Download Hypertension Systolic ≥140 or Diastolic ≥ 90 Stage I systolic=140

Hypertension
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Etiology (ET)
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Systolic ≥140 or Diastolic ≥ 90
o Stage I systolic=140- 159; Diastolic is 90-99
o Stage II is systolic= ≥160; Diastolic ≥100.
Hypertensive emergency - blood pressure > 180/120
mm Hg with evidence of end organ dysfunction
Hypertensive urgency
o blood pressure > 180/120 mm Hg without
evidence of progressive end-organ dysfunction
Can be primary or secondary.
Has no specific identifiable causes, pathogeneses is
multifactorial
o Genetic predisposition, more prelevant with
increased age and in blacks.
o Environmental factors excessive salt intake and
obesity
o Exacerbated in males, smokers, blacks and
sedentary lifestyle.
Onset usually 20-55.
Secondary Hypertension suspect those at early age or
patient experiencing symptoms for the first time is >50
yo.
causes of secondary hypertension include
o renal
 any cause of chronic kidney disease
 renovascular hypertension
o endocrine
 Cushing syndrome
 primary hyperaldosteronism
 hyperthyroidism
 hyperparathyroidism
 pheochromocytoma
o obstructive sleep apnea (OSA)
o coarctation of aorta
o medications
Course (CS)
capacity of system
increase renin, angiotensin and aldosterone secretion.
Wall may dilate or tear, forming aneurysm, or forming
MI
Cardiovascular
P are kidneys,
1
S/S
Physical Findings (PF)
Diagnostic testing (DT)
Treatment (Tx)
Cardiovascular
brain, and retina. Poor control of HTN can lead to chronic
renal failure, stroke due to hemorrhage, loss of vision, or
CHF.
 Frequently asymptomatic in early stages.
 Initial symptoms are vague and nonspecific.
o Fatigue, malaise, and at times morning headache
o Elevated bp under various conditions is key sign
of htn.
 Accelerated HTN- somnolence , confusion, visual
disturbance, n/v
 Most Pt asymptomatic common complaint is nonspecific headache.
 In untreated HTN you see end organ damage like- HF,
renal failure, stoke, dementia, aortic dissection,
atherosclerosis, retinal hemorrhage, av nicking
 Loss of peripheral pulses w/ atherosclerosis.
 Systolic BP ≥ 140 or diastolic BP ≥ 90 on ≥2 separate
occasions
 Once diagnosed diagnostic test are indicated to assess
end-organ damage, id and additional risk factors ,
exclude secondary causes of htn and assist with
medication choice.
o EKG may show LVH or HF
o CXR may show ventricular hypertrophy, but cxr
not considered necessary in uncomplicated HTN.
o
or UA) may indicate renal dz or diabetes.
o Lipid profile to assess atherosclerosis.
 Non-pharm Tx of essential htn should be stressed should
include DASH diet, weight loss, exercise, stop smoking,
limitation of Alc, limitation of sodium.
 Diabeic patients and those with renal dz = aggressive tx
to achive BP < 130/80
 For patients with prehypertension (120- 130/80-89) or
HTN stage one = lifestyle modification.
o If patient stage one patient is HTN after 3 months
of lifestyle mod start antihypertensive
medication.
o Stage II Pt and Pt with diabetes (with systolic bp
> 130 and diastolib >80 needs earlier pharm tx.
 The goal of HTN meds is to
o
o
 direct vasodilation =hydralazine
 inhibition of vasoconstriction.
 Block sns =alpha blocker
 Block ca activated smooth muscle
contraction=ccb
 Block aldosterone=aldosterone
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Cardiovascular
antagonist= spirolactone
 Block renin angiotensin system=
ACE inhibitors and ARB’s
Diuretics plasma volume and chronically reduce
peripheral resistance Recommended as initial tx for
HTN. K suppliments may be needed for some patients.
o Thiazides most conservative effective
o Loop diuretic used only with renal dysfunction
and when close electrolyte monitoring is assured.
Βeffective in younger white patients.
Angiotensin-Converting enzyme (ACE) inhibitors, also
inhibit bradykikin degredation and stimulate synthesis
of vasodilation prostaglandins= Initial drug choice for
Htn pt’s with diabetes and the tx of choice for mild or
moderate HTN, especially younger white pt, or when
diuretics are insufficient.
o Side effect= cough
o ARB’s= interaction of angiotensin 2 on receptors.
