cardiology i: hypertension...12/23/2013 1 cardiology i: hypertension, heart failure, endocarditis,...

12/23/2013

1

Cardiology I:

Hypertension, Heart Failure, Endocarditis, Pericarditis &

Effusion

Sally M. Hur, PA-C

Instructor, UMDNJ PANCE/PANRE Review Course

(becoming Rutgers University July 1, 2013)

UMDNJ PANCE/PANRE Review Course


Draft Finished Federal

Review

Expert

Review

Advisory

Council

Public

Com’t

HHS

Clear

Re-

lease

Lifestyle Completed Completed Completed In

progress

Risk Assess-

ment

Completed Completed Completed

In

progress

Cholesterol Completed

Completed Completed

In

progress

Blood

Pressure

Completed

In progress In progress

Obesity In progress

Progress of JNC 8

Essential Hypertension

Secondary Hypertension

Malignant Hypertension

Hypotension



Hypertension

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2

50 Million Americans (1 in 4)

Only 70% are aware

Only 50% are treated

Only 25% are treated adequately



Essential Hypertension

Normal <120 <80

Pre-HTN 120-139 80-89

Stage 1 HTN 140-159 90-99

Stage 2 HTN ≥160 ≥100

*Treatment Goal is <140/90

*Target is <130/80 in DM & Renal Disease UMDNJ PANCE/PANRE Review Course


Classification

Average of:

Two or more readings

on Two or more different occasions

No smoking or caffeine 30 minutes prior

Up to 30% have “white-coat HTN” home +/-

ambulatory BP monitor



Diagnosis

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Assess co-morbidities

Look for end-organ damage

EKG

U/A, BUN/CR, K+

Retinopathy

CVA/TIA/Peripheral Artery Disease

Look for reversible cause: (20 HTN)

CBC, lipids, Ca++ UMDNJ PANCE/PANRE Review Course


Work Up

Diabetes

Dyslipidemia

Smoking

Obesity (BMI ≥ 30)

Inactivity

Age (>55♂ >65♀)

Fam Hx of premature cardiovascular disease UMDNJ PANCE/PANRE Review Course


HTN Co-Morbidities

Aldosteronism

Chronic kidney disease

Renovascular disease

Pheochromocytoma

Cushing’s syndrome

Coarctation of Aorta

Medication induced

Sleep Apnea UMDNJ PANCE/PANRE Review Course



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Less than 5% of all HTN patients

Red Flags:

HTN starts at early age(< 25yrs) w/o

FamHx

HTN first develops > 50

Previously controlled HTN, now refractory UMDNJ PANCE/PANRE Review Course



Presents classically as HTN with hypokalemia

(~30% have normal K+)

May be 5-15% of pts DX with essential HTN

Best screening test: aldosterone/renin ratio > 25

Urine K+ > 40 mEq/L

Diagnose with CT or MRI of adrenal glands

shows: adrenal adenoma or hyperplasia



Aldosteronism

Renal parenchymal disease is most common

glomerular, tubular interstitial, polycystic dz

Diabetic Nephropathy

Tests: BUN/Cr, U/A

Diagnose with Renal biopsy



Chronic Kidney Disease

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Causes 1-2% of HTN

HTN > 50 y/o with bruits, PAD, refractory HTN

(suspect: renal artery atherosclerosis)

HTN < 30, female with renal artery bruits (suspect: fibromuscular dysplasia (FMD))

Dx: Arteriography is “Gold Standard”

Dx: US, CT, MRI, Nuclear also OK

Tx: Stent for young, Meds for most older pts. UMDNJ PANCE/PANRE Review Course


Renal artery stenosis

Less common cause - Glucocorticoid excess

PE: Truncal obesity with muscle atrophy

striae, acne, hyper-pigmented skin

Labs: Glucose (hyperglycemia)

K (hypokalemia)

