cardiovascular disorders

what can a combination of hypertension and dyslipidemia can lead to

stroke and coronary artery occlusion

during diastole, some blood flows backwards in the aorta but is blocked by the closed aortic valve. where does this blood go?

coronary arteries

the end of systole is marked by the ___

dicrotic notch: ventricular pressure falls below aortic pressure → aortic valve closes

what is pulse pressure 

difference betwene systolic and diastolic 

what is mean arterial pressure?

normal values?

equation

average pressure in arterial system at any time

90-100 mmHg

D + ((S-D)/3)

what is cardiac output?

equation?

amount of blood leaving the heart

SV x HR

neural mechanisms to regulate blood pressure 

vagal stimulation slows HR 

sympathetic stimulation increases HR: constrict small arteries and increases peripheral resistance 

how does the autonomic nervous system control blood pressure

intrinsic reflexes controlled within vessels - baroreceptors (carotid sinus) and chemoreceptors

extrinsic reflexes outside of vessels - pain and cold affect vascular diameter

humoral mechanisms to regulate blood pressure

RAAS

vasopressin/ADH → urea retention → increased BP → visceral vasoconstriction

catecholamines (epi, norepi) → vasoconstriction

aldosterone secretion is controlled by the ___ system

RAAS - renin angiotensin aldosterone system

describe the RAAS

BP in kidneys drop → juxtaglomerular apparatus secretes renin into blood 

renin: convert angiotensinogen to angiotensin I

angiotensin I: split into angiotensin II by ACE (angiotensin converting enzyme)

angiotensin II stimulates aldosterone secretion

aldosterone: cause increased reabsorption of Na and water retention → blood volume increases 

increased blood volume increases BP → RAAS stops 

what is the juxtaglomerular apparatus

connects distal convoluted tubule to afferent arteriole

what is the primary long term controller of BP

kidneys - regulate ECF volume

pressure diuresis vs naturesis

diuresis: kidney water excretion

naturesis: kidney salt excretion

what is dyslipidemia? 

what contributes to it? 

imbalance of lipid components in blood 

triglycerides, phospholipids, cholesterol

what do lipoproteins do

transporters

what are the 5 types of lipoproteins based on density (lowest to highest)?

and what do they do

chylomicrons: transport ADEK, triglycerides

VLDL: triglycerides from liver to periphery for storage

IDL

LDL: cholesterol from liver stored in periphery

HDL: cholesterol from periphery to liver for elimination

75% LDL removed by ___

25% LDL removed by ___

hepatocytes 

scavengers - macrophages, monocytes, endothelial cells 

normal, risky, and dangerous total cholesterol levels

under 200

200-239

240+

normal, risky, and dangerous LDL levels

under 100

100-159

160+

normal, risky, and dangerous HDL for males

60+

40-59

under 40

normal, risky, and dangerous HDL levels for females

60+

50-59

under 50

how may dyslipidemia present in an adult

xanthoma - fat stored abnormally as little balls around eye 

atheroslceroisis

what is primary dislipidemia

familial hypercholesterolemia

autosomal dominant - deficient LDL receptor

blood LDL levels in dyslipidemia 

heterozygous 1/500 cases - 350 mg/dL 

homozygous 1/1000000 cases - 1000 mg/dL

what is secondary lipidemia 

onset caused by dietary factors, obesity, T2DM

what is recommended for someone with secondary dyslipidemia

DASH (dietary approach to stop hypertension)

mediterranean diet

how is dyslipidemia diagnosed

3 or more:

elevated fasting blood glucose, blood pressure, waist circumference, increased triglycerides

decreased HDL

what is atherosclerosis? 

primarily occurs due to ___

hardening of arteries due to fibrofatty lesions 

hypercholesterolemia and elevated LDL 

risk factors of atherosclerolsis

age, family hx, males and postmenopausal women

smoking, HTN, DM, inactivity, homocysteins

if BOTH hypertension and diabetes are present, __x higher risk of atherosclerosis

8

what does homocysteine do

inhibit coagulant cascade, associated with endothelial damage

what is homocystinuria

rare autosomal recessive disorder - loss of metabolism of homocysteine

severe risk of atherosclerosis

how can atherosclerosis cause an embolus 

fat builds in lumen → moves into tunical media → inflammatory response (platelets and WBC) → grows fibrous cap → high pressure → breaks off to become embolus 

what is a fatty streak

early warning sign for atherosclerosis - thin, flat, yellow discolorations that grow in length with age → fibrous atheromatous plaque if endothelium is damaged

seen in children, increase in number til 20yo → static or regress in size

what is fibrous atheromatous plaque

fatty deposits grow into smooth muscle and limit lumen size - adhere circulating monocytes and lipids → thrombus

grey/early white

what is a complicated lesion

hemorrhage, ulceration, scar tissue deposition

thrombi occlude small arteries of heart and brain

may cause aneurysm too

activated macrophages release ___. 