Calcium Channel blockers = peripheral vasodilation,
preferable in blacks and elderly.
Aliskiren, renin inhibitor- recently approved for mom tx
or combo.
Aldosterone receptor antagonist, like spirolactone are
used for refractory HTN as addition.
Secondary HTN- TX underlying cause
Target BP
o target blood pressure (BP) < 140/90 for most
patients
o target systolic blood pressure < 150 mm Hg
recommended in older patients (age ≥ 60 years
or age ≥ 80 years varies by guideline)
o in patients with diabetes guidelines vary but
targets range from < 130/80 mm Hg to < 140/90
mm Hg
o in patients with chronic kidney disease, current
guidelines recommend < 140/90 mm Hg, with
multiple guidelines suggesting < 130/80 mm Hg
if proteinuria or diabetes present; lower blood
pressure targets associated with reduced risk of
end-stage renal disease in patients with
proteinuria
o in patients with coronary artery disease reaching
systolic blood pressure ≤ 130 mm Hg appears
associated with reduced risk of heart failure and
stroke but increased risk of hypotension .
IV saline if volume depleted for Urgency and
Emergency
3
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Follow up
Refer
Cardiomyopathy
Dilated Cardiomyopathy
Cardiovascular
Hyepertensive Urgency (no evidence of end organ
damage) may be treated with any of
o nicardipine 5 mg/hour orally, increase by 2
mg/hour every 15 minutes, maximum dose 15
mg/hour
o captopril 25 mg orally 2-3 times daily
o clonidine
 adults - initial dose 0.1-0.2 mg orally, then
increase 0.05-0.2 mg every hour up to
total dose 0.5-0.7 mg as needed
 children aged 1-17 years - initial dose
0.05-0.1 mg orally, repeat up to maximum
0.8 mg
o labetalol dose options include
 initial dose 20-80 mg IV, then additional
40-80 mg dose (range 20-80 mg) at 10minute intervals until desired blood
pressure achieved
 initial dose 0.5-2 mg IV infusion, adjust as
required
 initial dose 200 mg oral, then additional
200-400 mg dose after 6-12 hours as
needed
 Hypertensive emergency
o admit to intensive care unit for IV medications
o lower blood pressure by 10%-15% over first
o
 For patients receiving lifestyle modification advice alone
o follow-up at 3-6 month intervals
o if higher BP, follow-up at 1-2 month intervals
 For patients on antihypertensive drug treatment
o follow-up every 1-2 months depending on BP,
until readings on 2 consecutive visits are below
target
o for symptomatic patients or those with severe
hypertension, intolerance of antihypertensive
drugs, or target organ damage, follow-up more
frequently than 1-2 months
o see patients every 3-6 months after target BP is
reached
Referral to a hypertension specialist considered in severe
cases, or when secondary hypertension.
Dz of heart muscle characterized by their presentation and
pathophysiology.
 Dilated cardiomyopathy is a progressive disease of heart
muscle that is characterized by ventricular chamber
enlargement and contractile dysfunction with normal
left ventricular (LV) wall thickness.
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Etiology
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Course
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S/S
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PF
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DT
Cardiovascular
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The right ventricle may also be dilated and
dysfunctional.
Dilated cardiomyopathy is the most frequent reason for
heart transplantation
Middle age men most affected
Big and baggy not thick and strong.
decreased contractile function without pressure
overload, volume overload or coronary artery disease
Associated with reduced strength of ventricular
contraction, result in dilation of the left ventricle.
Causes include
o genetic abnormalities
o Secondary to other cardiovascular disease:
ischemia, hypertension, valvular disease,
tachycardia induced
o excessive alcohol consumption
o postpartum state
o Toxicity
o Endocronopathies- Thyroid, Pheochromocytoma.
o myocarditis
o may be idiopathic
Can lead to heart failure (cause of death in 70%),
embolism, atrial flutter, atrial fibrillation
dyspnea on exertion, fatigue, orthopnea, paroxysmal
nocturnal dyspnea, palpitations, chest pain, systemic
and pulmonary embolism.
Left or biventricular chf
Edema, increasing weight and abdominal girth
increased.
