Other Forms of Heart Disease

Other Forms of Heart Disease

Other Forms of Heart Disease

-Acute Bacterial Endocarditis

-Streptococcus virdans is the main bacteria from the mouth that has a tendency to affect heart leaflets

-Can come from procedures or instrumentation (oral, GU procedures, hemodialysis catheter, or IV catheters)

-Untreated Strep Tonsillitis and IV drug users 

-Bacteria lodge on heart valves that bear platelet fibrin thrombi and produce valve damage

-The ability to adhere fibrin thrombi comes from production of extracellular dextran by streptococcal strains

-May present 2-5 weeks after precipitating procedure or infection

-If organism slow growing symptoms may be slower up to 6 months

-Symptoms-fever, chills, shortness of breath, night sweats, weight loss, and anorexia

-TEE is useful for assessing vegetation

-Penicillin G and Gentamicin is ideal

-Vancomycin also helpful

-Surgery is needed for refractory infection or valvular heart damage

-Jones Criteria-Rheumatic Disease

-Major Criteria

-Carditis (Pleuritic pain, friction rub, heart failure

-Polyarthritis

-Chorea

-Erythema Marginatum

-Subcutaneous Nodules

-Minor Criteria

-Fever

-Arthralgias

-Previous Rheumatic Fever or rheumatic heart disease

-Acute rheumatic fever can be diagnosed if 2 major, or 1 major and 2 minor criteria are met

-Penicillin is indicated to treat strep infection

-Salicylates are helpful for fever and arthritis symptoms

-Acute Pericarditis

-most time the cause is unknown but presumed viral

-Pericardial friction rub may be present

-EKG-tachycardia with diffuse ST elevation 

-ECHO helpful if effusion present also

-Causes-viral, fungal, TB, bacterial, MI, post surgical, myxedema, drug induced, uremia, neoplasm, radiation

-Treatment with salicylates or NSAIDS help with pericardial inflammation and decrease chest pain

-Cardiac Tamponade

-dependent on the size of the effusion

-Pericardium can accommodate 80-100 mL of fluid before pressure rises

-Acute tamponade acutely ill with signs of cardiogenic shock

-Tachycardia to maintain CO

-Pulsus Paradoxus-rise and fall of more than 10 mmHg with inspiration

-The diagnosis is made on clinical findings-ECHO is useful to help 

-Treatment requires immediate drainage.  Vasopressors may be needed temporarily

-Pericardial Effusion

-Abnormal accumulation of fluid in the pericardial sac

-Drainage should be reserved (>2 weeks)

-If slow can accumulate 2 liters of fluid before increase in intracardiac pressure

Valvular Heart Disease

Valvular Heart Disease

Valvular Heart Disease

-Aortic Stenosis

-Can be congenital or acquired

-Most common congenital abnormality

-Causes LVH

-Symptoms-angina, syncope, CHF

-Systolic Murmur Crescendo-Decrescendo over right sternal border

-Diagnosis and determination of severity is by ECHO and physical examination

-Treatment is surgical replacement of the valve

-Aortic Regurgitation

-may be secondary to or primary disease of aortic leaflets or root.  

-Can come from rheumatic heart disease

-Symptoms-DOE, PND, and fatigue

-Decrescendo diastolic murmur head at left sternal border

-Medical therapy includes ACE inhibitors and Nifedipine (vasodilators) to help unload ventricle

-Valve Replacement for low ejection fraction (usually less than 14%)

-Mitral Stenosis

-thickening of the mitral leaflets impeding flow into left ventricle

-Rheumatic fever most common cause

other etiologies-congenital, connective tissue disease and carcinoid

-can cause right heart failure

-Dyspnea and orthopnea are common presenting symptoms

-Low pitched diastolic murmur heard best at apex with patient in left lateral decubitus position

-Medical treatment involve rate control because patients are prone to tachycardia

-Diuretics are helpful for decreasing pulmonary vascular resistance and helping after load

-Balloon Valvuoplasty or surgery for severe cases

-Mitral Regurgitation (MR)

-most common cause is rheumatic fever and mitral valve prolapse

-Fatigue and dyspnea on exertion common symptoms

-Right Heart Failure may occur

-Holosystolic murmur best heard at apex

-Medical therapy-ACE inhibitors, vasodilators and hydralazine

-Surgery is often difficult to time for severe cases and can cause more damage to left ventricle

-Many cases valve can be repaired

-Mitral Valve Prolapse

-Most common valvular abnormality.  

