Rheumatic Heart Disease: GAS

Acute Rheumatic Fever: MECCS

Migratory Polyarthritis

Erythema marginatum

Cardiac involvement: Pericarditis, CHF, Valve disease

Chorea

Subcutaneous Nodules

Tx streptococcal pharyngitis with penicillin/erythromycin to prevent Rheumatic Fever

Tx acute rheumatic fever with NSAIDs + Penicillin/Macrolide to prevent recurrence

Infectious Endocarditis

Acute Endocarditis: normal heart valve -> Usually Staph Aureus

Subacute Endocarditis: damaged heart valves -> S. Viridans or Enterococcus

-> Most common valvular abnormality associated is MVP w MR

Native valve endocarditis: S. Viridans MCC

Prosthetic valve endocarditis: S. Epidermidis > Streptococci MCC of late onset

Endocarditis in IVDU: S Aureus, Candida and Pseudomonas

Complications: Hematogenous spread/septic emboli -> splenic abscess etc

Dx: 3-4 Positive Blood cultures; TTE then TEE; Duke Criteria
Janeway lesions (painless lesions on palms and soles); Glomerulonephritis

Osler nodes (painful, raised lesions of fingers, toes, or feet)

Roth spots (oval, retinal hemorrhages with a clear, pale center)

Rheumatoid factor

Tx: A gentleman’s Vacation ....; IV antibiotics

Tx empirically with vancomycin + ceftriaxone/gentamicin (synergistic) if no prosthetic valve

If prosthetic valve: Vanc + gentamicin + rifampin

Vancomycin to cover MRSA, Strep and Enterococci —-> switch to IV Pen G if penicillin Sensitive

Gentamicin —> severe aerobic GN

Ceftriaxone covers HÁČEK ——->>>>> Culture negative endocarditis: Think HÁČEK

If stroke d/t emboli consider valve replacement

Prophylaxis: qualifying cardiac indication AND procedure to warrant antibiotics

Qualifying cardiac indications:

Prosthetic valves

Hx of Infective Endocarditis

Congenital heart disease

Cardiac transplant with valvulopathy (structurally abnormal valve)

Qualifying procedures:

Dental procedures; biopsy or incision or resp mucosa; involve infected skin or MSK tissue

Not: NATIVE VALVE prolapse/stenosis, routine GI or GU procedures

IVDU IE
Multiple nodular pulm lesions with small cavities, typically in periph; HIV increases risk


Nonbacterial thrombotic Endocarditis (Marantic Endocarditis)

Associated with debilitating illness eg metastatic cancer

Sterile deposits of fibrin and platelets -> can embolism to brain or periphery

Heparin has no confirmed efficacy

Nonbacterial Verrucous Endocarditis (Libman): AV in individuals with SLE

Vegetations on BOTH sides of valve leaflets

Rarely leads to IE but can be source of emboli; regurgitate murmurs

Tx SLE and anticoagulation

CARDIAC Myxoma: Benign -> 80% in LA

Mid Diastolic rumble d/t position dependent mitral valve obstruction

-> Worsened by sitting upright, relieved by lying down

Constitutional sx: Fever, weight loss

Embolisation of tumour fragments

Acute Pericarditis

Uraemia —-> tx w hemodialysis

Collagen vascular disease: SLE, Scleroderma, RA, Sarcoidosis

Neoplasm; Amyloidosis; Radiation

Drug induced lupus syndrome: procainamide, hydralazine

After surgery: postpericardiotomy syndrome

Complications: Pericardial effusion; Cardiac tamponade

Chest Pain: Radiates to trapezius ridge and neck; shoulder pain

VPositional: relieved by sitting up and leaning forward

Pericardial Friction Rub: Specific pathiognomic Heard best during expiration with pt sitting up

Scratching, high pitched sound with up to 3 components:

Atrial systole; Ventricular systole; Early Diastole

Dx: Clinical + ECG

ECG: Diffuse ST elevations and PR depression; T wave inverts

ST segment typically returns to normal after a week

ECHO needed: often normal but used to assess for effusion and tamponade

Tx: Self limiting (2-6 wks)

NSAIDs then Colchicine (lowers rate of recurrence) —> Glucocorticoids only if refractory

Constrictive Pericarditis: BP low/norm cf tamponade + calcifications

Fibrous scarring Restricts diastolic filling of heart: filling unimpeded in early diastole

NB Ventricular filling impeded in ENTIRE DIASTOLE in TAMPONADE

Causes: Similar to acute pericarditis

Patients appear very ill

Elevated JVD: Prominent x and y descents -> resembles square root sign (y absent in tamponade)

Kussmaul sign: JVD fails to decrease during inspiration

Pericardial knock (corresponds to abrupt cessation of filling): mid diastolic sound

Pulses Paradoxus (abnorm large decreases in SV during inspiration -> >10)

ECG: Low QRS voltages, T Wave flattening/inversion

ECHO (see acute)

CT and MRI show calcification and thickening

Elevated and equal diastolic pressures in all chambers

Tx: diuretics in fluid overload, surgical pericardiectomy

DDX Amyloidosis: nephrotic disease + increased LV wall thickness

Pericardial Effusion
Muffled heart sounds; Dullness at lung base (compressed by pericardial fluid)

Dx: ECHO

CXR: Enlarged cardiac silhouette -> water bottle appearance

ECG: Low QRS voltages and T wave flattening

Electrical Alternans: Massive effusion + tamponade

—-> Electrical alternans with Sinus tachycardia highly specific!