Tachypnea, tachycardia and hypertension, Hypoxia signs
(clubbing, Cyanosis)
small pulse pressure
Coronary artery dz
pulsus alternans typically seen with advanced
myocardial disease
jugular-venous distention (JVD) (heart failure)
Pulmonary edema with crackles and or wheezes
cardiomegaly
S3 galllop
murmurs aortic regurgitation, mitral regurgitation, less
commonly tricuspid regurgitation, arrhythmias
pulmonary rales (heart failure)
hepatomegaly (heart failure)
Goiter
ascites
peripheral edema (heart failure)
Chest x-ray - massive cardiomegaly, pulmonary vascular
congestion, interstitial pulmonary edema
5
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TX
FU/Referral
Hypertrophic Cardiomyopathy
Etiology
Course
S/S
PF
DT
Cardiovascular
EKG- S-T changes, , conduction abnormalities,
ventricular ectopy
 Echo= excludes valvular lesions, you will see LVH
dilation and dysfunction, low CO. Most useful study.
 Abstinence from alcohol is essential
 Underlying disease should be treated
 Congestive heart failure requires supportive treatment
Refer to cardiology
 Massive hypertrophy , particularly of septum, sm left
ventricle, systoloic anterior mitral motion, and diastolic
dusfunction.
Almost exclusively genetic
Hypertrophic cardiomyopathy and elderly is a distinct form.
Complications of HCM may include the following:
 Congestive heart failure
 Ventricular and supraventricular arrhythmias
 Infective mitral endocarditis
 A-fibrillation with mural thrombus formation
 Sudden death
 Sudden cardiac death (the most devastating
presenting manifestation) usually occurs impatience
younger than 30 years old.
 Dyspnea (the most common presenting symptom)
 Syncope and presyncope
 Angina
 Palpitations
 Orthopnea and paroxysmal nocturnal dyspnea (early
signs of congestive heart failure [CHF])
 CHF (relatively uncommon but sometimes seen)
 Dizziness
 Double apical impulse or triple apical impulse (less
common)
 Normal first heart sound; second heart sound usually is
normally split but is paradoxically split in some
patients with severe outflow gradients; S3 gallop is
common in children but signifies decompensated CHF
in adults; S4 is frequently heard
 Jugular venous pulse revealing a prominent a wave
 Double carotid arterial pulse
 Apical precordial impulse that is displaced laterally
and usually is abnormally forceful and enlarged
 Systolic ejection crescendo-decrescendo murmur
 Holosystolic murmur at the apex and axilla of mitral
regurgitation
 Diastolic decrescendo murmur of aortic regurgitation
(10% of patients)
 Echocardiography is the key to diagnosis
 MRI is also useful diagnostic tool
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TX
FU/Referral
Restrictive Cardiomyopathy
Etiology
Course
Chest radiograph is often not remarkable.
EKG abnormalities include nonspecific ST and T-wave
changes exaggerated septal Q waves and left ventricular
hypertrophy.
 Initial tx is Beta blockers or CCB; Diasopyramide is
usedfor its negative inotropic effects.
 Surgical or nonsurgical ablation of the hypertrophic
septa may be required
 Dual chamber pacing implantable defibrillators or mitral
valve replacement may be indicated.
Cardiology consultation for diagnosis
Restrictive cardiomyopathy is rare its principal abnormality
is diastolic dysfunction—specifically, restricted ventricular
filling, ventricles are stiff.
 Results from fibrosis or infiltration of the ventricle wall
because of collagen defects diseases most commonly
amylodoises, radiation post operative changes diabetes
and endomyocardial fibrosis.
 Left ventricle is small or normal with mildly reduced
function
Complications of RCM may include the following;
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S/S
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PF
DT
Cardiovascular
Thromboembolism
Dysrhythmias
Cardiac cirrhosis
Progressive deterioration of cardiac function
Patients may be more comfortable in the sitting position
because of fluid in the abdomen or lungs.
Weight loss and cardiac cachexia are not uncommon.
Easy bruising, periorbital purpura, macroglossia, and
other systemic findings, such as carpal tunnel syndrome,
should advise the clinician to consider amyloidosis.
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Patients present with decreased exercise tolerance
In advance dz patients developed right-sided congestive
failure
 Pulmonary hypertension usually it’s present
 Heart sounds S1 and S2 are normal, with a normal
S2 split.
o A loud early diastolic filling sound (S3) may be
present but is uncommon in amyloidosis
 Breath sounds are decreased due to pleural effusion,
frequently bilateral, and large in amyloidosis.
