2015 cardiology 1 - @mycme

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Cardiology I:Hypertension, Heart Failure,

E d diti P i diti & Eff i

Rutgers, The State University of New Jersey

Endocarditis, Pericarditis & Effusion

Steve McKenzie, MS, PA-CAssistant ProfessorPANCE/PANRE Review Course

PANCE/PANRE Review Course

• Essential Hypertension

• Secondary Hypertension

Hypertension

• Malignant Hypertension

• Hypotension


• 78 Million Americans (1 in 4)

• Only 78% are aware

Essential Hypertension

• Only 64% are treated

• Only 25% are treated adequately

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From: 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8)

JAMA. 2014;311(5):507-520. doi:10.1001/jama.2013.284427

Guideline Comparisons of Goal BP and Initial Drug Therapy for Adults With Hypertension

Figure Legend:

Date of download: 4/13/2015 Copyright © 2014 American Medical Association. All rights reserved.


Guideline Comparisons of Goal BP and Initial Drug Therapy for Adults With Hypertension

Figure Legend:

Date of download: 4/13/2015 Copyright © 2014 American Medical Association. All rights reserved.


JNC 8: Goal Blood Pressure

General < 60: <140/90

General > 60: <150/90

Chronic Kidney Disease (CKD): <140/90

Diabetes: <140/90*

* ADA recommends <130/80

for younger individuals

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JNC 8: Initial Drug Treatment Options

General

Non AA: Thiazide type diuretic AngiotensinNon-AA: Thiazide-type diuretic, Angiotensin converting enzyme inhibitors (ACE I), Angiotensin receptor blockers (ARB) or Calcium channel blockers (CCB)

AA: Thiazide-type diuretic or CCB


JNC 8: Initial Drug Treatment Options

CKD: ACEI or ARB

Diabetes: ACEI, ARB, Thiazide type diuretic, or CCB

*ADA 2015: Initial Treatment ACEI or ARB

» Patients with blood pressure >120/80 mmHg should be advised on lifestyle changes to reduce blood pressure


ADA 2015: Recommendations

Lifestyle therapy for elevated blood pressure:

Weight loss if overweight

Dietary Approaches to Stop Hypertension (DASH)

• style dietary pattern including: red cing sodi mreducing sodium

increasing potassium intake

Moderation of alcohol intake

Increased physical activity

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Cuff bladder should be 80% of arm circumference.

Average of:

• Two or more readings

• On Two or more different occasions

Diagnosis

On Two or more different occasions

• No smoking or caffeine 30 minutes prior

• Up to 30% have “white-coat HTN”

• Consider: home +/- ambulatory BP monitor

NOTE: In HIGH RISK PATIENTS…• SUPERIOR to office reading in predicting end-organ damage

• 3 month delay in Dx = two-fold increase in cardiovascular morbidity


Assess co-morbidities

Look for end-organ damage

EKG, Exam, CXR

U/A BUN/CR K+

Work Up

U/A, BUN/CR, K

Retinopathy

CVA/TIA/Peripheral Artery Disease

Look for reversible cause: (20 HTN)

CBC, Lytes (K, Na, Ca++), Lipids,

Blood Sugar, Uric Acid, Orthostatic BP


• Diabetes

• Dyslipidemia

• Smoking

• Obesity (BMI ≥ 30)

HTN Co-Morbidities

• Obesity (BMI ≥ 30)

• Inactivity

• Age (>55♂, >65♀)

• Family History of premature cardiovascular disease

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PROPERTIES

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• Less than 5% of all HTN patients

• Red Flags:

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

Secondary Hypertension

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

HTN first develops > 50

Previously controlled HTN, now refractory

HTN resistant to 3+ medications


• Aldosteronism

• Chronic kidney disease

• Renovascular disease

• Pheochromocytoma

Secondary Hypertension

• Cushing’s syndrome

• Coarctation of Aorta

• Medication induced

• Sleep Apnea

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Aldosteronism

• Most common treatable cause of HTN

• Most common presenting age 30-50

• Presents classically as HTN with hypokalemia (~30% have normal K+); aldosterone; renin

