cardiovascular disorders pfn: somcml05

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Slide 1JSOMTC, SWMG(A)

Cardiovascular DisordersPFN: SOMCML05

Hours: 8.0


Terminal Learning Objective

Action: Communicate knowledge of “Cardiovascular Disorders”

Condition: Given a lecture in a classroom environment

Standard: Received a minimum score of 75% on the written exam IAW course standards


References

Current Medical Diagnosis and Treatment(51st edition; 2012; McPhee; Papadakis)

Pathophysiology for the Health Professions(4th edition; 2011; Gould; Dyer)

Guide to Physical Examination and History Taking (10th edition; 2009; Lynn S. Bickley)

Pharmacology (3rd edition; 2010; Brenner; Stevens)

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Reason

Cardiovascular disease remains the leading cause of death in the USA today. One in four persons aged 45‐64 have some form of cardiovascular disease. One in three over the age of 64 will develop cardiovascular disease. While the majority of CVD affects those in middle age and older, a significant number of younger patients may be victims also.


Reason

In its early stages, CVD may produce little or no signs and symptoms. As it evolves, symptoms may remain subtle. As a Special Operations Medical NCO, your challenge will be the early recognition and initial management of various CVD entities in order to reduce morbidity and mortality in your patient population.


Agenda

Recall the anatomy and physiology of the cardiovascular system

Identify potential cardiovascular pathologies and the impact they may have on cardiovascular function

Identify normal and abnormal volumes and pressures related to cardiovascular function

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Agenda

Identify signs and symptoms that may suggest cardiovascular disease

Communicate the information that should be incorporated into a cardiovascular history

Identify the content of a cardiovascular oriented physical exam and the significance of exam findings


Agenda

Communicate normal and abnormal heart sounds

Identify the physiologic changes associated with ageing

Identify the risk factors associated with cardiovascular disease

Identify the pathogenesis of atherosclerotic vessel disease


Agenda

Communicate normal and abnormal lipid values, different types of hyperlipidemia, secondary causes, physical exam findings, management, and counseling of dyslipidemia patients

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Agenda

Communicate the etiology, signs and symptoms, diagnostic tests, and management of the three types of chest pain, to include: ischemic heart, acute coronary syndrome, and coronary artery diseases

Communicate the etiology, signs and symptoms, diagnostic tests, and management of congestive heart failure


Agenda

Communicate the etiology, signs and symptoms, diagnostic tests, and management of the inflammatory heart diseases, to include: pericarditis, infective endocarditis, rheumatic fever, and rheumatic heart disease


Agenda

Communicate the etiology, signs and symptoms, diagnostic tests, and management of vascular disorders, to include: hypertension (secondary and essential), peripheral vascular diseases, atherosclerosis, and aortic aneurysms

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Agenda

Identify diagnostic criteria and management guidelines for pulmonary emboli


The Anatomy and Physiology of the Cardiovascular System


Gross Anatomy

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Gross Anatomy


Coronary Vessels


Cardiac Circulation

Heart has very high oxygen and nutrient demands

Coronary arteries originate at base of aorta

Arterial anastomoses ensure constant blood supply

The great and middle cardiac veins carry blood from the coronary capillaries to the coronary sinus

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Heart Wall


Heart Wall

Components include:

Epicardium

Myocardium

Endocardium


Structural Differences Between Ventricles

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Internal Anatomy

Atria

Thin walled chambers that receive blood from vena cava and pulmonary vein

Ventricles

Thick walled chambers separated from the atria by AV valves


Internal Anatomy

Valves

Atrioventricular

• Tricuspid

•Mitral

Semilunar

• Pulmonic

• Aortic

Chordae tendinea

Papillary muscles / trabecular carnea


Heart Valves

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Heart Valves


Superficial Anatomy


Systemic Circulation

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The Conduction System

Comprised of two types of cells

Nodal cells (pacemaker cells)

• Establish rate of contractions

Conducting cells

• Distribute contractile stimulus to the myocardium


Conduction System

Nodal

SA node

AV node

Conducting

AV bundle

Bundle branches

Purkinje fibers


Conduction Pathways

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Conduction System ECG


Conduction SystemActivation Potentials

SA (sinoatrial) node *

60 to 100 bpm

AV (atrioventricular) node

40 to 60 bpm

Bundle of His

< 40 bpm

Purkinje Fibers

< 40 bpm


Cardioregulation

Basic heart rate established by pacemaker cells (modifiable by ANS)

Cardiac centers in medulla oblongata contain the autonomic centers for cardiac control

Cardio‐accelerator center: governs sympathetic neurons

Cardio‐inhibitor center: governs the parasympathetic neurons

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Cardioregulation

Neurotransmitters

Acetylcholine (Ach)

• Released by parasympathetic system

• Slows HR / reduces SV

Norepinephrine (NE) and Epinephrine:

• Released by sympathetic neurons

• Increase HR / SV

Note: Hypothalamus can provide additional input (allows emotion, fear, anxiety to affect HR)


Heart Innervation


Cardiac Contractility Frank‐Starling law

The heart will contract with greater force when preload (EDV ) is increased

Myocardial contractility

The squeezing contractile force that the heart can develop at a given preload

• Regulated by:

Sympathetic nerve activity (most influence)

Catacholamines (epi – norepinephrine)

Amount of contractile mass

Drugs

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Vascular Anatomy and

Physiology


Arteries


Sympathetic Innervation

Vascular smooth muscle is innervated by the sympathetic nervous system

Increase in stimulation > vasoconstriction

Injury to artery causes muscle contraction (vasospasm)

Decreased stimulation or certain chemicals such as nitric oxide / lactic acid leads to vasodilation

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Resistance Friction between the blood and walls of a vessel

Smaller vessels = increased resistance

Blood viscosity

Ratio of RBCs to plasma volume

Increased viscosity = increased resistance

• e.g., Dehydration / Polycythemia

Total blood vessel length

The longer the vessel, the greater the resistance


Total Peripheral Resistance (TPR)

TPR is the sum of resistance in all vessels of the arterial system

Note:Most of the TPR is in small arteries and arterioles as they are narrow and have high resistance


Veins

Thinner walls

No elastic lamina

Adaptable to volume and pressure

Contain valves to prevent backflow of blood

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Venous Return

Skeletal muscle pump Contraction of muscles and presence of valves

Respiratory pump Increased thoracic pressure and abdominal pressure during inhalation moves blood into thoracic veins and right atrium


Hemodynamics

Factors affecting circulation

Velocity of blood flow

Pressure differences

Resistance to flow

Venous return

Circulatory pressure generated by ventricles

Note: An interplay of forces creates blood flow


Potential Cardiovascular Pathologies and the Impact

They May Have on Cardiovascular Function

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Potential Pathologies

Cause

Pericarditis

Effect

Effusion

Tamponade

Restricted filling

Decreased cardiac output



Cause

Coronary arteries

• Atherosclerosis

• Atherothrombosis

Effect

Ischemia

Dysrhythmias

Decreased myocardial contractility

Reduced cardiac output



Cause

Cardiomyopathy

• Ischemia

• Toxic

• Infectious

Effect

Decreased contractility

Reduced cardiac output

Congestive heart failure

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Cause

Valvular dysfunction

• Stenosis

• Regurgitation

Effect


Cardiac failure



Cause

Arteriosclerosis

Atherosclerosis

Effect

Hypertension

Thrombosis

Stroke

Aneurysm / Dissection / Rupture



Cause

Peripheral vascular disease

Effect

Peripheral arterial disease

• Ischemia

• Necrosis / Gangrene

Peripheral venous disease

• Deep venous thrombosis

• Pulmonary embolism

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Normal and Abnormal Volumes and Pressures Related to Cardiovascular

Function


Volumes and Pressures

End Diastolic Volume (EDV)

Left ventricular volume at end of diastole (end of ventricular filling )

End Systolic Volume (ESV)

Left ventricular volume at end of systole (end of ventricular contraction)

Stroke Volume (SV)

EDV‐ ESV



Cardiac Output (Q): HR X SV

Preload

Diastolic filling volume of the left ventricle

EDV reflects stretch of the cardiac muscle cells

Afterload

Resistance to ventricular emptying during systole

The amount of pressure left vent. must generate to squeeze blood into the aorta

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Systolic Blood Pressure (SBP)

Pressure measured in the brachial artery during systole (ventricular emptying and ventricular contraction period)

Diastolic Blood Pressure (DBP)

Pressure measured in the brachial artery during diastole (ventricular filling and ventricular relaxation period)



Mean Arterial Pressure (MAP)