Tx: Pericardiocentesis not indicated unless evidence of tamponade/haemo instability

If effusion small and clinically insignificant a repeat ECHO in 1-2 wks will suffice

Cardiac Tamponade
Mechanical impairment of diastolic filling -> Elevated and equalised diastolic pressures

Decreased filling leads to decreased stroke volume and cardiac output —-> Decreased Preload

Iatrogenic (central line, PM insertion, pericardiocentesis, CABG)

Pericarditis; METASTASES; Post MI with free wall rupture

Elevated JVP (distended neck veins)

Narrowed pulse pressure d/t decreased stroke volume

Pulses Paradoxus: >10mg

Tachypnea, tachycardia and hypotension with onset of cardiogenic shock

—-> Increased contractility and HR; cold clammy peripheries w cyanosis

Beck Triad: Hypotension, muffled heart sounds, JVP

Dx: ECHO

CXR: Enlarged cardiac silhouette w clear lung fields

ECG: Electrical Alternans: Alternate beat variation in direction of ECG waveforms

D/t pendulum swinging of heart within pericardial space (motion artifact)

Cardiac catheterisation: Equalisation of pressures in all chambers; Loss of y descent

Tx: Hemostable: monitor + IV fluid boluses

Hemodynamically unstable: percutaneous pericardiocentesis first line

Emergent surgery if hemorrhagic tamponade

—> do not delay surgery for pericardiocentesis in traumatic tamponade

Surgical drainage if purulent

Hypertensive Emergency

Systolic >220 and/or diastolic >120 + end organ damage: immediate treatment

W/o end organ damage -> Hypertensive Urgency: BP lowered over 24hrs

Eyes -> papilledema ->>> Visual disturbances

CNS: altered mental status or intracranial hemorrhage. —> Severe HA

Hypertensive encephalopathy may develop: Altered mentation

End Organ damage: AKI; CHF with pulm oedema, aortic dissection; MI

Non compliance with BP medications/dialysis

Cushing syndrome; Alcohol withdrawal; Pheochromocytoma; Polycystic kidney disease

Renal artery stenosis (atherosclerosis/ fibromuscular dysplasia)

Reduce MAP by 25% in 1-2 hours; IV agents in emergency, PO in urgency

Short acting agents: esmolol, nitroprusside, labetalol or nitroglycerin

May lead to posterior reversible encephalopathy syndrome (PRES)

-> Elevated BP overwhelms autoregulatory mechanisms of cerebral vessels

—->> arteriolar dilation and extravasation of fluid into brain

 May not be reversible and affects areas other than posterior brain also

Insidious onset of headache, altered consciousness, visual changes and seizures

Classic radiology of posterior cerebral white matter oedema

Pts may be normotensive

Dx clinically + MRI

Tx: Lower BP with IV meds, correct electrolytes and seizure cessation

BBs; CCBs; Nitrates (Nitroprusside/nitroglycerin)

Resistant HTN
Renovascular HTN (renal artery stenosis) most common
Elevated Cr; RAAS activated-> hypokalaemia

Recurrent flash pulm oedema; Diffuse atherosclerosis (PAD)

Onset of severe HTN after age of 55; HTN ===> shrinks kidney (norm size =12cm)

Presence of continuous abdominal bruit

Aortic Dissection

Predisposing factors: Long-standing HTN MCC

Cocaine; Marfans / ED; Bicuspid aortic valve/ Coarctation of aorta

Third trimester of pregnancy

Type A (proximal) involves ascending aorta ——> widened cardiac silhouette

Type B (distal) limited to descending aorta (distal to subclavian artery) ->>> Type A

Severe tearing/ripping/stabbing pain: Anterior/back of chest (often interscapular region)

Diastolic Murmur in upper sternal area

D-Dimer elevation d/t fibrin degradation products

Most hypertensive but some hypotension

Pulse or BP asymmetry between arms (>20mmHg)

Aortic regurgitation (proximal extension) and pericardial effusion (esp Type A)

Distal extension into renal arteries: elevated Cr

Neurological manifestations: hemiplegia, hemianesthesia, d/t obstruction of carotid A

CXR show widened mediastinum

Dx: CT angiography initial study of choice if hemodynamically stable and no renal dysfunction:

Intimal flap separating true and false lumens

TEE can be done at bedside (hemodynamically unstable pt test of choice)

Tx: Medical tx immediately: IV beta blockers (initial tx of choice) + IV sodium nitroprusside

Type A: Surgical management

Type B: Medical management:

IV labetalol, esmolol, propranolol

Morphine or dilaudid for pain

Rupture of thoracic aorta (Incomplete/complete)

Hidden injury: Aortic isthmus most vulnerable

Rapid deceleration injury (eg fall), breakage of first rib

Widened mediastinum

Obstructive intimacy flap or intramural hematoma:

Impedes blood flow (pseudocoarctation)

Proximal HTN and distal hypotension (diminished femoral pulses)

Expansion of adventitious under high flow pressures compresses/stretches surrounding structures:

L recurrent laryngeal N: Hoarseness

Dx + Tx: See dissection

Widened mediastinum does not always indicate injury: confirm with CT angiography

Abdominal Aortic Aneurysm

Most occur between renal arteries and iliac bifurcation

Most cases there is atherosclerotic weakening of aortic wall

Smoking greatest RF

Syphilis and CT abnormalities (Marfans) associated with thoracic aneurysms but may affect lower aorta

Sense of ‘fullness’; Pulsatile mass on Abdo exam

Pain may be present (throbbing character) —> abdo, flank, back or groin

Prevertebral aortic calcification on plain X-RAY

Dx: Abdo CT w contrast in symptomatic patients and haemo stable + AAA known

FAST if unstable

Tx: Aneurysm >5.5 cm or symptomatic needs surgical resection with Syn graft placement

Asymp and <5.5cm: periodic US although even small ones can rupture

US Screening: 1 time in M 65-75 w any hx of smoking/family hx of AAA

Rupture/impending rupture/expansion of AAA:

Triad: Sudden onset of severe pain radiating to groin/buttocks/legs, hypotension and pulsatile mass

Emergent laparotomy

Umbilical/flank hematoma: Grey Turner and Cullens sign

Rapid expansion -> distal embolism of debris -> Distal ischemia/decreased pulse

Smoking cessation best intervention to minimise AAA progression!