Crepitations or rales are rarely heard, even in advanced
heart failure of amyloidosis.
 Echocardiogram is the key to diagnosis
 Chest x-ray may show a mild to moderately large cardiac
silhouette.
7
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FU/Referral
Endomyocardial biopsy may be necessary to
differentiate restrictive disease from other forms of
cardiomyopathies or pericarditis.
 No specific treatmen
 The mainstays of medical treatment include diuretics,
vasodilators, and angiotensin-converting enzyme
inhibitors (ACEs) as indicated, as well as anticoagulation
(if not contraindicated)
Cardiology
Conduction Disorders
Atrial Fibrillation
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TX
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Etiology
Course
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PF
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DT
Tx
Cardiovascular
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Atrial fibrillation is the most common chronic
arrhythmia
Incidents and prevalence increases with age
Called holiday heart when caused by excessive alcohol
use or withdrawal.
Hemodynamic stress
Atrial ischemia
Alcohol and drug abuse
Endocrine disorders
Genetic factors
Advanced aging
Non-cardiovascular respiratory causes
Can lead stroke and MI.
Patients may present with palpitations, angina, fatigue
or other symptoms of heart failure.
Patients may be completely asymptomatic
paroxysmal, persistent, or permanent
Patients with decompensated congestive heart failure
(CHF)
Patients with hypotension
Patients with uncontrolled angina/ischemia
Absence of P ways replaced by a regular leaves
Irregular ventricular rate
Heart rate typically will be from 110 240 beats per
minutes.
EKG
Acute atrial fib depends on the presentation and
includes electronic cardioversion , treatment of
underlying disease, and control of rate.
o Cardioversion if <48 hours
o Agents used for rate control in acute aphid
include
 Diltiazem
 Metopolol
 Digoxin- rarely mono tx
 Amiodarone (mainly for patients who are
intolerant of or unresponsive to other
8
Follow up/ Referral
A-Flutter
ET
Cardiovascular
agents)
o Anticoagulation is indicated as follows
 Patients with newly diagnosed AF and
those awaiting electrical cardioversion
can be started on intravenous (IV) heparin
or low-molecular-weight heparin (LMWH)
 Concomitantly, patients can be started on
warfarin in an inpatient setting while
awaiting a therapeutic INR value (2-3)
 Oral direct thrombin inhibitors may
present an alternative to warfarin in a
higher-risk population with nonvalvular
AF
 Treatment of chronic atrial fib includes control of rate
and prevention of thromboembolism
o Appropriate antithrombotic regimen should be
balanced between the risk of stroke and the risk
of bleeding.
 Warfarin- targer 2-3
 Alternatives if above can not be used
 adding clopidogrel to aspirin may
be considered
o Agents used for rate control include
 Beta blockers
 Nondihydropyridine calcium channel
blockers
 Digoxin
 Amiodarone
o Agents used for rhythm control include
 Flecanide
 Propafenone
 Dofetilide
 Amiodarone
 Sotalol
Cardiology
 A cardiac arrhythmia characterized by atrial rates of
242-400 beats per minute.
 Usually occurs in patience with chronic obstructive
pulmonary disease, CHF, atrial septal defect or coronary
artery disease.
 Associated with a variety of cardiac disorders
 Conditions also associated with a flutter
o Hypoxia
o COPD
o Pulmonary embolism
o Hyperthyroid
o Pheochromocytoma
o Diabetes
o Electrolyte imbalance
9
Course
S/S
PF
DT
TX
Follow up/Referral
Atrioventricular Block
Cardiovascular
o Alcohol consumption
o Obesity
o Digitalis toxicity
Any prolonged atrial arrhythmia can cause a tachycardiainduced cardiomyopathy
 Palpitations, fatigue or poor exercise tolerance, mild
dyspnea, presyncope.