-Systolic murmur

-it is when there is superior displacement of one or both leaflets across the plane of the mitral annulus towards left atrium

-Sometimes get palpitations, chest pain, anxiety and dizziness

-Tricuspid Stenosis

-Caused mainly by rheumatic fever

-Can cause right heart failure

-High pitched diastolic murmur

-Tricuspid Regurgitation (TR)

-most often due to dilation of the Right Ventricle secondary to right heart failure

-Pulmonary HTN can cause

-High Pitched Pansystolic murmur

-Pulmonic Stenosis

-Usually congenital. Rheumatic fever can cause on occasion

-Systolic murmur

-Pulmonic Regurgitation

-Usually from dilation of the annulus secondary to pulmonary hypertension

-Diastolic murmur

-Severe cases will present with right heart failure

-Treatment is usually at underlying cause of pulmonary hypertension

Vascular Diseases

Vascular Diseases

Vascular Diseases

-Aortic Aneurysm

-Aneurysm refers to the focal dilation of an artery

-Aortic aneurysm can be thoracic or abdominal 

-Usually from atherosclerotic disease 

-Occurs more frequently in men

-HTN, Connective Tissue disease and Family History of Aneurysm are risk factors

-Most AAA are infrarenal 

-Diagnosis of Aneurysm can be made on ultrasound in abdomen

-Transesophageal ECHO (TEE) can diagnose Thoracic Aneurysms

-CT or MRI may be used to diagnose Aneurysm

-CT with IV contrast or TEE needed for dissection

-AAA >5 cm should be resected

-Iliac artery aneurysms greater than 3 cm should be resected

-May try percutaneously placed prosthetic grafts

-Pseudo-aneurysm 

-localized tear in arterial wall that allows blood to accumulate in the vascular space

-Comes from trauma to vessel

-More prone to rupture

-Need treatment

-Aortic Dissection

-Tear in the aortic intima layer through which blood accumulates and dissects between the intima and the media creating a false lumen

-CT with IV contrast or TEE needed for diagnosis

-Beta Blockers even in normotensive patients

-Emergent surgery is needed for Type A (Proximal) Thoracic Dissections 

-Expandable endovascular stents are sometimes used

-Larger dissections need to go for operative repair in the OR

-Arterial Embolism/Thrombosis

-Presents as sudden onset of pain involved extremity

-The P’s of arterial occlusion pain, pallor, paresthesias, paralysis, and pulselessness

-Emboli originate from the heart (A-Fib) or atherosclerotic changes of vessel

-Thromboectomy or Thrombolysis need to be don with ischemic extremity.  

-Can also place stent in certain areas

-Long term anticoagulation needed after revascularization 

-Thromboangiitis obliterans (Buerger’s Disease)-disease of small arteries and veins in upper and lower extremities

-Common <40 in heavy smokers

-Needs risk factor modification

-Giant Cell Arteritis

-may either present as Takayasu’s Arteritis or Temporal Arteritis 

-Takayasu’s Arteritis usually effects young women and likes to affect the aortic arch and the great vessels

-Treatment is systemic corticosteroids.  

-Surgery is rarely needed to bypass affected vascular bed

-Temporal Arteritis

-Temporal Arteritis is another type 

-Presents with temporal headaches and unilateral vision changes

-Presents in older patients

-ESR usually >100 mm/hr

-Definitive dx is biopsy. Treatment steroids 

-Peripheral Artery Disease (PAD)

-Defined as chronic occlusive artery disease

-Presents with pain in affected extremity with exertion alleviated with rest (Claudication)

-Ischemic foot ulcers and hair loss of affected extremity may occur

-Diagnosis duplex ultrasonography ABI < 1.0.  >1.0 is normal in health patients

-Treatment is usually conservative Pentoxifyline (vasodilation and decreased platelet aggregation) or Cilostazol  (vasodilation and decreased platelet aggregation)

-Treatment also involves risk factor modification (smoking cessation and weight loss)

-Revascularization when disabling symptoms, ischemic ulceration, gangrene, or acute arterial occlusion

-Phlebitis/Thrombophlebitis

-Thrombophlebitis is when there is inflammation of a wall of a vessel from a thrombus

