HTN, HF, Carditis, hypotension, syncope Flashcards
Difference between essential (primary) and secondary HTN
Essential-Onset between 25-50
95% of HTN
Exacerbating factors (obesity, NSAIDS, sleep apnea, Increased Na+, Excessive ETOH, Smoking, Polycythemia)
Secondary causes think someone, not between 20-50, had well controlled and now has an increase, refractory HTN on multiple meds
Causes(OCPs, NSAIDs, decongestants, SSRIs and tricyclic, glucocorticoids, weight loss meds, erythropoietin, illicit drugs, Primary renal disease(most comon cause) renal artery stenosis, hyper/hypothyroid, pregnancy, coarctation of aorta(children))
Metabolic Syndrome
Abdominal Obesity Triglycerides >150mg/dL HDL <40mg/dL in Men HDL <50mg/dL in women Systolic BP >130 or diastolic BP >85 Fasting BGL >100mg/dL
Hypertensive urgency
Severe HTN in asymptomatic Pt no evidence of EOD
SBP>180
DBP>120
Hypertensive Emergency
Severe HTN with evidence of acute EOD
Life threatening needs immediate treatment
SBP>180
DBP>120
Lab tests for R/O secondary HTN
TSH-thyroid issues UA-checking for protein Renal artery bruits-stenosis Polysomnography-sleep apnea Excessive cortisol, moon face, obesity-bushings UA- illicit drugs
120-129/80
JNC 7-preHTN
2017 elevated
130-139/80-89
JNC 7-preHTN
2017 Stage 1 HTN
140-159/90-99
JNC-7-Stage 1 HTN
2017-Stage 2 HTN
> 160/>100
JNC7-STage 2 HTN
2017-Stage 2 HTN
HTN screening
Over 40 or with risk factors yearly
Ambulatory BP monitoring
24 hr BP monitoring, expensive
Preferred method for confirming the diagnosis oHTN/white coat HTN
How to diagnose HTN
Pt presents with HTN urgency or emergency
initial screening of >160/100 with target EOD
2ndary HTN causes
Sleep apnea Drug induced/related CKD Primary aldosteronism renovascular disease longterm corticosteroid use/ bushings syndrome pheochromocytoma coarctation of aorta thyroid/parathyroid
Think 2ndary HTN in Pt
Less than 20 older than 50
well controlled HTN with spike
HTN refractory to multiple treatments
Meds that causes 2ndary HTN
OCP, NSAIDs, Decongestants, Antidepressants, Glucocorticoids, Weight loss meds, EPO, Cyclosporine, stimulants
Most common cause of 2ndary HTN
Primary Renal disease
Complications of Untreated HTN
ESKD,
Strokes,
dementia/alzheimers
CVD-LVH, HF, arrhythmias, MI, sudden death
End Organ Damage(EOD)
LVH(early finding) CHF- AMI/CAD Demand ischemia Stroke Aortic dissection retinal hemorrhage
EOD on fundoscopy
optic disc swelling, cotton wool patches, hard exudates
HTN Pt clinical presentation
Asymptomatic for years-nonspecific headaches
Hypertensive Encephalopathy
HTN with somnolence, confusion, visual disturbances, N/V
EMERGENCY
Goal of initial assessment
Determine extent of EOD
Determine overall CVD risk
RO identifiable 2nd causes/often curable causes of 2nd HTN
Nonpharm approach
Weight reduction DASH diet Na reduction physical activity decrease alcohol/smoking
JNC 8 HTN goals >60 no DM or CKD
<150/90
Black-Thiazide or CCB
Nonblack-thiazide, ACE, ARB or CCB
JNC 8 HTN goals<60 no DM/CKD
<140/90
Black-Thiazide or CCB
Nonblack-thiazide, ACE, ARB or CCB
JNC 8 HTN goals DM or CKD
<140/90
DM no CKD
Black-Thiazide or CCB
Nonblack-thiazide, ACE, ARB or CCB
CKD- ACE or ARB along with another class
Hypotension-BP criteria
BP<90/60 MAP <65
Shock-definition
state of cell and tissue hypoxia due to a decrease in O2 delivery
Hypoperfusion state
Features of Hypotension
Tachycardia oliguria hyperlactatemia AMS Tachypnea Cool/clammy Cyanosis-Perioral cyanosis metabolic acidosis