Dx: 24 hr urine free cortisol >3x normal

Dx: MRI pituitary (>50%) CT lungs/ abdomen



Cushing’s Syndrome

Rare: causes <0.1% of HTN

Labile HTN, headaches, tachycardia, diaphoresis

Labs: plasma/24hr urine metanephrines

Dx: CT/ MRI of Adrenals (90% sensitivty)

Tx: Laparoscopic surgical resection

Alpha adrenergic blockade (phenoxybenzamine)

or CCBs UMDNJ PANCE/PANRE Review Course


Pheochromocytoma

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Uncommon cause of HTN

Usually young, cold feet, decreased or no

femoral pulses, high BP arms with low BP

legs.

Narrowing of aortic arch - distal to left

subclavian

Dx: Echocardiography/doppler (MRI/CT

useful)

Tx: stenting or surgery UMDNJ PANCE/PANRE Review Course


Coarctation of Aorta

Oral Contraceptive - sodium retention and

angiotensinogen

NSAID - Na++

retention, renal vasoconstriction

Corticosteroids - like Cushing’s

ETOH >2/day- activates sympathetic system

Sympathomimetics – cold/diet meds, cocaine..

Erythropoietin UMDNJ PANCE/PANRE Review Course


Medication Induced

OSA and HTN linked epidemiologically

Untreated OSA predisposes to new HTN

Treating OSA lowers BP

Possible mechanisms:

sympathetic activation

elevated angiotensin II and aldosterone

oxidative and inflammatory stress UMDNJ PANCE/PANRE Review Course


Sleep Apnea

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Treatment Goal is <140/90

Target is <130/80 in DM & Renal Disease

All patients must use lifestyle modification

Most patients will need two medications

Consider: DM, Renal Disease, CHF, post MI,

High CVD risk, CVA UMDNJ PANCE/PANRE Review Course


Treatment

Pre-HTN: 120-139/80-89

Weight Reduction: Target BMI= 18.5-24.9

DASH Diet: Fruit, veggies, low fat dairy

*8-14 point drop in SBP

Sodium reduction <2.4G sodium/day

* 2-8 point drop in SBP

Aerobic exercise 30min/daily (ideal)

* 4-9 point drop in SBP

Decreased ETOH <2 drinks/daily

* 2-4 point drop in SBP UMDNJ PANCE/PANRE Review Course


Treatment: Pre HTN

Stage 1 HTN: 140-159/90-99

Life Style Modification

Life Style Modification alone if low risk (2%)

Thiazide diuretics for others

May consider ACEI, ARB, BB, CCB, combo

Evaluate for “compelling indications”



Treatment: Stage 1 HTN

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Stage 2 HTN: ≥160/ ≥100

Life Style Modification WITH medications

Two drugs needed for MOST

Thiazide diuretic with: ACEI, ARB, BB, CCB

Evaluate for “compelling indications”



Treatment: Stage 2 HTN

Diabetes: Thiazide diuretic (Thiaz)

ACE inhibitor (ACEI)

Angiotensin receptor blocker (ARB)

Beta Blocker (BB)

Calcium channel blocker (CCB)

Chronic Renal Disease:

ACEI

ARB UMDNJ PANCE/PANRE Review Course


Treatment: Compelling Indications

CHF: Thiazides, b blockers, ACE I, ARB,

Aldosterone Antagonist (spironolactone)

Post MI: b blockers, ACE I, Aldosterone

Antagonist

High CVD risk: Thiazides, b blockers, ACE I,

Calcium Channel blockers

CVA prevent: Thiazides, ACE I



Treatment: Compelling Indications

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Hypertensive Urgency:

• No Sx, BP>220/125

Oral meds with partial reduction in BP=OK

Hypertensive Emergency:

Elevated BP with End Organ Damage

Malignant Hypertension:

Encephalopathy or Nephropathy w/

papilledema UMDNJ PANCE/PANRE Review Course



Hypertensive Emergency:

•Elevated BP with End Organ Damage

BP must be lowered within 1 hour to avoid

death

Hypertensive Encephalopathy/ICH

Hypertensive Nephropathy

Pulmonary edema/ MI/ unstable angina

Aortic dissection

Eclampsia – in pregnancy UMDNJ PANCE/PANRE Review Course



Parenteral meds to rapidly lower BP

Nitroprusside: controlled (agent of choice)

Nitroglycerin: less control (useful w/ ischemia)

Labetalol: potent a and ß-blockade

Too rapidly > cerebral, coronary, & renal ischemia

Reduce pressure 25% in 1st 1-2 hrs

Decrease additional 15% over next 3-12 hrs

Achieve ~160/110 by 12 hrs




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10

1. Diet and exercise

2. Hydrochlorothiazide

3. No treatment necessary



A 32-year old male with a history of Type 2

DM has a blood pressure averaging 135/85

on several measurements. What is the best

intervention for this patient?

1. Diet and exercise

2. Hydrochlorothiazide

3. No treatment necessary


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A 32-year old male with a history of Type 2

DM has a blood pressure averaging 135/85

on several measurements. What is the best

intervention for this patient?

Positional syncope or near-syncope

Lying to standing or motionless standing

Sx: lightheaded, weakness, visual

disturbance

Dx: Orthostatic BP drop > 20 mm Hg systolic

Causes: often elderly, DM, BP meds,

Parkinson’s, volume loss: blood loss, diuretic,

N/V

Cardiogenic Shock UMDNJ PANCE/PANRE Review Course


Orthostatic Hypotension

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1 in 4 Americans have HTN

95% of all cases are Essential (or primary) HTN

Co-morbidities

Primary Aldosteronism: most common treatable

cause of HTN

Chronic kidney disease - most common cause of

secondary HTN

Treatment Goal is <140/90, Target is <130/80 in DM

& Renal Disease

Compelling indications: CHF, post MI, High CVD

risk, DM, Renal disease, CVA UMDNJ PANCE/PANRE Review Course


Conclusion/Summary



Case 1

73 year old man presents with 2 day

history of shortness of breath on

exertion and paroxysmal nocturnal

dyspnea

Heart failure is defined as the poor contraction and/or relaxation of the heart resulting in insufficient blood volume to adequately meet oxygen demand.

This defective pumping mechanism results in accumulation and redistribution of fluids.



What is CHF

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Dyspnea on exertion

Orthopnea

Paroxysmal Nocturnal Dyspnea

Wheezing/Rales/Tachycardia

“Non-specific” Presentations:

Cough, Syncope

Fatigue, Weakness, Confusion

Insomnia, Nocturia UMDNJ PANCE/PANRE Review Course


Left

Heart

Failure

CHF: Symptoms and Signs

Peripheral edema

Jugular-Venous Distention (JVD)

Gastro-intestinal

N/V/D/Pain complaints

Hepatic and bowel edema

Hepato-Jugular Reflex (HJR)

Ascites



Right

Heart

Failure Sx

CHF: Symptoms and Signs



Case 2:

69 year old woman

with HTN and prior MI’s presents with 2

day history of

dyspnea on

exertion and

bilateral edema

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In US the most common cause of CHF:

Coronary Artery Disease Precipitated by HTN (more in US), DM,

hyperlipidemia

With myocardial injury

Leading to decreased myocardial function



CHF: Etiology

Common causes of New Acute CHF:

Massive MI:>40% = cardiogenic shock

Valve failure: ruptured chordae tendineae of

mitral valve

Myocarditis

Thyrotoxicosis/ thyroid storm



CHF: Etiology

Factors Determining Performance:

Preload: How full is the ventricle before it

squeezes?

Afterload: What is ventricle pushing against?