“Average” pressure throughout the cardiac cycle against the walls of the proximal systemic arteries (aorta)

[ (2 x diastole) + systole ] / 3

Total Peripheral Resistance (TPR)

The sum of all forces that oppose blood flow

Depends on

• Length of the vasculature and vessel radius

• Blood viscosity and hydrostatic pressure



Pulse Pressure

The change in blood pressure seen during a contraction of the heart

Systolic pressure minus the diastolic pressure

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Blood Pressure

Pressure exerted on walls of vessel

HR ↑ CO ↑ BP ↑

Pressure falls steadily with increased distance from ventricle

10% ↓ of BV then BP ↓

Water retention will increase BP


Local Regulation of Blood Pressure

Local factors cause changes in capillary beds

Autoregulation is ability to make these changes as needed by demand for O2 and waste removal

• Important for tissues that have major increases in activity (brain, cardiac, and skeletal muscle)


Local Regulation of Blood Pressure

Local changes in response to physical changes

Warming and decrease in vascular stretching promotes vasodilation

Vasoactive substances released from cells alter vessel diameter (K+, H+, lactic acid, nitric oxide)

Systemic vessels dilate in response to low levels of O2

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Neural Control of Blood Pressure


Cardiovascular Center Output Heart

Parasympathetic (vagus nerve)

• Decreases heart rate

Sympathetic (cardiac accelerator nerves)

• Causes increased contractility and rate

Blood vessels

Sympathetic vasomotor nerves

• Stimulation to arterioles in the skin and abdominal viscera produces vasoconstriction (vasomotor tone)

• Increased vasomotor tone results in increased blood pressure


Baroreceptor Reflex

Baroreceptors in the internal carotid artery, aortic arch, and other large arteries in the neck send impulses via the glossopharyngealnerve to the CV center in the medulla

If a drop in blood pressure is detected, baroreceptors are stretched less and slow their rate of impulse emission to the CV center

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Baroreceptor Reflex (cont.)

In response to decreased feedback, the CV center will reduce parasympathetic stimulation and increase sympathetic stimulation of the heart and blood vessels

As a result, HR and CO will increase, and arterioles will vasoconstrict ‐ resulting in a restoration of blood pressure


Baroreceptor Reflexes in BP Control


Chemoreceptor Reflexes

Carotid bodies and aortic bodies

Detect changes in blood levels of O2, CO2, and H + (hypoxia, hypercapnia, or acidosis)

Causes stimulation of CV center

• Increases sympathetic stimulation to arterioles and veins

Vasoconstriction and increase in BP

Changes breathing rate as well

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Hormonal Control of Blood Pressure

Renin‐angiotensin‐aldosterone system

Decrease in BP or blood flow to the kidneys

Release of renin results in formation of angiotensin II

Angiotensin II leads to

• Systemic vasoconstriction

• Release of aldosterone from the adrenal glands (Na+ and H2O reabsorption)


Hormonal Control of Blood Pressure (cont.)

Epinephrine and norepinephrine

Increased HR and force of contraction

Causes vasoconstriction in the skin and abdominal organs


The Renin‐Angiotensin System

Perfusion

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Hormonal Regulation of BP

ADH (anti‐diuretic hormone)

Released from the pituitary in response to low blood volume / increased plasma solute concentration

• Causes vasoconstriction and reabsorption of H2O in the kidneys

• Raises BP


Hormonal Regulation of BP (cont.)

ANP (atrial natriuretic peptide)

Released from heart in response atrialstretching

• Causes vasodilation and loss of salt and water from the kidneys

• Lowers BP


Signs and Symptoms that May Suggest Cardiovascular

Disease

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Chief Complaint

Chest Pain

Shortness of Breath

Exertional

Positional

Nocturnal

Fatigue / Weakness

Cough / Hemoptysis

Palpitations

Dizziness / Syncope

Weight gain / Edema

Claudication


The Information that Should be Incorporated into a Cardiovascular History


History of Present IllnessOriented to Pain

Onset

Provocative / Palliative Factors

Quality / Quantity

Region / Radiation

Severity

Timing

Associated Symptoms

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Past Medical History (PMHX)

CVRFs (cardiovascular risk factors)

Chest Trauma

Fever

Upper/ Lower Respiratory Symptoms

Gastrointestinal Symptoms


The Content of a Cardiovascular Oriented Physical Exam and the

Significance of Exam Findings


Physical Exam

General Appearance

Vital Signs

Eyes

Fundi

Exopthalmos

Lid lag

Xanthalasma

Neck

Carotid arteries

Goiter

Chest

Excursion

Deformity

Point tenderness

PMI

Thrills

Lifts / Heaves

Lungs

IPPA

Crackles (rales)

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Physical Exam

Heart

Rate / Rhythm

Sounds (S1, S2, S3, S4)

Murmurs • Systolic versus Diastolic

• Region / Radiation

PMI

Abdomen

Distention / Ascites

Hepatomegaly

Hepatojugular reflux

Bruits

Pulsations


Physical Exam

Extremities

Distal pulses

Embolic signs

Hair distribution

Temperature / Color

Lesions

Nail deformities


Additional Diagnostics

CXR

Infiltrates

Cardiomegaly

Widened mediastinum

ECG

Injury patterns

Dysrhythmia

Lab

CBC

Electrolytes

Lipids

Glucose

TFTs

U/A

Cardiac enzymes

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Skeletal LandmarksAuscultation Sites

Aortic2nd RICS

Pulmonic2nd LICS

Tricuspid4th LICS

Mitral5th ICS MCL


Normal Heart Sounds

Normally audible

S1 (Lubb)

Systole

Closure of AV valves

S2 (Dubb)

Diastole

Closure of semilunar valves


Cardiac Auscultation

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Normal and Abnormal Heart Sounds


Extra Heart SoundsGallops

S3

Rapid ventricular filling

Associated with left ventricular failure

S4

Forceful atrial ejection into a distended ventricle

Associated with left ventricular hypertrophy usually secondary to hypertension

Note: Gallops are not always audible; best heard over apex of heart

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Sounds like: TENN ‐ E ‐ SSEE

S1 S2 S3



Sounds like: KEN ‐ TU ‐ CKY

S4 S1 S2



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Murmurs Abnormal ausculatory sounds due to deformity of valvular structure

Types

Regurgitant

Stenotic

Systolic

Diastolic

Mitral and aortic valves most often affected due to higher pressures within left side of heart


Valvular Anatomy


Innocent Murmurs

S1 S2 S1

CharacteristicsEarly to midsystolicHeard best 2nd to 4th interspaceGrade 1‐2 intensityMusical, vibratory, or buzzingNo extra heart soundsOften decreases or disappears with sitting

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Aortic Stenosis

S1 S2 S1

CharacteristicsMachinery type sound, roughAortic, neck, and apex areasPatient sitting forwardUse diaphragm to auscultate


Aortic Regurgitation

S1 S2 S1

CharacteristicsHigh pitched blowing diastolic May radiate towards apexPatient upright, leaning forward, holding breath in fixed expirationUse diaphragm to auscultate


Systemic Hypertension

Aortic area (diaphragm)

S1 S2

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Mitral Stenosis

S1 S2

o.s.

S1

CharacteristicsLoud S1Opening high‐pitched snapMid‐diastolic low pitchedUse diaphragm for S1 at LLSB and apexUse bell for diastolic rumble over PMI


Mitral Regurgitation

S1 S2 S1

CharacteristicsBlowing, holosystolicRadiates from LLSB and apex to axillaryline and lung base


Mitral Valve Prolapse

S1 S2 S1

Click‐Murmur

CharacteristicsMurmur crescendos in late systoleSquatting pushes click/murmur closer to S2Use diaphragm

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The Physiologic Changes Associated with Aging


Aging Effects

Decreased aortic compliance

Reduced cardiac muscle fiber size, decreased PMI

Reduced cardiac output and maximal heart rate

Increased systolic blood pressure

Total cholesterol and LDL increased

HDL decreased

CHF, CAD, and atherosclerosis more likely


The Risk Factors Associated with Cardiovascular Disease

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Cardiovascular Risk Factors



Major Risk Factors

Age: Males > 45 y/o and Females > 55 y/o

Gender (Male >Female)

Smoking

Hypertension*

Dyslipidemia*

• LDL > 160mg/dL

• HDL < 35mg/dL

(Note: subtract one risk factor if HDL >60 mg/dL)

Diabetes*



Other Risk Factors

FHX CVD: Males < 55 y/o and Females < 65 y/o

Obesity

Physical Inactivity

Ethnics

Socio‐economics

Stress

Homocysteinemia

↑ C‐Reactive Protein (CRP)