• 30-50% caused by aldosterone producing adenomas;

• Best screening test: aldosterone/renin ratio

• Diagnose with CT or MRI of adrenal glands shows: adrenal adenoma or hyperplasia


• Most common cause of secondary HTN

• HTN is present in more than 85% and a major factor causing increased cardiovascular morbidity and mortality

M h i d d l l d

Chronic Kidney Disease

• Mechanism: expanded plasma volume and peripheral vasoconstriction

• Screening tests: BUN/Cr, U/A, microalbuminuria

• Diagnose with Renal sonography


• 1-2% of HTN causes

• Atherosclerosis (85%)

• Fibromuscular dysplasia (15%)

• Dx: CT with contrast, MRI (no gadolinium)

• Tx: Stent for young medication for most older patients

Renal artery stenosis

• Tx: Stent for young, medication for most older patients

• HTN >50 y/o with bruits, PAD, refractory HTN (suspect: renal artery atherosclerosis)

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

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Cushing’s Syndrome

• Less common cause of HTN –

Glucocorticoid excess

• Presentation: Truncal obesity with muscle atrophy, striae, acne, hyper-pigmented skin, , yp p g

• Labs: Glucose (hyperglycemia)

• Potassium (hypokalemia)

• Dx: 24 hr urine free cortisol >3x normal

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


Pheochromocytoma

• Catecholamine secreting tumors from adrenal medulla

• Rare: causes <0.1% of HTN; Men = women

• Presentation: Labile HTN, headaches, tachycardia, diaphoresis, orthostatic changes often present

• Labs: urine/plasma: increased concentration of• Labs: urine/plasma: increased concentration of fractionated catecholamines & metanephrines

• Imaging: CT/ MRI of Adrenals >95% sensitivity

(only if labs are positive)

• Tx: Laparoscopic surgical resection;

alpha adrenergic blockade (phenoxybenzamine)


• Uncommon cause of HTN

• Narrowing of aortic arch - distal to left subclavian

• Usually young, cold feet, decreased or no femoral pulses, high BP arms with low BP legs

Dx: CXR: “Number 3 sign” and rib notching

Coarctation of Aorta

• Dx: CXR: Number 3 sign and rib notching

• Tx: stenting or surgery

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Corticosteroids – like Cushing’s

Oral Contraceptive - sodium retention and angiotensinogen

NSAID - Na++ retention, renal vasoconstriction

Medication Induced

,

ETOH >2/day- activates sympathetic system

Sympathomimetics – cold/diet meds, cocaine..

Erythropoietin


Coarctation of Aorta: Figure 3 Sign

http://images.radiopaedia.org/images/2173775/6e811d3218a49cb6178245b4a2b78a.pngFrom WikiFoundry: http://www.wikiradiography.net/page/Coarctation+of+the+Aorta


OSA and HTN linked epidemiologically

Untreated OSA predisposes to new HTN

Treating OSA lowers BP

Possible mechanisms:

Sleep Apnea

sympathetic activation

elevated angiotensin II and aldosterone

oxidative and inflammatory stress

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• General > 60 years <150/90

• General < 60 years <140/90

Treatment Goals

• DM & Renal Disease <140/90

• ADA: DM <140/80

• All patients must use lifestyle modification


• Weight Reduction: Target BMI= 18.5-24.9

• DASH Diet: Fruit, veggies, low fat dairy

• Sodium reduction <2.4G sodium/day

• Aerobic exercise 30min/daily (ideal)

Treatment: Lifestyle Modifications

• Aerobic exercise 30min/daily (ideal)

• Decreased ETOH <2 drinks/daily

• Also Consider Initiating a Statin!