-May involve superficial or deep veins

-Superficial thrombophlebitis produces a firm tender cord at affected vein

-Treatment for superficial involves warm compresses and NSAIDs

-Thromboembolic events do not occur with superficial because of valves and endogenous TPA produced by the body

-Venous Thrombosis 

-DVT usually affects the lower extremities but can affect upper or come from pelvis veins

-Virchow’s Triad-venous stasis, hypercoagulability, and venous injury predisposes to DVT

-Diagnosis is accomplished with ultrasound

-DVT

-DVT risk factors

-Pregnancy

-Surgery

-Malignancy

-Immobility

-Inherited Hypercoagulable States

-Trauma

-Lupus anticoagulant 

-Central Venous catheters

-Anticoagulation is initially accomplished with bolus of heparin or lovenox.  

-Warfarin is started then until INR is 2.0-3.0

-Warfarin is continued for 3-6 months

-Pregnancy requires lovenox.  No warfarin in that it crosses placental barrier

-Consider repeating doppler study prior to discontinue treatment

-Second DVT requires lifelong treatment and/or Greenfield filter

-Venous Insufficiency 

-Varicose veins caused by incompetent valves in the saphenous veins

-May result from conditions increase in abdominal pressure (pregnancy, ascites, obesity)

-Conservative treatment is TED hose

-Surgical vein stripping/sclerotherapy

-Leg ulcers or chronic venous stasis dermatitis may develop

-Right sided heart failure or cirrhosis may be predisposing factors

-Lymphedema is different in that is non pitting and from incompetent lymphatic channels

Coronary Heart Disease

Coronary Heart Disease

Coronary Heart Disease

-Risk Factors for Heart Disease

-Non Modifiable Risk Factors

-Age

-Male Sex

-Family history of Premature Heart Disease

-High Elevated Lipoprotein A

-Elevated Fibrinogen Levels

-Decreased Fibrinolytic Activity
                        -Elevated homocysteine levels

-Risk Factors (Modifiable)

-Smoking

-Hyperlipidemia

-DM

-HTN

-Obesity and Inactivity

-Angina Pectoris 

-Discomfort in the chest related to myocardial ischemia

-Comes as a result of oxygen demand of myocardial tissue not meeting demand

-Can be from the jaw to the epigastrium

-May be associated with shortness of breath, diaphoresis, palpitations, or nausea

-If related to activity usually last less than 15 minutes

-Maybe improved with rest or nitroglycerin

-Stable Angina is when the pain is a chronic pattern and predictable with exertion

-The pain is alleviated with rest and does not occur at rest

-Unstable Angina

-Angina is consider unstable when it varies from baseline in terms of frequency, severity, duration of the episodes

-Occurs at rest

-Stable Angina

-Medical management involves risk factor modification

-Should be started on ASA therapy

-Nitrates, Beta Blockers, and calcium channel blockers can be used to help symptoms

-Should be on lipid lowering meds

-Beta Blockers inhibit catecholamine receptors and reduce myocardial oxygen demand

-Nitrates decrease systemic vascular resistance and help heart work more efficiently 

-Unstable Angina

-IV Nitroglycerin is used in the management of unstable angina

-Beta Blockers and Calcium Channel Blockers are used

-Oxygen, heparin/lovenox, ASA, and morphine are used

-Will need to be evaluated for re-vascularization

-Cardiac Catheterization Indications

-Unacceptable response to medical therapy

-Abnormal non invasive testing

-Angina in the setting of depressed LV function

-STEMI

-Chest pain with new onset LBBB

-Prinzmetal’s Angina

-Also called variant angina

-Caused by coronary artery spasm

-Presents similar to angina by discomfort described as a pain and episodes tend to occur at rest

-Treated with calcium channel blockers

-Acute MI

-ST elevation MI (STEMI)

-EKG shows ST elevation MI in Anterior Lateral Leads

-new ST elevation at the J Point at least 2 contiguous leads of >2 mm is diagnostic of with chest pain

-New LBBB with chest pain is a STEMI

-Treatment-ASA 325 mg PO, O2, Nitroglycerin, Morphine, Heparin, Beta Blockers.  Also glycoprotein IIb/IIIa inhibitors