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The Pathogenesis of Atherosclerotic Vessel Disease


Atherosclerosis

Disease of the muscular arteries (not veins)

Coronary

Cerebral vessels

Progressive deposition of cholesterol esters

Accounts indirectly for half of annual mortality

Ischemic heart disease leads to MI

Cerebrovascular disease leads to Stroke


Atherosclerotic Vessel Disease

Pathophysiology

Lesions start as fatty streaks (as early as adolescence)

• Subendothelial accumulation of large foam cells (derived from macrophages plus smooth muscle cells) filled with lipid

Fibrous plaque

•More advanced and the cause of disease

• Develops from fatty streaks

• Projects into arterial lumen

• Reduces blood flow

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ASVD Targets

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Atherosclerotic Effects

Calcification Pipe like rigidity with loss of compliance; decreases vessel lumen diameter

Rupture or Ulceration Clot formation

vessel occlusion

Hemorrhage into plaque

Embolization from plaque

Weakening of vessel wall with rupture

MI

Angina

Stroke

Aneurysm


Atherosclerosis Endpoints


Myocardial Infarct SiteOld

Scar

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Stroke

Hemorrhagic Zone


Aortic Aneurysm


Gangrene Arterial Occlusive Disease

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Normal and Abnormal Lipid Values, Different Types of Hyperlipidemia, Secondary Causes, Physical Exam

Findings, Management, and Counseling of Dyslipidemia

Patients


Dyslipidemia

Definition

An abnormal level of circulating lipids in the blood

Major risk factor for the development of atherosclerotic vessel disease

Types

Primary (genetic)

Secondary


Dyslipidemia

Secondary causes

Diet

Hypothyroidism

Pregnancy

Obesity

Excess ETOH intake

Obstructive liver disease

Meds (e.g., thiazides, BB, ocp’s, and steroids)

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CholesterolThyroid Connection

Hypothyroidism is common cause of secondary dyslipidemia

Nearly 90% of those with hypothyroidism have elevated cholesterol

Up to 10% of individuals have TSH

Only 60% of those on thyroid hormone have normal TSH


Lipid Levels

Total Cholesterol < 200 mg / dl (desirable)

LDL < 160 mg / dl (desirable)

HDL > 40 mg / dl (desirable)

TG < 150 mg / dl (desirable)


DyslipidemiaRisk Profile

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DyslipidemiaPhysical Exam Clues

Arcus juvenilis (in younger individuals)

Xanthomas


Arcus JuvenilisCornea


Xanthelasma

Note: 50% of patients with xanthelasmawill have significant hypercholesterolemia

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Xanthomatous Eruption


Xanthomatous Tuberosity

NOTE: Pathognomonic for familial hypercholesterolemia


DyslipidemiaManagement Guidelines

Diet for 6 months

Increased physical activity

Weight reduction

Medications

If no resolve with above

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Therapeutic Lifestyle ChangesDiet

Saturated fat < 7% calories

Polyunsaturated fat < 10% calories

Monosaturated fat < 20% calories

Total fat 25 ‐ 35% calories

CHO 50 ‐ 60% calories

Fiber 20 ‐ 30 gm/ day

Protein 15% calories

Cholesterol < 200 gm/ day


Therapeutic Life Style ChangeExercise

Aerobic exercise

> 20 minutes per activity

At least 3 days per week

Promotes weight loss and HDL


Therapeutic Life Style ChangeSmoking Cessation

Can lower oxidative stress

Reversal of endothelial dysfunction

HDL

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Therapeutic Life Style ChangeAlcohol Moderation

“French Paradox”

Related at least in part to ethanol‐induced HDL

Wine phenolics may confer additional benefits


The Appropriate Treatment Measures for Dyslipidemia


Cholesterol Lowering Drug Therapy

Bile acid sequestrants

Cholestyramine

Colestipol

Fibrates

Gemfibrozil

Clofibrate

Niacin

HMG CoA Reductase Inhibitors (statins)

Lovastatin

Pravastatin

Simvastatin

Fluvastatin

Atorvastatin

Rosuvastatin

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Bile Acid Sequestrants

Effect on lipids

TC, LDL, HDL, TG

Adverse effects

Constipation

Bloating

Abdominal cramping


Fibrates

Effect on lipids

TC, LDL, HDL, TG

Adverse effects

Nausea

Diarrhea

Cholelithiasis


Niacin

Effects on lipids

TC, LDL, HDL, TG

• Adverse effects

Flushing, pruritis, headache, and fatigue

• (PG‐mediated? ASA may lessen these side effects)

Gastritis, abdominal pain, aggravation of PUD, and hepatotoxicity

Impaired glucose control and uric acid concentrations

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Statin Effects

Improvement of endothelial vasodilation

Vascular smooth muscle proliferation

Platelet‐thrombus formation

Fibrinogen formation

Cholesterol accumulation in macrophages

LDL oxidation

Leukocyte and monocyte adherence

Blood viscosity


Statin Precautions

Major toxicities

Elevated liver enzymes

Myalgias

Rhabdomyolysis ( risk when combined with other agents)

Selected minor adverse effects

Dyspepsia/ heartburn

Headache

Taste disturbances


Rhabdomyolysis

Definition

Acute, potentially fatal skeletal muscle condition characterized by skeletal muscle destruction as evidenced by myoglobinuria and CK elevations at least 10x normal

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Rhabdomyolysis (cont.)

Complications

Hyperkalemia

Cardiomyopathy

Hyperuricemia

Respiratory and/or renal failure

DIC

Metabolic acidosis


MyotoxicityClinical Clues

Symptoms (primary)

Gradually decreased muscle strength

Localized or generalized muscle weakness

Note: Symptoms may occur days or months after initiating therapy and generally worsenswith every dose


Monitoring of Lipid Lowering Therapy

Lipid profiles

Before initiation and at 6‐12 weeks until stable

Every 6 months thereafter

Hepatic transaminases

Baseline and every 6‐12 weeks until stable

Every 6 months thereafter

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The Etiology, Signs and Symptoms, Diagnostic Tests, and Management of the Three Types of Chest Pain


Chest Pain

6 million patients seen annually for chest pain

1.5 million diagnosed with AMI

1 million diagnosed with unstable angina

50,000 missed diagnoses of AMI


Chest PainDifferential Diagnosis

Cardiac Angina

AMI

Pericarditis

Endocarditis

Valvular

Vascular Aortic Dissection

Mesenteric Artery Occlusion *

Pulmonary PE

Pneumothorax

Pneumonia

Pleurisy

Musuloskeletal Chostrochondritis

Muscle Strain

Gastrointestinal GERD

Integument Herpes Zoster

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Chest PainNON‐Ischemic Clues

Pleuritic pain

Localization with one or two fingers

Reproducible pain

Constant pain lasting days

Fleeting pain


Acute Coronary Syndromes

Epidemiology

> 6,000,000 Americans have CAD

500,000 deaths per year in the U.S. from CAD

250,000 patients with prehospital cardiac arrest

• 6% survive to hospital discharge

> 4,000,000 E.D. visits per year for acute chest pain

$100 billion per year

Platelet / Thrombi aggregation versus spasm


Acute Coronary Syndromes (cont.)

Etiology

Ischemia

• Imbalance between oxygen demand and oxygen supply

Fixed atherosclerotic lesion versus plaque disruption with embolic event

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Ischemic Heart DiseaseCategories

Definition

Closely related syndromes caused by an imbalance between myocardial oxygen demand and blood supply

* Most common etiology is atherosclerosis

1. Angina Pectoris

2. AMI (acute myocardial infarction)

3. Sudden Cardiac Death Syndrome


Ischemic Heart DiseaseEpidemiology

Peak incidence

Males > 60 y/o

Females > 70 y/o

Risk factors

Age

Gender

Hypertension

Dyslipidemia

Diabetes

Smoking

Family history


Ischemic Heart Disease Pathogenesis

Critical stenosis occurs when 75% (or greater) of the lumen of one or more coronary arteries is/are obstructed by atherosclerotic plaque

With this fixed level of obstruction, compensatory coronary vasodilation is insufficient to meet moderate increases in myocardial demand, leading to ischemia

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Ischemic Heart DiseasePathogenesis

Fixed obstruction (> 75% of lumen)

Superimposed plaque lesion

Change in plaque morphology

Platelet aggregation

Coronary artery thrombosis

Coronary artery spasm


Angina Pectoris

Definition

Intermittent chest pain caused by reversible myocardial ischemia

Types

Typical (stable) angina

Prinzmetal’s (variant) angina

Unstable (crescendo) angina


Angina Pathophysiology

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Angina PectorisTypical (Stable)