Orthostatic/postural hypotension
After 5 min of lying down, delay of the normal compensatory mechanism of ANS
Clinical presentation of orthostatic hypotension
SBP drops >20mmHg
DBP drops>10mmHg
Orthostatic Hypotension-etiology
Drop in blood volume Drop in cardiac output Arrhythmia Medications endocrine, neurological or metabolic disorders
Orthostatic Hypo initial work up
CBC, BMP, ECG,
Consider- tilt test, echo, neuro and cardiology consults
Management of orthostatic hypotension
treat underlying cause asymptomatic pt may not need treatment D/C causative med IV or PO fluid treat infection, arrhythmia, anemia
Orthostatic hypotension Pt ed
Stand up slowly, maintain hydration, increase Na+ intake, raising head of bed, compression socks, reduce alcohol, increase caffine
Vasovagal hypotension
Stimulation of vagus nerve causes drop in BP and HR(stimulation of parasympathetic nervous system)
DVT etiology
prolonged immobilization, thrombophilia, neoplasm, Fhx, increases with age
DVT clinical finding
swelling of leg or calf, warmth and erythema
pain increasing with standing or walking
DVT diagnosis
H&P Hollman’s test, ultrasound, can do d Dimer
DVT treatment
Depends on location
Fem-pop or more distal- determine if provoked or unprovoked- Anticoag with warfarin or DOAC/NOAC-
Ileofemoral- refer for mechanical thrombectomy vs thrombolysis
chronic Arterial occlusive disease etiology/pathology
chronic and progressive- atherosclerotic plaques, stenosis, ruptured plaques(emboli)
chronic arterial occlusive disease- clinical findings
typically chronic and progressive-claudication, collateral circulation
PAD is normally asymptomatic-can progress to become life-threatening if risk factors are not treated
chronic Arterial occlusive disease- Dx
H&P, specific pattern Pt has with Sx development,
Ankle-brachial index
imaging if indicated
Chronic arterial occlusive disease treatment
Tx risk factors- Especially statins and controlling DM. Walking program can help to create collateral circulation and train muscles to depend on less O2.
acute arterial occlusive disease treatment
emergency(NPO) discuss anticoag with surgeon(heparin) Angiogram, open embolectomy vs endovascular
Acute arterial occlusive disease -Dx
Cardiac exam, abdominal exam, pulse exam, imaging -CT
acute arterial occlusive disease clinical findings
cold leg, painful, no collateral flow
acute arterial occlusive disease etiology
result of clot
phlebitis/thrombophlebitis-eti
a clot formed in superficial venous return-no risk of DVT
phlebitis/thrombophlebitis clinical findings
pain, redness, and inflammation (locally not to entire lower limb as with DVT)
phlebitis/thrombophlebitis Dx
Clinical, use duplex ultrasound if suspicious for DVT
phlebitis/thrombophlebitis treatment
NSAIDs and localized heat
Chronic venous insufficiency etiology/pathology
MC FMHx, then DVT and trauma, occurs in men and women equally-rarely congenital
Venous insufficiency, reflux of blood flow through valves
Chronic venous insufficiency clinical findings
spider or reticular telangiectasia, varicose veins, edema, skin changes, ulceration, thrombophlebitis
-pain edema, aching, throbbing fatigue-consider venous stasis ulcer
chronic venous insufficiency Dx
Ultrasound can measure size and flow (antegrade/retrograde)-reflux is retrograde flow for more than 500ms
chronic venous insufficiency Tx
lifestyle modifications- elevation and compression socks
minimally invasive techniques- ablation
invasive- vein stripping
