Cardiac Flashcards
1
Q
Prehypertension measurements
A
120-139/80-90
2
Q
What is primary hypertension?
A
- Sustained elevation of 140/90 or higher
- Results from environmental or genetic factors
- Affects 90-95% of individuals with hypertension
- Also called essential or idiopathic hypertension
3
Q
Modifiable Risk Factors for Hypertension
A
- Smoking
- DM
- HLD
- Obesity
- Physical inactivity
- Unhealthy diet
- Excessive sodium intake
- Excessive alcohol intake
4
Q
Non-modifiable Risk Factors for Hypertension
A
- Chronic kidney disease
- Family history
- Increased age
- Low socioeconomic status
- Low educational status
- Male sex
- OSA
- Psychosocial stress
- Pregnancy
5
Q
HTN increases the risk of developing…
A
- heart disease
- kidney disease
- hardening of the arteries (atherosclerosis or arteriosclerosis)
- eye damage (retinopathy)
- stroke (ischemic and hemorrhagic)
6
Q
What is end-organ damage?
A
A complication of hypertension
- called this because damage to these organs is the end result of chronic (long duration) high blood pressure
7
Q
What to ask for evaluation of hypertension?
A
- duration and levels of elevated BP
- past treatments (both successes and failures)
- associated symptoms that suggest secondary HTN
- symptoms of stress
- weight control
- physical activity/sedentary lifestyle
- tobacco use
- dietary intake
- medications
- psychosocial and environmental factors that may impact BP
8
Q
Associated symptoms that suggest secondary HTN
A
- palpitations
- sweating
- dizziness
- abdominal pain
- back pain
9
Q
Medications to ask about when evaluating HTN
A
- illicit drug use
- oral contraceptives
- NSAIDs (can increase BP)
- decongestants
- steroids
10
Q
Diagnosis of HTN
A
- obtain 2 or more BP with patient in chair after 5 minutes of rest (no caffeine or smoking 30 minutes prior)
- measure height, weight, waist circumference with waist/hip ratio and BMI
- excess body fat: waist >34 in. for women and >39 in. for men there is an increased risk for CVD
- perform funduscopic exam
- perform complete heart exam (bruits, thrill, edema)
- perform complete neuro exam
- ECG
11
Q
Lab Tests to do for HTN patients
A
- UA (may reveal proteinuria)
- electrolytes
- calcium
- creatinine
- fasting lipid profile
** Goal is to identify target organ damage, any underlying cause and/or additional risk factors
12
Q
Hypertension Prevention
A
- maintenance of healthy weight and BMI
- smoking cessation
- regular aerobic exercise
- alcohol in moderation (<1 oz per day)
- stress management
- adherence to medication regimen
- assess for and treat OSA
13
Q
Why is it important to assess medication adherence for HTN treatment?
A
It is important to identify obstacles to effective treatment
- cost?
- hard to get?
- sexual dysfunction/side effects?
**Ask them to bring their medications in to the office
14
Q
Treatment strategy for HTN Stage 1
A
if no history of CVD, and risk score is <10%, initiate lifestyle changes first
15
Q
Treatment strategy for HTN Stage 2
A
lifestyle changes AND medication
16
Q
Things to consider when starting BP medications…
A
- ACE inhibitors can increase potassium
- Avoid beta blockers in individuals with DM and reactive airway disease
- Avoid ACE inhibitors in childbearing women: CategoryX
- Start low, go slow
- Maximize one medicine then consider adding a new medication (start at lowest dose, then increase)
- If cannot control BP… REFER!
17
Q
How often to reassess HTN patients?
A
Reassess monthly until patient reaches goal, then every 3-6 months
18
Q
Peripheral Artery Disease (PAD)
A
- atherosclerotic disease of arteries that perfuse the limbs, especially lower extremities
- especially prevalent in patients with DM
- often asymptomatic
- could have intermittent claudication
19
Q
What is intermittent claudication?
A
Obstruction of arterial blood flow in the iliofemoral vessels resulting in pain with ambulation
- fatigue, discomfort and/or pain that occurs in specific leg muscle groups during walking because of exercised induced ischemia
20
Q
What is critical limb ischemia?
A
- can occur with PAD
- it is pain that occurs at rest or impending loss of limb caused by severe restriction in blood flow.