 Less common symptoms
o Angina, profound dyspnea, or syncope.
o Tachycardia may or may not be present,
depending on the degree of AV block associated
with the atrial flutter activity
 The heart rate is often approximately 100-150
beats/min because of a 2:1 AV block
 The pulse may be regular or slightly irregular
 Hypotension is possible, but normal blood pressure is
more commonly observed
 Saw tooth pattern in EKG
 ECG – This is an essential diagnostic modality for this
condition
General treatment goals for symptomatic atrial flutter are
similar to those for atrial fibrillation and include the
following
 Control of the ventricular rate
o Ventricular rate control achieved with drugs that
block the AV node. IV calcium channel blockers
(eg, verapamil and diltiazem) or beta blockers
can be used, followed by initiation of oral agents
o The success rate of electrical cardioversion is
higher than 95%
o Pharm cardioversion tx Dofetilide and Ibutilide
 Restoration of sinus rhythm
o RFA is often used as first-line therapy to achieve
permanent restoration of sinus rhythm
o The main difference between atrial fibrillation
and atrial flutter is that most cases of atrial flutter
can be cured with radiofrequency ablation (RFA)
 Prevention of recurrent episodes or reduction of their
frequency or duration
 Prevention of thromboembolic complications
o Anticoagulation tx
 Minimization of adverse effects from therapy
Cardiology
 Atrioventricular (AV) block occurs when atrial
depolarizations fail to reach the ventricles or when
atrial depolarization is conducted with a delay. Three
degrees of AV block are recognized
 First-degree AV block
o atrial-ventricular (AV) conduction delayed
10
ET
Course
Cardiovascular
o PR interval prolonged, greater than 0.2
seconds
o >65 most affected
 Second degree AV block
o Mobitz I (Wenckeback)
 bradyarrhythmia with progressive
prolongation in PR interval until P
wave not conducted
o Mobitz II
 almost always due to organic disease
involving the infra-nodal conduction
system.
 bradyarrhythmia
 sudden interruption of
atrioventricular (AV) conduction with
constant PR interval
 Third degree Block
o bradyarrhythmia
o complete absence of conduction between
atria and ventricles
o atrioventricular dissociation
 First degree and Mobiz I may occur in
o normal individuals with heightened vagel tone
o may also occur as a drug effect especially
 digitalis
 calcium channel blockers
 beta blockers or sympatholytic agents
 Clonidine
 Methyldopa
o Organic disease
o Disturbances also occur transiently or chronically
due to ischemia, infarction, inflammatory
process, fibrosis, calcification or infiltration.
 Mobitz II
o degenerative change in His-Purkinje system
o MI
o calcific valvular stenosis
 Third Degree
o Idiopathic
o myocardial infarction
o postsurgical
 valve replacement
 correction of congenital heart disease
 heart transplant
o carotid sinus hypersensitivity
o metallic metabolic abnormalities
First Degree block no clinical consequences
Mobiz I
 Syncope
11
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PF
DT
Tx
Cardiovascular
 Progression to third-degree block uncommon.
Mobitz II to can lead to complete heart block.
Third Degree Heart Block
 Ventricular tachycardia
 asystole
 heart failure
 syncope
First-degree AV block
 Usually asymptomatic
Mobiz I
 Often asymptomatic
 Syncope or presyncope
 Dizziness
Mobitz II
 Syncope or presyncope
 Dizziness
 fatigue and weakness
Third degree Block
 syncope or presyncope
 dizziness
 palpitations
 Stokes-Adams syncopal attacks
 angina
 dyspnea
 edema
First-degree AV block
 Normal physical exam
Mobiz I
 Pulse ≤ 60 p/min
Mobitz II
 pulse ≤ 60
 May have a regular irregular heartbeat
 fixed PR intervals before and after blocked beats on
electrocardiogram
Third degree Block
 Pulse <50
 complete absence of relationship between p waves
and QRS.
EKG
First-degree AV block
 Usually no treatment necessary.
Mobiz I
 Usually no treatment needed
 Atropine in emergency situations
Mobitz II
 Cardiac pacemaker
 Atropine IV if symptomatic
 epinephrine infusion maybe use after atropine
12
FU/ Referral
Bundle Brach Block
ET
Course
S/S
PF
DT
TX
Cardiovascular
 dopamine
Third degree Block
 immediate cardiac pacemaker if symptomatic
 Atropine is a temporizing measure while awaiting a
transcutaneous pacemaker.
First-degree AV block
 No screening indicated
Mobiz I
 No screening indicated
Mobitz II
 Cardiology
Third degree Block
 Cardiology, Routine checks every 6-12 months
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Bundle branch block is a condition in which there's a
delay or obstruction along the pathway that
electrical impulses travel to make your heart beat.
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The delay or blockage may occur on the pathway
that sends electrical impulses to the left or the right
side of your heart.
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Bundle branch block sometimes makes it harder for
your heart to pump blood efficiently through your
circulatory system.