Complication of AAA repair: Bowel ischaemia d/t inadequate perfusion d/t loss of IMA

Peripheral Vascular Disease (Chronic Arterial Insufficiency)

Sites of occlusion/stenosis: Superficial femoral artery most common

Popliteal artery

Aortoiliac occlusive disease (Leriche syndrome):

—->>> atheromatous occlusion of distal aorta just above bifurcation

Bilateral claudication, impotence and absent/diminished femoral pulses

Risk Factors: SMOKING!!!!!!!

Intermittent claudication -> pain completely relieved by rest

Rest pain (continuous)

Felt over distant metatarsals (arteries smallest)

Often prominent at night (awakens pt)

Hanging foot over side of bed/standing relieves pain (extraperfusion d/t gravity)

Hair loss/decreased growth, thickened toenails, decreased skin temperature, muscular atrophy

Ischemic ulceration (usually toe) -> Tissue infarction/gangrene in late disease

Bruits, often cocomittant with renal artery stenosis

Complication: Compartment syndrome

Ankle-to-brachial index (ABI): initial test of choice and dx (not gold standard)

Ratio of systolic BP at ankle to systolic BP at arm (Norm is between 0.9 and 1.3)

ABI>1.3 d/t noncompressible vessels (severe disease)

Claudication ABI <0.7

Rest pain ABI <0.4

Patients with calcified arteries (esp DM) have false ABI readings (vessels not compressible)

Arteriography (contrast) is gold standard for dx and locating PVD —->>> invasive

Tx: Stop smoking!!!!!! Graduated exercise; Foot care

Anti Plt tx: stroke/MI prevention and mild sx relief

 Cilostazol (PDEI) suppresses Plt aggregation and dilates arterioles

Surgery if rest pain, ulceration, refractory to medical therapy -> Angioplasty; stenting; Bypass graft

Acute Arterial Occlusion: IV heparin

Usually d/t embolisation

Common femoral artery most common site of occlusion

Six P’s: Pain, Pallor, Polar, Paralysis, Parathesias, Pulselessness

Immediate anticoag prior to any dx scans: IV heparin

Dx: Clinical; Arteriogram/ CT Angiograpy to define site of occlusion

ECHO to evaluate cardiac source of emboli

Tx: Skeletal muscle can tolerate 6 hrs ischemia (thrombolytic window)

Emergent embolectomy -> Bypass if refractory

Cholesterol Embolisation Syndrome

D/t cholesterol crystals originating from a proximal source eg atherosclerotic plaque

Often triggered by a surgical or radiographic intervention (eg arteriogram) or thrombolytic therapy

Eosinophilia with poss eosinophiluria

Livedo reticularis (bilaterally in legs typical), gangrene, ulcers, amaurosis fugax,

Blue toe syndrome: cyanotic toes with intact pulses

Hollenhorst plaques (ocular): bright yellow refractive plaques in retinal artery

AKI, pancreatitis, intestinal ischemia -> GI Bleeding

Tx is supportive, do not anticoagulate

Mycotic Aneurysm

D/t damage to aortic wall secondary to infection

Tx: IV antibiotics+surgical excision

Luetic Heart: syphilitic aortitis

Usually affects men in their 40s and 50s

Aneurysm of aortic arch with retrograde extension

AR and stenosis of aortic branches, commonly coronary arteries

Tx: IV penicillin and surgical repair

Coarctation of Aorta

Narrowing/constriction of aorta

Leads to obstruction between proximal and distal aorta and thus increases LV afterload
—> sustained apical impulse

Midsystolic murmur heard best over back (interscapular) or continuous d/t collateral vessels

Cold extremities, claudication with exercise and leg fatigue

Prevalence increased in Turner syndrome (bicuspid too)

Epistaxis and HA d/t HTN

ECG shows LV hypertrophy: S4 —-> High voltage QRS, ST depression, T wave inversion

CXR: notching of ribs: Figure 3 appearance

Dx: ECHO

Tx: surgical decompression, balloon angioplasty +/-stent

Complications: Severe HTN; Rupture of cerebral aneurysm; Aortic dissection

Deep Vein Thrombosis

Virchow triad: endothelial injury, venous stasis and hypercoagulability

Risk Factors:

Malignancy; Obesity; Prior DVT, PE or varicose veins

Hypercoagulable states, Prolonged immobilisation or bed rest

Major surgery, esp surgery of pelvis (orthopaedic procedures); Major trauma

Leg pain and swelling that improves with rest/elevation

Homans sign: calf pain on dorsiflexion; Palpable cord

Dx: Compression US recommended as initial test prior to anticoag unless PE suspected

Doppler and Duplex US

Intermediate-high protest probability of DVT

If Doppler + start anticoagulation; If Doppler - repeat for 2 weeks

Low-intermediate probability of DVT

If Doppler - then no anticoagulation, repeat in 2 days

Complications: PE (femoral vein most likely source)

Postthrombotic syndrome (chronic venous insufficiency)

Phlegmasia cerulea dolens (painful, blue, swollen leg)

Major venous obstruction -> leg oedema compromises arterial supply to limb

Venous thrombectomy indicated

Tx: Oral Heparin

Start warfarin once aPTT therapeutic and continue for 3-6 months

+ Continue heparin until INR has been therapeutic for 48 hrs

Thrombolytic therapy Indicated if massive PE and hemodynamically unstable and no CI

IVC filter: If CI to anticoagulation or failure of anticoagulation

Prophylaxis post surgery:

Unfractionated Heparin or LMWH until patient ambulatory (warfarin second line)

Upper extremity DVT:

PICC related/Central catheter DVT; Spontaneous (Young athletic M); Thoracic outlet syn

Dx: Doppler/duplex US

Tx: 3 months anticoagulation

NB: Use of multivitamins can decrease efficacy of warfarin as most contain Vit K!