Definition

Intermittent chest pain caused by reversible myocardial ischemia

Characteristics

75% or > occlusion

Onset with exertion or emotional upset

Relieved with rest or nitrates (NTG)

ECG ST segment depression

Brief pain duration (often < 5 minutes)


Angina PectorisPrinzmetal’s Variant

Definition

Intermittent chest pain caused by reversible myocardial ischemia due to vasospasm near a plaque

Characteristics

Occurs at rest or during sleep

Coronary spasm near plaque

Relieved with nitrates (NTG)

Transient ST segment elevation


Angina PectorisUnstable Angina

Definition

Crushing chest pain caused by an acute change in plaque morphology (ulceration, bleeding, thrombosis)

• Also known as crescendo or pre‐infarction angina

Characteristics

Occurs at rest or with exertion

Acute plaque changes

No relief with nitrates (NTG)

Longer duration (typically > 20 minutes)

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Myocardial Infarction (MI)

Definition

Is the development of a defined area of myocardial necrosis caused by local ischemia

• The most common cause is coronary thrombosis due to atherosclerotic plaque

Leading single cause of death in industrialized nations

In USA, 1.5 million have AMI annually, of which 500,000 are fatalities


Atherosclerotic Plaque Thrombosis


Coronary Artery Thrombosis

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AMIClinical Features

Preceding angina in approximately 50%

Crushing substernal chest pain

Radiating to neck, jaw, shoulder, and arm

Dyspnea

No relief with nitrates (NTG)

Longer duration of pain

ECG changes: ST segment and Q waves


Cardiac Markers Enzymes

Myoglobin No 1‐3 hrs. 12‐24 hrs.

CK‐ Total No 4‐8 hrs. 36‐48 hrs.

CK‐ MB ++ 3‐4 hrs. 24‐36 hrs.

Troponin T ++++ 3‐4 hrs. 10‐14 days

Troponin I ++++ 4‐6 hrs. 4‐7 days

Marker Cardiac? 1st Rise Duration


AMI Diagnostic criteria

Cardiac enzyme elevation

• CK‐MB

• Troponin

Ischemic symptoms

•Diaphoresis

• Dyspnea

• Pain patterns

ECG changes of ischemia

• ST segment changes

• Q waves

56


AMIComplications

Sudden Death (25%) Cemetary

75% ‐ 90% Arrhythmias

10% ‐ 50% Thromboembolism

10% ‐ 20% No Complications

10% Cardiogenic Shock

~ 10% Cardiac Rupture


AMI Management (Initial)

Oxygen via nasal cannula 2‐4 LPM

IV

ASA 325 mg (chewed and swallowed)

NTG (sublingual or spray) 0.4 mg q 5 minutes

• Unless systolic BP < 90 mmHg

Morphine 2‐4 mg IV if pain not relieved after 3 sublingual NTG tablets

Beta blockers*

Thrombolytics* or PCI


Sudden Cardiac Death

Most causes are due to heart disease typically within 6 hours of presentation, but defined as <24 hours

Most common cause is ischemic heart disease, usually in the form of ventricular arrhythmias

Sudden death accounts for 50% of all cardiac deaths

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Sudden Cardiac DeathMorphology

Atherosclerosis

Two or more coronaries > 75% occlusion

? Vasospasm Ventricular arrhythmia

< 50% have occlusive thrombosis

Morphology may be elusive

Other cardiac causes

Conduction system abnormalities

Cardiomyopathy

Valvular disease


The Etiology, Signs and Symptoms, Diagnostic Tests,

and Management of Congestive Heart Failure


Congestive Heart Failure

Multisystem derangement when the heart can no longer eject the blood delivered by the venous system leading to organ hypoperfusion

Affects 3‐4 million patients annually

Most common diagnosis in hospitalized patients over 65 years old

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CHF Etiology

Right sided

LVD*

Cor pulmonale

Pulmonary vascular disease

Valve disease

Left sided

Myocardial damage

Hypertrophic cardiomyopathy*

Congenital heart disease

Constrictive pericarditis

Valve disease*


Cardiac Remodeling

NORMALHYPERTROPHIC DILATED


CHF Signs

Right‐sided

Distended neck veins (JVD)

Kussmaul's sign

Hepatomegaly

Ascites

Peripheral edema

Abdominal Jugular Reflux (AJR)

Left‐sided

Tachycardia

Cool, clammy skin

Pulmonary edema (crackles)

Cardiomegaly

Third heart sound (S₃)

Murmur

Dyspnea / Cough

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JVD Measurement


Pulmonary Edema


CardiomegalyNormalEnlarged

60


Borderline Cardiomegaly


Cardiomegaly


CHF Compensatory MeasuresLocal

Sympathetic Response

Hypertrophy CO Compensated

Heart Failure

Cardiac Elongation

Note: If CO, then decompensated HF exists

61


Physiologic Response to Heart Failure

Carotid and LABaroreceptors

Renal ‐Adrenal

LV Dysfunction

Vasoconstriction

Aldosterone

Sodium and FluidRetention

Tachycardia

Renin‐Angiotensin System(See next slide)

Sympathetic Output


Physiologic Response to Heart FailureRenin‐Angiotensin‐Aldosterone System

DeceasedRenal Perfusion Renin

Angiotensin I

Angiotensin II

SympatheticActivity

Vasoconstriction

H2O Retention

Na Retention

NE releaseAldosterone


Acute CHF Management

Lasix (diuretic)

Decrease preload and diuresis

Morphine

Decrease preload and afterload; anxiolytic

Nitrate

Decrease preload and afterload

Oxygen

Increase PO2 and pulmonary vasodilation

Positioning

Semi‐reclining; increased lung volume

Inotropic agents

Strengthen contractions

62


The Etiology, Signs and Symptoms, Diagnostic Tests, and Management of the

Inflammatory Heart Diseases


Pericarditis

Definition

Acute pericarditis is a syndrome caused by inflammation of the pericardium and characterized by chest pain, distinctive ECG changes, and a pericardial friction rub on physical examination

Etiology

Most often viral in origin


PericarditisClinical Manifestations

Preceding upper respiratory infection (URI)

Sudden onset chest pain

Retrosternal

Pleuritic

Decrease pain with sitting position / leaning forward

Radiation to trapezius / neck region

Aggravated by swallowing

Fever, myalgias, and fatigue

63


Pericarditis Exam and Labs

Pericardial friction rub

ECG changes

Diffuse ST segment elevation

PR segment depression

Elevated ESR


PericarditisComplications

Cardiac tamponade

Increase of pericardial fluid volume

Impaired ventricular filling



Cardiac Tamponade

Physical exam

“Becks Triad”• Elevated JVP

• Systemic hypotension

• Muffled heart sounds

Pulsus paradoxis

Narrowed pulse pressure

Tachypnea

Tachycardia

Diagnostics

CXR• Water bottle effect

ECG• Tachycardia

• Low QRS amplitude

Echocardiogram

64


Cardiac TamponadeTreatment

Pericardiocentesis

Intravenous volume expansion

Vasopressors (dopamine)

Note: following pericardial drainage, rapid recovery is the rule


PericarditisManagement

Non‐steroidal anti‐Inflammatory drugs (NSAIDs)

Indocin 25‐50 mg PO tid

Ibuprofen 800 mg PO tid

Naprosyn 250 mg Po tid

Physical profiling

Note: Symptoms will usually subside within several days


Infective Endocarditis Definition

Condition characterized by infection of the endocardium and heart valves (May be indolent or acute)

Etiology

Bacteremia

• Dental procedures

• Urethral catheterization endoscopy

• Prostatic massage

Staphylococci and Streptococci

• 80% of occurrences

65


Infective EndocarditisHistory

Fever

Chills

Night Sweats

Fatigue and malaise

Anorexia

Weight loss


Infective EndocarditisPhysical Exam

Regurgitant murmur

Fever

Vascular phenomena

Janeway lesions

Splinter hemorrhages

Subconjunctival hemorrhages

Immunological phenomena

Osler nodes

Roth spots


Janeway Lesions

66


Splinter Hemorrhages


Conjunctival Hemorrhages


Osler Nodes

67


Roth Spots


Infective EndocarditisLab

Positive blood cultures

Elevated WBC count

Elevated erythrocyte sedimentation rate (ESR)

Anemia with sub‐acute endocarditis

Hematuria / Proteinuria

Glomerulonephritis


Rheumatic Fever

Definition

An immune mediated inflammatory disease that occurs as a result of untreated group A beta‐hemolytic streptococcal pharyngitis