Left bundle branch block
 heart disease
 congestive heart failure
 cardiomyopathy
 high blood pressure
Right bundle branch block
 Congenital
 MI
 Myocarditis
 hypertension
 scar tissue that develops after surgery
 pulmonary embolism
Can lead to a sudden onset cardiac death if person have MI
and then develop Bundle branch block.
may need pacemaker.
Syncope presyncope bradycardia
Atherosclerosis, cardiomyopathy ischemic heart disease,
Htn.
EKG
No specific treatment, treat underlying condition
Some people may benefit from the pacemaker
13
FU/ Referral
Paroxysmal Supraventricular
tachycardia (PSVT)
Cardiology
PSVT is the most common paroxysmal tachycardia and
usually occurs in persons without structural problems.
episodic condition with an abrupt onset and termination
o supraventricular arrhythmia which may include(1)
 atrioventricular nodal reciprocating tachycardia
(AVNRT)
 atrioventricular reciprocating tachycardia (AVRT)
 atrial tachycardia
ET
triggered by a reentry mechanism. This may be induced by
premature atrial or ventricular ectopic beats. Other triggers
include hyperthyroidism and stimulants, including caffeine,
drugs, and alcohol.
It is usually a narrow-complex tachycardia that has a
regular, rapid rhythm
 usually bening.
 Tachycardia may induce ischemia
 May precipitate heart failure or hypotension during
acute MI.

Usually asymptomatic

palpitations
 fatigue
 lightheadedness
 chest pain
 dyspnea
 presyncope
 syncope
o pulse > 140-250 beats/minute during acute episode of
paroxysmal supraventricular tachycardia(1)
o pulse > 100 beats/minute with sinus tachycardia
EKG
Mechanical measures to interrupt a cute PSVT include
 Valsalva maneuver, coughing, breath holding,
stretching, putting the head between the knees,
applying Coldwater to face and unilateral carotid
sinus massage
 Synchronize shock
 Adenosine
 Verapamil
Cardiology
 form of ventricular tachycardia characterized by
"twisting of the peaks" morphology on
electrocardiogram (QRS complex rotation around an
isoelectric baseline)
 often associated with a prolonged QT/QTC interval
 Drugs that prolong QT
o Disopyramide
Course
S/S
PF
DT
Tx
FU/referral
Torsades de Pointes
ET
Cardiovascular
14
Course
S/S
PF
DT
TX
FU/ Referral
Ventricular Tachycardia
ET
Course
S/S
PF
Cardiovascular
o Dofetilide
o Ibutilide
o Procainamide
o Quinidine
o Sotalol
 Prolongation of QT interval can be congenital
Sudden cardiac death
 Recurrent episodes of palpitations, dizziness, and
syncope;
 Sudden cardiac death can occur with the first
episode.
 Nausea, cold sweats, shortness of breath, and chest
pain also may occur but are nonspecific and can be
produced by any form of tachyarrhythmia
o Rapid pulse, low or normal blood pressure, or
transient or prolonged loss of consciousness.
o This could be preceded by bradycardia or
premature ventricular contractions
o Pallor and diaphoresis may be noted, especially with
a sustained episode
EKG
Magnesium Sulfate
None
 3 or more beats of ventricular origin (wide QRS) at rate
100-200
 for wide QRS tachycardia in adult, consider ventricular
tachycardia until proven otherwise
 oronary artery disease
 cardiomyopathy
 electrolyte abnormalities
 myocardial ischemia
 hypoxemia
 acidosis
 idiopathic
 syncope
 heart failure
 angina
 ventricular fibrillation
 Palpitation
 Light-headedness
 Syncope
 Chest pain
 Anxiety
 tachycardia (regular rhythm with pulse > 120),
hypotension
 Tachypnea
 Signs of diminished perfusion, including a diminished
level of consciousness, pallor, and diaphoresis
15
DT
TX
Follow up
Ventricular Flutter
Etiology
Course
S/S
PF
DT
TX
Follow up
Wolff-Parkinson-White syndrome
ET
Cardiovascular
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 High jugular venous pressure
 Abnormal splitting of S2
EKG
 no treatment if asymptomatic
 if unstable - O2, IV access, consider sedation (unless
hemodynamically unstable, for example, hypotension,
pulmonary edema or unconscious), cardiovert 50 joules
(unsynchronized if hemodynamically unstable to avoid
delay, consider precordial thump if hemodynamically
stable), cardiovert 100 joules, cardiovert 200 joules,
cardiovert up to 360 joules, if recurrent add lidocaine
and cardiovert at previously successful energy level then
add procainamide or bretylium
 if stable - O2, IV access, lidocaine, procainamide,
cardiovert
 No driving for six months
Life-threatening ventricular tachyarrhythmia
Associated with coronary artery disease
Can lead to cardiac arrest