Chronic Venous Insufficiency (postphlebitic syndrome)

May involve superficial, deep or both venous systems

Hx of DVT: Causes destruction of venous valves in deep venous system

Ambulatory HTN

Induration and brown/black pigmentation of skin -> stasis dermatitis

Reduced local capillary blood flow and hypoxia of tissues

Lower leg swelling: Leg elevation provide relief (opp in arterial insufficiency)

Skin changes: Skin becomes thin, dystrophic, shiny and cyanotic

Varicose veins: Serpentine cord like lesions

Venous ulcers: Less painful than arterial insufficiency ones; itchy?

Usually just above medial malleolus

Dx: Duplex US

Tx: Leg elevation and knee length stockings (compression therapy)

If ulcers: wet saline dressings,

Superficial Thrombophlebitis:

In legs associated with varicose veins (greater saphenous system), secondary to blood stasis

Pain, tenderness, induration and erythema along course of vein -> Tender cord may be palpable
No anticoagulation needed as rarely causes PE (use sc if DVT risk factors for progression)

Mild analgesic (aspirin or NSAIDs); elevation and hot compresses, continue activity

If suppuratve thrombophlebitis

Septic phlebitis often d/t infection of IV cannula

Redness extends beyond area of vein with purulent drainage

Remove cannula and give systemic antibiotics

Decompression Sickness

Sx within 12 hrs surfacing

Mottling and cyanosis of extremities

Resp distress and localised ischemia ——->>> pulm oedema

Brain, heart etc: obstructive shock, confusion; sx of stroke etc etc

Flu like sx; Swelling/pain in muscles and joints

—-> remember association of decompression sickness and avascular necrosis

Tx: IV hydration, Trendelenburg positioning (feet above head in supine)

Immediate admin of O2 ——> facilitates absorption of Nitrogen gas from bloodstream

Hyperbaric O2 therapy

Fibromuscular Dysplasia
Can involve any artery

Renal A stenosis: Abdo bruit; Resistant HTN w Flank pain

Increase Cr after starting ACEI or ARB

Onset of HTN >35

Aldosterone levels and renin levels both increase (norm ratio)

Cerebrovascular compromise can cause sx of brain ischemia —> subauricular bruit

——>>> TIA, headache, pulsatile tinnitus, dizziness etc

Dx: CT/MR Angiography, duplex US —-> string of beads on angiography

Tx: ACEIs/ARBs first line; Angioplasty

Renal Artery Stenosis

RFs: Atherosclerosis and fibromuscular Dysplasia

Dx: Best initial test is US; Best dx is CT Angiography

Tx: ACEIs/ARBs (CI if bilateral/only 1 kidney); CCBs; Revascularisation

Cyanosis

Central cyanosis

Significant amount of deoxygenated Hb in blood —>> low arterial O2 saturation

Bluish discolouration of nail beds, lips and tongue

Warm extremities

Peripheral cyanosis: Extremities cool and clammy

Normal arterial oxygen saturation and increased extraction d/t sluggish blood flow through capillaries

Bluish discolouration of distal extremities only

Subclavian Steal Syn

Stenosis of subclavian artery proximal to vertebral artery

Blood flows retrograde typically down LEFT vertebral artery to supply distal subclavian

BP in LEFT ARM < BP in RIGHT ARM; Upper extremity claudication

Dx: Doppler US

Tx: surgical carotid subclavian bypass

Congestive HF: Elevated BNP and S3 Gallop specific signs

Systolic Dysfunction (decreased EF): EF < 55% ischemic heart disease MCC

Less commonly: Alcohol, radiation, Hemochromatosis, thyroid disease

Alcoholic Dil CO is reversible with alcohol cessation! Dilated CO: Eccentric hypertrophy

Diastolic Dysfunction: Increased filling P

Either d/t impaired relaxation, increased ventricular stiffness (hypertrophy) or both

HTN -> (most common cause) —-> Concentric Hypertrophy

Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis)

—-> Hemachromatosis restrictive CO reversible with phlebotomy

High Output HF:

Increased cardiac output (systolic murmur) in response to disturbance causing reduced SVR:

Peripheral vasodilation d/t unmet metabolic demand

——-> Chronic anemia; Hyperthyroidism; Pregnancy, Wet Beri Beri

Increased quantity of peripheral vessels: Paget disease of bone; morbid obesity

Bypass of systemic arteriolar resistance: AV fistulas

MR; Aortic insufficiency

High EF eg 70%; widened pulse pressure

Eccentric LV HTN may occur —> laterally displaced point of max impulse

Left Sided HF:

Orthopnea; Paroxysmal nocturnal dyspnea; Nocturnal cough (nonproductive)—> worse lying down

Diaphoresis and cool extremities at rest—-> NYHA class IV

Displaced PMI d/t cardiomegaly

S3 (ventricular gallop)—-> ken-tuck-Y: Heard best at apex. May be norm in children

S4 gallop (TEN-nes-see): Heard best at Apex with bell

Right HF:
Nocturia d/t increased venous return with elevation of legs

JVD; Hepatomegaly/hepatojugular reflux (specific); Ascites

RV heave

New York Heart Association (NYHA) Classification:

• NYHA class I: Patients are nearly asymptomatic

• NYHA class II: Symptoms occur with activities such as climbing a flight of stairs

• NYHA class III: Symptoms occur with usual activities of daily living

• NYHA class IV: Symptoms occur at rest. Incapacitating

Dx: CXR: Use initially if pneumonia sx eg consolidation

Cardiomegaly

Kerley B lines: horizontal lines nr periph of lung nr costophrenic angles

-> pulm congestion secondary to dilation of pulm lymphatic vessels

Echo (TTE): Initial test of choice; ECG often nonspecific

Radionucleotide ventriculography using technetium-99m (MUGA)

BNP Levels >150pg/ml support decompensated HF

Tx: Combo of diuretic and ACEI should be initial tx

Systolic dysfunction: Diuretic, ACEI, BB, Aldosterone antagonist (in that order)

Diuretics: Most effective symptomatic relief -> Do not improve mortality or prognosis

Spironolactone: decrease mortality in CHF classes III and IV

Alternative is eplerenone (doesn’t cause gynecomastia)

ACE Inhibitors: Block aldosterone remodelling -> Reduce mortality

Decrease Preload and Afterload

Beta blockers: Decrease mortality -> Metoprolol, Bisoprolol, Carvedilol (best choice)

Slows progression of HF by slowing tissue remodelling (d/t epinephrine/NE)

Digoxin: pts with EF <40% who continue to have sx despite optimal therapy

No effect on mortality (decreases hospital admissions)

Increases vagal tone; common issue is atrial tachy with AV block

Hydralazine and isosorbide dinitrates —> reduce preload and afterload

Pts who cannot tolerate ACEI

Improves mortality if Black

Following are CI in patients with CHF

Metformin—-> potentially lethal lactic acidosis

Thiazolidinediones——-> fluid retention

NSAIDs——-> may increase risk of CHF exacerbation

ICD lowers mortality in pts with EF <35%

Diastolic Dysfunction: Symptomatic tx only

No medication proven to decrease mortality

Beta Blockers and diuretics only drugs that have clear benefit

Signs of digoxin toxicity: More likely if pt hypokalaemia/renally impaired

Nausea/vomiting, anorexia: Tachycardia w AV block; Visual disturbances

Inciting event (viral illness) can cause volume depletion or renal injury

—->>>>> Acute elevation of digoxin levels occurs

NB: Digoxin increase contractility but decreases HR!

Tachycardia mediated cardiomyopathy

AF, Flutter, VT, AVRT etc

Chronic tachycardia causes structural changes in heart inc LV dilatation and myocardial dysfunc

Tx underlying arrhythmia —> normalises LV function

Acute Decompensated HF

Worsening/exacerbation of sx

Flash pulm oedema

Tx: Oxygenation and ventilatory assistance needed

If BP norm/elevated: diuresis and poss vasodilator

Low BP: Diuresis and vasopressor!

Use dobutamine if inotrope needed

Early use of Noninvasive ventilation if resp distress gives rapid improvement

Digoxin not used in acute setting as takes several weeks to work

HF w preserved EF (>50%) common cause for acute decompensated HF

Signs of HF with norm/near normal LV EF

HF w reduced EF —-> EF <40%

Peripartum Cardiomyopathy (form of Dil. Cardiomyopathy)

Rapid Onset of HF during final month (>36 wks) of pregnancy or within 5 months of delivery

S3 (decomp HF)

Mitral regurgitation

Dx: Transthoracic Echo

Urgent/immediate delivery only if adv HF or hemodynamic instability

Isolated ambulatory HTN (Masked HTN)

Evidence of hypertensive end organ damage:

Hypertensive retinopathy; increased QRS Voltage (LV Hypertrophy)

Dx: Ambulatory BP Monitoring: Useful for unexplained syncope and dizziness

HTN: First Line DOCs: Thiazides and beta blockers

Metabolic Syn X: insulin resistance d/t obesity; hyperuricaemia

Syndrome X: Exertional angina with NORMAL coronary arteriogram -> Excellent Px

Exercise testing and nuclear imaging show evidence of myocardial ischemia

Stable Angina Pectoris: Form of CAD

Major Risk Factors: DM——> WORST risk factor; HTN——> MOST COMMON

Angina Pain: Substernal; Worse on exertion; Improves with rest/nitroglycerin

Typical: All 3. Does not change with breathing or body position, no chest wall tenderness!

Atypical: <3 Dyspnea, nausea/vomiting, epigastric pain

Dx of CAD: Best initial test for all forms of chest pain: ECG!

Resting ECG: Often norm in stable angina; Q waves indicate previous MI

Stress ECG (high sensitivity)

Exercise induced ischemia causes subendocardial ischemia: ST depression

Pts with a positive stress test should undergo cardiac catheterisation

Stress test considered positive if pt develops any of the following during exercise:

ST depression, chest pain, hypotension or significant arrhythmias

LBBB and digoxin make ECG interpretation difficult: Stress Echo
Stress Echo

Exercise induced ischemia: wall motion abnormalities (akinesis/dyskinesis) not present at rest

Pts with positive stress ECHO should undergo cardiac catheterisation

Thallium 201 or Technetium during exercise (nuclear perfusion imaging)

MUGA: myocardial perfusion imaging after IV radioisotope

Pharmacological stress test: Pt cannot perform exercise

IV adenosine, dobutamine or dipyridamole

Adenosine/dipyridamole cause coronary vasodilation: Diseased arteries already maximally dilated

Dobutamine increases myocardial O2 demand via increasing HR, BP and contractility