-Patients need Reperfusion Therapy ASAP

-TPA should be reserved for when reperfusion therapy not readily 

-Non ST Elevation MI

-Non Q Wave MI usually do not have occlusion of the infarct related coronary artery

-Higher mortality

-Elevated Troponin without ST elevation on EKG.  Must also have Angina type chest pain

-Medical management involves ASA, Beta Blockers, nitrates, oxygen, and morphine

-Oral diltazem may decrease risk of reinfarction

-ACE inhibitors for those with decreased ejection fraction

-Identifying the Area Infarcted

-Inferior MI-ST Elevation seen in leads II, III and avF

-At least two contiguous leads

-Anteriolateral STEMI- ST elevation in anterior leads (V3, V4) and lateral leads (I, aVL, V5 and V6)

-ST elevation in at least 2 contiguous leads

-Septal Wall MI-ST elevation in septal leads (V1 and V2) 

-ST elevation in at lease two contiguous leads

-Posterior Wall STEMI-1 mm ST depression occurring in leads V1-V4

-These occur in at least 2 contiguous leads 

Hypotension

Hypotension

Hypotension
-Cardiogenic Shock
-Defined as widespread failure of inadequate tissue perfusion resulting in metabolic demands not being met
-Caused by inadequate cardiac output
-Usually form left sided heart failure except with right ventricular infarct
-Hypotension and Tachycardia present
-Signs of left side failure-JVD, pulmonary edema, diaphoresis
-Primary cause-myocardial ischemia
-Valvular dysfunction, persistent tachycardia, or trauma can cause
-Treat by supporting blood pressure, correcting underlying cause, and oxygenation
-May need to intubate and place on mechanical ventilator
-Support blood pressure with vasopressors (dopamine, levophed)


-Orthostatic Hypotension
-Means a decrease in both systolic and diastolic pressure on standing.
-Most clinicians consider a 20 mmHg drop positive
-Can be acute or chronic
-Causes for acute orthostatic hypotension
-anatomic variation
-altered body chemistry
-drug effect
-Volume depletion *****
-Antidepressants
-physical exhaustion
-pregnancy

-Chronic-can be idiopathic or secondary to another disease state
-Diseases-adrenal insufficiency, diabetes, porphyria, intracranial tumors, cerebral infarcts, Wernickes encephalopathy

-Treatment can include volume replacement, stopping offending medicine if possible, or treating underlying disease
-Make sure fall precautions are in place

Hypertension

Hypertension


Hypertension

-For adults over 18 defined as SBP > 140 mm Hg and DBP > 90 mmHg
-Diagnosis requires elevated reading on 3 separate visits
-Essential HTN known as Primary Hypertension
-Defined as hypertension with no identifiable cause

-Secondary Hypertension
-Caused by an underlying problem
-Renal Parenchymal Disease
-Renal Artery Stenosis
-Aortic Coarctation
-Carcinoid Syndrome
-Pregnancy
-Hypothyroid or Hyperthyroidism
-Hyperparathyroidism
-Cushing Syndrome
-Pheochromocytoma
-Hormone Replacement Therapy
-Brain Tumor
-Pain, stress, and anxiety
-Sleep Apnea
-Porphyria
-Lead Poisoning
-Hypoglycemia
-Alcohol withdrawal
-NSAIDS
-Alcohol
-Ephedrine
-MAO inhibitors
-Corticosteroids


-HTN Treatment

-Lifestyle Modifications

-JNC Guidelines

-Stage I HTN (SBP 140-159 or DBP 90-99) Thiazide Diuretics first
-May also consider ACE inhibitors, ARB’s, Beta Blockers or Calcium Channel Blockers
-Stage 2 HTN (SBP >160 mmHg or DBP >100 mmHg)
-2 Drug Combination for most
-Combination with ACE inhibitor, ARB, Beta Blocker or Calcium Channel Blockers


-Accelerated HTN
-Also known as hypertensive urgency
-SBP >200 mmHg and DBP >120 mmHg.
-May need admitted


-Hypertensive Emergency
-Also known as malignant hypertension
-When patients have elevated blood pressure (>200 SBP and DBP > 120 mmHg) and have evidence of end organ damage
-May reverse when BP is lowered