Palpitations
Fatigue or poor exercise tolerance
Mild dyspnea
Presyncope
The heart rate is often approximately 150 beats/min
The pulse may be regular or slightly irregular
Hypotension is possible, but normal blood pressure is more
commonly observed
EKG
o immediate nonsynchronized direct current (DC) shock if
loss of consciousness
o lidocaine may be useful in post-myocardial infarction
setting to suppress symptomatic ventricular
arrhythmias(1)
o consider placement of implantable cardioverterdefibrillator
Cardiology
o beta blockers
o amiodarone may be indicated for patients with history
of acute sustained ventricular arrhythmias
 congenital condition involving abnormal conductive
tissue between the atria and the ventricles that provides
a pathway for a reentrant tachycardia circuit
 wide QRS (> 0.12 second) with initial slurring (delta
wave), sinus rhythm, short PR (< 0.12 second)
 accelerated conduction due to accessory atrioventricular
(AV) pathway, leading to ventricular preexcitation
 congenital phenomena that are related to a failure of
insulating tissue maturation within the AV ring—even
16
Course
S/S
PF
though their manifestations are often detected in later
years, making them appear to be acquired
Risk of recurrence after a single episode of supraventricular
tachycardia (SVT) is uncertain
Once identified and appropriately treated, WPW syndrome
is associated with an excellent prognosis, including the
potential for permanent cure through RF catheter ablation
 palpitations
 anxiety
 light-headedness
 chest pain
 pounding sensation in the neck and chest
 dyspnea
 Normal cardiac examination findings in the vast
majority of cases
 During tachycardic episodes, the patient may be cool,
diaphoretic, and hypotensive
 Crackles in the lungs from pulmonary vascular
congestion
 In many young patients, only minimal symptoms (eg,
palpitations, weakness, mild dizziness) despite
exceedingly fast heart rates
 pulse uniformly rapid, often > 220 beats/minute

Follow Up/Refer
"frog sign" is presence of prominent jugular venous
pulsations (cannon a-waves) due to atrial contraction
against closed tricuspid valve
 occasionally expiratory splitting of S2
 ECG diagnosis
o short PR interval
o delta wave - initial slurring of QRS
o wide QRS complex
 f atrial fibrillation - lidocaine, procainamide, DC shock
after Versed
 digoxin and verapamil are contraindicated with
refractory period < 300 milliseconds(1)
 if unresponsive to vagal maneuver - drug of choice
is adenosine (Adenocard) IV 6 mg
 radiofrequency catheter ablation
Cardiology
Heart failure

DT
TX

Cardiovascular
Inability of the heart to deliver sufficient oxygenated
blood to meet the needs of tissues and organs
heart failure with reduced ejection fraction
o ejection fraction ≤ 40%
o Also called systolic heart failure.
o Absolute/relative impaired myocardial
contractility with decreased ejection fracture
17

ET
Course
S/S
Cardiovascular






heart failure with preserved ejection fraction
o typically ejection fraction ≥ 50%
o Also called diastolic heart failure
o Normal myocardial contractility and ejection
fraction with impaired relaxation and feeling.
o coronary artery disease (resulting in myocardial
infarction and ischemic cardiomyopathy) causes about
two-thirds of systolic heart failure
o systemic hypertension
o valvular heart disease including aortic stenosis, aortic
regurgitation, mitral regurgitation
o severe renal failure
o constrictive pericarditis
o dilated cardiomyopathy
 genetic causes
 viral infection (recognized or unrecognized)
 alcohol use disorder (alcoholic cardiomyopathy)
 chemotherapy (doxorubicin or trastuzumab)
o hypertrophic cardiomyopathy
o restrictive cardiomyopathy
o infiltrative disorders (cardiac
sarcoidosis, hemochromatosis, amyloidosis)
o peripartum cardiomyopathy
o myocarditis
o infectious endocarditis
o arrhythmia
o tachycardia-induced heart failure
o beriberi
o HIV infection
o muscular dystrophy
o causes of right ventricular failure
 most common cause is left ventricular failure (rightsided failure usually late in course)
 mitral stenosis
 pulmonary arterial hypertension (may be due
to chronic obstructive pulmonary
disease, pulmonary embolism)
 right-sided infective endocarditis
 right ventricular infarction
o high output cardiac failure - anemia, thyrotoxicosis,
arteriovenous fistula, Paget disease of bone
Can lead to cardiac arrhythmias, salt and water retention
and and organ damage.