- ischemia exceeds 2 weeks
21
Q
What is acute limb ischemia?
A
- occurs with PAD
- has rapid onset (hours)
- urgent recognition with prompt revascularization is required to prevent loss of limb
22
Q
What is OLDCARTS?
A
Used for PAD assessment
O - onset
L - location
D - duration
C - characteristics
A - alleviating/aggravating factors
R - radiation/relieving factors
T - timing
S - severity
23
Q
Raynaud Phenomenon
A
- PAD
- episodic vasospasm (ischemia) in arteries and arterioles of the fingers, less commonly in the toes
- is secondary to other systemic diseases or conditions (exposure to cold, pulm htn, smoking, scleroderma)
24
Q
Raynaud Disease
A
- PAD
- is a primarily vasospastic disorder of unknown origin
25
Thromboangniitis obliterans (Buerger disease)
- causes pain, tenderness, and hair loss in the affected area
- symptoms are caused by slow sluggish blood flow
- can often lead to gangrenous lesion
- occurs mainly in young men who smoke
- inflammatory disease of peripheral arteries resulting in nonatherosclerotic lesions (spasm, thrombi, T-cell activation)
- digital, tibial, plantar, ulnar, and palmar arteries
- obliterates the small and medium-sized arteries
26
PAD Clinical Presentations
- often have no complaints
- intermittent claudication or atypical leg pain (atypical pain usually due to co-morbidities)
- patients may present initially with a threatened limb (critical limb ischemia)
- may have non healing wound/ulcer
- skin discoloration and gangrene
- lack of hair growth on lower limbs
- thickened toenails
- diminished or absent pulses
- bruits in abdominal, femoral, or popliteal area
- pale, cool extremities
- muscular atrophy
- prolonged capillary refill
27
PAD Diagnostic Tests
- Ankle Brachial Index (ABI)
- Doppler ultrasound
- CBC
- BMP
- C reactive protein (CRP)
- erythrocyte sedimentation rate (ESR)
- X ray (especially if there are wounds [osteomyelitis])
- contrast angiography
28
Ankle-Brachial Index (ABI)
- used for PAD diagnostics
- a comparison of upper extremity BPs to lower extremity BPs
- looking at vascular health
- <0.9 diagnostic for occlusive arterial disease
- > 1.3 suggests presence of calcified vessels and need for additional testing such as exercise ABI
29
PAD Treatment
- lifestyle modifications
- stop smoking (smokers have a particularly strong risk of PAD)
- control DM
- control BP
- be physically active (including a supervised exercise program)
- eat a low saturated-fat, low-cholesterol diet
- drug treatment includes medicines to help improve walking distance (cilostazol, pentoxyfyline)
- antiplatelet agents
- cholesterol lowering agents (statins)
- angioplasty or surgery may be necessary
30
Consultation/Referral for patient with PAD
- refer to vascular surgeon for persistent symptoms or moderate or severe ischemia
- refer if exercise and meds have not helped after 3-6 months (75% of patients will improve on this regimen)
- refer all non healing ulcers
- critical limb ischemia, gangrene, ulceration or pain at rest are present
31
Complications of PAD
- amputation
- intractable pain
- immobility
- ischemia leads to necrosis leads to gangrene
32
Orthostatic Hypotension
- decrease in systolic (by 20 mm Hg or more) and diastolic (by 10 mm Hg or more) blood pressure upon standing
- lack of normal blood pressure compensation in response to gravitational changes on the circulation
- 2 types (acute and chronic)
33
Acute Orthostatic Hypotension
- common in diabetics, blood loss, and elderly
34
Chronic Orthostatic Hypotension
- primarily seen in older men
35
Atrial Fibrillation
- supraventricular tachyarrhythmia characterized by rapid uncontrolled uncoordinated atrial activation with deterioration of atrial mechanical function
- can reduce cardiac output by as much as 30%; blood can pool in the atrium, causing a clot in the left atrial appendage
- increases the risk of ischemic stroke fivefold
- up to 25% of all strokes in older adult population occur secondary to Afib
36
Types of Atrial Fibrillation
1. paroxysmal