Myocardial Contractility: The force that the

muscle can exert

Heart Rate: too fast or too slow = increased

demand



Pathophysiology

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Measures of Cardiac performance:

Arterial Blood Pressure

Cardiac Output (SV x HR)

Cardiac Index (CO/ BSA)

Ejection Fraction (100 x SV/EDV)



Pathophysiology

In most cases - Ejection fraction refers to left

ventricular ejection fraction.

50 - 70% = Normal

36 - 49% = Below Normal

35 - 40% = may confirm diagnosis of systolic

heart failure

<35% - patient may be at risk of life-threatening

arrhythmias



Ejection Fraction

Heart performance is poor: cannot provide

sufficient blood flow to meet demands:

All of these inter-react



Preload

Afterload

Contractility Rate

Decreased pump

function

Altered Filling Increased Demand

Multi-factorial Syndrome

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Mechanical abnormality: •Valve dysfunction, shunts

Rate/rhythm disorders: •Bradyarrhythmia/tachyarrhythmia

High Output States: •Thyrotoxicosis, fever, chronic anemia, blood

loss



Pathophysiology

Impaired Systolic Function

Decreased Contractibility (Low EF)

Ischemic Damage (MI)

Chronic Pressure Overload (HTN, AS)

Chronic Volume Overload (AR)

Dilated Cardiomyopathy



Pathophysiology

Impaired Diastolic Function

Poor filling (Decreased Preload)

Myocardial Hypertrophy

1o -Hypertrophic Cardiomyopathy

2o -Hypertension

Ischemic Fibrosis (post MI)

Restrictive Cardiomyopathy



Pathophysiology

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Impaired Systolic Function


Impaired Diastolic Function


Hypertrophic Cardiomyopathy



Cardiomyopathy

Causes ~25% of all CHF cases

African American> whites; men > women

Cause - usually idiopathic

Alcoholic Cardiomyopathy

Peri-partum Cardiomyopathy

Toxins? infections?

Poor EF, large heart

Thin, dysfunctional LV Wall

H/O thromboembolic disease – anticoagulate




Right heart failure predominates

Pulmonary HTN present

Usually caused by - Amyloidosis

Sarcoidosis

Scleroderma

Loffler’s syndrome

Normal EF, normal heart size, large atria

Normal LV wall, early diastolic filling




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Often present in early adulthood

Cause in young: genetic - IHSS (HOCM)

Cause in elderly: chronic HTN

Very good EF, large heart

Thick LV Wall (asymmetric hypertrophy)

Decreased diastolic filling

Bisferins Pulse

Avoid intense physical activity reduce

risk of sudden death



Hypertrophic Cardiomyopathy

“Broken Heart Syndrome”

• LV apical ballooning following a high catacholamine stress.

• Presents with Acute chest pain or SOB similar to an acute anterior myocardial infarction, but has normal coronaries on catheterization.

• Most patients recover completely



Taku-Tsubo Cardiomyopathy



Taku-Tsubo Cardiomyopathy

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Acute Decompensation of “Stable”

CHF

A Disease of the Elderly

75% of case in persons over 65

Caused by ischemic cardiomyopathy



Common Presentation

Acute Decompensation of “Stable” CHF

Altered cardiovascular condition:

- Infarction, Arrhythmia, Worsened HTN

New metabolic stress:

- Fever, Infection, Blood loss, Anemia

Medication discontinued

- non-compliance with medications?



