bpm.
¡Rarely seen in adult patients
¡Etiology (common causes).
§Digitalis toxicity
§Theophylline
Dopamine

¡Irritability of the myocardium due to the following:
¡Electrolyte imbalance
¡Hypoxia
¡Acidosis
¡Myocardial infarction
§Other.
¡A stimulus from the ventricle replaces the sinoatrial (SA) node as the pacemaker for one or more beats, and contraction occurs without the usual transmission from the atrium.
¡Clinical manifestations.
§Patients may or may not be aware of PVCs.
§Symptoms are usually related to the number and frequency of abnormal beats.
§Patients may complain of "fluttering" or "palpitations" of the heart.
§On the monitor, PVCs exhibit a wide, bizarre configuration that is very different from that of the normal beat.
¡ Implications.
§PVCs that occur infrequently or have the same focus (i.e., have the same shape), are unifocal
¡An increase in the frequency of these beats is more significant, especially if the PVCs occur more often than 6 times per minute, or if the patient has had a very recent myocardial infarction. PVCs that are the result of more than one focus (i.e., multifocal) are more serious and may precede ventricular tachycardia or ventricular fibrillation.
§The risk is minimal if the beats are isolated.
§The danger increases if beats do the following:
▪ Are frequent (i.e., more than six per minute) I
▪Are multifocal (have different shapes)

§Irritability of the myocardium
§Series of ectopic electrical impulses from the ventricles assumes control of the heart rhythm.
¡Clinical manifestations.
§The monitor pattern shows a series of beats with wide, bizarre complexes.
§If conscious, the patient may feel palpitations or may be light-headed or dizzy, or have chest pain.
§Blood pressure usually drops significantly.
§A weak pulse may be present.
§If unconscious, the patient may appear clinically dead and may not have a pulse (if so, treat as ventricular fibrillation) or may demonstrate seizure-like activity.
§ Ventricular rate is 120 to 250 bpm.
¡Implications.
§If untreated, VT produces rapid hemodynamic decompensation caused by inadequate filling and emptying of the ventricles.
§If untreated, VT leads to VF, asystole, and death.

§Delay in the impulse from the atria to the ventricles characterized by a PR interval of longer than 0.20 second
§Rhythm is regular, and the QRS complex is not affected.
¡Etiology.
§Occurs in all ages in both normal and diseased hearts
§Drugs.
▪Digoxin
▪Beta blockers
▪Calcium channel blockers
▪Damage to the junction
¡Clinical manifestations: usually asymptomatic

Second-degree block (Mobitz type I) (Wenckebach)
¡Characteristics.
§Usually transient and occurs at the AV node
§Progressive prolongation of the PR interval until an impulse is completely blocked (dropped)
§Then, the pattern usually repeats.
§ R-R interval decreases prior to the blocked beat. 5. Atrial rhythm is usually regular, and the ventricular rhythm is usually irregular, with progressive shortening of the R-R interval before the blocked impulse.
§QRS complex is not affected.
¡Etiology
§Usually from drug effects (e.g., digitalis, verapamil, propranolol), or
§Myocardial infarction
¡Clinical manifestations.
§Often asymptomatic
§If symptomatic, may see the following:
▪ a. Decreased cardiac output
▪b. Hypotension
c. Loss of consciousness

Second-degree block (Mobitz type II)
¡Characteristics.
§Usually occurs below the level of the AV node
§Associated commonly with an organic lesion in the conduction pathway
§Associated with poorer prognosis than Mobitz type-I
§PR interval does not lengthen prior to a dropped beat.
§More than one dropped beat may occur in succession. 6. Sometimes associated with widened QRS complex
§Overall, the atrial rate is unaffected, but the ventricular rate is less than the atrial rate.
¡Etiology.
§Most often due to conduction path lesion
§Usually anterior myocardial infarction
§Clinical manifestations: same as second-degree type I.