PROPERTIES


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Hypertensive Urgency

• Persistent asymptomatic SBP > 220mmHg or DBP > 125mmHg

• Plus optic disc edema, progressive target organ complications and severe perioperative hypertensioncomplications and severe perioperative hypertension

• Must be reduced with a few hours

• TREATMENT: Parenteral drug therapy is not required and goal is partial reduction of blood pressure with relief of symptoms


Hypertensive Emergency

• DBP > 130 mmHg

• Requires substantial reduction within 1 hour to avoid morbidity or death

• Include: intracranial hemorrhage aortic dissectionInclude: intracranial hemorrhage, aortic dissection, preeclampsia-eclampsia, pulmonary edema, unstable angina, myocardial infarction,

• malignant hypertension (hypertensive encephalopathy, hypertensive nephropathy)


Malignant Hypertension

• A Type of Hypertensive Emergency Characterized by:

• encephalopathy or

• nephropathy with papilledema

• Sustained elevated arterial blood pressure: p

• Diastolic: 130mmHg or greater

• Systolic: 200mmHg or greater

• Treatment is identical with all hypertensive emergencies

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Other Hypertensive Emergencies

• Unstable Angina/ Myocardial Infarction

• Acute Pulmonary Edema

• Ischemic Stroke

• Intracranial Hemorrhage• Intracranial Hemorrhage

• Aortic Dissection

• Preeclampsia-eclampsia

• Cocaine Induced


Hypertensive Emergency: Treatment

• Labetalol IV: Combined beta and alpha-blocking agent; most potent for rapid blood pressure reduction

• Nicardipine IV: most potent and longest acting calcium channel blocker. Vasodilator with potential to precipitate reflex tachycardia. Often used w/ b-blocker

• Esmolol: Less potent B-Blocker than Labetalol

• Clevidipine: CCB without vasodilation or reflex tachycardia

• Nitroprusside: is no longer treatment of choice, useful with aortic dissection in combo with beta-blocker


Hypertensive Emergency: Treatment• Ischemic Stroke Nicardipine OR Labetalol

• Intracranial Hemorrhage Nicardipine OR Labetalol

• Acute Nephropathy Nicardipine

• Unstable Angina/ MI: Labetalol w/ Nitroglycerin

• Pulmonary Edema: (diastolic) Labetalol w/ Nitroglycerin +Lasix

• Pulmonary Edema: (systolic) Nicardipine w/ Nitroglycerin +Lasix

• Aortic Dissection Labetalol OR Esmolol w/ Nipride

• Preeclampsia-eclampsia Labetalol OR Nicardipine +Mg

• Pheochromocytoma/ Cocaine Nicardipine w/ Benzodiazepine

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Hypertensive Emergency: Treatment

• Reduce pressure by no more than 25% within 1-2 hours

• Then reduce towards 160/100 within 2-6 hours

• If reduced too fast may precipitate coronary, renal or cerebral ischemia

• Avoid the use of sublingual or oral fast acting nifedipine• Avoid the use of sublingual or oral fast-acting nifedipine


Orthostatic Hypotension

• Orthostatic drop of SBP by > 20 mmHg

• Positional syncope or near-syncope:

lying to standing or motionless standing

• Symptoms: lightheaded weakness visual disturbanceSymptoms: lightheaded, weakness, visual disturbance

• Causes: often elderly, DM, BP meds, Parkinson’s, volume loss: blood loss, diuretic, vomiting, diarrhea


Summary

• 1 in 4 Americans have HTN

• 95% of all cases are Essential HTN

• JNC 8 Treatment Goal:

> 60 y/o <150/90

/ / < 60 y/o <140/90

DM & CKD <140/90

• Primary Aldosteronism: most common treatable cause

• Chronic kidney disease: most common cause of 2dary HTN

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• Poor contraction and/or relaxation of the heart • Defective pumping results in:

insufficient blood volume to adequately meet oxygen demands.accumulation/ redistribution of fluids.