Epidemiology

Uncommon in developed nations

Usually affects age group 5‐15 years of age

68


Rheumatic FeverPathogenesis

Organs involved

Heart

• Valvulitis often a result, causing regurgitant or stenotic lesions

Large joints

Brain

Skin

Sub Q tissues


Rheumatic Fever Clinical Features

Preceding case of streptococcal pharyngitis

Signs and symptoms of RF begin several weeks after pharyngitis

Carditis

Arthritis

Erythema marginatum

Subcutaneous nodules

Chorea (involuntary, irregular movements)


Erythema Marginatum

69


Rheumatic FeverTreatment

Referral

Echocardiography

Antimicrobials

Anti‐inflammatories

Antibiotic prophylaxis


The Etiology, Signs and Symptoms, Diagnostic Tests, and Management of Vascular

Disorders


Hypertension Epidemiology 50 million Americans have > 140/90 BP

Prevalence increases with age

Average age at onset: 32 y/o

At age 65: 30% whites and 50% blacks affected

Increased risk for:

Stroke ‐ Congestive heart failure

Peripheral vascular disease (PVD)

Atrial fibrillation

Erectile dysfunction

Dementia

70


Hypertension TreatmentRational

A little reduction goes a long way

A meta‐analysis showed that decreasing DBP by 5‐6 mm/Hg decreases mortality by 42% over 4‐6 years

Treatment reduces the risk of stroke, ischemic heart events, CHF, and renal failure

Only 59% of patients with HTN are under treatment and < 1/3 are controlled to 140/90 BP


Definition of Hypertension

Systolic (mm Hg) Diastolic (mm Hg)

Normal <120 <80

Prehypertension 120‐139 80‐89

Stage 1 HTN 140‐159 90‐99

Stage 2 HTN >160 >100

Stage 3 HTN > 180 > 110

Isolated Systolic > 140 < 90Systolic with wide > 160 < 70pulse pressure


BP Regulation

BP = CO x TPR

BP ‐ blood pressure

CO ‐ cardiac output

TPR ‐ total peripheral resistance

Treatment of hypertension seeks to lower CO and/or TPR

71


BP Regulation

CO = heart rate x stroke volume

Heart rate controlled by parasympathetic and sympathetic nervous systems

Stroke volume is the volume of blood pumped by the heart on each beat

• Contractility (force generated by the muscle)

• Frank‐Starling length‐force relationship (preload)

• Afterload (resistance or force that the heart works against)


ContractilityInotropy

The force of cardiac muscle contraction

Stimulated by sympathetic NS activation (release of norepinephine, activation of beta 1‐adrenergic receptors)

Stimulated by circulating catecholamines(adrenal gland release of epinephrine, “fight or flight”)

Occurs via increased influx of Ca2+ through voltage‐gated Ca2+ channels


Frank‐Starling Relationship

Venous filling pressure (preload) is a key determinant of stroke volume

72


Afterload

The force the heart works against

Aortic pressure

Systemic arterial pressure

Total peripheral resistance

BP = CO x TPR


TPR Determinants

TPR increases when vessels (arterioles) constrict

Arteriolar constriction depends upon Ca2+

influx through voltage‐activated Ca2+ channels

• Increased by SNS activity (via alpha1‐adrenergic receptors)

• Increased by angiotensin II (via AT1 receptors)


TPR Determinants

TPR increases when plasma volume increases

The kidney is responsible for salt and water homeostasis

Majority of blood volume is contained in the distensible venous circulation (which sets preload)

73


History

Symptoms

HTN is generally asymptomatic

Assess other CV risks

Tobacco use

Dyslipidemia

Glucose intolerance

Family history of premature coronary disease

Lifestyle

Diet

Alcohol

Drugs / Medications (prescription and OTC/herbal)

Exercise (inactivity increases risk by 20‐50%


History

Evaluate for end organ damage (EOD)

Visual changes

Headaches

Neurological symptoms

Chest pain

Dyspnea

Palpitations

Weight gain / edema

Abdominal pain


Physical Exam

Height, weight, and appearance

BMI > 25‐29 is overweight, >30 is obese

Fundus exam

Thyroid exam

Neck exam

Cardiac exam

Abdominal exam

Vascular exam

Bruits

Extremities

Pulses, cyanosis, and edema

Neurological exam

74


Blood Pressure Measurement



Measurement of BP should be obtained:

In all adults (age > 18) at each visit

> 30 minutes after use of nicotine or caffeine

After 5 minutes of rest with arm supported at heart level

With appropriately sized cuff

• Bladder should encircle 80% of the arm

• Cuff should cover 2/3 of upper arm



False positives

Cigarettes, caffeine, pain, and anxiety

Drugs ‐ amphetamines, cocaine, cold remedies, NSAIDS, estrogen, steroids, TCAs, licorice, ma huang, and ephedra

Consider “white coat” hypertension in patients with office‐home mismatch (about 25% of patients with mild office HTN)

• Ambulatory BP monitoring may be helpful

75


Hypertensive Patients Laboratory Evaluation

Na, K, BUN, and Creatinine

Renal disease and hyperaldosteronism

UA

Red cells, casts, and proteinuria

Glucose

Diabetes and Cushing’s

Cholesterol

Risk factor

EKG

Evaluate for hypertrophy and ischemia

Special tests for secondary hypertension

Renal artery duplex; renin/aldosteroneratio; 24‐hour urinary cortisol; plasma free metanephrine


Hypertension Categories

Essential (primary)

> 96% of hypertension

Secondary

< 4% of hypertension


Primary (Essential) Hypertension

Etiologies Neural factors

Increased SNS activity

Decreased PNS activity

Renal factors

R‐A‐A system imbalance (high renin)

Lowered antihypertensive function of kidney

Imbalance in salt excretion

Endocrine / Metabolic

Increased norepinepherineand/or epinepherine

Increased aldosterone

76


Primary (Essential) Hypertension Etiologies

Cardiovascular factors

Force and rate of cardiac contraction

Mechanical properties of vessel wall

Genetic factors

Familial ‐ genetic mutations

High rate of HTN in African Americans

Polygenic disease

•Many genes involved in BP regulation


Secondary Hypertension“ABCDE” Mnemonic

Accuracy

Apnea

Aldosteronism

Bad kidneys

Catacholamine excess

Coarctation of aorta

Diet and Drugs

Endocrinopathy


Secondary HypertensionDiagnostic Clues

Apnea (Obstructive Sleep Apnea)

Snoring

Central obesity

Daytime somnolence

Early morning headaches

Nocturia

77



Aldosteronism

Hypertension

Hypokalemia

Weakness

Abdominal distention

Ileus



Bad kidneys

Abdominal bruits

Labs

• Blood Urea Nitrogen (BUN) elevation

• Creatinine elevation



Catacholamine excess

Pheochromocytoma

• Sudden blood pressure elevation

• Flushing

• Diaphoresis

• Headache

• Sporadic pattern

• Palpitations

• Anxiety attacks

78



Coarctation of aorta

Brachial pulse stronger than femoral pulse

• BP difference between upper and lower extremity greater than 20 mmHg

Note: Condition usually diagnosed during infancy. Clues include poor feeding, tachypnea, tachycardia, and cyanosis.



Endocrinopathies

Hyperthyroidism

•Goiter

• Hypereflexia

• Resting tachycardia

• Diaphoresis

• Exopthalmos



Cushing’s syndrome

Central obesity

Hirsutism

Amenorrhea

Moon face

Dorsal hump (“Buffalo Hump”)

Hypokalemia

Hyperglycemia

79


TreatmentLifestyle Modifications

Weight reduction

Alcohol moderation

Aerobic exercise

Dietary modification

Sodium restriction

DASH diet

Tobacco cessation


Antihypertensive Drug Strategies Reduce cardiac output

‐adrenergic blockers Ca2+ channel blockers

Dilate peripheral blood vessels

Ca2+ channel blockers

Angiotensin converting enzyme (ACE) inhibitors

Angiotensin II receptor blockers (ARBs)

a1‐antagonists

Nitrates


Antihypertensive Drug Strategies (cont.)