Precipitating Factors

Acute Decompensation of “Stable” CHF

Dietary indiscretion

- salty food, alcohol

Iatrogenic volume overload

- transfusion, IV NS

New medication initiated

- NSAID, B-Blocker, CCB



Precipitating Factors

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Chest X-ray

Cardiac silhouette enlargement

If Acute:

Enlarged pulmonary veins

Upper lobe redistribution of fluid

Interstitial edema with central haziness

Peri-hilar or patchy peripheral infiltrates

Pleural effusions are common (R>L) UMDNJ PANCE/PANRE Review Course


CHF: Studies & Labs

http://www.radiologyassistant.nl/en/p4c132f36513d4



http://www.radiologyassistant.nl/en/p4c132f36513d4



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(becoming Rutgers University July 1, 2013) http://www.radiologyassistant.nl/en/p4c132f36513d4

Electrocardiogram (EKG)

Evaluate rate and rhythm

Evaluate for acute or prior MI

Evaluate for Ventricular Hypertrophy



CHF: Studies & Labs

Echocardiography: The most useful and

practical test to diagnose and evaluate

suspected CHF

Determine Ejection Fraction

LV function and wall motion (?prior MI)

Evaluate valve function

Dx: dilated, restrictive, or hypertrophic

cardiomyopathy UMDNJ PANCE/PANRE Review Course


CHF: Studies & Labs

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Angiography

Angiogram: invasive but..

In presence of evidence of ischemia..

Patients benefit from diagnosis and

intervention (angioplasty and/or stenting)



CHF: Studies & Labs

Labs:

BNP (B-type Natriuretic Peptide)

released by heart muscle in fluid overload

sensitive & specific: <100 rules out CHF

CPK and Troponin (MI)

CBC (anemia)

Electrolytes

Renal Function (BUN/ Creatinine)



CHF: Studies & Labs

Control HTN:

• focus on systolic pressure

• reduces incidence of heart failure by 50%

Prevent first MI

Post MI:

• b-Blocker, lower cholesterol,

• anti-thrombotic, revascularization



Prevention

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Determined by Stage of Heart Failure

AHA/ACC NYHA

Stage A (Pre CHF - at risk) N/A

Stage B (asymptomatic) Stage I

Stage C (symptomatic) Stage II-III*

Stage D (marked sx at rest) Stage IV

*(NYHA depended on patient reported symptoms)



Treatment

Stage A: Pre CHF (ACC/AHA)

No structural heart abnormality

No signs or symptoms of heart failure

Presence of risk factors:

HTN, CAD, DM, ETOH Abuse,

Rheumatic fever, FHx of

cardiomyopathy



Treatment

Stage A (ACC/AHA):

Control HTN (focus on systolic pressure)

Lower cholesterol

ACE inhibitors (for appropriate patients)

Lifestyle Changes:

•Smoking cessation

•Exercise

•Decrease ETOH



Treatment

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Stage B: Early CHF (ACC/AHA)

Structural heart abnormality present

No signs or symptoms of heart failure

Example:

• LV Hypertrophy or Fibrosis, Valvular disease

• LV Dilation or Hypocontractility, prior MI



Treatment

Stage B (ACC/AHA):

All - Stage A measures

ß-Blockers (for appropriate patients)

ACE inhibitors (for appropriate patients)



Treatment

Stage C – CHF (ACC/AHA)

Underlying structural heart disease

Current/prior signs or symptoms of heart

failure

Examples: LV Dysfunction managed w/meds



Treatment

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Stage C (ACC/AHA)

All- Stage A measures

Medications for routine use:

• Diuretics

• ACE inhibitors

• b- Blockers

• Digitalis

Dietary salt restriction



Treatment

Stage D – End Stage CHF (ACC/AHA)

Advanced structural heart disease

Marked symptoms of heart failure at rest

Example:

patients awaiting transplant

pts require continuous IV meds

pts require mechanical assist device UMDNJ PANCE/PANRE Review Course


Treatment

Stage D (ACC/AHA)

All - Stage A thru C measures

Mechanical Assist devices

Transplant

Continuous IV infusion of inotropic

medication



Treatment

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Loop Diuretic: Lasix (double current po

dose)

SL/IV NTG: ensure normotensive

O2, CPAP

ACE inhibitor

Treat Cause: MI? HTN?