varicose veins pathology
venous insufficiency- causing dilation of veins and blood pooling
Varicose veins clinical findings
squishy +/-painful veins
Varicose veins Dx and Tx
Ultrasound- minimally invasive (ablation) to invasive(vein stripping)
Venous ulceration EPI/Patho
the result of venous insufficiency
Venous ulceration clinical /Dx
typically on medial malleolus, will have swelling, will have a palpable pulse
Reynaud’s disease Epi/
F>M, FMHx, smoking, autoimmune disease, some meds
Reynaud’s pathology
vasospastic disorder
Reynaud’s clinical and Dx
pallor, cyanosis, hyperemia
H&P Sx
Reynaud’s treatment
Lifestyle changes-gloves and socks-smoking cessation, D/C BB if HTN and give CCB
Temporal arteritis EPI/ETI
Autoimmune vasculitisF>M 4:1
caucasions
temporal arteritis clinical findings
HA, malaise/fatigue, some fever and neck/jaw claudication
Temporal arteritis Dx
ESR/CRP- Rheumatology referral
Temporal arteritis Tx
temporal artery biopsy, Oral corticosteroids (PO Prednisone)
Aortic Aneurysm Epi/Eti
M>F >60yo, Caucasians, Hx of smoking, FMHx
Aortic Aneurysm Clinical findings
Usually none - can cause back and abd pain
can embolize to legs
RUPTURE- very rapidly becomes hemodynamically unstable
Pulsatile mass in abd
Aortic Aneurysm Dx
Imaging or ultrasound
Aortic Aneurysm Tx
Treat HTN (BB) antiplatlets and statins(prevent emboli and further stenosis) Endovascular repair: stent graft EVAR or open repair
Aortic Dissection Epi/Eti
Trauma, penetrating atherosclerotic plaque, HTN
Aortic Dissection Patho
Fenestrated intima allows blood into other layers of the blood vessel creating a false lumen
Aortic Dissection Clinical findings
Ripping, tearing pain in back, depending on location can have unequal BP(check bilateral BP)
Aortic Dissection Dx
Imaging
Aortic Dissection Tx
BP management, may need endovascular or open repair if causing end organ damage
HF NYHA Class I
Pt with heart disease w/o limitation of physical activity-no signs of HF
HF NYHA Class II
Pt with heart Disease resulting in slight limitation of physical activity-Symptoms of HF develop with activity but go away with rest
HF NYHA class III
Pt with heart disease resulting in marked limitation of physical activity, Symptoms develop w/ less than ordinary physical activity- no symptoms at rest
HF NYHA Class IV
Symptoms of HF at rest
HF AHA Stage A
At high risk for HF no structural damage and no Sx of HF
HF AHA Stage B
Structural HD w/o signs or symptoms of HF,
HF AHA Stage C
Structural HD w/ prior or current signs and symptoms of HF
HF AHA Stage D
Refractory HF requiring specialized intervention
HFpEF
Diastolic HF-enlarged muscle doesn’t allow enough blood into the ventricle, Ejection fraction is normal but Cardiac output is decreased-dizziness, orthostatic hypotension
HFrEF
Systolic HF- weak ventricular muscle is not able to push out causing a decrease in CO and EF
Left-sided HF
SOB, pulmonary edema
Can have right sided failure symptoms as well due to the severity of HF
Right Sided HF
Systemic edema-JVD-
Can have Left sided symptoms as well depending on the severity
HF ECHO
Can monitor proper contraction and movement of heart and valves- can give an EF and determine which part of the heart is damaged
HF Brain Natriuretic peptide(BNP)
Is released from the ventricle in response to increases in ventricular stretch
Acute HF
Decompensated HF
Chronic HF
Stable- treat underlying causes
Treatment approach to Chronic HF
1-ACE, ARB or ARNI
2-BB-carvedilol or metoporlol ER