Reduce vascular volume

Diuretics

Direct vasodilators

80


Hypertension Therapy

Grade 1

Trial of therapeutic lifestyle changes (3 to 6 months)

• Aerobic exercise

• Dietary modification

• Tobacco cessation

•Weight reduction

•Moderation of ETOH usage



Grade 2

Confirm with 3 day blood pressure screen and initiate pharmaceutical treatment

Immediate pharmaceutical treatment in following:

• Grade 3 Hypertension

• Systolic HTN with widened pulse pressure

• Evidence of end organ damage



“First Line” medications

Ace inhibitor (ACEI)

Angiotensin receptor blocker (ARB)

Calcium channel blocker (CCB)

Thiazide diuretic

• Risk of glucose intolerance as side effect

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“Second step”

ACE inhibitor plus thiazide diuretic

ACE inhibitor plus calcium channel blocker

Angiotensin receptor blocker plus calcium channel blocker

Note: Allow at least three weeks with each medication initiation or adjustment. Most will require more than one medication.


Diuretics

Thiazides

hydrochlorothiazide HCTZ (Hydrodiuril)

chlorthalidone (Hygroton)

K+ sparing

triamterene (Dyrenium)

amilioride (Midamor)

eplerenone (Inspra)


Thiazide Diuretics

hydrochlorothiazide, chlorothiazide, and chlorothalidoneMechanism of action

• Inhibits the Na+‐ Cl‐ absorption in the distal convoluted tubule

• Leads to loss of Na+, K+ , and water in the urine

• Reduces aldosterone levels

82


Thiazide Diuretics

Side Effects

Hypokalemia, hypercalcemia, hyperuricemia, and hyperlipidemia

Postural hypotension

Diminished glucose tolerance

Idiosyncratic pancreatitis and rashes


Hypokalemia Precautions

Caution at plasma K+ below 3.5 mEq/L

Predisposes to:

Cardiac arrhythmias

Muscle cramping/weakness

Lethargy

May need prescription K+ supplementation

or switch to a K+ sparing diuretic


Potassium Sparing Diuretics

Amiloride, triamterene, spironolactone, and eplerenone

Mechanism of action

• Amiloride and triamterene block Na+ channels in the distal convoluted tubule, blocking K+ secretion

• Spironolactone and eplerenone are aldosteroneantagonists

83


Potassium Sparing Diuretics

Side Effects

Hyperkalemia

GI disturbances

Rash and headache (amiloride)

Renal calculi (triamterene)

Fatigue, dizziness, flu‐like symptoms, diarrhea, and cough (eplerenone)


Beta‐blockersMechanism of Action

All ß‐blockers reversibly antagonize ß‐adrenergic receptors to:

() CO • () HR• () Contractility

() CNS outflow () renin release (direct inhibition of juxtaglomerular cell secretion)


Beta‐blockersMechanism of Action

Drugs without ISA

(intrinsic sympathomimetic activity)

Initial reduction of CO

Reflex rise in peripheral resistance that fades over time

Drugs with ISA

Less reduction in CO

Fall in vascular resistance due to vasodilationvia activation of ß2‐adrenergic receptors

84


Beta‐blockers

Additional considerations

‐blockers

May have favorable effects on:

• Atrial tachycardia and A‐fib

• Essential tremor

• Thyrotoxicosis and migraine

• Anxiolytic effect

May have unfavorable effects on:

• Asthma

• 2nd or 3rd degree heart block


Beta‐blockersAdverse Effects

Bronchospasm

ß2AR relax airway SM

Bradycardia

Decreased conduction and AV Block

Depression, bad dreams, and fatigue

Impotence

Elevated tryglycerides, lowered HDL

Less in drugs with ISA

Glucose intolerance


Inhibitors of Renin‐Angiotensin

ACE Inhibitors (Captopril and other ‐prils)

Prevent conversion of angiotensin I to angiotension II by blocking angiotensin converting enzyme (ACE)

Angiotensin II Receptor Blockers (ARBs) (Losartan [Cozaar] and other ‐tans)

Block AT1 receptors to induce vasodilation

Also increase Na+ and water excretion

85



ACE Inhibitor Pharmacology

African‐Americans respond less favorably

Thiazide + ACE = highly effective

Preserves renal function in diabetics

Advantage: Little effect on lipids, glucose, or sexual function

Caution: Feto‐toxicity… do not give to pregnant women and those expecting to conceive or breastfeeding


Ace InhibitorAdverse Effects

CommonDry Cough

Na+ depletion

Angioedema*Allergic skin/mucosa disease (life threatening)

Incidence in African‐American 2‐4 x greater

Renal failure

Proteinuria, rashes, reduction in blood cell counts, and fever (10%)

Hepatotoxicity and pancreatitis

86


Calcium Channel Blockers

These drugs inhibit Ca2+ channels in the heart and vasculature, reducing contraction

Lower contractility and CO (heart)

Reduced vasoconstriction and TPR (vascular)

Preparations

Verapamil

Diltiazem

Nifedipine


Calcium Channel Adverse Effects

Headache

Flushing

Palpitations

Ankle edema

Note: Does not adversely affect lipids, glucose metabolism, cause Na+ or H2O retention, or activate the renin‐angiotensin system


a1 Antagonists

These drugs work by blocking a1‐adrenergic receptors*, resulting in arteriolar dilation

Reduction in TPR

Preparations

Prazosin (e.g., Minipress)

Terazosin (e.g., Hytrin)

87


a1 AntagonistsAdverse Effects

First‐dose syncope

Orthostatic hypotension

Use with caution in the elderly

Note: Have beneficial effects on lipids, reduce total cholesterol and triglycerides, elevate HDL


Hypertensive CrisisEmergency versus Urgency

Hypertensive emergency

Average BP > 220/140 mm Hg

• Severe BP elevations with evidence of progressive target organ damage

• Requires immediate BP reduction

Hypertensive urgency

Average BP > 180/110 mm Hg

• Severe BP elevations but without evidence of progressive target organ damage

•May benefit from BP reduction within a few hours


Target Organ DamageManifestations

Cardiac Cerebro‐vascular

Peripheral‐vascular

Renal Retinopathy

EKG and/or X‐ray evidence of CAD

EKG evidence of LVH

LV dysfunction

Heart failure

TIAs

Stroke

Absence of one or more distal pulses with or without intermittent claudication

Aneurysm

Serum creatinine

> 1.5 mg/dL

Proteinuria (1+ or greater)

Albuminuria

Hemorrhages or exudates with or without papilledema

88


Hypertensive EmergencyClinical Characteristics

BP Fundi Neuro Cardiac Renal

> 220/140 Hemorrhages

Exudates

Papilledema

HA

Confusion

Somnolent

Stupor

Visual Loss

Seizure

Neuro Def.

Apical impulse

shift

Cardiomegaly

CHF Sxs

Proteinuria

Oliguria


Hypertensive Crisis Management

Considerations

Autoregulation set point

Hypoperfusion risk

• Cerebral

• Coronary

• Renovascular

Treatment goal

Gradual BP reduction

• Initial redux no greater than 20‐25% of initial BP

•MAP redux to 110‐115 mm Hg first 30‐60 minutes



Oral agents

Captopril (ACE‐I)

• Dose: 25mg po / sublingual

• Effective within 15‐30 minutes; may repeat in 1‐2 hours

• Greater effect in combination with Lasix

• Side effects: reflex tachycardia

89


Hypertensive CrisisManagement

Oral agents (cont.)

Clonidine (central acting alpha‐adrenergic agonist)

• Dose: 0.1 ‐ 0.2 mg ; followed by 0.1 mg per hour until BP goal obtained

• Onset of action within 30 ‐ 60 min; max effect 2 ‐ 4 hours

• Side effects: drowsiness most common



Oral agents (cont.)

Labetolol (alpha / beta‐adrenergic blocker)

• Dose: 200 ‐ 400 mg PO

• Onset within 2 hours

• Precautions

Bronchospasm

Heart block

Bradycardia


Aortic Dissection

Definition

Intimal tear with entry of blood into the media

“Dissects” between the intima and adventitia

#1 site: Ascending aorta

Stanford classification

A: Involves Ascending aorta (with or without descending)

• 80% of dissections

B: Descending aorta only

90


Aortic Dissection


Aortic Dissection


Aortic Dissection

Increased risk

Group A: >50 y/o with hypertension

Group B: Younger patients with Marfan’s, Ehler‐Danlos, and pregnancy

Mortality

Type A

•Untreated: 75%

• Surgically treated: 15‐20%

Type B

• 32 ‐ 36% with or without surgery

91


Aortic Dissection

History

>90% with abrupt and severe pain in the chest or between the scapulae

• “Tearing” or “Ripping”

• Can be dull or pressure‐like

• Anterior chest ~ ascending aorta

• Back ~ descending aorta

Nausea, vomiting, and diaphoresis common


Aortic DissectionPresentation

Associated symptoms based on progression of dissection:

Carotid arteries stroke

Spinal arteries paraplegia

Abdominal aorta/renal arteries/iliacs Abdominal/flank pain

Coronary arteries aortic insufficiency

pericardial effusion

Laryngeal nerve compression hoarseness

Tracheal compression dyspnea

stridor

wheezing

Esophageal compression dysphagia


Aortic Dissection Presentation

Physical exam

Most common

•Normal heart and lungs

Aortic insufficiency murmur in 16‐20%

Unequal, decreased, or absent peripheral pulses and blood pressure

92


Aortic DissectionPresentation

CXR

85% with some abnormality

•Widened mediastinum most common

• Left pleural effusion; indistinct aortic knob; displaced, calcified intima > 6mm from outer aortic wall


Aortic DissectionAortic Knob


Aortic DissectionTreatment

Considering it?

