Cardiovascular Conditions Flashcards
What is coronary artery disease?
cardiovascular condition, involves narrowing or blockage of coronary arteries due to atherosclerosis.
-impedes blood flow to myocardium, leading to ischemia (with pain: angina pectoris)
-potentially resulting in ACS or MI
What is acute coronary syndrome?
term used to describe a range of conditions associated with sudden, reduced blood flow to the heart.
-3 entities: STEMI, NSTEMI, and unstable angina
What causes ACS?
What is the pathophys?
the rupture of an atherosclerotic plaque in a CA, leading to partial or complete blockage of blood flow
-disruption of plaque triggers platelet aggregation and thrombus formation. results in ischemia and potential necrosis of myocardial tissue. extent of damage depends on duration and severity of ischemic event.
CAD can lead to _________ , or progress to ______.
angina pectoris
ACS
s/s ACS
CP or discomfort that may radiate to shoulders arms, neck, jaw, back.
-described as pressure or squeezing
-dyspnea, diaphoresis, nausa, syncope
Dx of ACS
ECG
cardiac biomarkers
Why ECG for dx ACS?
differentiates between stemi and nstemi/ unstable angina
What does NSTEMI ECG usually show?
ST segment depression or T wave inversion
Cardiac biomarkers for dx ACS
Troponins.
-elevated indicate myocardial necrosis and help differentiate between NSTEMI and unstable anginga
ACS management
pharm:
1. antiplatelet agents (aspirin and P2Y12 inhibitors)
2. anticoagulants
3. beta blockers
4. ACE inhibitors
5. statins
reperfusion therapy:
-PCI
-thromobolysis
What do ST segement elevations signify?
COMPLETE blockage of one or more CAs
(indicates acute transmural ischemia)
Pathophys of STEMI
results from rupture of atherosclerotic plaque followed by thrombosis, leading to occlusion of the CA.
risk fac
Risk Factors of STEMI (preluding one)
- HTN
- HLD
- smoking
- DM
- family hx CAD
clinical manifestations of STEMI
CP (pressure or squeezing) radiating to left arm, neck, or jaw
diaphorsis
dyspnea
nausea
sometimes syncope
post STEMI reperfusion management
- antiplatelet therapy with aspirin and P2Y12 ihibitors (clopidogrel)
- AC with heparin or LMWH
- BB to reduce myocardial oxygen demand
- ACE inhibitors prevent ventricular remodeling
- statins for lipid management
NSTEMI is characterized by
partial blockage of a CA, result is reduced blood flow to heart muscle
How is a NSTEMI identified?
by cardiac biomarkers, such as troponins, indicating myocardial injury
Pathophy of NSTEMI
CA plaque ruptures or erodes, leading to thrombus formation. Not completely obstructied, so some perfusion of myocardium is allowed, BUT insufficient to meet metabolic demands, esp during exertion or stress.
mismatch between o2 supply and demand causes ischemia and myocardial necrosis
clinical manifestations of NSTEMI
similar to other forms of ACS, including CP or discomfort that may radiate to arm, neck, jaw, back. (often pressure like)
dyspnea, diaphoresis, nausea, fatigue
Dx of NSTEMI
- ECG: may show nonspecifc changes (ST depression or T wave inversion)
- cardiac biomarkers ** (Troponin I or T)
Management/ Tx of NSTEMI
Pharm:
1. antiplatelet agents (aspirin and P2Y12 inhibitors)
2. AC (heparin)
3. BB
4. statins
5. nitrates**
procedure (not all cases)
- PCI
What diagnostic tool helps differentiate between NSTEMI and unstable angina?
cardiac biomarkers (Troponin I or T) as they are sensitive indicators of myocardial cell injury
Unstable angina is characterized by_______
and indicates________
unexpected CP or discomfort typically at rest or with minimal exertion.
indicates sudden reduction in blood flow to heart muscle, often due to plaque rupture and subsequent thrombus formation in CA
How do stable and unstable angina differ?