this damages endothelium and exposes collagen fibers → ___

free radicals that oxidize LDL 

clotting cascade

activated macrophages ingest oxidized LDL to form ___

foam cells - macrophages that accumulate oxidized LDL bc inability to breakdown

lipids get released from foam cells, foaming a lipid core of an ubstable plaque.

this unstable plaque consists of ___

large lipid core

inflammatory infiltrate

thin fibrous cap

manifestations of atherosclerosis are not usually noted til ___ years old after evidence of__.

20, fatty streaks 

what effects do atherosclerosis plaques produce

narrowed vessel → ischemia

sudden obstruction ← plaque rupture

thrombus and embolus ← vessel endothelium damage

aneurysm ← vessel wall damage

what is common in atherosclerosis of a larger vessel?

medium vessels?

thrombi and aneurysm

ischemia and infarction (heart, brain, kidneys, LE, small intestine

5 main Ps of arterial occlusion presentation 

pain 

pallor

pulse

paresthesia

paralysis 

how to treat an arterial occlusion

surgical removal of emboli

thrombolytics may dissolve the clot

anticoagulants prevent clotting

what as an aneurysm

dilation of a blood vessel

describe a true aneurysm

bound by vascular wall, blood remains inside

describe a false aneurysm/pseudoaneurysm 

localized dissection of inner wall → extravascular hematoma 

describe a berry aneurysm.

where are they most common?

true aneurysm - spherical dilation

brain, circle of willis 

describe a fusiform aneurysm.

where are they most common?

true aneurysm - entire vessel circumference dilates

thoracic aorta

describe a saccular aneurysm 

true aneurysm over vessel circumference - looks liek a sac, similar to berry 

describe a dissecting aneurysm

false aneurysm - tear in intimal layer - life threatening

blood pools within vessel wall → blood filled cavity

2 most common causes of aortic aneurysm

atherosclerosis

degeneration of tunica media

clinical presentation of thoracic aortic aneurysm

substernal/back/neck pain with stridor/cough

hoarseness from recurrent laryngeal nerve compression

difficulty swallowing from esophageal compresison

SVC compression → face/neck vein distension

where and how big are abdominal aortic aneurysms 

infrarenal aorta 

2cm normally, >3cm is aneurysm 

signs/symptoms of an abdominal aortic aneurysm

abdominal/low back pain unchanged with position, may radiate into LE 

pulsating mass (>4cm normally palpable)

calcification and/or eroded vertebrae seen on xray

stasis of blood → thrombus 

how to diagnose aortic aneurysm?

manage?

imaging - ultrasouns, CT, MRI, echocardiograph 

surgical repair 

what size aneurysm does rupture risk skyrockey

5-5.9cm

what is the rupture risk % for the following aneurysm sizes:

3-3.9cm

4-4.9cm

5-5.9cm

6-6.9cm

>7cm

0

<1%

1-11%

10-22%

30-33%

who is an aortic dissection most common in 

40-60 yo 

males 

95% aortic dissections tear through ___.

most common in ___ aorta then ___ aorta.

intima and internal media

ascending, thoracic

major risk factors for aortic dissection

hypertension and media degeration

connective tissue disorders (marfan)

pregnancy (extensibility changes)

classify the levels of aortic dissection 

type A: more common - ascending aorta

type B: begin distal to subclavian artery emergence 

acute: within 14 days of symptom onset 

clinical presentation of an aortic dissection

abrupt onset of sharp, excruciating, ripping pain

anterior chest of ascending aorta, low back if descending aorta

blood pressure elevated until lack of arterial blood flow

rapid onset syncope, paralysis, hemiplegia

how to diagnose aortic dissection?

acute vs chronic treatment?