2. persistent
3. longstanding persistent
4. permanent
5. nonvalvular
37
Paroxysmal A fib
AF ends spontaneously or after intervention within 7 days of onset
38
Persistent A fib
AF continues for more than 7 days
39
Longstanding Persistent A fib
continuous A fib for more than 12 months
40
Permanent A fib
AF when no longer attempting to restore or maintain sinus rhythm
41
Nonvalvular A fib
AF in the absence of rheumatic mitral stenosis, heart valve replacement, or mitral valve repair
42
A-Fib Risk Factors
- increasing age
- hypertension
- DM
- vascular disease
- smoking
- inactivity
- hyperthyroidism
- heart failure or left ventricular hypertrophy (LVH)
- obesity
- obstructive sleep apnea
- genetic variants (fam hx, euro descent)
- cardiothoracic surgery
- valvular heart disease (VHD)
- increased pulse pressure
- LVH on EKG
- enlarged left atrium (LA), increased thickness of LV wall, decreased LV fractional shortening on echocardiogram
- increased CRP or BNP
** Reversible causes include pulmonary embolism, caffeine intake, alcohol, fevers, and infectious origin
43
Assessment Findings for Afib
- irregular or rapid heart tones
- irregular peripheral pulses
- subjective symptoms include unusual heartbeats (racing, fluttering, palpitations), shortness of breath, lightheadedness
- hypotension (due to poor blood perfusion)
- elevated jugular venous pressure (blood is pooling, so there is backflow)
44
Diagnostic Studies for Afib
- 12 lead EKG
- Holter monitor
- Pulse oximeter
- TSH, CMP, CBC
- transthoracic echocardiogram
- chest xray
- PT/INR
- stress test
- transesophageal echocardiogram
45
Who manages initial care of Afib patients?
Cardiologist
46
Afib Treatment
- Anticoagulation
- Rate control meds
- Rhythm control meds
- digoxin
47
Anticoagulation for Afib
- new/novel oral anticoagulants (NOACs) are recommended over warfarin where eligible, except in patients with moderate to severe mitral stenosis or mechanical heart valve
- initiation based on risk for thromboembolism independent of Afib type, on stroke/bleed risks, basis of Afib (valvular or nonvalvular), renal function, and patient preferences
- warfarin is the only approved anticoagulant for valvular Afib
- NOAC (dabigatran, rivaroxaban, apixaban)
48
Rate control meds for Afib
- Beta blockers (-olol's)
- Calcium channel blockers
49
Types of CCBs used for Afib
- verapamil
- diltiazem
50
Rhythm control meds for Afib
- amiodarone
- dronedarone
51
Complications of Afib
- hemorrhagic stroke
- ischemic stroke
- bleeding secondary to anticoagulation
- bradycardia secondary to rate control medications
- pulmonary fibrosis, hypothyroidism with long-term use of amiodarone
52
Chest Pain
- discomfort or a sensory pain response to noxious stimuli associated with actual or potential tissue damage involving the chest wall, thoracic organs, and adjacent structures
- location may be anywhere along the front and back of the body between neck and upper abdomen
53
Origins of chest pain
- chest wall
- lungs
- cardiac
- GI
- psychogenic/psychosomatic
54
Chest wall origin of chest pain
- bones
- muscles
- nerves
- cartilagenous tissue
- skin
55
Lung origin of chest pain
- lung
- pleura
- diaphragm
- infection
- neoplasm
55
Cardiac origin of chest pain
- heart
- pericardium
- epicardium
- mediastinum
56
GI origin of chest pain
- stomach
- esophagus
- gallbladder
- duodenum
- hiatal hernia
57
Psychogenic/Psychosomatic origin of chest pain
- anxiety
- depression
- panic attack
58
Chest Pain Treatment
- plan/management
- pain relief
- treatment of underlying cause
- referral for proper follow up (cardio, GI, psych)
- educate patient and family about cause
59
Heart Failure
- general term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood-borne nutrients
60
Types of Heart Failure
1. Congestive HF
2. Diastolic HF
3. Right sided HF
4. High-output failure
61
Congestive HF
- systolic heart failure
- inability of the heart to generate adequate cardiac output to perfuse tissues
62
Diastolic HF