stable: predictable pattern and relieved by rest or nitro
unstable: unexpected. occurring at rest or with minimal exertion
pathophy of unstable angina
disruption of atherosclerotic plaque, leading to platelet aggregation and partial occlusion of CA
(so there is an imbalance between O2 supply and demand)
What is the difference between unstable angina and MI?
the partial occlusion of unstable angina does not result in myocardial necrosis
s/s unstable angina
-new onset CP (may radiate)
-worsening anginal symptoms (dyspnea, diaphoresis, nausea, syncope)
-angina at rest lasting more than 20 min
*immediate medical eval as may escalate to MI
Dx of unstable angina
- ECG (may show ST depression or T wave inversion)
- cardiac biomarkers (Troponin) remain normal or only slightly elevated since no myocardial necrosis
Management unstable angina
- anti-ischemic therapy with nitrates and BB
- antiplatelet therapy (aspirin, possibly P2Y12 inhibitors like clopidogrel)
- AC (heparin)
depending on risks: coronary angiography, PCI, CABG
What is cardiac tamponade?
accumulation of fluid in pericardial space, which exerts increased pressure on the heart
impairs ability to fill properly during diastole, leading to *decreased cardiac output and hemodynamic instability *
What are some causes of tamponade?
trauma, malignancy, infection, uremia, post MI syndrome
pathophy of cardiac tamponade
rapid or excessive accumulation of pericardial fluid overwhelming compensatory mechanisms of heart.
-as intrapericardial pressure rises, it surpasses intracardiac pressures, leading to impaired ventricular filling.
-result is reduced stroke volume and CO (manifests as hypotension and shock)
What is Beck’s Triad? What does it indicate?
hypotension, JVD, muffled heart sounds
tamponade
Dx of tamponade
assessment, but confirmed with imaging (echo)
Echo shows pericardial effusion and signs of chamber collapse (RA and ventricualr collapse during diastole)
ECG changes: low voltage QRS complexes and electrical alterans due to swinging movement of heart within fluid-filled pericardium
M
Management of tamponade
hemodynamics stabilization with IV fluids to augment preload and maintain CO.
-pericardial fluid drainage through pericardiocentesis (using echo guidance) or sx intervention (pericardial window)
What are cardiomyopathies?
a group of diseases that affect the heart muscle, leading to impaired cardiac function
resulting in HF, arrhythmias, sudden cardiac death
4 main types of cardiomyopathy
- dilated
- hypertrophic
- restrictive
- arrythmogenic RV cardiomyopathy (ARVC)
described dilated CM.
causes?
s/s?
enlargement and impaired contraction of LV, leading to systolic dysfunction.
-idiopathic or secondary to ischemic heart disease, alcohol abuse, or viral infections
-s/s of HF (dyspnea, fatigue, peripheral edmea)
described hypertrophic CM (HCM).
causes?
s/s?
abnormal thickening of myocardium, particular affecting interventricular septum. It can obstruct blood flow out of the LV.
-often inherited in an autosomal dominant pattern.
-CP, syncope, palpitations. *risk for sudden cardiac death due to arrhythmias
described restrictive CM.
causes?
s/s?
stiffening of ventricular walls, leading to impaired disatolic filling *without * significant systolic dysfunction
-can be caused by infiltrative diseases such as amyloidosis or hemochromatosis
-s/s:exercise intolerance and right sided HF symptoms (ascites, hepatomegaly)
Dx of cardiomyopathies
clinical evaluation
imaging (echo, MRI)
somtimes genetic testing
described arrhythmogenic RV CM.
causes?
s/s?
replacement of myocardial tissue with fibrofatty tissue in RV, leading to arrhythmias
-genetic disorder
-palpitations or syncope. risk for sudden cardiac death.