Characteristics.
¡Complete absence of conduction between the atria and the ventricles
¡Atrial rate is unaffected, and the ventricular rate is slower than the atrial rate.
¡Ventricular rate is usually 40 to 60 bpm.
¡PR interval will vary because the atria and the ventricles are depolarized from different pacemakers.
¡Etiology.
§MI is the most common cause.
§May also be caused by digitalis toxicity or any other degeneration of the conduction system
¡Clinical manifestations.
§Otherwise, progressive decrease in cardiac output, loss of consciousness
Asymptomatic if the ventricular rate is adequate

¡Levine Sign":
§Clenched fist over chest, classic finding
¡BP often elevated during symptoms
¡Physical exam often uninformative
§occasional S3/S4,
§mitral regurgitation or new murmur (papillary muscle dysfunction)
diminished peripheral pulses

¡Standard 12 lead
§ Ideally should be obtained and read within 10 min of presentation for patients with acute chest pain
¡Mostly helpful in detecting acute MI, less so UA
¡Compare to prior ECG if available
§If normal or unchanged, serial ECGs every 10-30 min
¡New ST changes or T-wave inversion suspicious for UA
§T-wave flattening or biphasic T-waves
§≤1 mm ST depression 80 msec from the J point, is characteristic in UA
§Can see evidence of old ischemia, strain or infarct, such as old TWI, Q-wave, ST depression
§Single ECG for acute MI is about 60% sensitive and 90% specific
¡ECG can also be helpful to diagnose other causes of chest pain
§Pericarditis: Diffuse ST elevations, then T wave inversions and pulse rate depression
§Pulmonary embolus S1Q3T3 pattern, unexplained tachycardia and signs of right heart strain

Labs
¡For stable angina, cardiac enzymes not indicated, but if history suspicious for acute MI, should obtain.
¡CK-MB and troponin I or T <50% of patient with UA will have low level troponin elevations CK-MB peaks 12-24 hr, return to baseline in 2-3 days Troponin peaks in 12 hr, return to baseline 7-10 days
¡Hematocrit (anemia increases risk of ischemia)
¡Coagulation profile
¡Electrolytes, especially Cr and K+

Imaging
¡CXR:
§Usually nonrevealing
§May show cardiomegaly, or pulmonary edema, CHF suggests UA or MI.
§May be helpful in identifying other etiologies such as pneumonia, pneumothorax, or aortic dissection
¡Coronary CTA:
§Good for low-risk patients with no known CAD to rule out ischemia as cause of pain in patient if no coronary stenosis
§"Triple rule-out" for ACS, PE, and aortic dissection
¡Bedside echo: To detect wall motion abnormalities and other etiologies of shock, pericardial effusion, pneumothorax
¡Technetium Tc-99 sestamibi (rest): Radionucleotide whose uptake by myocardium is dependent on perfusion

Diagnostic Procedures/Surgery
¡Exercise stress testing: Not appropriate if active chest pain with moderate to high likelihood of ischemia Imaging stress test (sestamibi, thallium, or echo) if baseline ECG abnormalities Early positive (within 3 min) concerning for UA Coronary angiography: Gold standard of diagnosis for CAD

¡Chest pain:
§Most common presentation of MI
§Substernal pressure
§ Heaviness
§Squeezing
§Burning sensation
§ Tightness

¡Anginal equivalents (MI without chest pain):
§Abdominal pain
§Syncope
§Diaphoresis
§Nausea or vomiting
§Weakness
¡May localize or radiate to arms, shoulders, back, neck, or jaw
¡
¡
¡
¡Associated symptoms:
§Dyspnea
§Syncope
§Fatigue
§Diaphoresis
§Nausea
§Vomiting
¡Symptoms are usually reproduced by exertion, eating, exposure to cold, or emotional stress.
¡Symptoms commonly last 30 min or more.
¡Symptoms may occur with rest or exertion.
¡Often preceded by crescendo angina
¡May be improvedelieved with rest or nitroglycerin
¡Symptoms generally unchanged with position or inspiration

§EKG changes (ST-elevation, Q-waves (at least 0.04s and 25% of R wave), T- waves inversion
§Cardiac enzyme
CK-MB (increases during the first 4-8 hours; returns to normal values after 48-72 hours)
Troponin I/T (increases in the first 3-5 hours; returns to normal values after 5-14 days)* CK-MB is an important marker for reinfarction

Ischemia -T wave inversion, peaked T waved, and ST segment depression *with angina, cardiac changes usually do not persist once pain has been alleviated.