Exertional dyspnea and/or dyspnea at rest
Orthopnea
Acute pulmonary edema
Chest pain/pressure and palpitations
Tachycardia
Fatigue and weakness
18











PF
DT
TX
Cardiovascular
Nocturia and oliguria
Anorexia, weight loss, nausea
Exophthalmos and/or visible pulsation of eyes
Distention of neck veins
Weak, rapid, and thready pulse
Rales, wheezing
S3 gallop and/or pulsus alternans
Increased intensity of P2 heart sound
Hepatojugular reflux
Ascites, hepatomegaly, and/or anasarca
Central or peripheral cyanosis, pallor
 Rails heard over lungs
 JVD
 Hepatomegaly
 Edema
 S3 , S4, Gallup, cardiomegaly, pulsus alterans
 Cyanosis
 Echocardiogram is diagnostic standard for identifying
heart failure
 BNP
o guideline-directed medical therapy for symptomatic
heart failure with reduced ejection fraction
 angiotensin-converting enzyme (ACE)
inhibitors (or angiotensin receptor blockers [ARBs])
recommended for all patients
o ACE inhibitors appear to reduce mortality and
rates of myocardial infarction and hospital
admission in patients with left ventricular
dysfunction or symptomatic heart failure
o ARBs reduce heart failure hospitalization and
possibly mortality
o ARBs may have similar clinical outcomes
compared with ACE inhibitors, but may be better
tolerated
 beta blockers recommended for all patients
o beta blockers (bisoprolol, carvedilol, or
sustained-release metoprolol succinate) reduce
mortality in stable patients with class II and III
heart failure and possibly class IV heart failure
 loop diuretics for all volume overload, NYHA class IIIV patients
o such as furosemide (Lasix) 20-40 mg/day in 1-2
doses initially, maximum 600 mg/day
o diuretics may reduce risk of death and worsening
heart failure and improve exercise capacity
 hydralazine plus isosorbide dinitrate for persistently
symptomatic, NYHA class III-IV, African-American
patients
o addition of isosorbide dinitrate plus hydralazine
19
Follow up/referral
Cardiovascular
(BiDil) to standard heart failure therapy reduces
mortality in black patients with advanced heart
failure
 aldosterone antagonist for NYHA class II-IV patients
with serum creatinine < 2.5 mg/dL (221 mcmol/L) in
men or < 2 mg/dL (177 mcmol/L) in women and
potassium < 5 mEq/dL
o monitor for hyperkalemia and impaired renal
function
o aldosterone blockers (eplerenone [Inspra] or
spironolactone [generic, Aldactone]) reduce allcause mortality and hospitalizations in patients
with left ventricular dysfunction and heart failure
or postmyocardial infarction including patients
with mild symptoms
o other medications commonly used in heart failure
 digoxin may be considered for patients with heart
failure and reduced ejection fraction and persistent
or severe symptoms on guideline-directed medical
therapy
o digoxin reduces hospitalization and clinical
deterioration in symptomatic patients with
systolic heart failure
 aspirin
o aspirin 75-100 mg/day (or clopidogrel 75
mg/day) recommended if established coronary
artery disease but not suggested if no coronary
artery disease
o aspirin may increase hospitalization rates in
patients with heart failure
 anticoagulant therapy
o in patients with atrial fibrillation, chronic
anticoagulant therapy recommended if additional
risk factor for cardioembolic stroke and
reasonable if no additional risk factor for
cardioembolic stroke, in absence of
contraindications
o anticoagulation not recommended in patients
without atrial fibrillation, prior thromboembolic
event, or cardioembolic source
o warfarin reduces risk for ischemic stroke but
increases risk for major bleeding compared to
aspirin in patients with ejection fraction ≤ 35%
and in sinus rhythm
Cardiology
20
Cardiovascular
21