management of CM
depending on the type and severity
may include meds like BB or ACE inhibitors
lifestyle mod
ICDs
sx: septal myectomy for HCM
contributors to dysrhythmias
electrolyte imbalances, ischemic heart disease, MI, congenital heart defects
generalized tx of arrhythmias
antiarrhythmic drugs, AC for thrombus prevention, cardioversion, catheter ablation, pacemaker or defibrillator
classic HF symptoms
dyspnea, fatigue, fluid retention (leading to pulmonary congestion or peripheral edema)
two main types of HF
Heart Failure with Reduced Ejection Fraction (HFrEF) and Heart Failure with Preserved Ejection Fraction (HFpEF)
HFrEF: systolic or diastolic dysfunction?
systolic. heart muscle weakens and cannot contract effectively
HFpEF: systolic or diastolic dysfunction?
diastolic. heart loses ability to relax and fill properly during diastole.
Pathophys of heart failure overview
involves neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system. These initially compensate for decreased CO, but eventually exacerbate myocardial damage and worsen HF.
compensatory mechanisms lead to vasoconstriction, sodium and water retention, and increased cardiac workload.
Dx of HF
- history and physical exam
- dx tests like echo to asses EF and identify structural abnormalities
- Biomarkers (B-type Natriuretic Peptide BNP or N-terminal pro-BNP) crucial for diagnozing and monitoring severity of HF
management of HF overview
-lifestyle mod (sodium restrict, fluid management, exercise, no smoking)
-pharm
-device therapy or surgery
Pharm management of HF
-ACE inhibitors
-BB
-diuretics
-aldosterone antagonists
-and sometimes ARNIs (angiotensin receptor-neprilysin inhibitors)
advanced HF therapies (devices and surgeries)
-CRT cardiac resynchronization therapy
-implantable cardioverter-defibrillators (ICDs)
-mechanical circulatory support (LVADs)
-transplant
Hypertensive urgency criteria
and s/s
SBP > 180mmHg or DBP >120 mmHg without evidence of acute target organ damage.
-severe headache, SOB, epistaxis
TX HTN urgency
GRADUALLY reduce blood pressure over 24 to 48 hours using oral antiHTN meds
(rapid= possible cerebral hypoperfusion)
hypertensive emergency criteria and s/s
similar BP parameters but accompanied by acute, life threatening target organ damage. ex: hypertensive encephalopathy, acute MI, acute LV failure with pulm edema, aortic dissection, acute renal failure
management of hypertensive emergency
prompt reduction of MAP by 20-25% within first hour, using IV antiHTN agents
-sodium nitroprusside, labetalol, or nicardipine
subsequent BP reduction should be gradual over next 24 to 48 hours to minimze risk of ischemic complications
What can cause hypertensive emergencies?
nonadherence to meds
autonomic dysregulation
secondary causes like pheochromocytoma or renovascular hypertension
examples of inflammmatory and infectious heart conditions
myocarditis, pericardities, endocarditis, rheumatic heart disease
What is Myocarditis?
Causes?
inflammation of the heart muscle (myocardium), often caused by viral infections such as Coxsackievirus.
-also bacterial inx, autoimmune dz, exposure to toxins
s/s myocarditis
range from mild CP to fatigue to severe HF and arrhythmias
Dx myocarditis
markers for inflammation
ECGs
echo
cardiac MRI
Tx myocarditis
symptom management
address cause
may need mechanical support
What is pericarditis?
causes?
inflammation of pericardium (fibrous sac around heart)
-idiopathic
-infections
-post MI infarction (Dressler’s syndrome)
-systemic inflammation like lupus
s/s pericarditis
sharp BP, worse with inspiration or lying flat
pericardial friction rub
ECG changes (diffuse ST elevation)
Tx pericarditis
NSAIDs
colchicine
corticosteroids (in refractory cases)
What is endocarditis?
causes?
infection of inner lining of heart chambers and valves
-bacteria entering bloodstream and adhering to damaged endocardial tissue or prosthetic valves
s/s endocarditis
fever
new or changed heart murmurs
petechiae
embolic phenomena
dx endocarditis
BCx
echo
Tx endocarditis
prolong abx therapy
surgery if need valve repair or replacement
What is rheumatic heart disease?
sequela of rheumatic fever, an inflammatory disease following group A streptococcal pharyngitis.