Pulmonary Edema/CHF

Shock caused by the Heart’s diminished CO

“Pump failure” 2o to MI, CHF, Cardiomyopathy

Dysrhythmia: Tachy or Brady

Acute valve dysfunction - (regurgitant)

Rupture of ventricular septum or wall UMDNJ PANCE/PANRE Review Course


Cardiogenic Shock

General Treatment Measures

Continuous IV infusion of inotropic medication

** Dopamine is pressor agent of choice

Mechanical assist devices

Intra-Aortic balloon pump

maintains adequate perfusion and circulation

Transplant?



Cardiogenic Shock

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Cardiac output decreases.

Neurohormonal mechanisms attempt to increase

perfusion of the kidneys Renin is released: BP is

raised & fluid retained

• HTN increases afterload (decreases EF) and work (increases

demand)

• Volume overload decreases contractility (decreases EF)

Low CO causes catecholamine release:

• Heart rate increases= less filling/preload (decreased EF) and

increases work (increased demand)

• BP increases= causing higher afterload (decreased EF) and

increases work (increased demand) UMDNJ PANCE/PANRE Review Course


Cycle of CHF

Diuretics – (furosemide):

Reduce peripheral vascular resistance

Reduce plasma volume

take off excess salt and fluid

control fluid retention

decrease volume overload

Negative: electrolyte depletion, hypotension, increase neurohormonal activation…



Medications

ACE inhibitors: Interfere in the renin-angiotensin

system (RAS)

Block angiotensin - a potent vasoconstrictor

Decrease aldosterone mediated sodium

retention

Slow myocardial remodeling and fibrosis

(also ARBs and spironolactone)



Medications

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b-Blockers: Interfere w/ changes caused by

catecholamine release

Slow heart rate

Decrease afterload/blood pressure

Decrease cardiac output

Cause rise in EF and reduction in LV size



Medications

Digitalis : Controls symptoms of decreased contractility

Inotropic effects

Controls rate in afib

Useful with CHF Symptoms despite ACE and b-Blockade

Negative: dig toxicity, arrhythmia



Medications

5 year survival: <50% after acute onset of CHF.

Only 35% of men and 50% of women are alive

after 5 years.

Worse prognosis: older patients, men, pts with CAD,

pts with reduced EF

Class D (IV) > 30% annual mortality

Class B-C (I-II) >5% annual mortality



Prognosis

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A 73-year old presents with a 2-day history of

shortness of breath on exertion and

paroxysmal nocturnal dyspnea. What is the

most likely underlying diagnosis?



1. Coronary artery

disease

2. Pheochromocytoma

3. Sarcoidosis

4. Systemic infection

A 73-year old presents with a 2-day history of

shortness of breath on exertion and

paroxysmal nocturnal dyspnea. What is the

most likely underlying diagnosis?



1. Coronary artery

disease

2. Pheochromocytoma

3. Sarcoidosis

4. Systemic infection

Coro

nary arte

r...

Pheoch

rom

ocyto

...

Sarc

oidosis

Syst

emic

infe

c...

100%

0%0%0%

Infective Endocarditis

Acute Pericarditis

Pericardial Effusion

Cardiac Tamponade



Endocarditis, Pericarditis & Effusion

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Preexisting Heart Lesion (Valvular)

Fever (>380 C)

New Heart Murmur

Positive Blood Cultures

Evidence of Septic Emboli

Echocardiography w/ Vegetation




Classic Signs:

Petechia - palate, conjunctiva, subungual

Subungual splinter hemorrhages

Osler node: (painful lesion- finger/toes/feet)

Janeway lesion: painless red lesion palm/sole

Roth spot: exudative retinal lesion (25%) UMDNJ PANCE/PANRE Review Course



Which Lesion is painful?



Osler Janeway

Osler = Ouch

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Acute bacterial infection typically Staph. aureus.