• ~ 5 million patients in the US

Heart Failure

p• Disease of the aging population (75% are > 65)• Commonly a chronic disease with acute exacerbation


Heart Failure Symptoms Left sided:

Low output with elevated pulmonary venous pressure

• SOB, Dyspnea on Exertion,

• Orthopnea Paroxysmal Nocturnal DyspneaOrthopnea, Paroxysmal Nocturnal Dyspnea

Right sided:

Primary cause is left ventricular dysfunction

Fluid retention with:

• edema, hepatic congestion,

• loss of appetite, nausea


Heart performance is poor: cannot provide sufficient blood flow to meet demands:

All of these inter-react

HF is a Multi-factorial Syndrome

PreloadAfterload ContractilityRate

Increased DemandDecreased pump

functionAltered Filling

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Factors Determining Performance:

• Preload: How full is the ventricle before it squeezes?

• Afterload: What is ventricle pushing against?

HF is a Multi-factorial Syndrome

• Myocardial Contractility: Force the muscle can exert

• Heart Rate: too fast or too slow = increased demand

PROPERTIES



Factors/ Causes Leading to HFMechanical abnormality:

• Valve dysfunction

• Shunts

Rate/rhythm disorders:

Bradyarrhythmia• Bradyarrhythmia

• Tachyarrhythmia

High Output States:

• Thyrotoxicosis,

• Fever

• Blood loss/ Chronic anemia

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Factors/ Causes Leading to HF

Impaired Systolic Function:

Impaired myocardial contractility

with decreased LV ejection fraction (< 40%).

• Most common cause: Coronary artery disease

leading to MI and loss of functioning myocardium.

• Chronic Pressure Overload (HTN, AS)

• Chronic Volume Overload (AR)

• Dilated Cardiomyopathy


Impaired Diastolic FunctionImpaired relaxation and filling with normal contractility and ejection fraction (> 50%). Poor Filling = Decreased Preload

• Most common cause: Left Ventricular Hypertrophy

Factors/ Causes Leading to HF

Most common cause: Left Ventricular Hypertrophy secondary to hypertension

• Hypertrophic Cardiomyopathy• Ischemic Fibrosis (post MI) • Restrictive Cardiomyopathy


Impaired Systolic Function

• Dilated Cardiomyopathy

Cardiomyopathies

Impaired Diastolic Function

• Restrictive Cardiomyopathy

• Hypertrophic Cardiomyopathy

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Dilated Cardiomyopathy

• Most common form of cardiomyopathy

• Symptoms: DOE, orthopnea, PND, palpitations, CP

• Signs: pulsus alternans, JVD, S3/S4, mitral regurgitation

• African American > Caucasian

M• Men > women

• Cause: usually idiopathic

Alcoholic, Peri-partum, toxins/infections?


Dilated Cardiomyopathy, continued

• CXR: cardiomegaly, pulmonary vascular congestion

• Echo: Poor EF (<50%, but often less than 30%),

large dilated, thin, dysfunctional left ventricle

EKG L f i l h h• EKG: Left ventricular hypertrophy,

ST and T wave abnormalities, LBBB/RBBB, Arrhythmia (a-fibrillation, PVC, PAC)

• Treatment: w/ thromboembolic disease – anticoagulate


Restrictive Cardiomyopathy

• Symptoms: Right heart failure Sx predominate

• Signs: JVD, hepatomegaly, ascites, edema

• Pulmonary HTN present

• Usually caused by - AmyloidosisUsually caused by Amyloidosis

Sarcoidosis

Scleroderma

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Restrictive Cardiomyopathy, continued

• CXR: pulmonary vascular congestion with normal heart size to moderate cardiomegaly, pleural effusion

• EKG: low QRS voltages, ST and T wave abnormalities, frequent arrhythmias

• Echo: Normal EF, normal heart size, large atria, Normal LV wall, early diastolic filling


Hypertrophic Cardiomyopathy

• Hypertrophic Obstructive Cardiomyopathy (HOCM): inherited autosomal dominant trait

• Left Ventricular hypertrophy with narrowed LV outflow tract

• Obstruction is worsened with increase myocardial contractility.

• Symptoms: Dyspnea and chest pain. Syncope is common.Symptoms: Dyspnea and chest pain. Syncope is common.

• Signs: bisferiens carotid pulse, a loud S4, systolic murmur that with Valsalva maneuver or with squatting.