What is the primary valve impacted by rheumatic heart disease?
mitral valve
leads to chronic valvular damage
Tx for rheumatic heart disease
prevention through early abx tx of streptococcal infections
What is pericardial effusion?
accumulation of excess fluid in pericardial cavity, the space between the heart and pericardium (double walled sac surround heart)
How much fluid is normally in the percardial sac?
15-50ml
etiology of pericardial effusion
so many.
- inflammatory conditions (pericarditis)
- infectious dx (bact, fung, viral)
- malignances (primary or metastatic)
- autoimmune disorders (lupus, RA)
- trauma
- Dressler’s syndrome (post MI)
- hypothyroidism
- renal failure
- certain meds
- radiation therapy
pathophys of pericardial effusion
imbalance in fluid production and reabsorption, or due to pathological processes, excess fluid accumulates
s/s of pericardial effusion
asymptomatic
CP, SOB, orthopnea, cough, fatigue
(due to compression of nearby structures and impaired cardiac function–> can lead to tamponade)
dx of pericardial effusion
echo
CXR
CT scan
MRI
ECC: low voltage QRS complexes or electrical alterans can suggest significant effusion
tx pericardial effusion
small: observation
large: pericardiocentesis and drainage via pericardial window or pericardiectomy in recurrent cases
What is pulmonary edema?
accumulation of excess fluid in the alveoli and interstitial spaces of the lungs, leading to impaired gas exchange and respiratory distress.
often associated with left sided HF–> increased pressure in pulm circulation
pathophys of pulmonary edema
imbalance between hydrostatic and oncotic pressures in pulmonary capillaries. When LV function is compromised, like in MI or CM, there is backflow of blood into pulmonary veins and capillaries. This increased hydrostatic pressure forces fluid out of the capillaries into the alveolar spaces, overwhelming the lymphatic drainage system and leading to edema.
s/s pulmonary edema
dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough (may = frothy pink sputum)
crackles or rales
tachypnea
tachycardia
signs of hypoxia (cyanosis)
Dx pulmonary edema
CXR- bilateral infiltrates
echo
ABG: hypoxemia and resp alkalosis (hyperventilation)
Management pulmonary edema
underlying cause and symptom relief
oxygen
diuretics (reduce fluid overload via renal excretion of sodium and water)
vasodilators like nitroglycerin to decrease preload and afterload (increase CO)
mech vent or NIPPV
What is syncope?
sudden, temporary loss of consciousness typically caused by decrease in blood flow to the brain. It is a symptom. Can indicate cardiac and non-cardiac conditions.
How does syncope happen?
there is a transient drop in cerebral perfusion, which can result form
-decreased CO
-vasodilation
-hypovolemia
cardiac related usually stems from arrhythmias, structural heart diseases, or ischemic heart conditions
(ex. sick sinus syndrome (bradyarrhythmia) or VT, aortic stenosis, HCM)
Noncardiac causes of syncope
vasovagal reactions
orthostatic hypotension
situational triggers (coughing, swallowing)
most prevalent type of syncope
vasovagal syncope. due to exaggerated autonomic response that causes vasodilation and bradycardia
What is orthostatic hypotension a result of?
inadequate autonomic response to postural changes, leading to blood pooling in lower extremities,
syncope management
underlying cause
cardiac: may need med or device
vasovagal: lifestyle mod (more salt), hydration, avoid triggers
orthostatic: gradual position changes and compression garments
describe mitral stenosis
blood flow is not able to pass through valve from left atrium to left ventricle properly, leading to increased pressure in the left atrium and pulmonary circulation
s/s mitral stenosis
SOB, fatigue, palpitations
What causes mitral stenosis?
often rheumatic fever leading to thickening and fusion of the valve leaflets
Describe mitral regurgitation and
blood flow flows backward into left atrium during systole, leading to volume overload in left atrium and ventricle, potentially resulted in left sided heart failure
what causes mitral regurgitation?