3-Aldosterone Antagonist-Spironolactone
ACE/ARB-MOA
afterload reducers
ARNI-moa
potentiate ARB effects
Aldosterone antagonist MOA
Diuretic
BB moa
decrease afterload and myocardial O2 demand
Loop diuretics
Symptom relief
Digoxin moa
positive inotrope and negative chronotrope
Non pharm treatments of HF
ICD- BiVentricular pacing Case management- daily weigh-ins Coronary revascularization LVAD Transplants
Treatment of acute HF
O2, BiPAP-CPAP
Vascular support- MSO4-venodilation, Nitrates-venodilation, Diuretics-excrete fluid, Dobutamine-increase inotropy, Slowly reintroduce ACE, BB and other meds once stablized
S1
Closure of the AV valves-beginning of systole
S2
Closure of the Semilunar valves- the beginning of diastole
S3
Extra sound- HF or dilated cardiomyopathy-blood rushing into the ventricle “Ken Tuck Y”
Gallop
S4
Extra heart sound- immediately precedes S1- stiff ventricle, infiltrate-HFpRF
“Ten es see”
Gallop
Systolic murmurs
Aortic stenosis
Pulmonic Stenosis
Mitral/tricuspid insufficiency/regurge
Mitral valve prolapse
Diastolic murmurs
Always pathologic
Aortic/pulmonic insufficiency/regurge
mitral/tricuspid stenosis
Aortic Stenosis murmur
Harsh crescendo/decrescendo over aortic region
Aortic Stenosis eti/
MC valve disease, degeneration due to calcification
RHD, congenital bicuspid aortic valve, atherosclerosis, elderly-radiation/collagen diseases(rare)
Aortic stenosis signs
rales- cool extremities, angina, syncope-Life expectancy decreases rapidly when symptoms arise
Aortic stenosis Dx
Murmur heard best with Pt leaning forward, decreased w/volume reduction(standing) and increased with volume increase(squating)
Aortic stenosis grading
Normal-3-4cm^2
Mod 1.15cm^2
Severe<1cm^2
Aortic stenosis Tx
Valve replacement or repair
Aortic stenosis management
Avoid Negative inotropes
Observe yearly w/echo-asymptomatic every 2-5 years
Replacement for severe(10-30y expectancy)
Aortic stenosis Pt ed
Pt needs to tolerate elevated BP to maintain CO
Pulmonic stenosis murmur
crescendo/decrescendo over pulmonic area
with Pt leaning forward and with the release of Valsalva
Pulmonic stenosis ETI
heart surgery or congenital MC
Tetralogy of Fallot
Mitral insufficiency/ regurge murmur
Best heard at apex-radiates to axilla
systolic murmur-opening snap blowing holosystolic murmur
increases with increased peripheral resistance
Mitral regurge insufficiency ETI
leaflet, annulus chordae tendonae/papillary muscle abnormalities
Mitral regurge Sx
Asymptomatic —exercise intolerance, IHD(angina), severe dyspnea(L HFrEF) afib
Mitral regurge management
yearly echo, avoid atrial remodeling
Mitral valve prolapse murmur
late systolic click with a crescendo murmur
click will occur sooner when standing, later with squatting
Tricuspid regurge murmur
difficult to hear-use bell when standing
tricuspid regurge eti
pulmonary HTN leading to HF
infective endocarditis, Epstein barr, pacemaker leads, Rheumatic fever
Aortic insufficiency/regurge
Quiet blowing decrescendo heard on left sternal border, increases with peripheral resistance
Aortic insufficiency ETI
congenital leaflet-bicuspid aortic valve
endocarditis, marfans, Rheumatic HD, dilation of aortic root, rarely syphilis
Aortic insufficiency sings/sx
exercise intolerance, dyspnea, orthopnea, CHF, angina, bounding peripheral pulses
Aortic stenosis tx/management
yearly echos
replacement
Mitral valve stenosis murmur
Opening snap, diastolic murmur, rumbling decrescendo low pitch heard best at apex with bell in left recumbent