Injury-ST segment elevation greater than 1mm above baseline

Infarction- may produce Q waves (pathologic) greater than 25@ of QRS complex height or more than 1 mm wide (0.04s).

§Acute endocarditis is a febrile illness that rapidly damages cardiac structures, seeds extracardiac sites hematogenously, and can progress to death within weeks. Subacute endocarditis follows an indolent course, rarely causes metastatic infection, and progresses gradually unless complicated by a major embolic event or a ruptured mycotic aneurysm.

Causes/ Risk factors:
§Bacteria

Classification
§Acute Endocarditis (less than 6 weeks): The culprit is staphylococcus aureus (more common in IV drug abusers)
§Subacute Endocarditis is caused by:
▪Streptococcus viridians, most prone to dentistry procedures
▪Enterococcus (bacteria arise from GI tract)

Clinical Symptoms And Signs
¡Fever
¡Roth spots (retinal lesions due to vasculitis)
¡Osler's nodes (painful nodes in the pads of the finger or the toes due to vasculitis)
¡Murmur
¡Jane way lesions (lesions on the palm and the soles due to emboli)
¡Anemia
¡Nail bed hemorrhages/ Splinter hemorrhages
¡Emboli

Diagnosis
¡Blood culture
¡Transesophageal echocardiogram

¡Clinical symptoms and signs
§Retrosternal chest pain (pleuritic pain which radiates to trapezius or scapula)
§Leaning forward lowers the pain.
§Swallowing, cough, and lying down increase the pain.
§Fever
§Pericardial rub
§
¡
¡Diagnosis
§EKG
▪Diffuse S-T elevation
▪P-R depression (the most specific for pericarditis)
▪T wave inversion
§Echocardiogram

¡Malar flush ("mitral facies")
¡Prominent jugular
¡A-waves
¡Right ventricular lift
¡Loud S1
¡Opening snap
¡Low-pitched diastolic rumble
¡Exertional dyspnea
¡Fatigue
¡Palpitations
¡Paroxysmal nocturnal dyspnea
¡Orthopnea
¡Hemoptysis
¡Systemic emboli
¡Pulmonary edema

¡Acute pulmonary edema
¡Jugular venous pressure (JVP) exhibits cannon
¡A-waves and giant V-waves.
¡Harsh blowing apical crescendo-decrescendo murmur radiating to the axilla
¡Palpable thrill at apex
¡S3 and S4
¡Palpitations
¡Atrial fibrillation
¡Dyspnea
¡Orthopnea
¡Nocturnal paroxysmal dyspnea
¡Peripheral edema
¡Systemic emboli
¡Normal JVP
¡ Left ventricular hypertrophy (LVH)
¡Apical high-pitched pansystolic murmur
Decreased or obscured

¡Exertional angina
¡Syncope (during exercise)
¡CHF (initially diastolic failure, then systolic)
¡Sudden death secondary to ventricular fibrillation
¡Harsh crescendo-decrescendo (diamond-shaped) systolic murmur at aortic focus radiating to carotids
¡Absent aortic component of S2
¡Delayed upstroke in peripheral pulse (pulsus parvus et tardus)
¡S4 gallop
¡Ejection click

¡Fatigue
¡Dyspnea on exertion
¡Paroxysmal nocturnal dyspnea
¡Orthopnea
¡Syncope
¡Acute pulmonary edema
¡High-pitched blowing decrescendo diastolic murmur at aortic area
¡Accentuated A2 heart sound
¡Wide pulse pressure
¡Corrigan pulse (collapsing pulse)
¡Duroziez sign (to-and-fro murmur)
¡De Musset sign (head bobbing with systole)
¡Quincke pulse (nail bed pulsations)
¡Austin Flint murmur (soft diastolic rumble)

§Cardiac tamponade is impaired ventricular filling due to excessive pericardial effusion.

s/s: §Beck's triad:
▪JVD
▪Hypotension
▪Muffled heart sounds
§Narrowed pulse pressure (due to low stroke volume)
§Pulsus paradoxus (blood pressure decrease for >10mmHg during inspiration)
§Tachycardia

Diagnosis
¡Echo
¡Chest Xray
§Increased cardiac silhouette
§Clear lung fields