mitral valve prolapse
ischemic heart disease
infective endocarditis
describe aortic stenosis
calcification and narrowing of the aortic valve restricts blood flow from LV into aorta
s/s aortic stenosis
exertional dyspnea, angina, syncope due to reduced CO
describe aortic regurgitation
occurs when aortic valve fails to close properly during diastole, causing blood to leak back into left ventricle. results in volume overload and eventual left ventricle dilation and hypertrophy
name some causes of tricuspid and pulmonary valve disorders
-congenital defects (usually pulmonary)
-secondary to other cardiac conditions like pulmonary hypertension
-RV enlargement or failure (tricuspid)
Dx and Tx of valvular disorders
echo (structure and function)
depending on severity. pharm (diuretics, vasodilators). surgery (repair/replacement)
common vascular conditions
atherosclerosis, PAD, aneurysms, venous insufficiency, DVT, PE
describe atherosclerosis
buildup of plaque within arterial walls, leading to narrowed or blocked arteries. Can result in CAD, CVA, PAD. PAD specifically affects arteries in legs and feet, causing pain, cramping, and potential tissue loss due to inadequate blood flow
describe aneurysms
abnormal dilation or ballooning of a blood vessel wall, most commonly seen in aorta.
can rupture–> hemorrhage
describe venous insufficiency
occurs when veins are unable to efficiently return blood to heart, often due to damaged valves within the veins. can lead to varicose veins, swelling, skin changes, and ulcers.
Chronic venous insufficiency may require compression or surgery to improve venous return.
dx and tx of vascular conditions
-doppler US or angiography
-lifestyle mod
-pharm: antiplatelet or AC
-endovascular interventions
-surgical procedures
describe acute arterial occlusion
sudden blockage of an artery, usually in lower extremities, resulting in rapid decrease in blood flow to the affected area. medical emergency due to potential for tissue necrosis if not treated. blockage can occur due to an embolus, which is often a blood clot that travels from another part of the body, or a thrombus, which forms at the site of occlusion
s/s of acute arterial occlusion
6 Ps
-pain (severe and sudden)
-pallor
-pulselessness
-paresthesia (result of nerve ischemia)
-paralysis (result of severe ischemia affecting motor function)
-poikilothermia
Dx of acute arterial occlusion
clinical exam and imaging
doppler US.
gold standard: angiography to visualize arterial blockage and plan tx
Tx of acute arterial occlusion
including long term management
initially: AC with heparin to avoid clot propagation
thromolytic therapy to dissolve if within timeframe
Sx: embolectomy or thrombectomy
sometimes- bypass if direct removal not feasible.
long term: Antiplatelet therapy and lifestyle modification
risk factors for arterial occlusion
HTN, HLD, DM
the pathophysiology of acute venous thrombosis involves what traid?
Virchow’s triad
-venous stasis (prolong immobility, long flight, bedrest)
-endothelial injury (trauma, surg procedure)
-hypercoagulability (genetic factors- factor V Leiden mutation or malignancy, pregnancy)
s/s DVT
Dx DVT
swelling, pain, warmth, redness in affected limb
some asymptomatic
Doppler US
Tx DVT
focus is on preventing clot propagation and embolization while minimizing bleeding risks
AC cornerstone of treatment with LMWH, UFH, or DOACs
if sig risk for limb ischemia or massive PE: thrombolytic therapy or surg.
DVT prevention
compression stockings, pharm prophylaxis for hospitalized patients. education on lifestyle mod (exercise, hydration)
describe aortic aneurysm
dilation of the aorta, occurring anywhere along its length. Arises due to weaking of arterial wall, leading to localized enlargement.
how are aneurysms classified?
by location:
TAA- chest
AAA- abdomen
risk factors for aneurysms
age
HTN
smoking
genetics: Marfans
atherosclerosis
s/s of aneurysms
asymptomatic until pressing on structures or rupture
describe aortic dissection
tear in intimal layer of aorta’s wall, allowing blood to flow between the layers of the vessel walls. This creates a false lumen and can compromise blood flow to vital organs.