Cardiac catheterisation with coronary angiography———> DEFINITIVE test for CAD

CONTRAST used to visualise any stenosis lesions

Coronary stenosis >70% can produce angina

Tx: SMOKING CESSATION halves risk within a year of quitting

HTN esp if DM

Hyperlipidaemia: lifestyle and statins

ASPIRIN (all pts with CAD): Decreases morbidity and reduces risk of MI

Beta blockers: angina prophylaxis (reduce O2 demand)

Nitrates: Generalised vasodilation

Pain relief via decrease in heart wall stress

Side effects: Headache, orthostatic hypotension, tolerance, syncope

CCBs: Secondary tx if beta blockers and/or nitrates ineffective

May increase mortality can reflex increase HR!!!! —> Use concurrent beta blocker

Ranolazine:

Decreases myocardium calcium level by inhibiting late phase Na influx into ischemic myocytes

Revascularisation: PCI (angioplasty) and CABG -> Does not reduce incidence of MI

PCI -> Restenosis in up to 40% within 6 months -> Drug eluting stents prevent this

Unstable Angina USA (ACS along with MI)

May lead to total occlusion (MI) —->>> Give all IV LMWH + Aspirin +/- clopidigrel

Distinction between Unstable Angina and NSTEMI based solely on cardiac enzymes:

—>>> Troponin and/or CK-MB

Both lack ST elevation and pathological Q waves

Dx: See Stable Angina

Pts with unstable angina at higher risk of adverse events during stress testing:

-> Should be stabilised medically before stress testing or undergo catheterisation initially

Tx: Tx as MI except for thrombolysis

Aspirin; Nitrates (CI in RHF); O2 if hypoxic

Clopidogrel (reduces incidence of MI aspirin alone)

Beta blockers: First line therapy if no CI

IV LMWH -> Enoxaparin DOC

Morphine can mask worsening sx (CI in RHF)

Cardiac catheterisation/revascularisation

Controversial if superior to medical management

After acute tx: Continue aspirin/anti platelet drug, beta blocker and nitrates

Pts with any form of CAD regardless of LDL levels should be put on a STATIN

Prinzmental Angina

Transient coronary vasospasm usually accompanied by a fixed atherosclerotic lesion

->>> Can occur in norm coronary arteries also

Episodes of angina at rest associated with ventricular dysrhythmias -> May be life threatening

Classically occurs at night ->> Classically F who also has migraines

Transient ST elevation on ECG during chest pain, represents transmural ischemia

Coronary angiography is definitive test w Stimulation Tests

—->> Shows vasospasm when pt given IV ergonovine/Ach (provokes vasoconstriction):

Vasodilators: CCBs and nitrates proven helpful

Risk factor modification where appropriate

Myocardial Infarction

Chest pain: Typically does not respond to nitroglycerin

Painless or atypical infarcts more likely in postoperative pts, elderly, diabetic and F

Sense of impending doom

Sudden cardiac death (usually d/t VFib)

ECG:

Peaked T Waves: occur v early and may be missed

ST elevation indicates transmural injury

Q Waves: Specific for necrosis: seen late (not acutely): last forever

ST depression: Subendocardial injury

New LBB Block

S4 d/t ishaemia induced myocardial dysfunction

RV infarct: Inf ECG changes, CLEAR LUNGS

Preload dependent so avoid nitrates, morphine or diuretics as will cause CV collapse

Acute Inferior infarct: Papillary muscle displacement and subsequent MR and pulm oedema

STEMI: 2mm in 2 + anatomically contiguous leads

Cardiac enzymes: Dx Gold Standard for MI

Myoglobin: Rises in first hr, peaks in 2hrs, norm by 24hrs

Troponins: Most important to order

Increases within 3-5hrs and returns to norm in 5-14 days

CK-MB

Increases within 4-8hrs and returns to norm in 3 days;

Useful in detecting recurrent infarct

Tx: Similar to USA: MONA BASH C

ASPIRIN; Reduces mortality; Part of LT maintenance tx

Beta Blockers; Reduce remodelling of myocardium post MI; Part of LT maintenance tx

ACE Inhibitors; Reduce mortality; Part of LT maintenance tx

Statins; Reduce risk of further events; ATORVASTATIN superior; Part of LT maintenance tx

Oxygen

Nitrates: Dilate coronary arteries + Venodilation (decrease preload and thus demand)

Morphine Sulfate: Analgesic; decreases preload and thus O2 demand

Heparin: prevents progression of thrombus; NOT shown to decrease mortality

Enoxaparin superior in decreasing risk of further MI

In MI only aspirin, Beta blockers and ACE Inhibitors reduce mortality

Revascularisation: Thrombolysis, PCI or CABG

PCI superior than thrombolysis but if delayed presentation tPA may be better

Urgent/Emergent CABG NOT used in acute setting on a stable patient

Clopidogrel: Benefit is additive to effects of aspirin

PCI: Door to balloon < 90min by skilled personnel (only available at specialised centres)

STEMI Sx developed <12hrs

Reduces mortality more than tPa

Thrombolytic therapy: Up to 24hrs after onset of chest pain: Used if PCI window lost

Outcome best if given within first 6hrs

Alteplase has best outcome and is first choice but expensive

Absolute CI to tPA:

Recent head trauma or traumatic CPR/ Previous stroke in last 3 months

Hx of hemorrhagic stroke

Recent invasive procedure/surgery

Dissecting aortic aneurysm

Active bleeding or bleeding diathesis

Complications of acute MI:

Pump Failure —-> cardiogenic shock

VFib: Sudden death d/t reentrant arrhythmia IMMEDIATELY post MI (post ischaemic damage)

Or d/t abnorm automaticity (10-60 min post MI)

Acute MR: Immediate cf papillary muscle rupture 3-5 days post-> Rapid pulm oedema and CHF