Rapid onset of high fevers, rigors

New regurgitant murmur

Labs: leukocytosis & positive blood cultures

Sx: 2o to emboli to lungs, kidneys, joints, bones:

cough, CP, back/flank pain, arthritis

Rapid deterioration with CHF (70%)



Acute Infective Endocarditis

Slow insidious bacterial infection of heart valve

Typically Strep. viridans

Patients have weeks of constitutional Sx

• nausea, vomiting, fatigue, and malaise

• (-) fever: w/ elderly, CHF or renal patients

Regurgitant murmur

Labs: anemia of chronic dz, normal WBC UMDNJ PANCE/PANRE Review Course


Subacute Infective Endocarditis

Prosthetic Valve Disease: Fever or Prolonged Constitutional Sx

Agent = (early) soon after valve implant

• Staph, Gram neg., Fungi

Agent = (late) after 2 months

• Strep and Staph

Treatment = 6 weeks of treatment

• Staph = 6wk Vanco + Rifampin +

2wkGent UMDNJ PANCE/PANRE Review Course



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Injection Drug Users

All febrile IDU’s should be evaluated for IE

Agent = 60% Staph aureus

• Also Enterocci/Streptococci

Treatment = 2-4 wk Depends on the Agent




Bug Specific Treatment Empiric = Vancomycin + Ceftriaxone

Strep. viridans

4 wk PenG or 2 wk PenG + Gent

4 wk Ceftriaxone or Vancomycin

Staph. aureus

6 wk Nafcillin or Oxacillin

6 wk Vancomycin

HACEK - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

4-6 wk Ceftriaxone




Lesions Requiring Prophylaxis

High Risk

Prosthetic Valves

Prior Infective Endocarditis

Cyanotic Congenital Heart Disease

Moderate Risk

Rheumatic (or other acquired) valve disease

Hypertrophic Cardiomyopathy *

Mitral valve prolapse WITH regurgitation * UMDNJ PANCE/PANRE Review Course



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Lesions NOT Requiring Prophylaxis:

ASD/ VSD/ PDA- post repair CABG MVP without regurgitation Rheumatic fever without valve dysfunction Previous Kawasaki’s/ Pacemakers/ AICD-Defibrillators Hypertrophic Cardiomyopathy * Mitral valve prolapse WITH regurgitation* UMDNJ PANCE/PANRE Review Course



Procedures Requiring Prophylaxis:

• Dental: Extraction/ Root Canal/ Tonsillectomy

• GI: Surgery/ ERCP/ Colonoscopy w/ Biopsy

• GU: Prostate surgery/ cystoscopy




Procedures NOT Requiring Prophylaxis:

Respiratory: Flexible Bronchoscopy*

GI: Endoscopy w/ Biopsy*

GU: Hysterectomy, C-section/ Vaginal delivery*

Dental fillings/ local injection/ fluoride/ orthodontic adjustment

Respiratory: flex bronchoscopy/ tympanostomy/ ET Tube

CV: TEE, angioplasty UMDNJ PANCE/PANRE Review Course



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Major Criteria:

Two (+) Blood Cultures with typical agent

TEE Demonstrates Endocarditis

New Murmur

Minor Criteria:

Fever >38C

Vascular phenomena

Immunologic phenomena

(+) Blood Culture UMDNJ PANCE/PANRE Review Course



Modified Dukes Criteria

Definitive Dx: 2 major OR 5 minor OR 1 major + 3 minor

Possible Dx: 1 major + 1 minor OR 3 minor




Complications: depend on organism, valve and

time to diagnosis

Staph aureus: more valve damage, more

abscesses and emboli

Aortic valve: embolization to brain/

myocardium embolization to spleen/ kidneys

Tricuspid: septic pulmonary emboli

Damage leads to rapid deterioration with CHF UMDNJ PANCE/PANRE Review Course



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Prognosis: Medical treatment is usually

effective

Valve replacement surgery indicated

if:

• Valve regurgitation with CHF

• Infections not responding to ABX

• Recurrent infection with same agent

• Fungal endocarditis

• +/- continued embolization




1. Exudative retinal lesions

2. Painful lesion on finger

3. Painless lesion on sole

4. Subungual splinter

hemorrhages



A patient with a diagnosis of infective

endocarditis tells you that they have a

history of Janeway lesions. What will most likely be found on physical exam?