Mitral valve stenosis ETI
second most common murmur-
Rheumatic fever, 4x more males-females have more symptoms
endocarditis
Mitral valve stenosis sx/signs
rales, cool extremities, subtle exercise intolerance, palpitations, chf, hoarsness, a fib
Mitral valve stenosis Dx
EKG, Echo, CBC, BMP, Mg++, TSH, CXR, BNP
Mitral valve stenosis grading
Normal 4-5 cm^2
mild <2.5cm^2
Critical<1 cm^2
Mitral valve stenosis Tx and Management
Replacement
prevent clots, control HR(BB, CCB), prophylaxis against endocarditis(dental procedures)
Yearly echo
Pulmonic regurge murmur
caused by pulmonary HTN MC
quiet murmur low flow- Descrescendo best heard in pulmonic area increases with release of valsalva
Tricuspid stenosis murmur
Pan diastolic at L sternal border
increases with exercise(increased venous return to heart
Dilated cardiomyopathy
MC type- ischemia, HTN, thick ventricular walls with dialation inside then becomes thin and weak
Hypertrophic cardiomyopathy HOCM
think sudden cardiac death by athlete, inborn deffect of left ventricle hypertrophy near the outflow track into the aorta
need exercise restriction(can have surgery to remove portion(Septal myomectomy)
ICD and BB
Restrictive cardiomyopathy-
rare -deposits of things in the heart muscle, amylooidosis-plaques heart muscle causing issues with conduction and contraction
tako tsubo cardiomyopathy
broken heart-after catecholamine discharge dilation and ballooning of LV-mainly postmenopausal women
EKG findings in cardiomyopathy
50% sensitive 90% specific
Criteria for LVH
V1 S+V5/6 R >35mm(7big boxes)
Radiology findings in cardiomyopathy
CXR- gives an indication of an enlarged heart but no cause
Echo can calculate EF and specify which part of Heart is affected
Cardiac MRI-expensive and slow-more detailed than echo
Lab studies in cardiomyopathy
BNP/Nt-ProBNP-higher the BNP the more stretch of the ventricles- causes vasodilation-drop in BP
Causes decrease in renin causing more diuresis decreasing blood volume
Endocarditis
Patho-Infection/inflammation of valve or prosthetic valve
ETI-TB, mycobacteria, HACEK, Staph and Strep
Risks-indwelling catheters, central lines, iv drug users, prolonged infections
S/S- fever, malaise, splinter hemorrhages, Osler nodes(painful) Janeway lesions(not painful), new murmur, sepsis
Dx-blood culture(3 separate locations), echo
Tx-based on blood culture results, replace valve if damaged
Myocarditis
Patho-inflammation/infection of muscle
ETI- HX recent uri, febrile illness, drugs, vaccination
Dx- Echo, MRI, myocardial biopsy
Tx- typically self limiting, if not treat as HF and treat cause
Pericarditis
Patho- inflammation/ infection of pericardial sac
ETI- viral infection, systemic disease, infrections, autoimmune, drugs, uremia
Clinical pres- pericardial friction rub, fever, tamponade, tachypnea, tachycardia, narrow pulse pressure, pulsus pardoxus, diffuse ST elevation, pleuritic chest pt increases in supine position decreases when leaning forward
Dx- elevated erythrocyte sediment rate(ESR) and c reactive protein(CRP)
Tx NSAIDs, ASA, colchicine(post MI), ABX for infective, dialysis for uremic
Consideration- Colchicine can cause severe ADE, effusion vs tamponade
Rheumatic heart disease tx
PCN, Tx chorea, CHF management, surgery to replace valves
Endocarditis prophlylaxis
Dental procedures, respiratory tract procedures, procedures on infected skin/tissue -prosthetic cardiac valve, previous infective endocarditis, Congenital heart disease, cardiac transplants