- pulmonary congestion despite normal stroke volume and cardiac output
63
Right HF
- commonly caused by diffuse hypoxic pulmonary disease
- can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation
64
High-output Failure
- inability of the heart to supply the body with blood-borne nutrients, despite adequate blood volume and normal or elevated myocardial contractility
65
Left-sided HF symptoms
F - fatigue
O - orthopnea
R - rales/restless
C - cyanosis/confusion
E - extreme weakness
D - dyspnea
66
Right-sided HF symptoms
B - bloating
A - anorexia
C - cyanosis/cool legs
O - oliguria
N - nausea
E - edema
D - distended neck veins
67
Disorders caused by HF
- pneumonia
- COPD
- bronchitis
- cirrhosis
- venous insufficiency
- dependent edema
- pulmonary embolism
68
Diagnostic Studies for HF
- BNP
- NT-proBNP
** Both are important and are not interchangeable
69
When to hospitalize patients with HF
- pulmonary edema
- cardiogenic shock
- MI
- O2 saturation > 90%
- anasarca
- pneumonia
70
HF Treatment
- goal of ejection fraction > 40%
- First line therapy is for all patients regardless of severity is both an ACE inhibitor and a Beta Blocker (start low...go slow)
- diuretics to manage fluid retention
71
Loop Diuretics
* used for HF
- lasix
- torsemide
- bumetanide
72
Aldosterone receptor antagonist
* used for HF
- spironolactone
- eplerenone
73
Heart Murmur
-the sound detected during turbulent blood flow through the heart or the great vessels due to one of the following
- blood forced through narrow passages (valvular stenosis)
- regurgitation through incompetent or abnormal valves (mitral valve regurgitation)
- increased blood flow across normal structures (anemia)
- shunting of blood from an area of high pressure to an area of lower pressure (ventricular septal defect)
74
Risk Factors for Heart Murmur
- age (common in children, older adults)
- fever
- anemia
- pregnancy
- thyrotoxicosis
- HTN
- rigid carotid arteries
- MI
- atrial tumor or thrombus (usually causes "tumor flop")
- congenital heart disease
- valvular disease
- bacterial, viral, or fungal infection of heart
75
Grade 1 Heart Murmur
barely audible with intense concentration
76
Grade 2 Heart Murmur
faint, soft, audible immediately
77
Grade 3 Heart Murmur
moderately loud, no thrill palpable
78
Grade 4 Heart Murmur
loud with palpable thrill
79
Grade 5 Heart Murmur
very loud, audible with part of stethoscope off the chest; thrill palpable
80
Grade 6 Heart Murmur
audible without a stethoscope on chest wall; thrill palpable
81
Heart Murmur Diagnostic Testing
- cardiac auscultation
- electrocardiogram
- chest xray
- doppler echocardiography (transthoracic or thransesophageal)
- stress echocardiography
- angiography
- cardiac catheterization
- cardiac CT (or MRI)
82
Physiologic Maneuvers useful in Diagnosing Heart Murmurs
- respiration
- abrupt standing and squatting
- valsalva
- hand grip
- post extra systolic potentiation
83
Heart Murmur: Respiration maneuver
systemic and pulmonary venous return change reciprocally with inspiration and expiration; alter certain heart sounds and murmurs
84
Heart Murmur: abrupt standing and squatting maneuver
systemic venous return and arterial pressure change reciprocally; alters certain heart sounds and murmurs
85
Heart Murmur: Valsalva maneuver
induces decrease in intensity of murmur of aortic stenosis and increases intensity of systolic ejection murmur of hypertrophic cardiomyopathy
86
Heart Murmur: hand grip maneuver
increase in systemic vascular resistance: tends to decrease intensity of murmur of aortic stenosis and increase intensity of murmur of mitral regurgitation
87
Heart Murmur: post extra systolic potentiation
clues to valvular heart disease
88
Transient Ischemic Attack (TIA)
a transient episode of neurologic dysfunction due to the focal brain, spinal cord, or retinal ischemia, without acute infarction
89
Three subtypes of TIA
1. Cardioembolic
2. Atherothrombotic
3. Lacunar
90
TIA Risk Factors
- HTN
- advanced age
- prior TIA
- smoking/tobacco use
- DM
- HLD