2 large bore IV’s, monitor, T & C, and ECG

Blood pressure

Reduction decreases dissection advance

Goal

• SBP 100 ‐ 120 mmHg

• Pulse rate < 60 bpm

Surgical referral ASAP

93


Peripheral Vascular Disease


Peripheral Arterial Disease (PAD) Definition

Restriction of arterial blood flow to extremities (especially lower extremities)

Etiology

Atherosclerosis

Clinical presentation

Claudication

Pallor

Diminished peripheral pulses

Ulcerative lesions


Peripheral Artery Occlusion“The Five Ps”

Pain

Parasthesia

Paralysis

Pallor

Pulselessness

Poikilothermia

Note: Constitutes medical emergency

94


Gangrene Secondary to Arterial Occlusive Disease


Assessment of PAD

Note CV risk factors

Evaluate peripheral pulses

Check capillary refill time

Extremity warmth and color

Non‐healing ulceration

Sensory examination


Treatment of PADBy Referral

Modify risk factors

Exercise

30 minutes of walking 3 or 4 times a week (reassess after 8 weeks)

pentoxifylline (Trental)

400 mg PO tid (reassess after 8 weeks)

Note: surgery may be required if above measures are unsuccessful

95


Venous InsufficiencyVaricose Veins / Stasis Dermatitis

Presenceof hemosiderin

deposits


Venous Insufficiency / Varicose VeinsRisk Factors

Age

Family history

Obesity

Smoking

Pregnancy


Venous Insufficiency / Varicose VeinsMedical History

Commonly associated medical conditions

PAD

Heart failure

Diabetes

Arthritis

Note: Increased risk for developing coronary artery disease and development of DVT

96


Venous Insufficiency / Varicose VeinsSymptoms

Limb discomfort “heavy sensation”

Pain

Numbness and tingling

Pruritis

Swelling

Increased with standing


Venous Insufficiency / Varicose VeinsSigns

Skin hyperpigmentation

Dry and scaly skin

Ulcerations


Venous InsufficiencyStasis Ulcer

97


Arterial versus Venous Disease

Arterial

Cool temp

Pallor

Decreased pulse

Sharp pain

Pain increase with exercise or elevation

Dry ulcer development

Venous

Warm

Flushed (red)

Edematous

Aching pain

Increased pain with dependency

Weeping venous ulcers


Deep Venous Thrombosis (DVT)

Definition

Development of thrombus within a deep vein

Usually involves the lower extremities

Predisposing factors include stasis, vascular injury, and hypercoagulability (Virchow’s Triad)

Complications

Pulmonary Embolism

•Associated with 30% mortality rate

• ~300,000 cases annually in USA

• ~50,000 ‐ 150,000 deaths per year


Deep Venous ThrombosisRisk Factors

Prolonged immobility

Thrombogenic factors

Pregnancy

Nicotine use

Oral contraceptive use

Lower extremity trauma

Recent surgery

Obesity

98


Deep Venous ThrombosisRisk Factors

Prolonged immobility

Thrombogenic factors

Pregnancy

Nicotine use

Oral contraceptives

Lower extremity trauma

Recent surgery

Obesity

Arrhythmias


Deep Venous Thrombosis Clinical Manifestations

Calf pain and tenderness

Homan’s Sign

Pain in the calf when the foot is passively dorsiflexed (diagnostic reliability is limited)

Palpable cord in the posterior calf

Unilateral leg swelling

Erythema and warmth

Note: Diagnostic test of choice is duplex ultrasonography


Deep Venous Thrombosis

99


Deep Venous ThrombosisDifferential Diagnosis

Muscle strain, tear, or twisting injury to the leg

Leg swelling in a paralyzed limb

Lymphangitis or lymph obstruction

Venous insufficiency

Cellulitis

Popliteal (Baker's) cyst


Deep Venous Thrombosis Management

Heparin therapy initiation immediately

Low molecular weight heparin (LMWH*)

• Subcutaneous dosing every 12 hours

• Lab monitoring not necessary

Warfarin (coumadin) therapy

Hospital

• Oral route

• Four to five day overlap with heparin

• Continued for 3 months


Deep Venous Thrombosis Management

Elevate legs

Apply heat

Analgesics

Note: No massage

100


Thromboangiitis ObliteransBuerger’s disease

Definition

Obstructive inflammatory disease of superficial distant arteries, usually involves digits of hands or toes

Typical patient is male, age 20‐40 years old, and is invariably a heavy smoker

Symptoms include intermittent numbness, tingling, or pain


Thromboangiitis ObliteransBuerger’s disease

Signs include pallor of affected digits and eventual ulcerative or gangrenous tissue changes

Treatment is to discontinue smoking


Thromboangiitis ObliteransBuerger’s Disease

101


Raynaud’s Syndrome

Definition

Periodic vasospastic events causing pallor or cyanotic color changes of the fingers

• Occasionally may involve the ears or nose

Symptoms include cold digits, numbness, and eventually pain



Signs are variable color changes of affected digits, which include pallor, cyanosis, and rubor

Treatment includes protection from cold and stress

May also require vasodilator drugs such as calcium channel blockers



102


Diagnostic Criteria and Management Guidelines for

Pulmonary Emboli


Pulmonary Embolism

650,000 cases per year in the U.S.

Mortality

2 ‐ 10% if diagnosed and treated

30% if undiagnosed

#3 cause of death overall

#1 cause of nonsurgical maternal death in the peripartum period


Pulmonary Embolism

The source is lower extremity DVT in 80 ‐90% of cases

Upper extremity DVT in 10 ‐ 15%

Others:

• Pelvic vein thrombosis

• Fat emboli

• Septic emboli

• Right heart thrombosis

103


Pulmonary EmbolismEtiology

Virchow’s triad

Venous stasis

• Prolonged travel

• Bed rest

Hypercoagulability

• Pregnancy, malignancy, estrogen therapy, and nicotine use

Endothelial damage

• Recent surgery and trauma


Pulmonary EmbolismEtiology

#1 Risk Factor

Prior DVT or PE

10 ‐ 15% of patients will have no identifiable risk factor at the time of presentation


Pulmonary Embolism Clinical Presentation

“Classic Triad”

Dyspnea, hemoptysis, and pleuritic chest pain in only 20% of patients

Three notable findings

Pleuritic chest pain in 74%

Dyspnea in 84%

Respiratory rate > 16 in 92%

104


Pulmonary Embolism Clinical Presentation

The presence of any one of these should make you consider PE

The absence of all three argues strongly against PE

• But then why would it be in your differential diagnosis?

Heart rate > 100 in only 44%


Pulmonary EmbolismClinical Presentation

Clinical suspicion very important*

ECG

Often normal

>40% with nonspecific ST and T wave abnormality

Sinus tachycardia is the most common rhythm disturbance


Pulmonary EmbolismCXR Findings

Normal in ~30%

A concerning finding in the setting of dyspneaand hypoxemia without RAD

Atelectasis in ~50%

Elevated hemidiaphragm in 40%

Greatest roles of the CXR in PE are to rule out other causes of patient’s symptoms (i.e., pneumothorax or pneumonia)

105


Pulmonary Embolism Treatment

Initial

IV

O₂

ECG monitor and pulse oximetry

High pretest probability

Anticoagulate first, then order your study

• LMWH (Low molecular weight heparin*)

Does not require lab

Subcutaneous administration every 12 hours

Vasopressors


Questions ?