How are dissections classified?
2 main systems: Stanford and DeBakery
Stanford: Type A (involves ascending aorta) and Type B (not involving ascending aorta)
DeBakery: also includes location and extent
pathophysiology of aortic dissection and aneurysm
degeneration of elastic fibers in arterial wall and increased proteolytic activity that weakens structural integrity.
aneurysm: leads to dilation
dissection: rupture under hemodynamic stress
s/s of aneurysms and dissections
aneurysm: back or abdominal pain when big enough
dissection: sudden onset severe chest or back pain (tearing/ripping)
dx of aneurysms and dissections
US for AAA
CT angio for dissections
Management of aneurysms and dissections
larger aneurysm: open repair or endovascular stent grafting
dissection:
A: emergent surgical repair
B: BP control
hyperlipidemia is
a medical condition with elevated levels of lipids in the blood, including cholesterol and triglycerides.
HLD is a significant risk factor for
cardiovascular diseases, such as CAD, stroke, PAD
How is HLD classified?
primary: often genetic
secondary: from lifestyle factors or other medical conditions
how is cholesterol transported in the blood?
by lipoproteins, primarily low-density lipoprotein (LDL) and high density lipoprotein (HDL).
LDL vs HDL
low density cholesterol: often referred to as bad cholesterol as high levels can lead to plaque buildup in arteries, increasing risk of atherosclerosis,
high density cholesterol: considered good as it helps remove LDL cholesterol from bloodstream
What do high triglycerides contribute to?
hardening or thickening of the arterial walls, increasing risk of CV events
contributors to HLD
-poor diet
-obesity
-sedentary
-smoking
-excessive alcohol consumption
-certain conditions like diabetes and hypothyroidism -
dx of HLD
-fasting lipid panel test: assesses total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides
HLD management: list possible medications
statins:
ezetimibe:
fibrates and omega 3 fatty acids:
PCSK9 inhibitors:
HLD management: lifestyle modification
heart healthy diet low in sat fat and cholesterol, physical activity, healthy weight, no smoking
how do statins work?
lower LDL by inhibiting the enzyme HMG-CoA reductase, involved in cholesterol synthesis
how does ezetimibe work?
reduces intestinal absorption of cholesterol
how do fibrates and omega 3 fatty acids work?
lower triglycerides
who are PCSK9 inhibitors for?
those with familial hypercholesterolemia or those not responding to statins alone.
complications that can occur post vascular intervention (angiography, angioplasty, stent placement)
hematoma
pseudoaneurysm
arteriovenous fistula
RP bleed
arterial occlusion
describe hematoma
s/s
tx
accumulation of blood at site of vascular access, often due to inadequate hemostasis post procedure.
localized swelling, bruising pain
small: resolve spontaneously; large: may compress structures/ need intervention
what is a pseudoaneurysm?
occurs when blood leaks out of an artery but is contained by the surrounding tissue, forming pulsatile mass. Also results often from inadequate closure of arterial puncture site.
clinical presentation and tx of pseudoaneurysm
palpable mass with bruit on auscultation
US guided compression or thrombin injection
what is an arteriovenous fistula?
presentation
tx
occurs when there is abnormal connection between an artery and a vein, usually due to inadvertent puncture during procedure. can lead to altered hemodynamics and may have bruit/thrill over site.
sx intervention if large or symptomatic
What is retroperitoneal hemorrhage?
serious complication where there is bleeding in RP space.
can occur due to high puncture sites in femoral artery, leading to vessel injury.
s/s RP bleed
tx
back pain
hypotension
tachycardia
prompt fluid resuscitation and possible sx
what is an arterial occlusion?
s/s
tx
blockage of an artery used for access, often due to thrombosis or dissection
limb ischemia: 6 Ps
AC or surgical revascularization