-HTN Treatment

-Diuretics
-Loop Diuretics (High Ceiling)
-Thiazide Diuretics
-Potassium Sparring Diuretics
-Loop Diuretics
-Furosemide and Bumex
-Mechanism-works on the ascending loop of Henle to block reabsorption of sodium and chloride
-This then prevents passive reabsorption of water
-Reserved for when there is a need for fluid removal
-Adverse Effects-hyponatremia, dehydration, hypotension, hypokalemia, ototoxicity, hyperglycemia, and elevated uric acid levels

-Thiazide Diuretics
-Hydrochlorothiazide (Hctz)
-Mechanism-blocks the reabsorption of sodium and chloride in the early segment of the distal convoluted tubule
-This passively causes an increase of flow of water and increased urinary output
-Generally considered first line in essential hypertension
-Other indication is benign peripheral edema
-Adverse effects-low Na, Cl, and low K.  Also dehydration, hyperglycemia, and elevated uric acid levels

-Potassium Sparing Diuretics
-Spironolactone and Triamterene
-Mechanism-blocks the sodium potassium exchange in the distal nephron
-Indicated for hypertension or benign peripheral edema
-Adverse Effects-hyperkalemia, leg cramps, and dizziness
Caution when in use with ACE inhibitors

-Osmotic Diuretics
-Mannitol
-Mechanism-creates osmotic force within the lumen of the nephron
-Indications reduction of intracranial pressure (ICP), intraocular pressure, and prophylaxis of renal failure
-Adverse Effects
-Adverse Effects
-Headache
-nausea and vomiting
-fluid and electrolyte imbalances


-ACE Inhibitors

-Mechanism-blocks ACE which inhibits production of angiotensin II
-Prevents the breakdown of Bradykinnin a vasodilator.
-Elevates Prostaglandins  (vasodilator)

-Indications
-HTN
-Heart Failure
-Nephropathy

-Adverse Effects-dry cough (bradykinnin), hyperkalemia, first dose hypotension, renal failure, and angioedema

-Angioedema can be from C1 Esterase Deficiency

-Angiotensin Receptor Blockers (ARB's)
-Block Angiotensin II Receptor
-No elevated Bradykinnin Elevation
-Vasodilator

-Indications
-Hypertension
-Heart Failure
-Myocardial Infarction
-Renal Impairment
-Adverse Effects
-Dizziness
-No dry cough because of  no Bradykinnin elevation


-Calcium Channel Blockers
-Classifications
-Dihydropyridines (Nifedipine)
-Non Dihydropyridines
-Phenylalkamines (Verapamil)
-Benzothiazepines (Diltazem)

-Dihydropyridines-dilate arterioles. Nifedipine, Amlodipine, Nicardipine, and Felodipine
-Non Dihydropyridines- diltazem and verapmil block calcium channels in the heart and arterioles (slows heart and dilates arterioles)

-Adverse Effects-constipation, bradycardia, edema, AV Blocks
-Can also cause gingival hyperplasia
-Diltazem and Verapmil good for rate control with Atrial Fibrillation
-Verapmil used for Prinzmetal’s Angina


-Vasodilators
-Hydralazine-selectively dilates arterioles
-Indications-HTN, Hypertensive crisis, and Heart Failure
-Adverse effects-reflex tachycardia, increase in blood volume, and hypotension, and dizziness

-Nitroprusside-dilates the venous and arterial systems.
-Used for hypertensive urgency
-Metabolizes can accumulate and cause cyanide poisoning.
-Adverse effect-hypotension, cyanide poisoning and thiocyanate toxicity

-Nitroglycerin-mainly causes dilation of veins
-Used to treat angina, heart failure and myocardial infarction
-oral form is isosorbide

-Alpha Adrenergic Blocking Agents- (Prazosin)
-prevent stimulation of alpha adrenergic receptors on veins and arterioles
-Used in HTN, Peripheral Vascular Disease, and pheochromocytoma

-Centrally Acting Agents-(methyldopa and clonidine) inhibit outflow of impulses along sympathetic nerves
-Used for hypertension
-Can cause rebound hypertension if discontinued abruptly.

-Beta Blockers
-work by blocking primary Beta 1 receptors in the heart and slow heart rate (Propranol, Atenolol, Metoprolol)
-Indications-HTN, MI, CAD, CHF, Tachycardia, SVT, severe recurrent VT, migraines, and stage fright
-Adverse effects-AV block, bradycardia, bronchospasm, heart failure