Terminal Learning Objective

Action: Communicate knowledge of “Cardiovascular Disorders”

Condition: Given a lecture in a classroom environment

Standard: Received a minimum score of 75% on the written exam IAW course standards

106


Agenda

Recall the anatomy and physiology of the cardiovascular system

Identify potential cardiovascular pathologies and the impact they may have on cardiovascular function

Identify normal and abnormal volumes and pressures related to cardiovascular function


Agenda

Identify signs and symptoms that may suggest cardiovascular disease

Communicate the information that should be incorporated into a cardiovascular history

Identify the content of a cardiovascular oriented physical exam and the significance of exam findings


Agenda

Communicate normal and abnormal heart sounds

Identify the physiologic changes associated with ageing

Identify the risk factors associated with cardiovascular disease

Identify the pathogenesis of atherosclerotic vessel disease

107


Agenda

Communicate normal and abnormal lipid values, different types of hyperlipidemia, secondary causes, physical exam findings, management, and counseling of dyslipidemia patients

Identify the appropriate treatment measures for dyslipidemia


Agenda

Communicate the etiology, signs and symptoms, diagnostic tests, and management of the three types of chest pain, to include: ischemic heart, acute coronary syndrome, and coronary artery diseases

Communicate the etiology, signs and symptoms, diagnostic tests, and management of congestive heart failure


Agenda

Communicate the etiology, signs and symptoms, diagnostic tests, and management of the inflammatory heart diseases, to include: pericarditis, infective endocarditis, rheumatic fever, and rheumatic heart disease

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Agenda

Communicate the etiology, signs and symptoms, diagnostic tests, and management of vascular disorders, to include: hypertension (secondary and essential), peripheral vascular diseases, atherosclerosis, and aortic aneurysms


Agenda

Identify diagnostic criteria and management guidelines for pulmonary emboli


Reason

Cardiovascular disease remains the leading cause of death in the USA today. One in four persons aged 45‐64 have some form of cardiovascular disease. One in three over the age of 64 will develop cardiovascular disease. While the majority of CVD affects those in middle age and older, a significant number of younger patients may be victims also.

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Reason

In its early stages, CVD may produce little or no signs and symptoms. As it evolves, symptoms may remain subtle. As a Special Operations Medical NCO, your challenge will be the early recognition and initial management of various CVD entities in order to reduce morbidity and mortality in your patient population.


Break


Check on Learning

Which of the following most accurately describes the vertical span of the heart?

A. From the 3rd to the 6th intercostal space

B. From the 1st to the 5th intercostal space

C. From the 1st to the 6th intercostal space

D. From the 2nd to the 5th intercostal space

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Check on Learning

Select the correct heart valve position during systole.

A. Atrioventricular valves open

B. Semilunar valves open

C. Atrioventricular and semilunar valves open

D. Atrioventricular valves closed


Check on Learning

Which of the following may cause a narrowed and reduced pulse pressure?

A. Age related vessel changes

B. Hypertrophic Obstructive Cardiomyopathy

C. Intravascuscular volume depletion

D. Young age


Check on Learning

Select the normal range for Mean Arterial Pressure.

A. 30 to 40 mmHg

B. 20 to 30 mmHg

C. 30 to 50 mmHg

D. 70 to 100 mmHg

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Check on Learning

Select the normal range for Pulse Pressure.

A. 100 to 130 mmHg

B. 70 to 100 mmHg

C. 30 to 50 mmHg

D. 10 to 30 mmHg


Check on Learning

Which of the following best reflects mean arterial pressure?

A. (2 times systolic pressure plus diastolic pressure) divided by 3

B. (2 times diastolic pressure times systolic pressure) divided by 3

C. 2 times diastolic pressure times systolic pressure

D. (2 times diastolic pressure plus systolic pressure) divided by 3


Check on Learning

Which of the following best represents Cardiac Output?

A. Pulse pressure plus heart rate

B. Pulse pressure divided by diastolic pressure

C. 2 ml times pulse pressure times heart rate

D. 2 ml times diastolic pressure times heart rate

112


Check on Learning

Which of the following is true regarding cardiac preload?

A. Increased preload increases the force of cardiac contraction

B. Reduced heart rate increases preload

C. Increased heart rate decreases preload

D. All of the above


Check on Learning

Which position does a patient with impaired cardiac function prefer to sleep?

A. Prone

B. Right side

C. Supine

D. Left side


Check on Learning

Which of the following forms of dyspnea represents more advanced staged congestive heart failure?

A. Paroxysmal Nocturnal Dyspnea

B. Orthopnea

C. Trepopnea

D. Eupnea

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Check on Learning

Which of the following PMI (point of maximal impulse) is normal?

A. 4th intercostal space, midclavicular line

B. 5th intercostal space, midclavicular line

C. 6th intercostal space, midclavicular line

D. 5th intercostal space, anterior axillary line


Check on Learning

Identify the correct ausculatory site for the aortic valve.

A. 2nd right intercostal space

B. 2nd left intercostal space

C. 4th left intercostal space

D. 5th intercostal space, midclavicular line


Check on Learning

Select the correct ausculatory site for the mitral valve.

A. 2nd right intercostal space

B. 2nd left intercostal space

C. 4th left intercostal space

D. 5th intercostal space, mid‐clavicular line

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Check on Learning

Which of the following causes a systolic murmur?

A. Mitral stenosis

B. Aortic stenosis

C. Tricuspid stenosis

D. Aortic regurgitation


Check on Learning

Which of the following cause a diastolic murmur?

A. Pulmonic stenosis

B. Ventral septal defect

C. Aortic stenosis

D. Mitral stenosis


Check on Learning

Which of the following heart sounds is always abnormal?

A. Systolic murmur

B. Diastolic murmur

C. Split S2 sound

D. S3 sound

115


Check on Learning

Which of the following lipids plays the primary role in the development of atherosclerotic plaque?

A. HDL (high density lipoprotein)

B. LDL (low density lipoprotein)

C. TG (triglycerides)

D. All of the above


Check on Learning

Where is xanthalasma normally located?

A. Cornea

B. Olecranon surface

C. Medial to the inner canthus of the eye

D. None of the above


Check on Learning

Which of the following lipid reduction medications has the potential for inducing Rhabdomyolysis?

A. Niacin

B. Statins

C. Bile Acid Sequestrants

D. Fibrates

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Check on Learning

Which of the following lipid reduction medications can cause pruritis as a side effect?

A. Fibrates

B. Statins

C. Bile Acid Sequestrants

D. Niacin


Check on Learning

Jugular venous distention represents pressure in which cardiac chamber?

A. Left atrial

B. Right ventricle

C. Left ventricle

D. Right atrial


Check on Learning

Which of the following may be seen in Endocarditis?

A. Migratory arthritis

B. Janeway lesion

C. Chorea

D. Roth spots

E. A and C

F. B and D

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Check on Learning

Which of the following may be seen in rheumatic fever?

A. Erythema migrans

B. Janeway lesions

C. Osler nodes

D. Migratory arthritis


Check on Learning

Kussmaul’s Sign can be seen in which of the following conditions?

A. Hypertension

B. Congestive heart failure

C. Pericarditis

D. Cardiac tamponade

E. B and C

F. B and D


Check on Learning

Which of the following causes of secondary hypertension manifests with sporadic blood pressure elevations, severe headache, and diaphoresis?

A. Obstructive sleep apnea

B. Pheochromocytoma

C. Aldosteronism

D. Cushing’s disease

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Check on Learning

Which of the following causes of secondary hypertension is associated with hypokalemia and muscle weakness?

A. Obstructive sleep apnea

B. Pheochromocytoma

C. Cushing’s disease

D. Aldosteronism


Check on Learning

Which of the following antihypertensive meds may cause ankle edema as a side effect?

A. Beta blockers

B. Calcium channel blockers

C. ACE inhibitors

D. Angiotensin receptor blockers


Check on Learning

Which of the following antihypertensive medications has a negative effect on cardiac chronotropy?

A. ACE inhibitors

B. Beta blockers

C. Angiotensin receptor blockers

D. Calcium channel blockers

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Check on Learning

Which of the following antihypertensive meds can adversely effect glucose tolerance?

A. Calcium channel blockers

B. Beta blockers

C. ACE inhibitors

D. Thiazide diuretics

E. B and D

F. All of the above


Check on Learning

During the initial management of a hypertensive crisis, blood pressure reduction should not exceed ___ %.

A. 10%

B. 25%

C. 35%

D. 45%


Check on Learning

A patient presents with history of sudden onset of severe central chest pain. Physical exam reveals blood pressure difference of 30 mmHg between both arms. CXR reveals a widened mediastinum. Diagnosis?

A. Myocardial infarction

B. Angina pectoris

C. Aortic dissection

D. Pulmonary embolus

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Check on Learning

Which of the following factors is not thrombogenic?

A. Pregnancy

B. Smoking

C. Prolonged immobility

D. Alcohol use

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