1. Exudative retinal lesions

2. Painful lesion on finger

3. Painless lesion on sole

4. Subungual splinter

hemorrhages



A patient with a diagnosis of infective

endocarditis tells you that they have a

history of Janeway lesions. What will most likely be found on physical exam?

12/23/2013

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Myocardial Inflammation (Focal or Diffuse)

Sudden onset Heart Failure

Sx: SOB/ pleuritic chest pain

PE: Edema/ S3 gallop

EKG: Nonspecific ST changes w/ conduction

delay

Echocardiogram > Dilated Cardiomyopathy

Dx: Myocardial biopsy = gold standard UMDNJ PANCE/PANRE Review Course


Myocarditis

Myocardial Inflammation (Focal or Diffuse)

1o = viral Infection or immune response

Coxsackie B (measles/ influenza/ varicella)

Kawasaki’s

2o = Bacteria/ Toxins/ Systemic illness

Lyme/ RMS fever/ Syphilis/ Chagas

Radiation/ doxorubicin/ cocaine

Lupus



Myocarditis

Localized

inflammation of

anterior, lateral and

inferior walls may

cause ST elevations

in multiple areas



Pericarditis

12/23/2013

36

Common: Viral/ often post URI

Coxsackie B (echo/ influenza/ varicella)

Men under 50 most common (post URI)

Pleuritic/ positional chest pain

Pericardial friction rub

Treatment - ASA/ indomethacin/ NSAID

<5% develop tamponade



Acute Pericarditis

Pericardial Inflammation

Uremia/Renal Failure need dialysis

Post cardiac surgery

2-5 days Post MI / Dressler’s Syndrome

- CP relieved by leaning forward

Often with associated Myocarditis

Lyme/ Lupus/ radiation/ cancer/ RA/ drugs

Hypothyroid (myxedema) UMDNJ PANCE/PANRE Review Course


Acute Pericarditis



Disease: Pericarditis

http://www.the-

hospitalist.org/details/article/2785031/How_is_Acute_Pericarditis_Diagnosed_and_Treated.html

12/23/2013

37

Accumulation of fluid in pericardium

Rapid accumulation = tamponade

Fluid 2o to inflammatory process = painful

Slow accumulation (neoplasia/uremia)= no

pain

Large effusion >1000cc w/ neoplasia




Diagnostic Studies

PE: JVD/ muffled sounds/ paradoxical pulse

CXR: enlarged/ globular cardiac silhouette

EKG: low voltage/ T-wave Δ’s,

maybe electrical alternans

Echo: Primary method for detecting effusion




Paradoxical pulse – exaggeration of the normal variation in the pulse during respiration, in which the pulse becomes weaker as one inhales and stronger as one exhales; it is characteristic of constrictive pericarditis or pericardial effusion.

Electrical alternans - describes alternate-beat variation in the direction, amplitude, and duration of any component of the ECG waveform




12/23/2013

38

↑ Intrapericardial pressure

↓ venous return and ↓ ventricle filling

• Stroke volume falls > BP falls > Shock > Death

• Dyspnea and cough

• Tachycardia

• Narrow pulse pressure

• Paradoxical pulse / Electrical Alternans



Cardiac Tamponade

Treatment Tamponade:

Urgent pericardiocentesis

Sub-xiphoid with echocardigraphy

Small effusions:

Follow clinically (JVD) and serial echo

Large effusions:

Pericardial window






Thank you!! Enjoy the rest of the review and good luck on your boards!

cardiology i: hypertension...12/23/2013 1 cardiology i: hypertension, heart failure, endocarditis,...

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