• Presents in early adulthood

• Not to be confused with hypertrophy of elite athlete

• In elderly: usually associated with chronic hypertension


Hypertrophic Cardiomyopathy, continued

• CXR: normal or cardiomegaly

• EKG: left ventricular hypertrophy (LVH), exaggerated septal q waves infero-laterally mimicking an MI

• Echo: Asymmetric LVH systolic anterior motion of mitral• Echo: Asymmetric LVH, systolic anterior motion of mitral valve, septal thickening with motion

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• “Broken Heart Syndrome”

• LV apical ballooning following a high catacholamine stress.

P i h A h i SOB i il

Taku-Tsubo Cardiomyopathy

• 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, continued

PROPERTIES


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Question: With so many causes…, How will I know my patient has Heart Failure?

Answer: Start with Signs and Symptoms

Signs:

• Tachypnea >> Respiratory distress

• Fluid retention with Edema, JVD, Hepatic Congestion

Symptoms:

• SOB, Dyspnea on Exertion,

• Orthopnea, Paroxysmal Nocturnal Dyspnea

• Loss of appetite, Nausea, Weight gain (water)

These can by Chronic OR Acute…


Chronic Heart Failure: Classification

New York Heart Association (NYHA) Classification• Class I (mild): (AHA/ACC=B)

No limitation of physical activity • Class II (mild): (AHA/ACC=C)

Slight limitation of physical activity.Comfortable at restComfortable at restOrdinary physical activity results in symptoms

• Class III (moderate): (AHA/ACC=C)Marked limitation of physical activity.Comfortable at rest Less than ordinary activity causes symptoms

• Class IV (severe): (AHA/ACC=D)Symptoms of heart failure at restUnable to carry out any physical activity


• Cardiac output (CO) decreases:

• Neurohormonal mechanisms attempt to increase perfusion of the kidneys

• Renin is released: BP is raised & fluid retainedHTN increases afterload (decreases EF)

Classic Cycle of Chronic Heart Failure

HTN increases work (increases demand)

Volume overload decreases contractility (decreases EF)

• Low Cardiac output causes catecholamine release:Heart rate increases= less filling/preload (decreased EF)

Rate increases work (increased demand)

BP increases= causing higher afterload (decreased EF)

HTN increases work (increased demand)

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AHA/ACC NYHA

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

Stage B (asymptomatic) Stage I*

Treatment is Determined by Stage of HF

Stage C (symptomatic) Stage II-III*

Stage D (marked sx at rest) Stage IV

*(NYHA depended on patient reported symptoms)


Stage A: Pre CHF (ACC/AHA)

• No structural heart abnormality

• No signs or symptoms of heart failure

• Presence of risk factors: (HTN, CAD, DM, Obesity, FHx)

Stage A Intervention:

Treatment

g

• Control HTN ACEI/ ARB for appropriate patients (CAD and DM)

• Lower cholesterol with Statin

• Lifestyle Changes:Smoking cessation

Exercise

Decrease ETOH


• Control HTN:

• focus on systolic pressure

• reduces incidence of heart failure by 50%

Prevention

• Prevent first MI

• Post MI- Preserve Muscle:

• anti-thrombotic, revascularization

• b-Blocker, lower cholesterol,

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Stage B: Early CHF (ACC/AHA)

• Structural heart abnormality present

• No signs or symptoms of heart failure

• Examples:LV Hypertrophy or Fibrosis, Valvular disease

LV Dil ti H t tilit i MI

Treatment

LV Dilation or Hypocontractility, prior MI

Stage B Intervention:

• All - Stage A measures

• ACE inhibitors/ ARB (for appropriate patients)

• ß-Blockers (for appropriate patients)

• Valve repair (for appropriate patients)

• CABG/Stent (for appropriate patients)


Stage C: Symptomatic CHF (ACC/AHA)• Underlying structural heart disease• Current or prior signs or symptoms of heart failure• Examples:

LV Dysfunction managed with medication Stage C Intervention:• All- Stage A and B measures

Treatment

g• Medications for routine use with preserved EF:

Diuretics to relieve Sx of congestion• Medications for routine use with low EF:

Diuretics to relieve fluid retentionACE inhibitor/ ARBβ- BlockersAldosteroneConsider for appropriate patients: Digitalis, CRT, ICD


Stage D: Refractory HF (ACC/AHA)

• Advanced structural heart disease

• Marked symptoms of heart failure at rest

• Example: patients requires continuous IV meds

Stage C Intervention:

Treatment

• All - Stage A thru C measures

• Continuous IV infusion of inotropic medication

• Temporary or Permanent Mechanical Circulatory Support

• Heart Transplant

• Experimental Surgery of Drugs

• Consider: Palliative Care/ ICD deactivation

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PROPERTIES



ACE inhibitors: Interfere in the renin-angiotensin system (RAS)

• Block angiotensin - a potent vasoconstrictor

• Decrease aldosterone mediated sodium retention

Medications

Decrease aldosterone mediated sodium retention

• Slow myocardial remodeling and fibrosis

NOTE: ARBs and spironolactone work in a similar manner


-Blockers: Interfere w/ changes caused by catecholamine release• Slow heart rate

• Decrease afterload/blood pressure

Medications

• Decrease cardiac output

• Cause rise in EF and reduction in LV size

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Diuretics – (furosemide):• Reduce peripheral vascular resistance• Reduce plasma volume• Take off excess salt and fluid

Medications

• Control fluid retention• Decrease volume overload

• Negative: electrolyte depletion, hypotension, increase neurohormonal activation…


Digitalis : Controls symptoms of decreased contractility

• Inotropic effects

Medications

p• Controls rate in afib• Useful with CHF Symptoms despite ACE and β-

blockade

• Negative: dig toxicity, arrhythmia


• Most common cause is acute or subacute deterioration of chronic heart failure.

Precipitated by discontinuation of medication, excessive salt intake, myocardial ischemia, tachyarrhythmia (a.fib) or infection

Acute Heart Failure

infection.

• Severe dyspnea, pink, frothy sputum, diaphoresis and cyanosis.

• Wheeze and rhonchi

• CXR: pulmonary vascular redistribution, butterfly pattern of alveolar edema, increased interstitial markings

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Acute Decompensation of “Stable” CHFPrecipitating Factors

• Altered cardiovascular condition:

Infarction, Arrhythmia, Worsened HTN

• New metabolic stress:

Fever, Infection, Blood loss, Anemia

• Medication Change:g

Non-compliance with medications

New medication initiated

NSAID, B-Blocker, CCB

• Dietary indiscretion

Salty food, alcohol

• Iatrogenic volume overload

Transfusion, IV NS


Acute Decompensation of “Stable” CHF

CXR: Cardiac silhouette enlargement

If acute:

• Enlarged pulmonary veins

• Upper lobe redistribution of fluid

I t titi l d ith t l h i• Interstitial edema with central haziness

• Peri-hilar or patchy peripheral infiltrates

• Pleural effusions are common (R>L)


Massive MI:>40% = cardiogenic shock

Valve failure:

ruptured chordae tendineae of mitral valve

M diti

Other Causes of Acute CHF:

Myocarditis

Thyrotoxicosis/ thyroid storm

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





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Electrocardiogram (EKG)

• Evaluate rate and rhythm

• Evaluate for acute or prior MI

• Evaluate for Ventricular Hypertrophy

CHF: Studies & Labs

Evaluate for Ventricular Hypertrophy

Remember Angiography:

• in the presence of STEMI etc.


Labs:

• BNP (B-type Natriuretic Peptide)

• released by heart muscle in fluid overload

• sensitive & specific: <100 rules out CHF

CHF: Studies & Labs

• CPK and Troponin (MI)

• CBC (anemia)

• Electrolytes

• Renal Function (BUN/ Creatinine)

• Consider TSH


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

CHF: Studies & Labs

• Evaluate valve function

• Dx: dilated, restrictive, or hypertrophic Cardiomyopathy

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In most cases

EF refers to left ventricular ejection fraction.