imaging to confirm - CT

surgical - remove and replace (acute), BP stabilization (chronic)

what is virchow triad

major risk factors for DVT

stasis of blood - immobility

increased coagulability - oral contraceptices, smoking, cancers

vessel wall injury - trauma, surgery, inflammation

physical exam findings based on site of DVT occlusion

venous sinus in soleus, posterior tibial, peroneal veins

swelling of foot and ankle may occur

calf pain and tenderness noted, not diagnostic

diagnosing and treating a venous thrombosis 

diagnose: ultrasound, venography, plasma d dimer 

treat: minimize valve drainage, prevent embolus

how to prevent a venous thrombosis

early ambulation after surgery

support stockings, pneumatic compression

prophylactic anticoagulation

IVC filter

nonmodifiable risk factors for primary hypertension

age: adults more common - stiffened arterial walls - kidneys lose effectiveness to excrete sodium, retained, HTN

gender: males and postmenopausal females

race: AfAm

modifyable risk factors for primary hypertension 

diet: avoid salts, fats, cholesterols, >5 servings red meat/wk

dyslipidemia: avoid high cholesterol, triglycerides, LDLs - veggie diets good 

tobacco: toxins and nicotine cause arterial stiffness 

alcohol: excess account for 10% — 1/day associated with mild reduction in BP 

fitness level: 150min/wk moderate or 75min/wk vigorous 

obesity: waist to hip ratioi 

insulin resistance:

obstructive sleep apnea: disrupted sleep → dip blood pressure / less dip → higher RHR 

secondary hypertension is most common in what age group

younger than 30, older than 50

most common cause of secondary HTN

renal hypertension:

retained salt/water

reduced renal blood flow and RAAS activation (plaque build up, kidney thinks you have low BP, activate RAAS)

atherosclerosis of proximal renal artery, fibromuscular dysphagia (females and 30-50yo commonly)

what is adenocortical hormone dysfunction

can cause secondary hypertension

primary hyperaldosteronism or excess glucocorticoid (cortisol) → increased adrenocortical hormones

what is pheochromocytoma 

can cause secondary hypertension 

tumor of chromaffin cells of adrenal medulla → execss catecholamines → hypertensive crisis

what is aortic coarctation

can cause secondary hypertension

overactive changes in ductus arteriosus → narrowed aorta

relationship between oral contraceptives and secondary hypertension

estrogen

-promotes sodium and water retention

-increases vascular tone

-stimulates angiotensin production → more angiotensin II

what organs are most commonly targeted with hypertension

kidneys, heart, eyes, blood vessels

relationship between nephrosclerosis and hypertension 

high BP damages nephrons → glomerular dmage prevents adequate filtration 

relationship between dementia and hypertension

narrowing and sclerosis of snall arteries in subcortical brain → white matter demyelination

relationship between retinopathy and hypertension

increased vasomotor tone

arteriole narrows → hyperplasia from persistent contraction → permanent degeneration, blindness

normal, elevated, HTN1, HTN2, severe, crisis blood pressure values

normal: less than 120 AND less than 80

elevated: 120-129 AND less than 80

HTN1: 130-139 OR 80-89

HTN2: ≥140 OR ≥90

severe: >180 AND/OR >120 and asymptomatic

crisis: >180 AND/OR >120 and symptomatic

how to manage hypertension 

focus on modifyable risk factors - diet, exercise, lifestyle modifications 

hypertension is a complication in up to ___% all pregnancies.

when in pregnancy does it normally occur?

10

late stage, third trimester

what are reticulocytes

immature RBCs, normally around 10%

what is hemolysis

RBC breakdown → increased reticulocytes

what is preeclampsia-eclampsia

multisystem disorder

≥140 and/or ≥90

proteinuria after 20 weeks gestation

what is hypothesized to be the cause of preeclampsia

placental dysfunction with inadequate angiogenesis causing placental ischemia

___is the most common cause of death in the US 

cardiovascular disease

what are the three layers of pericardium (superficial to deep)

fibrous parietal

parietal serous

visceral serous

what is pericarditis?

what makes acute pericarditis acute?

inflammation of pericardium

less than 2 weeks

most common cause of pericarditis 

viral infection 

what happens to capillary permeability with acute pericarditis 

increased → capillaries allow proteins into space

typical triad of acute pericarditis presentation

chest pain - abrupt, constant, sharp, radiates into neck/back/abdomen/side, worsens with deep breathing/coughing/swallowing

pericardial friction rub

ECG changes

4 stages of ECG changes with acute pericarditis

diffuse ST elevation with PR depression → normalization

widesperad T wave inversions → normalizations

what kind of imaging will show fluid around the heart

echocardiogram

how to treat acute pericarditis

normally self limiting

symptoms treated with NSAIDs → colchicine if NSAID response is slow

how to treat acute pericarditis if infection is present 

antibiotics 

how to treat acute pericarditis with a connective tissue disorder or other idiopathic disorder unresponsive to NSAIDs

corticosteroids

relapsing pericarditis occurs in ___% of cases that respond to treatment

30