New holosystolic murmur

Cannon A waves (JVP): AV dissociation (V Fib/Third degree heart block)

Acute Pericarditis -> prevention via early coronary reperfusion

NSAIDs and corticosteroids are CI (may hinder myocardial scar formation); use aspirin

Dressler Syndrome (Post MI Syndrome)

Immmunologically based syndrome weeks to months post MI

Fever (low grade), malaise, pericarditis, leukocytosis and pleuritis

Aspirin most effective tx, ibuprofen second

Mechanical complications

Free wall rupture: Acute SEVERE hypotension and Murmur 5 days + post MI

Usually leads to hemipericardium and tamponade

Rupture of IV septum: Step up in O2 concentration from RA to RV —-> normally 75-80%

Biventricular failure
Papillary muscle rupture: Produces MR (new murmur)

Few days post MI cf acute MR -> Emergent surgery

Ventricular Pseudoaneurysm: Bedside ECHO

Incomplete free wall rupture (myocardial rupture contained by pericardium)

Surgical emergency as tend to progress to free wall rupture

Ventricular Aneurysm: Persistent ST elevation months after

D/t scar tissue deposition several months post transmural MI

Rarely rupture but can lead to progressive LV enlargement —-> decomp HF

Medical management protective

Deep Q Waves and systolic murmur —-> D/t flow in and around aneurysm

ECHO: thin, dyskinesia myocardial wall

Hypertension
Smoking Cessation has no effect; moderate chronic smokers tend to have lower BP

Modification. Decrease in Systolic BP

Weight Loss. BMI <25. 5-20 per 10kg loss

DASH Diet. 8-14

Exercise. 4-9

Dietary Sodium. <3g/dy. 2-8

Limit alcohol intake <1/2 M/F. 2-4

Bundle Branch Blocks

Axis

ST elevation in:

V1-V4. LAD. ANTERIOR

I, AVL, V4-V6. CIRCUMFLEX LATERAL

II, III, AVF. RCA. INFERIOR

Third degree heart block:

Regular P-P Intervals (atria) and R-R Intervals (ventricles)

But not associated -> AV Dissociation —> cannon A waves

Multi focal Atrial Tachycardia

Varying PR Interval with 3 or more morphologically distinct P waves in same lead

Seen in old person with chronic lung dz in pending resp failure

Tx underlying cause eg COPD

No cardiac medications

V tach

Unstable: Shock them

Medical Tx if stable: amiodarone or lidocaine

Ventricular Arrhythmia

Sudden onset syncope w/o prodrome (most likely torsades)

Electrolyte disturbances can predispose eg diarrhoea (hypokalaemia and hypomagnesium)

Sotalol and other meds prolong QT and increase risk

Torsades

Electrolytes abnormalities: Low K/Mg; TCA overdose

Tx: Mg sulfate (effective at preventing torsades also even if norm serum Mg)

Temp PM and/or IV isoproterenol if Mg ineffective

WPW: Palpitations
Ventricular preexcitation d/t accessory conduction path

—> directly connects atria and ventricles ——> bypasses AV node

Short PR (<0.12) w wide QRS and slurred upstroke (delta wave)

Tx: Procainamide

CI: Anything that slows AV conduction as exacerbates accessory path: CCBs, BBs, Digoxin etc

Mobitz Type 1 (Progressing): Constant P-P w Increasing PR

A Flutter

Regular rhythm with ventricular rate of 125-150bpm and atrial rate 250-300bpm —-> 2:1

Tx: Unstable: Shock them

Stable: Rate control: BBs, CCBs or digoxin

A Fib: No P waves appreciated (no A waves) ->>>> Undulating Baseline

RATE CONTROL: BB/CCBs/Digoxin

Warfarin 4 wks before cardiovert and 4 weeks after if >48hrs (Same for flutter)

Lone AF: No evidence of valvular; CV or resp disease (score 0) -> no further tx

SVT: Sudden, transient palpations/dizziness in young adult

Tx: Carotid massage; kids splash cold water on face: increases vagal tone

———>>> decreases AV node conductivity

Adenosine: Slows HR, increases AV conduction delay/transient block,

Terminates paroxysmal SVT by interrupting nodal AV reentrant circuit

—-> buried P waves/pseudo S wave on ECG

Hyperkalaemia

Peaked T waves; AV block + Bradycardia; QRS wide

K released from damaged cells -> Burn victim

Hypokalaemia

Premature ventricular beats, U waves and flat broad T waves

MURMURS: Diastolic and continuous murmurs usually pathological: ECHO!

Anticoagulants:

Warfarin and DOACs/NOACs superior to aspirin and clopidigrel in AF to prevent thromboembolism

—> inhibit Factors IIa and X

Premature Ventricular Contractions

Use Beta Blockers or CCBs

AS: Parvus et Tardus; reduced/absent carotid upstroke; SAD; Altered S2 splitting

Replace if symptomatic; <0.8cm valve area or EF <50%

D/t sclerocalcific age related changes/bicuspid (earlier onset)

Supravalvular AS: Congenital Outflow obstruction d/t narrowing of ascending aorta

Different BPs in arms

Palpable thrill in suprasternal notch

Associated with coronary artery stenosis

MVP: Late systolic murmur with click louder w valsalva AND handgrip (cf HOCM)

 Softer with squatting

D/t myxomatous degeneration of valve leaflets and chordae

MVP syndrome

Associated with nonspecific sxs like palpitations, SOB, dizziness, panic/anxiety, numbness/tingling

MS: Normal LVEP

MR: Holosystolic radiating to axilla

Secondary MR (Functional MR): Reversible

Decompensated HF can cause this d/t increased LV EDV Preload

——>> dilation of MV Annulus w lateral displacement of papillary muscles

AR

Most commonly d/t aneurysm (—> aortic root dilatation) or biscuspid AV in developed countries