- physical inactivity
- cardiac disease
- chronic kidney disease
- afib
- family history of TIA or stroke
- oral contraceptive use
- sickle cell disease
- sleep apnea
- carotid artery stenosis
- hypercoagulable state
- obesity
91
TIA Assessment Findings
- aphasia
- visual field defects
- confusion
- amnesia
- diplopia
- dysphagia
- dysarthria
- unilateral weakness
- symptoms of typically last < 60 minutes
- transient global amnesia
92
Diagnostic Studies for TIA
- Brain imaging with CT and/or MRI of head: rule out hemorrhage or stroke
- carotid studies (U/S and/or angiography); 70% blockage may cause symptoms
- neurovascular studies such as CT angiography, MR angiography and/or ultrasound: may demonstrate atherosclerosis
- 12 lead EKG, 24-hr Holter monitor, echocardiogram if underlying cardiac problem suspected
- EEG if seizure is suspected
- laboratory studies to rule out medical causes: CBC, PT/PTT, ESR, glucose, lipid profile, serum electrolytes, creatinine
93
TIA Prevention
- control BP
- weight loss for vascular risk reduction
- aerobic activity 3-4 times weekly
- smoking cessation
- limit alcohol consumption
- antiplatelet therapy
- statin therapy
- sleep study (due to OSA correlation)
94
TIA Treatment
- use of antiplatelet agents rather than oral anticoagulants is recommended
- recommended for 50-99% stenosis of a major intracranial artery (ASA, BP <140 mm HG, high intensity statin therapy)
- apixaban, dabigatran
95
Angina
syndrome characterized by short episodes of deep, poorly localized chest pain or arm discomfort associated with physical exertion or emotional stress and relieved with rest
96
Acute Coronary Syndrome
any constellation of clinical symptoms suggestive of unstable angina or acute myocardial infarction
97
Examples of Acute Coronary Syndromes
- transient ischemia
- unstable angina
- sustained ischemia
- MI
- myocardial inflammation and necrosis
98
Stable Angina
- episodic
- crescendo - decrescendo pattern
- occurs on exertion and relieved by rest
- last 2-5 minutes
99
Unstable Angina
- severe and new onset
- crescendo pattern
- occurs at rest
- last > 10 minutes
100
Myocardial Infarction
- sudden and extended obstruction of the myocardial blood supply
- subendocardial infarction (NSTEMI)
- transmural infarction
101
Myocardial Infarction Diagnosis
- clinical assessment
- complete CV and neuro exam
- EKG changes
- cardiac enzymes (troponins most specific, see in 2-4 hrs, speaks in 24hrs, remains elevated for 7-10 days)
- CK-MB (see in 2-4 hr, peaks in 24 hrs)
- LDH (will show tissue damage)
- hyperglycemia 72 hrs post MI
102
Acute Myocardial Infarction Treatment
M - morphine
O - oxygen
N - nitrates
A - aspirin
**Caveat: if patient is having inferior MI, perform right sided EKG and do NOT give morphine
103
Post Myocardial Infarction Treatment
- beta blockers are recommended (do not give in acute heart failure)
- ACE inhibitors (ARBs if cannot tolerate ACEs)
- antiplatelet therapy (aspirin or plavix)
- DM management
- lipid management
- nitroglycerin and calcium channel blockers can be used to treat ischemic symptoms without significant renal dysfunction
104
Cardiovascular Syncope Causes
associated with decreased cardiac output or obstruction
105
Electrical Causes of Syncope
- arrhythmias
- heart block
- Brugada syndrome
106
Mechanical Causes of Syncope
- idiopathic subaortic stenosis
- hypertrophic obstructive cardiomyopathy
- valvular diseases
- myxoma
- MI
- pulmonary embolus
107
Syncope Diagnostic Studies
- goal is to identify life-threatening conditions or those associated with significant risk of injury
- detailed history and physical exam
- EKG
- CMP: glucose, calcium, sodium
- Holter monitor
- measure BP in both arms (a difference of 20 mm Hg or more is considered abnormal)
108
When to hospitalize syncope patients...
- known or serious CV disease
- significant EKG changes
- acute symptoms of chest pain or symptoms of PE
- disabling episodes of recurrent syncope
- syncope involving injury, rapid pulses or exertional syncope