50 - 70% = Normal

36 - 49% = Below Normal

Ejection Fraction

36 49% Below Normal

35 - 40% = may confirm diagnosis of systolic heart failure

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


• Loop Diuretic: Lasix (double current po dose)

• SL/IV NTG: ensure normotensive

• O2, CPAP

• ACE inhibitor

Treatment of Acute CHF/Pulmonary Edema

• Find and Treat Causes: MI? HTN?


• Shock caused by the Heart’s diminished CO

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

• Dysrhythmia: Tachy or Brady

• Acute valve dysfunction - (regurgitant)

R t f t i l t ll

Acute CHF with Cardiogenic Shock

• Rupture of ventricular septum or wall

Possible with Massive MI

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General Treatment Measures

• Continuous IV infusion of inotropic medication

Dopamine is pressor agent of choice

• Mechanical assist devices

T i t i d t f i d i l ti

Treatment of Cardiogenic Shock

To maintain adequate perfusion and circulation

Intra-Aortic balloon pump

Ventricular assist device

• Transplant?


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

Only 35% of men and 50% of women are alive after 5 years.

Prognosis

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


• Infective Endocarditis

• Acute Pericarditis

Endocarditis, Pericarditis & Effusion

• Pericardial Effusion

• Cardiac Tamponade

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• Preexisting Heart Lesion (Valvular)

• Fever (>380 C)

• New Heart Murmur

Infective Endocarditis

• New Heart Murmur

• Positive Blood Cultures

• Evidence of Septic Emboli

• Echocardiography w/ Vegetation


Classic Signs:

• Petechiae: 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%)


• Acute bacterial infection typically Staph. aureus.

• Rapid onset of high fevers, rigors

• New regurgitant murmur

Acute Infective Endocarditis

• 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%)

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• Slow insidious bacterial infection of heart valve

• Typically Strep. viridans

• Patients have weeks of symptoms

iti f ti d l i

Subacute Infective Endocarditis

nausea, vomiting, fatigue, and malaise

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

• Regurgitant murmur

• Labs: anemia of chronic disease, normal WBC


Prosthetic Valve Disease:• Fever or prolonged constitutional symptoms

• Organism = (early) soon after valve implantStaph, Gram neg., Fungi


• Organism = (late) after 2 monthsStrep and Staph

• Treatment = 6 weeks of treatment Staph = 6wk Vanco + Rifampin + 2wkGent


• Injection Drug Users

• All febrile IDU’s should be evaluated for IE

O i 60% St h


• Organism = 60% Staph aureusAlso Enterocci/Streptococci

• Treatment = 2-6 weeks depending on the agent

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Organism Specific Treatment• Empiric = Vancomycin + Ceftriaxone

• Strep. viridans4 wk PenG or 2 wk PenG + Gent4 wk Ceftriaxone or Vancomycin


y

• Staph. aureus6 wk Nafcillin or Oxacillin6 wk Vancomycin

• HACEK - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella4-6 wk Ceftriaxone


Lesions Requiring Prophylaxis

High Risk• Prosthetic Valves • Prior Infective Endocarditis • Cyanotic Congenital Heart Disease


• Cyanotic Congenital Heart Disease

Moderate Risk• Rheumatic (or other acquired) valve disease • Hypertrophic Cardiomyopathy • Mitral valve prolapse WITH regurgitation


Lesions NOT Requiring Prophylaxis:

• ASD/ VSD/ PDA- post repair• CABG• MVP without regurgitation• Rheumatic fever without valve dysfunction


• Rheumatic fever without valve dysfunction• Previous Kawasaki’s/ Pacemakers/ AICD-

Defibrillators• Hypertrophic Cardiomyopathy • Mitral valve prolapse WITH regurgitation

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Procedures Requiring Prophylaxis:

• Oral: Dental Extraction/Root Canal/Tonsillectomy

• GI: Surgery/ERCP/Colonoscopy with biopsy

• GU: Prostate surgery/Cystoscopy


Procedures NOT Requiring Prophylaxis:

• Oral: Dental injection/filling/fluoride/ orthodontic adjustment

• GI: Endoscopy with biopsy

• GU: Hysterectomy, C-section/ Vaginal delivery

• CV: TEE, angioplasty

• Respiratory: Flexible Bronch/ tympanostomy/ ET Tube


Modified Dukes CriteriaDefinitive Dx: 2 major OR 5 minor OR 1 major + 3 minorPossible Dx: 1 major + 1 minor OR 3 minor

Major Criteria:Two (+) Blood Cultures with typical agent


• Two (+) Blood Cultures with typical agent• TEE Demonstrates Endocarditis• New MurmurMinor Criteria:• Fever >38C• Vascular phenomena• Immunologic phenomena• (+) Blood Culture• predisposing heart condition or IV drug use


Complications: depend on organism, valve and time of DX

• Valve Damage leads to rapid deterioration with CHF

• Aortic valve: embolization to brain/ myocardium


Aortic valve: embolization to brain/ myocardium embolization to spleen/ kidneys

• Tricuspid: septic pulmonary emboli

• Staph aureus: more valve damage, abscesses and emboli

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• Prognosis: Medical treatment is usually effective

• Valve replacement surgery indicated if: • Valve regurgitation with CHF • Infections not responding to ABX


p g• Recurrent infection with same agent• Fungal endocarditis• +/- continued embolization


Myocardial Inflammation (Focal or Diffuse)

• Sudden onset Heart Failure

• Sx: SOB/ pleuritic chest pain

• PE: Edema/ S3 gallop

Myocarditis

• EKG: Nonspecific ST changes w/ conduction delay

• Echocardiogram > Dilated Cardiomyopathy

• Dx: Myocardial biopsy = gold standard


Myocardial Inflammation (Focal or Diffuse)

1o = viral Infection or immune response

• Coxsackie B (measles/ influenza/ varicella)

• Kawasaki’s

Myocarditis

Kawasaki s

2o = Due to:

• Bacteria: Lyme/ RMS fever/ Syphilis/ Chagas

• Toxins: Radiation/ doxorubicin/ cocaine

• Systemic illness: Lupus/ Rheumatoid Arthritis

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Localized inflammation of anterior lateral and

Pericarditis

anterior, lateral and inferior walls may cause ST elevations in multiple areas


Common: Viral/ often post URI

• Coxsackie B (echo/ influenza/ varicella)

• Men under 50 most common (post URI)

Pl i i / i i l h i

Acute Pericarditis

• Pleuritic/ positional chest pain

• CP relieved by leaning forward

• Pericardial friction rub

• Treatment - ASA/ indomethacin/ NSAID

• <5% develop tamponade


Pericardial Inflammation

• Uremia/Renal Failure need dialysis

• Post cardiac surgery

• Post MI (2-5 days) Dressler’s Syndrome

Acute Pericarditis

May present with associated Myocarditis

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Disease: Pericarditis

http://www.the-hospitalist.org/details/article/2785031/How_is_Acute_Pericarditis_Diagnosed_and_Treated.html


Accumulation of fluid in pericardium

• Rapid accumulation = tamponade

• Fluid 2o to inflammatory process = painful

Pericardial Effusion

• 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 ∆’s,

• maybe electrical alternans

• Echo: Primary method for detecting effusion

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Paradoxical pulse exaggeration of normal variation during respiration;Pulse becomes weaker as one inhales and stronger as one exhales.


Electrical alternansalternate-beat variation in direction, amplitude, and duration of the ECG waveform


↑ Intrapericardial pressure ↓ venous return and ↓ ventricle filling

• Stroke volume falls > BP falls > Shock > Death

• Dyspnea and cough

Cardiac Tamponade

• Tachycardia

• Narrow pulse pressure

• Paradoxical pulse / Electrical Alternans


Treatment• Tamponade:

• Urgent pericardiocentesis• Sub-xiphoid approach with echocardigraphy


• Small effusions: • Follow clinically (JVD) and serial echo

• Large effusions:• Pericardial window

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PROPERTIES



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2015 cardiology 1 - @mycme

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