Developing countries: Rheumatic Heart Disease

Accentuated by sitting up and leaning forward

Abrupt carotid distension & collapse, ‘pistol shot’ femoral pulses

Rapid rise-rapid fall (water hammer) pulsation; Widened pulse

pressure

Valvular AR best heard at L Sternal border at 3rd and 4th ICS

AR d/t aortic root dilatation: Murmur also radiates towards R

side and best heard at R Sternal border

—-> can signal impending dissection

HOCM: Midsystolic murmur at L Lower sternal Border; S4

IV Septal hypertrophy

Does not radiate to carotid cf AS

Syncope; SOB and chest pain

TR: Adverse effect of PM

S4 only pathologic

ACLS

PULSE +:

Unstable: SBP <90, Chest Pain, SOB, Altered Mental Status

FAST rhythm = Shock (synchronised cardioversion)

Machine wont drop a shock on a T wave (causes Q on T phenomenon—> torsades and death)

SLOW rhythm = PACE (IV drugs): Atropine > DA/Epi

A Fib/ Flutter = Fast+Narrow

If no CHF: BB/CCB

CHF: Digoxin/ Amiodarone

VT/V Fib: Can Shock -> Alternate between Epi and Amiodarone after each 2 MIN CPR

PEA (any pulseless activity that’s not VT/V Fib) and ASYSTOLE (Flat line): CANNOT SHOCK
2 MIN CPR: Pulse Check/Rhythm Check/Shock if indicated: Repeat

In PEA/ASYSTOLE give epi every 2 cycles and compressions only

Shock

Hypovolaemic Shock

Cardiogenic Shock eg Post MI. —> tachy and hypotension

—> acute R Heart dysfunction —> elevated CVP

—> acute L heart dysfunction —> refractory hypotension

Obstructive (tamponade) Shock

Preload decreased but PCWP paradoxically increased d/t external compression

SVR increases as perceives decreased Preload

Distributive Shock: Loss of vasomotor tone or dysfunctional ANS (neurogenic)

Eg septic Shock; spinal trauma; anesthesia; anaphylaxis

Warm extremities and low BP

==> CO usually increased (not in. Neurogenic shock d/t impaired sym reflexes)

SvO2= mixed venous oxygenation

Decreased in all except non neurogenic distributive shock

Septic Shock

Fever/Hypothermia not always present esp in older patients!

Decreased SVR (afterload) d/t periph vasodilation

Decreased/low normal PCWP (LA pressure) d/t capillary leakage (decreased Preload)

Elevated mixed venous oxygen saturation d/t hyperdynamic circulation:

CO increased in response to decreased SVR to maintain periph perfusion

Inability of tissues to adequately extract O2

May develop lactic acidosis d/t tissue hypoperfusion

Impaired contractility

CO can decrease in late septic shock but initially it is increased

CHA2DS2VASc

C. Congestive HF (or LV sys dysfunction). 1

H. HTN. 1

A. Age >74. 2

D. DM. 1

S. Prior stroke/TIA/thromboembolism. 2

V. Vascular disease 1

A. 65-74yrs. 1

Sc. Sex (F). 1

LONE AF: Non valvular AF (no cardiopulmonary or structural disease) = 0

Modified Wells:
3 points: Clinical signs of DVT

Alt Dx less likely than PE

2 points: Previous PE/DVT

HR>100

Recent surgery/immobilisation

1 point: Hemoptysis

Cancer

Marfan Syndrome: AD Fibrillin 1

Aneurysmal aortic root dilation —-> Type A dissection prior to 40

——-> Aortic Regurgitation

MVP

Arachnodactyly; Pectus deformity, scoliosis or kyphosis; Joint hypermobility

Ectopic lentis (upward lens dislocation); myopia

Spontaneous pneumothorax d/t apical blebs —-> ipsilateral tracheal deviation

——> also seen in COPD

Recurrent/incisional hernia; Skin striae

Cong contractural arachnodactyly: AD Fibrilin 2

Multiple contractures of large joints

Arachnodactyly

Homocystinuria: AR (Marfans is AD)

Defect in cystathione synthase (methionine metabolism)

Fair complexion + Marfanoid

Thromboembolic vents and intellectual disability

Downward lens dislocation

Megaloblastic anemia

Cyanide toxicity: Altered mental state, lactic acidosis, seizures and coma

Arteriovenous fistula:
Strong peripheral arterial pulsation: Brisk carotid upstroke

Flushed extremities

High output HF; LV hypertrophy; Systolic flow murmur

Can be iatrogenic or d/t trauma

Mediastinitis

Complication of cardiovascular surgery characterised by infection of deep tissues

Chest wall edema/crepitus, Purulent discharge/wound drainage, leukocytosis

Can also present atypically: anyone with copious drainage from serial wound should undergo imaging
Widened mediastinum

Blunt Cardiac injury

Rapid deceleration or direct blow to precordium —>> shearing, compression, abrupt Pressure change

Persistent tachycardia and new arrhythmia (despite norm BP)

Norm resp and O2 SATS

ACS d/t coronary dissection or thrombosis

Myocardial dysfunction (myocardial contusion)

Cardiac tamponade (obstructive shock)

Can also lead to cardiogenic shock

Dx: ECG (continuous cardiac monitoring for

24-48hrs) -> best initial test

FAST if d/t trauma; ECHO (TTE)

Intercostal vessel injury -> hypovolaemic

shock + heamothorax

ASCVD risk >7.5% 10 year risk and over 40

all given statin

Any actual diagnosis of atherosclerotic

disease eg PAD —> Low dose aspirin +
STATIN

——-> prevention of CV events